<<

PATTERN OF ALOPECIA AND THE EFFECT OF ALOPECIA ON THE QUALITY OF LIFE OF PATIENTS

BY

DR. EKPUDU, VIOLET IDONNI

A DISSERTATION SUBMITTED TO THE NATIONAL POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PARTIAL FUFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF FELLOWSHIP OF THE COLLEGE IN INTERNAL MEDICINE (IN THE SUBSPECIALTY OF DERMATOLOGY).

MAY 2008

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TABLE OF CONTENTS Page Title Page ------i Declaration ------ii Supervisor’s Certification ------iii Head of Department’s Signature ------v Table of contents ------vi List of Figures ------vii List of Tables ------viii List of Abbreviations ------ix Dedication ------x Acknowledgement ------xi Summary ------xii Chapter 1. Introduction ------1 Chapter 2. Literature Review ------4 Chapter 3. Aim and Objectives ------49 Chapter 4. Materials and Methods ------50 Chapter 5. Results ------62 Chapter 6. Discussion ------113 Chapter 7. Conclusion and Recommendations ----- 131 References ------135 Appendix I. Questionnaire ------152 Appendix II. Ethical approval ------161

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LIST OF FIGURES

1. Fig I - Sex Distribution of Patients and Controls 2. Fig II - Age Distribution of Patients and Controls. 3. Fig III - Age and Sex Distribution of Patients. 4. Fig IV - Clinical Severity of Alopecia. 5. Fig V - Symptoms associated with loss. 6. Fig VI - Places Treatment were sought by Patients. 7. Fig VII - . 8. Fig VIII - Central centrifugal cicatricial alopecia. 9. Fig IX - Chronic cutaneous lupus erythematosus. 10. Fig X - Dissecting .

11. Fig XI - keloidalis nuchae. 12. Fig XII - .

13. Fig XIII - Dada hair in a young child.

14. Fig XIV - with .

15. Fig XV - Scleroderma.

16. Fig XVI - Lichen planopilaris.

17. Fig XVII - Male pattern baldness I.

18. Fig XVIII - Male pattern baldness II. 19. Fig XIX - .

20. Fig XX - Histology of lichen planopilaris.

21. Fig XXI - Histology of CCLE. 22. Fig XXII - Histology of .

23. Fig XXIII - Histology of Pseudopelade.

24. Fig XXIV - Anagen hair.

25. Fig XXV - Telogen hair.

26. Fig XXVI - Employment status of patients and controls 27. Fig XXVII - Marital Status of Patients and controls.

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LIST OF TABLES

1. Table 1 - Top ten groups of skin disorders observed at study site.

2. Table II - Age of onset, sex and clinical severity of alopecia.

3. Table III - Skin diseases co-existing with alopecia.

4. Table IV - Clinical diagnoses of alopecia versus gender.

5. Table V - Literacy levels of patients and controls.

6. Table VI - Diagnoses, sex, mean age distributions and mean

and sum of total DLQI scores of patients.

7. Table VII- Distribution of subscale scores of DLQI for patients.

8. Table VIII- DLQI scores for clinical and socio-demographic

characteristics of patients.

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LIST OF ABBREVIATIONS

VDRL - Venereal Disease Research Laboratory

LUTH - Lagos University Teaching Hospital

DLQI - Dermatology Life Quality Index

DOP - Dermatology Outpatient Clinic.

QOL - Quality of Life.

ARV - Antiretroviral.

DLE - Discoid Lupus Erythematosus.

CCLE - Chronic Cutaneous Lupus Erythematosus.

KFSD - Keratosis follicularis spinulosa decalvans.

CCCA - Central Centrifugal Cicatricial Alopecia. t - Student’s t-test value.

Χ2 - Χ2 value.

F - Analysis of variance value.

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DEDICATION

This work is dedicated to God Almighty, my Hope and my Strength.

The One whose own I am and always will be.

Amen.

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ACKNOWLEDGEMENTS

I wish to express my gratitude to my supervisor, Professor

Y.M Olumide, who has been both a teacher and a role model.

I also wish to thank Dr.J.D Adeyemi, my supervisor also, for his support, time and attention given to this project.

I am also deeply indebted to Professor M.A Danesi and Dr. J.N.A Ajuluchukwu for their encouragement and support.

To my teachers at the University of Benin Teaching Hospital- Professor E. Okpere, Professor L. Ojogwu and Dr. A. Onunu who stimulated my interest in Internal Medicine and Dermatology respectively, I am most grateful.

I also wish to thank Professor C. Ukoli, Professor B. Okeahialam, my teachers and colleagues at the Jos University Teaching Hospital for being there for me.

I also appreciate Drs. Ahamefule and Ayanlowo and Residents doctors in the Dermatology unit, Department of Medicine, LUTH, for their support.

To Drs A.Uloko and N.Essen, my ‘big brothers’ in residency, you are very much appreciated.

Professor A.Y Finlay is gratefully acknowledged for permitting the use of the Dermatology Life Quality Index and its translation.

To my family and loved ones, who have encouraged and supported me in the place of prayer, I am deeply indebted.

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SUMMARY

Background

Skin disease is a significant problem in developing countries but its effect on quality of life has rarely been investigated. Multiethnic developing countries provide valuable opportunities to assess the influences of socio- demographic factors like social class, age and gender on the impact of skin diseases on quality of life. Lagos, Nigeria provides an ideal setting for such a study. The present study is aimed at determining the pattern of alopecia and the effect of alopecia on the quality of life of patients. This would increase awareness about possible underlying psychopathologic disorders in dermatological patients with a view to facilitating early recognition, treatment and optimizing patient management.

The study population consisted of 100 consecutive adult patients who presented with alopecia to the dermatology outpatient clinic of the Lagos University Teaching Hospital. An age and sex matched control group consisting of 100 persons with no dermatologic or chronic medical disorders were also recruited from patient relatives, colleagues, friends and medical students.

Structured pretested questionnaires incorporating the Dermatology Life Quality Index, modified to meet the language and cultural needs of the population were administered to both the cases and controls, followed by a dermatological examination and laboratory investigations where relevant.

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Results One hundred patients were studied who were aged between 16-61 years. The mean age was 33.65 + 10.82 years. There were 60 (60%) and 40 (40%) females. The controls also consisted of 100 patients who were age and sex matched for the patients. Most of the patients seen (68%) were aged between 21 and 40 years.

Generally, all patients presented with alopecia of the scalp with just a few having involvement of other body sites (ninety seven patients had only their scalp affected, two (2%) had both scalp and eye brow alopecia and only 1 patient had involvement of all body sites). The most frequent symptoms associated with were pruritus and pain, though 30% of patients reported no symptoms at all.

The most frequent causes of alopecia were keloid folliculitis (acne keloidalis nuchae and acne folliculitis nuchae) (28%), followed by alopecia areata (15%), CCLE (14%), folliculitis decalvans (9%), lichen planopilaris (6%) and dissecting folliculitis (5%).Mostly male patients presented with keloid folliculitis.

Twenty one (21%) patients were observed to have sought the services of a dermatologist only after having been elsewhere for treatment.

The mean score of the DLQI was 7.3 + 7.16. The total DLQI scores were significantly higher for patients (median 4, range, 0-30), than for controls (median 0, range 0-1). (P< 0.0001).The Highest DLQI scores were obtained for keloid folliculitis, alopecia areata, Chronic Cutaneous Lupus Erythematosus and lichen planopilaris.

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There was no significant increase of DLQI scores with increasing severity of alopecia. Majority of patients (54%) had a moderate to extremely large impairment of their quality of life. Female patients had more impairment in their quality of life than the male patients. Patients had their greatest impairment in the symptoms and feelings subscale of the DLQI. Females had the highest scores here and they were also more affected in the daily activities domain.

Conclusion A wholistic approach has become increasingly relevant in the management of patients with alopecia as this condition can have a severe psychological impact on an individual’s well being. This study has shown that Alopecia negatively affects the quality of life of affected patients and those with the most cosmetic disfigurements have the greatest impairment in their life quality.

CHAPTER ONE

INTRODUCTION

Hairs are a human characteristic that convey aspects of self image, identity and health among other attributes. Alopecia which can be described as the visible result of hair loss cuts across all ages, socio economic class and gender. It has a varied presentation and its causes are myriad. It may be classified as non-scarring and scarring, diffuse or patchy.

Unlike other dermatological conditions, which may be limited to areas covered by clothing, alopecia is quite apparent. Due to great emphasis placed on physical appearance by most cultures, patients usually are bothered about their appearance and actually believe that their hair loss generates social stigmatization. This leads to feelings of shame, embarrassment and even guilt.

For some women, the loss of hair is reported as being psychologically more difficult than the loss of a breast through breast cancer. Individual and social perception of this condition can affect its impact on patients thus leading to a number of non-dermatological problems. Quality of life is the degree of enjoyment or satisfaction experienced in everyday life. Many studies evaluating the quality of life in some dermatological conditions have been carried out. These employ validated instruments that are either generic or disease specific. Generic instruments have the advantage of allowing for direct comparison with other populations, though they are usually bulky and lack disease specificity. Disease specific instruments are more sensitive than generic instruments and are applied to specific diseases. They however do not allow comparison with non-dermatological populations.

For the purpose of this study, the Dermatology Life Quality Index was employed to evaluate the effect of alopecia on the quality of life of affected patients.

Most quality of life studies in dermatological conditions have been carried out in the western world. A Nigerian study assessing the pattern of alopecia and its effect on patient’s life quality has become increasingly needful as patient management has become more wholistic incorporating social relations, psychological status, beliefs, physical health among others. Awareness of the possible psychosocial factors associated with alopecia would enable the dermatologist recognize these symptoms early, manage properly and refer appropriately.

Evaluating the pattern of alopecia would help in setting out appropriate treatment modalities, counseling patients on possible precipitating factors, harmful hair practices and offering genetic counseling when appropriate.

This study also seeks to promote collaboration between various subspecialties in the management of dermatology patients.

CHAPTER TWO

LITERATURE REVIEW 2.1 HISTORICAL BACKGROUND Through the ages, human hair and perceptions about it have

had significant socio-cultural impact and religious influences.

Dating as far back as the Mesopotamian and Persian era, hair had served as a means of differentiating between nobility and persons of other class, with the nobles curling, dyeing, and even plaiting their long hair and beards, sometimes adding gold dust and other precious ornaments.1

In biblical times, the Hebrews were prohibited from cutting their hair or beard, and even today, orthodox Jewish males wear their hair and beard long.1

In Islam, both males and females are behoven to cover their hair in public under a headcloth, turban, fez or veil.1

In the oriental culture, hairstyles showed regional variations and also indicated the age, class, marital status, profession and social status of the wearer.

In sub-Saharan African women, intricate patterns of braiding and beading adorned their hair and till date, this style is still quite fashionable and has even gained popularity amongst men and women in other parts of the world.

In Yoruba land, South Western Nigeria, ritual shaving of the head of newborns is said to mark the crossing of separation between the spirit world and the world of the living.2 However, some children do not have their head shorn. These are the ‘Dada’ children who are born with a full head of hair. Their hair is allowed to grow into uncombed, uncut and washed locks which snarl into dreadlocks.

These children are considered sacred as their hair is likened to cowries, literally gifts of money from the gods.2

The way hair is worn and perceived has evolved over many years and in modern times, it is still being influenced by social, cultural and even religious factors.

2.2 ALOPECIA are found over the entire surface of the human skin except on the palms, soles, glans penis and vulval introitus.

, Hairs are contained in a unit called the , which embryologically has an input from the epidermis which gives rise to the matrix cells and hair shaft, the dermis which contributes the papillae with its nerves and blood vessels. The hair follicle is divided into the infundibulum, isthmus and the inferior part.

There are 3 types of hairs. The lanugo hair: these are fine and long, appearing in the fetus at 20 weeks gestation and are shed before birth. Vellus hairs are short, fine and light coloured covering most body surfaces. The terminal hairs are longer, darker and thicker and are usually found on the scalp, eyebrows, eyelashes, pubic, axillary and beard areas. They originate as vellus hair, and then at puberty under the influence of androgens differentiate into terminal hair3.

Human hair may also be categorized into 3 major distinct groups based on ethnic origin4 viz; Asian, Caucasian and African. This is especially important because the kinky nature of African hair predisposes the scalp to some forms of alopecia, notably, acne keloidalis nuchae. In a bid to straighten the African hair, central centrifugal cicatricial alopecia and traction alopecia may develop.

Use of hair chemicals like ‘relaxers’ also predispose to chemical induced alopecia.

The human hair goes through a cycle of three phases3: Anagen,

Catagen and Telogen. The Anagen is the growth phase. Its duration and rate of growth differs in individuals, body sites, and at various ages. It lasts about 3-7 years. In catagen, which is the transitional phase, the hair follicle becomes more superficial ready to be shed. It lasts about 2-3 weeks3. Telogen is the resting phase in which the hair is finally shed and the growth cycle begins all over.

At any given time about 85% of scalp hair is in anagen, 14% in telogen and 1% in catagen3. Human terminal hair growth rate is about 0.37mm daily. Normally, about 100 hairs are lost daily, when this is exceeded it may either be due to changes of the physiologic cycle of hair growth or damage of the hair apparatus by systemic or local influences.

Alopecia is the visible result of hair loss. It can result from a congenital defect in the production of a normal hair follicle; aberrations in the production of a normal hair shaft and even destruction of the hair follicle5.

2.3 CLASSIFICATION OF THE ALOPECIAS Alopecia can be classified as patchy or diffuse, scarring and non- scarring3. Some authors6 also classify alopecias based on the prognosis of hairloss i.e. permanent or temporary. Currently, the classification into scarring and non-scarring is universally accepted

7. Non-scaring alopecia usually results in a diffuse or focal pattern of hair loss whilst the scaring alopecias are usually focal.

2.3.1 Non-Scarring Alopecias In these types of alopecia, the hair follicles remain intact and retain their ability to produce hair, though the patient may never regrow hair. These can be further sub-classified into the following5.

Diffuse non-

A. Failure of follicle production

- Congenital universal atrichia

- Atrichia with papular lesions

- Hereditary Vit D- resistant rickets.

B. Hair shaft abnormality

- Hair breakage

o

o

o etc.

- Unruly hair

o Wooly hair

o etc.

C. Abnormality of cycling (shedding)

-

- Anagen effluvium

-

- Alopecia areata

Focal non-scarring hair loss

A. Production decline

- Triangular alopecia

-

B. Hair breakage

- Trichotillomania

- Traction alopecia

- Tinea capitis

- Primary or acquired hair shaft abnormality

C. Unruly hair

- Hair shaft abnormality

o Wooly hair nevus

o Acquired progressive kinking etc.

D. Abnormality of cycling

- Alopecia areata

- Syphilis

E. Other conditions causing a focal non-scarring alopecia include

, severe scalp , cutaneous T-cell

lymphoma and Histiocytosis X.

Diffuse non-scarring hair loss

(A) Failure of follicle production i. Atrichia

This is a genetic cause of diffuse alopecia which usually presents in infancy and childhood. It is caused by an abnormality of the human homologue of the mouse hairless (hr) gene5,6,8. It presents as an abnormality in recapitulation of the anagen follicle after the first pelage as seen in hairless knockout mice. This is a putative multifunctional transcription factor on chromosome 8p 12.

In atrichia with papules, the patients develop follicular about

3-18 years after the onset of alopecia. ii. Vit D – resistant rickets

This is sometimes accompanied by universal hair loss in the first year of life with cutaneous cysts which develop in later years. It is due to mutations in the zinc finger domain of the Vit. D receptor, which acts as a transcription factor.

(B) Hair Shaft Abnormality

Hair breakage

The following hair shaft abnormalities may be associated with hair breakage. i. Trichorrhexis Nodosa

This is the commonest of these defects. It may be congenital or acquired.

Microscopically the affected hair develops a breach in the cuticle, with eventual separation and fraying of the exposed cortical fibres leading to a nodal swelling 9. The fibres then fracture and the shaft breaks with the resultant appearance of a splayed paintbrush or fan like array 5.

Congenital trichorrhexis nodosa may be present at birth or present in the first few months of life.

It may present alone or in association with follicular hyperkeratosis or teeth detects10 and other metabolic disorders like argininosuccinic aciduria, citrullinemia and Menkes syndrome.

Acquired trichorrhexis nodosa may be proximal or distal. The proximal type usually results from repetitive chemical or hot comb straightening mostly in African American women 10.

Distal trichorrhexis nodosa is usually secondary to excessive brushing, back combing or sporadic use of permanent waves 5.

Treatment of this condition is by avoidance of chemical or physical trauma to the hair. ii. Trichoschisis

This condition presents as a clean transverse fracture through the entire shaft at a location where there is focal absence of cuticle. It may be a marker for the sulphur deficient hair of in which the hairs of the scalp, eyelashes and brows are short and brittle 10. In affected patients the cystine content of the hair is less than half normal. About 50% of these patients have associated photosensitivity and are advised to practice sun protection. No treatment is currently available for this condition. iii Pili Torti

In Pili torti, the hairs appear short and brittle. This condition is also referred to as “twisting hair dystrophy” 11.

Microscopically, the hairs appear flattened and twisted through 900 to 3600. Pili torti can be seen in many different syndromes and other hair shaft abnormalities. When it occurs as an isolated finding, it is usually hereditary being mostly autosomal dominant, though it may occasionally be recessive or sporadic. In this case it is present at birth or develops over the first two years of life. The associated syndromes include Menkes syndrome and trichothiodystrophy. iv.

Also referred to as bamboo hair. This condition may occur in normal hair with other hair shaft anomalies or even in Netherton’s syndrome where it serves as a marker. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing intussuception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft12. This results in a ball and socket deformity or a golf tee shaped distal end of the shaft if it fractures. v. Netherton’s Syndrome

This syndrome consists of a triad of ichthyosis, atopic diathesis and trichorrhexis invaginata10. It is an autosomal recessive disorder. The affected hairs are short and brittle and may be irregularly distributed over the scalp.

vi. Monilethrix

The hairs in this condition are extremely short, brittle and emerge from keratotic follicular papules 13. Hair loss may be local or diffuse and start in the patient’s teens. Microscopically the hairs show elliptical nodes with a regular periodicity of 0.7-1mm10. The hair usually fractures at the points of constriction between the nodes. Monilethrix is caused by mutations in the genes for type 11 hair keratins hltbl or hHb6 on chromosome 12q1312,13. Most cases are of autosomal dominant inheritance with variable expression.

Monilethrix may occur alone or in association with keratosis pilaris, physical retardation, syndactyly, cataracts and nail or teeth abnormalities.

Treatment is with retinoids and topical minoxidil, though spontaneous recovery may occur.

Unruly hair i. Uncombable hair syndrome

Patients may present at any time from infancy to puberty. The hair here is slow growing, silvery blonde, and looks like spun glass. The hair though quite unmanageable and disorderly is not unduly fragile 10, 16.

This defect may be secondary to an abnormal configuration of the inner root sheath, which keratinizes before the hair shaft and thus determines its shape 16.

Biotin has been suggested as treatment 17, though generally there is no effective treatment for this syndrome.

ii. Wooly Hair

This is the presence of Negroid hair on the scalp of non-Negroid persons. May present at birth or in infancy being autosomal dominantly inherited. These hairs appear tightly curled and are usually thinner than normal hair thus creating an impression of reduction in hair density. iii. Maria-Unna type of Hereditary Hypotrichosis

The scalp hair in this condition has a variable course. It may be sparse or absent at birth, with wiry hair regrowth in childhood and probable loss again at puberty 18.

Body hair may be scanty or even absent. Diffuse follicular hyperkeratosis and facial milia-like lesions may be present and a distinct gene in chromosomal region 8p21 close to the hairless (hr) locus has been noted19.

iv. Other hair shaft abnormalities unassociated with breakage or unruly hair

These include and pseudo pili annulati. In pili annulati an autosomal dominantly inherited condition, the hair shows alternating light and dark bands both morphologically and microscopically, due to air filled spaces in the cortex 20.

Pseudo pili annulati is non hereditary and has no hair shaft cortex anomaly21however, it morphologically resembles pili annulati.

The above two conditions are seen primarily in blonde hair and are not associated with hair breakage.

(C) Abnormality of Cycling i. Telogen Effluvium

This is a diffuse form of hair loss where an abnormal number of hair follicles enter the telogen stage early and shed their fibres several months later 6. Telogen effluvium can be caused by high fever, hemorrhage, surgery, trauma, shock, drugs, crash diets, malabsorption (of proteins, vitamins, iron, zinc), endocrine imbalance (hyper and , hyperparathyroidism and hypopituitarism). It can also be seen pre and postpartum. In about

33% of acute cases, no cause is found 22.

Telogen effluvium is almost always potentially reversible and will not lead to total scalp hair loss, thus complete recovery is expected.

ii. Anagen effluvium

This is always pathological and it indicates the shedding of anagen hairs, though in actual fact, the hairs are usually broken rather than shed.

This condition can be caused by radiation therapy to the head, systemic chemotherapy especially with alkylating agents, mercury intoxication, Boric acid intoxication and thallium poisoning. Also implicated is toxic exposure to colchicines.

Chemotherapy induced anagen is potentially reversible on stopping the drugs. iii. Loose anagen syndrome

This has been primarily described in fair-haired children with a positive family history and may occasionally manifest in later life

23.

This condition is said to be due to a keratin mutation and it may be accompanied by uncombable hair. The hair should be handled gently and traction avoided. Though no causative treatment is

available, improvement with topical 5% minoxidil solution has been reported 24. iv. Alopecia areata

Alopecia areata is manifested as sudden loss of hairs without any or scarring. Its incidence is about 0.2% and prevalence is estimate to be 1.7% 25.The patches of hair loss spread centrifugally and can involve the eyebrows and eyelashes. When it involves the whole scalp it is called and if total body and scalp hair is lost, it is called 26.

Ophiasis is hair loss in the occipital and temporal scalp region usually in a band like pattern.

The scalp hair appears normal, though the near pathognomonic

“exclamation mark” hairs may be seen especially around the periphery of areas of hair loss. White or graying hairs may be found and this is referred to as .

Alopecia areata has been associated with some autoimmune disorders like thyroid related disease 27, pernicious anaemia and Addison’s disease. An increased prevalence of pigmentary defects has also been observed in patients with Alopecia areata 28.

Nail findings may include fine pitting, mottled lunula, or onychomadesis 29.

Alopecia areata is characterized by an aberrant autoimmune response of lymphocytes (mainly CD4 positive T-lymphocytes) and macrophages toward certain antigens of the anagen hair follicle 30.

There is a correlation with several HLA genes, which suggests a genetic predisposition for the disease like there is for many autoimmune processes 31.

Spontaneous remission is common in patchy Alopecia areata, but less so for Alopecia totalis or universalis and even less for .

Prognosis is worse in patients who develop alopecia at less than 5 years of age, alopecia totalis or universalis, associated atopy and prolonged duration of hair loss.

Treatment modalities which have been tried for Alopecia areata include immunosuppressives, irritants or immunogens, intralesional steroids, PUVA and 5% topical minoxidil.

Patients with Alopecia areata may need emotional support and physical means of camouflaging their hair loss usually with wigs.

Focal Non-Scarring Hair Loss

(A) Production decline

(i) Triangular alopecia

This is also referred to as temporal Alopecia. It may be congenital but usually appears in childhood as a focal patch of hair loss

which may either be complete or with remnants of fine vellus hair

32, 33. The underlying scalp is normal. The temporal area is favoured with hair loss being frequently bilateral. The Alopecia is usually persistent. ii. Pattern hair loss (androgenetic alopecia)

This is the commonest cause of hair loss in men and women (about

50-80% of post pubertal whites) 6.

In men, this usually starts at age 30-40 years with a hairline recession in the frontoparietal region and eventually followed by vertex balding.

Male pattern hair loss is classified using the Hamilton-Norwood system5, which distinguishes seven types with various subtypes.

Type 1 is the adolescent or juvenile hairline with no recession, this progresses to Type II with fronto temporal recession and worsen in

Type III. A Type III vertex (crown) pattern may also be seen. In Type

IV, the fronto temporal and vertex areas are involved. This progresses to Type VI where the frontal and vertex balding areas merge into one and increase in size, ending in Type VII where a narrow horseshoe shaped band of hair remains. The subtypes include a frontal recession which keeps advancing backwards, a single area of balding and another subtype in which the eventual extent of balding tends to be more limited than in regular classes.

In some cases this androgenetic hair loss is accompanied by pruritus, seborrhea and . These later two being typically androgen driven conditions.

In men, this male pattern baldness is hereditary (likely autosomal dominant) and androgen dependent specifically dihydrotestosterone related 34,35.

In androgenetic alopecia, the cycle of hair growth is accelerated, which results in a shortened anagen stage. The hair follicles produce thinner, shorter and depigmented hair shafts. This process is called miniaturization. Only a minority of follicles actually shed their hair shafts.

Women have a lesser degree of miniaturization and thus rarely have any balding when compared to men.

Three patterns have been described in women by Ludwig34. This hair loss pattern is localized on the crown, usually more diffuse and less intense. It starts after menopause due to the relative increase of androgens. Other authors like Olsen 36 have described a frontal accentuation hair loss pattern.

Some women with profound hyperandrogenemia, usually from tumours may develop a Hamilton pattern of hair loss and women with polycystic ovarian syndrome may develop pattern hair loss in their second to third decades 36. In the majority of patients with

female pattern hair loss, they have no increased serum androgens

34,36.

Pattern hair loss is related to an increased activity of 5- reductase especially type 2 in males and of specific dehydrogenases in females within the dermal papillae. These enzymes convert testosterone (dehydroepiandrosterone in females) to dehydrotestosterone, which has a strong affinity for the androgen receptors of the papilla 37.

Pattern hair loss usually is a visual diagnosis confirmed by a thorough history 38.

Oral type 2-selective 5- reductase inhibitors such as finesteride have been successfully applied in early stages of androgenetic

Alopecia 39.

Cyproterone acetate, an anti androgen has proved beneficial in the treatment of hyperandrogenic Alopecia in women40,41.

Topical minoxidil (2%) has also been used as an adjuvant therapy for both men and women, though hair loss recurs with interruption of application.

Co-existent seborrhoeic accelerates hair loss and should always be treated concomitantly.

Surgical hair restoration with follicular grafting, scalp reduction and flap rotation 42 have been tried.

Spironolactone and flutamide which are anti androgens have also been employed.

(B) Hair breakage i. Trichotillomania

Trichotillomania which is Greek for “hair pulling madness” is an impulse control disorder in which patients pull, pluck or cut their hair 43,44.

Clinically, there is a confluence of very sparse short hairs within an otherwise normal area of the scalp. Microscopically, the ends of cut or plucked hairs generally reveal either the tapered tips of newly regrowing anagen hairs or bluntly cut hairs.

Scalp biopsy shows an increased number of catagen hairs, trichomalacia and within the follicular canal secondary to traumatic hair removal and the absence or sparsity of a perifollicular inflammatory infiltrate45,46.

Treatment usually would include a psychological intervention and medications like clomipramine may be particularly effective.

ii. Traction Alopecia

This is caused by prolonged traction on the scalp by the physical pressure of tight braids, rollers etc. It can be reversible though may persist if the traction is unrelenting over months to years. iii. Tinea capitis

This is a common cause of hair loss especially in children. It may present as a seborrhoeic dermatitis, non-inflammatory “black dot ringworm” or a pyoderma-like kerion.

Treatment usually is with systemic antifungals. iv. Primary or acquired hair shaft abnormalities.

(a) Acquired trichorrhexis nodosa.

This may be seen in hairs subject to repetitive rubbing like

in lichen simplex chronicus or trichotillomania. May also

result from chemical hair processing.

(b) Acquired pili torti

This may result from trauma, scarring scalp abnormalities,

or from retinoids.

(c) Bubble hair

This is characterized by rows of bubbles seen microscopically

within localized areas of brittle hair47. It is caused by

prolonged exposure to high temperatures from curling irons or

hair dryers. This defect is completely reversible.

(C) Unruly Hair i. Wooly hair nevus

This is a non-hereditary focal condition, which appears within the first 2 years of life but can occur as late as adolescence 48. Fifty percent (50%) of cases may have an associated epidermal, verrucous or pigmented nevus. Patients may also have ocular abnormalities, like a persistent papillary membrane or retinal abnormality10.

Spontaneous improvement in the hair may occur with age. ii. Acquired Progressive Kinking

This condition is primarily seen in post pubescent males with androgenetic Alopecia 49.

Clinically, it presents with gradual curling and darkening of the frontal, temporal, auricular and vertex hairs. Microscopically, these hairs have kinks and twists with or without a longitudinal grooving.

(D) ABNORMALITY OF CYCLING i. Alopecia Areata

This is also a cause of focal non-scarring hair loss and has been discussed above. ii. Syphilis

Hair loss may be the sole presenting feature of syphilis. It may present as patchy “moth eaten” alopecia or as a generalized thinning.

A scalp biopsy may show either a superficial and deep perivascular mixed lymphocytic/macrophage/plasma cell infiltrate, a peribulbar, perifollicular, lymphocytic infiltrate mimicking alopecia areata, or a non-inflammatory telogen effluvium picture 50, 51.

Syphilis serology should be positive and treatment with the appropriate antibiotics reverses the hair loss.

Others

Other scalp conditions causing a focal non-scaring Alopecia include: i. Pityriasis amiantacea

This usually presents with thick adherent scaly infiltrate and surrounds the base of a group of scalp hairs 52. This condition is clinically similarly to psoriasis. However attempts to physically remove the scales leads to dislodgment of hair in the affected areas unlike in psoriasis.

Treatment is usually with keratolytics.

Other conditions include: i. Severe scalp psoriasis. ii. Cutaneous T-cell lymphoma iii. Histiocytosis X

2.3.2 Scarring Alopecias Scarring or cicatricial alopecias cause permanent hair loss with destruction of the hair follicles. Scarring alopecias may be primary

or secondary. Primary cicatricial alopecias arise as a result of compromise in the integrity of the pilosebaceous unit, whilst the secondary scarring alopecias are the result of a hereditary problem or an acquired disease53.

Biopsies usually confirm the diagnoses and show replacement of the hair follicles with fibrotic stellae and either fibrosis or hyalinization of surrounding collagen 54,55

The Primary Cicatricial Alopecias

These may be classified based on the type of inflammatory infiltrates seen on biopsy. This classification was developed by the

North American Hair Research Society 5.

The primary cicatricial alopecias can be classified based on the type of inflammatory infiltrate seen on biopsy. Other classification systems are based on age of onset and clinical features.

(A) Lymphocytic i. Chronic cutaneous lupus erythematosus ii. Lichen planopilaris

- Classic lichen planopilaris

- Frontal fibrosing Alopecia

- Graham little syndrome iii. Classic . iv. Central centrifugal cicatricial Alopecia. v. vi. Keratosis follicularis spinulosa decalvans

(B) Neutrophilic i. Folliculitis decalvans ii. Dissecting cellulitis/folliculitis (perifolliculitis capitis

abscedens et suffodiens)

(C) Mixed i. Folliculitis (acne) keloidalis ii. Folliculitis (acne) necrotica iii. Erosive pustular dermatosis

(D) Non-specific

(A) Lymphocytic i. Chronic cutaneous lupus erythematosus (CCLE)

This may present in the scalp as coin-shaped scaly, erythematous lesions. These scales are very adherent as they are anchored by hyperkeratotic plaques within the follicle openings. Thirty to fifty percent (30-50%) of cases present with atrophic hypopigmented hairless patches.

Patients may have no serologic evidence of the disease.

The diagnosis may be confirmed by scalp biopsy which shows vacuolar degeneration of the basal cell layer, a perivascular and peri-adnexal lymphoid infiltrate, increased dermal mucin and loss 33.

Direct immunofluorescence detects granular deposits of IgG and C3 at the dermal-epidermal junction and follicular epithelium.

Treatment comprises topical, intralesional or systemic steroids, retinoids and antimalarials.

Recent studies have shown promising results with thalidomide in refractory CCLE56.

ii. Lichen Planopilaris

Lichen planopilaris also known as rubra follicularis is characterized by a perifollicular erythema and sometimes hyperkeratotic follicular papules with a violaceous discoloration of the scalp.

The vertex is favoured and middle-aged women are preferentially affected.

This condition may sometimes co-exist with .

Histology shows vacuolar degeneration of the basal cell layer and lichenoid infiltrates in the dermis along the epidermo dermal junction and around the follicular epithelium.

Treatment is with topical or systemic corticosteroids, retinoids or

PUVA. Cyclosporin A, Antimalarials and thalidomide have also been employed.

Frontal fibrosing Alopecia is characterized by fronto-temporal hairline recession and eyebrow loss in postmenopausal women. It is associated with perifollicular erythema.

Histological findings are as for the classic lichen planopilaris.

Treatment is as for classic lichen planopilaris.

Graham-Little syndrome is characterized by lichen planus like lesions and a follicular “spikes” / keratosis pilaris-like picture that develop in areas of alopecia on the scalp, eyebrows, axillary and public areas 54.

Treatment is as for lichen planopilaris. iii. Pseudopelade of Brocq

This is a diagnosis of exclusion as its clinical picture is applicable for numerous alopecias of different aetiologies in their end stages

57,58.

It is characterized by few, irregularly shaped depressed, hairless patches usually located in the vertex region. The patches appear atrophic without any signs of acute inflammation. The follicular orifices are usually missing.

Elastin stains differentiate it from lichen planopilaris and lupus erythematosus.

Direct immunofluorescence is mostly negative. Specific treatment modality is however unclear. iv. Central Centrifugal Cicatricial Alopecia.

Commonly found in African Americans with a skew towards women.

This condition also known as hot comb alopecia and follicular degeneration syndrome is a cause of scarring central scalp hair loss. There is usually no associated bogginess or tautness to the scalp, However inflammation has been reported more commonly in affected males.

Histology shows premature desquamation of the inner root sheath with migration of the hair shaft through the outer root sheath, a mononuclear infiltrate and loss of the follicular epithelium with replacement by fibrous tissue. v. Alopecia mucinosa

This condition may present as erythematous plaques or flat patches without hair mostly on the scalp and face 59.

Histology shows prominent follicular, epithelial and sebaceous gland mucin and perifollicular lymphohistiocytic infiltrate without concentric lamellar fibrosis 54,55. vi. Keratosis follicularis spinulosa decalvans.

This is an X-linked disorder characterized by follicular hyperkeratosis, scarring alopecia of the scalp, absence of the eyebrows and eyelashes, severe photophobia and corneal dystrophy.

Starts in early childhood with symptoms subsiding with age.

Histology reveals plugging of the pilosebaceous orifices with keratinaceous debris and superficial and deep perivascular and periappendageal infiltrate of lymphocytes and plasma cells.

Treatment is with retinoids.

(B) Neutrophilic i. Folliculitis decalvans

This is an inflammatory alopecia, which presents with bogginess or induration of involved parts of the scalp with pustules, erosions, crusts and scales.

Staphylococcus aureus is usually cultured from these pustules.

Histology reveals an acute suppurative folliculitis with neutrophils and eosinophils, which may later be mixed with lymphocytes and histiocytes 54,59.

Loss of sebaceous epithelium and perifollicular fibrosis is common

54.

Folliculitis decalvans has been shown to be very resistant to antibiotic treatment.

Powell and Dawber 60 introduced a new treatment regimen consisting of rifampicin (300mg) and clindamycin (300mg) twice daily for 10 weeks. This combination has been successfully applied in many cases 61. ii. Perifolliculitis capitis abscedens et suffodiens (of Hoffman)

This condition also known as dissecting folliculitis is commonest amongst young African – American males.

Suppurative follicular and perifollicular abscesses lead to sinus tract formation. Foreign body giant cells can be found in large numbers. Histologically, the follicles are invaded by inflammatory cells. Once the follicles are destroyed, the inflammatory process is replaced by dense fibrosis of the dermis.

Treatment is with antibiotics. Systemic retinoids, dapsone and short-term steroids have also been employed. Topical disinfectants are thought to support systemic medications.

Some authors suggest x-ray, surgery or laser therapy as an alternative to systemic medication.

(C) Mixed

i. Acne Keloidalis

This condition seen primarily in African – American males is a destructive scarring alopecia. It presents with follicular based papules concentrated on the lower occiput 62 which progress to keloid – like plaques. This may be because of the kinky nature of

African hair and the fact that most African and African-American males have their hair closely shaven or cropped to the scalp.

On histology, there’s follicular dilatation, a mixed peri-infundibular infiltrate that goes into follicular rupture and foreign body granulomas, loss of sebaceous glands and lamellar fibroplasias.

Treatment is with systemic antibiotics, topical and/or intralesional steroids, and cryosurgery.

ii. Acne Necrotica

This presents as pruritic or painful erythematous follicle-based papules that develop central necrosis and crusting, healing with a varioliform scar. Found mostly on the nose, forehead, and anterior scalp and may spread to the trunk.

Tetracyclines and Cis-retinoic acid may be helpful with its treatment.

iii. Erosive pustular dermatosis

This presents as pustular, erosive and crusted lesions on the scalp of older Caucasian females. Bacteria and fungi may be cultured from these sites, though these may be secondary infections.

Biopsy reveals a lymphoplasmacytic infiltrate with or without foreign body giant cells and pilosebaceous atrophy.

Treatments with antibacterial and antifungal drugs have been disappointing. However potent topical steroids, zinc sulfate or isotretinoin may be useful54.

Secondary Cicatricial Alopecias These cicatricial Alopecias may present as a hereditary problem, alone or as part of a syndrome.

Causes of these include Aplasia cutis congenita, Conradi-Hunerman chondrodysphasia punctata, incontinentia pigmenti, ankyloblepharon, ectodermal defect, cleft lip or palate (AEC) syndrome and generalized atrophic benign epidermolysis bullosa.

Aplasia cutis congenita is the commonest congenital cicatricial alopecia. It presents as a congenital focal absence of epidermis with or without absence of other layers of the skin32.It may present

at birth with ulceration, crusting, scarring or with a parchment – like membrane.

Most lesions are on the scalp and may be singular. They are usually small and round but may occasionally be large and extend to the dura or meninges.

Unless these lesions are very large, no specific treatment is required.

2.4 PATTERN OF ALOPECIA

Hair loss can be caused by quite a number of conditions as seen from the preceding section. Age, sex, race, culture, medical conditions and even hair practices63 influence hair loss. Evaluating the pattern of alopecia seen in dermatology clinics would help the dermatologist counsel his patient on the above influences, set out appropriate treatment modalities and even offer genetic counselling when appropriate.

Some Nigerian studies64,65 have been done on pattern of skin diseases.

However literature review revealed none specific for pattern of alopecia.

Traore A et al66 working in Burkina Faso found Tinea to be the

commonest cause of alopecia, followed by alopecia areata, keloid folliculitis, androgenetic alopecia, traction alopecia and cosmetic alopecia.

A survey done by the American Hair Loss Association67 showed that the commonest form of alopecia seen in dermatology clinics was androgenetic alopecia (male or female pattern baldness), closely followed by telogen effluvium, alopecia areata, scarring alopecias and then hair loss due to cosmetic over processing. Some workers at the Cleveland clinic68 also observed a similar pattern as that described above.

This study sought to find out how the Nigerian picture compares with the above and in addition to describe the epidemiologic, clinical and possible aetiologic aspects of the pattern of alopecia seen.

2.5 EFFECTS OF ALOPECIA ON QUALITY OF LIFE

2.5.1 Quality of life in Dermatology

Quality of life measurements have recently become an integral part of dermatological studies. Quality of life analysis began to be developed in the 1970s in order to describe and measure the impact of different disease conditions on peoples’ daily lives, taking into account emotional and social functions as well as purely physical functions69. The application of this concept has given rise to a field of research called “health-related quality of life”.

Quality of life measurements could be generic or disease specific.

Generic measures assess the impact of any treatment or disease process whilst disease specific measures are designed to assess treatment and the disease process of a particular condition. These instruments help the carer to monitor and evaluate the effect of a treatment or condition from the patient’s perspective and also provide information for planning multidisciplinary care packages with those responsible for different aspects of the patient’s care.

These instruments are usually pretested for their validity, reliability and sensitivity. Validity refers to the tool’s capacity to correctly measure that for which it was designed. Reliability refers to the instrument’s reproducibility whilst sensitivity is the instrument’s ability to detect changes that occur in the study to which it is being applied.

Some examples of quality of life measurements include70

 Dermatology life Quality Index

 Health Assessment Questionnaire

 Sickness impact profile

 General Health Questionnaire

 Nottingham Health Profile

 Asthma Quality of Life Questionnaire

 Hairdex

 Skindex 29

The skin is the largest and most vulnerable organ in the body.

Diseases of the skin, hair and nails though rarely life threatening can be both physically and psychologically disabling for the patients due to their chronicity.

Many studies have pointed out the complex mutual relationships between the “psyche” and the “soma” and there exists extensive literature on the relationship between emotional stress and skin diseases71.

Skin diseases have been shown to greatly affect quality of life of patients72 particularly those, which run a chronic course, are recurrent or even disfiguring.

Sprangers et al73 working on “which chronic conditions are associated with better or poorer quality of life” found a significant impact on life quality in patients with Eczema and Psoriasis comparable to that of cardiovascular diseases. Gupta and Gupta 74 in their study on depression and suicidal ideation in dermatology patients with acne, alopecia areata, and psoriasis observed an increase in depression and suicidal ideation in acne patients. Van der Meeren et al75 also showed the profound psychological impact of acne on affected patients. Similar results

were also seen for alopecia areata, atopic dermatitis and psoriasis

75.

2.5.2 Quality of Life in Alopecia

Alopecia is quite apparent unlike other skin diseases, which may not be readily visible to people as they may be covered by clothing.

Hair loss may be seen by the affected individual as failure to conform to the norms of physical appearance in society or even as a sign of ageing. This has the potential to reduce the individual’s self esteem, affect his ability to enjoy and maintain personal and work relations, and also stop him from participating in social activities.

This fact is buttressed by the fact that sexuality, attractiveness and personality have been symbolically linked to human hair and in women it is regarded as feminine attribute76.

Egele and Tauschke 77 in their study found that some patients with hair loss experienced an ongoing feeling of loss, showing that for some individuals, coping with alopecia may be equated with grieving after bereavement. Yet another study has shown that alopecia may lead to a social anxiety disorder78.

However, some studies75 do not fully support the notion that alopecia is distressing to the affected individual, though they do

admit that these individuals usually have more “problems” than the controls recruited in the studies. These problems usually include higher levels of anxiety, lower self esteem and poorer body image.

It has become increasingly obvious that in the management of patients with hair loss, attention should not only be on the disease itself but should also encompass their psychological well-being.

This calls for collaboration between the dermatologist and the psychiatrist in the management of these patients. However, many patients reject the idea of being referred to a psychiatrist as they want to avoid the social stigma attached to visiting a psychiatric facility.

Koblenzer79 has advised that the patient be seen several times by the dermatologist for them to gain trust in their physician before being referred to the psychiatrist who preferably should see the patient for the first time in the office of the dermatologist. Many dermatology – psychiatry clinics have been established in developed countries and these have been shown to be of immense benefit to the patients80. Unfortunately this is not the case in developing countries.

Most documented quality of life studies were carried out by workers in developed countries. There is a dearth of information on the quality of life of dermatological patients in Nigeria. A study carried out by some workers in South Africa81 showed significant impact of dermatological

diseases like contact dermatitis, atopic dermatitis, acne, alopecia areata on patients’ quality of life, with females experiencing more effects on self esteem, clothing choice, treatment problems and anxiety. These findings were comparable with those from western literature.

2.6 RELEVANCE OF THE STUDY

It has become increasingly important that patient management should not just be limited to their physical ailments but should also encompass their psychosocial wellbeing. This wholistic medical care would be enhanced by results from studies which show the effects of psychosocial factors on medical conditions. A number of dermatological conditions have been studied to assess their impact on patients’ quality of life. Unfortunately, most of these works have been by our western counterparts.

In Nigeria today, there is a paucity of studies on health related quality of life. There is also very little collaboration between dermatologists and psychiatrists in the management of dermatological patients. In addition, not many dermatology-psychiatry liaison clinics currently exist in our country.

It is hoped that this study would highlight this necessity and create more awareness on the need for this liaison in the management of

dermatological patients with a view to providing them the best possible care.

CHAPTER THREE

AIM AND OBJECTIVES

I. AIM

To determine the pattern of alopecia and its effect on the quality of life of patients presenting to the Lagos University Teaching Hospital[LUTH] dermatology out-patient clinic[DOP], Yaba.

II. OBJECTIVES

1. To determine the pattern of alopecia in patients presenting to the LUTH Dermatology out-patient clinic (DOP), Yaba.

2. To determine the effects of alopecia on the quality of life of patients presenting to the LUTH DOP Clinic, Yaba.

3. To determine the influence of socio-demographic variables on the quality of life of patients with alopecia.

CHAPTER FOUR

MATERIALS AND METHODS

4.1 STUDY AREA This study was carried out at the Lagos University Teaching

Hospital (LUTH) Dermatology Out-patient Clinic Yaba. This hospital is situated in Lagos, the economic nerve centre of Nigeria with an estimated population of 9 million persons. The LUTH outpatient clinic is one of the few government owned facilities, which provide dermatological services in Lagos. The clinic is very well patronized and has patients drawn from different ethnic and socio-economic backgrounds, from all parts of Lagos State and adjacent states. The clinic sees an average of sixty (60) new patients per week with alopecia patients making up a sizeable proportion of this number.

4.2 STUDY POPULATION 4.2.1 Patient selection

i. All consenting patients with alopecia aged 16 years and above

who presented to the LUTH dermatology outpatient Clinic,

Yaba. ii. A control group matched for sex and age was recruited from

consenting individuals aged 16 years and above who did not

have any known chronic medical problems and had not had

any dermatologic consultations in the preceding 3 months.

4.2.2 Inclusion Criteria i. Patients 16 years of age and above who presented with

alopecia to the LUTH dermatology outpatient Clinic.

4.2.3 Exclusion Criteria i. Patients with alopecia who were younger than 16 years of age. ii. Patients who did not give informed consent. iii. Patients who had known chronic medical conditions. iv. Patients who had had a dermatologic consultation in the

preceding three months for any other .

4.2.4 Sample Size 82

The minimum sample size was determined using the formula:

N = Z2PQ d2

N = minimum sample size

Z = a constant which is 1.96 at 95% confidence interval. p = estimated prevalence of alopecia

Q = 1-p d = absolute precision which is 0.05

Nigerian studies which sought to determine the prevalence of different skin diseases have been carried out. Ogunbiyi et al64 working in South

Western Nigeria, calculated prevalence of alopecia to be 3.4%. Alabi83 working in the same centre had also found prevalence of alopecia to be

3.3%.

In south Eastern Nigeria, Nnoruka65 in her study calculated prevalence of hair disorders to be 1.3%. Onayemi et al84 working in North-Western

Nigeria, calculated prevalence of disorders of skin appendages to be 2.4%.

For the purpose of this study, estimated prevalence of alopecia was taken to be 3.4%. Of all the cited prevalence values, this was the highest and is also specific for alopecia.

Thus with 95% confidence interval, p of 0.034 and an error margin of 5%;

N = (1.96)2 (0.034) (1-0.034) (0.05)2

= 50.46 patients

≈ 51patients.

With default and non-response rate assumed to be 10%.

N = 50 x (100 + 10) = 55.56 patients 100 ≈ 56 patients.

Sample sizes from two quality of life studies in alopecia carried out in developed countries, were seventy five (75)85 and seventy (70)86 respectively. The sample size for this study was marked up to hundred

(100) in order to aid the researcher address all the objectives of the study, increase study precision and allow for matched comparison with studies carried out in western countries.

An age and sex matched control group of hundred (100) was also recruited.

4.3 ETHICAL CONSIDERATION Ethical clearance was sought and obtained from the research and ethical committee of the Lagos University Teaching Hospital (LUTH).

The aims and objectives of the study including how it would be carried out were fully explained to each participant. While participation was voluntary, patients were assured that non- participation would in no way affect their management. They were also guaranteed about confidentiality of information and data obtained from them.

4.4. METHODOLOGY

This was a prospective, observational study with a case control design. All consecutive patients who met the inclusion criteria were recruited. After each patient had been reviewed and a definitive diagnosis of alopecia made, the questionnaire was administered to them. This structured questionnaire (provided in appendix 1, pages 152-154) was pretested. It was designed to elicit socio-demographic data from the patient, past medical history and other relevant information. It also incorporated the Dermatology Life Quality Index87 which is an instrument consisting of 10 items. It is designed for use in persons aged 16 years and above.87 The DLQI evaluates the effects of dermatological conditions on the quality of life in a standardized and objective manner. It is analyzed under six headings

(i) Symptoms and feelings (ii) Daily activity

(iii) Leisure (iv) Work and school

(v) Personal relationships and (vi) Treatment

Each of these headings may have a score ranging from 3-6. The

DLQI is calculated by summing the score of each question to a maximum of 30 and a minimum of 0.

The DLQI scores for each participant was computed and interpreted as follows87.

0-1 = no effect at all on patient’s life.

2-5 = small effect on patient’s life

6-10 = moderate effect on patient’s life

11-20= very large effect on patient’s life

21-30= extremely large effect on patient’s life

Williamson, Gonzalez and Finlay86 employed the DLQI in quantifying the effect of hair loss on quality of life. Seventy patients were recruited. Mean DLQI score was found to be 8.3[s.d

=5.6, range 0-23].

The DLQI has also been found to have high reliability and internal consistency88.

4.4.1 Translation of the DLQI

For this study, three versions of the DLQI were employed:

i. A Yoruba language translation.

ii. A modified version in every day spoken `Nigerian’ English.

iii. The original DLQI instrument.

A translation was deemed necessary by the researcher to overcome the differences in culture and language between our Nigerian society and the western society for which the instrument was developed. Words and habits were substituted to those used in western societies. This would improve measurements and also allow for cross cultural comparison of results.

The translation and modified version were the result of a process of two forward and two back translations by several linguists and a bilingual

dermatologist after permission had been sought and obtained from the copyright owners of the DLQI instrument.87

The appropriate version was administered to each patient after validation by a pilot study.

4.4.2 Pilot Study

A pilot study was carried out by the researcher in which 30 healthy subjects with no skin diseases were administered the DLQI and their scores computed. The mean DLQI score for them was calculated to be

0.5.This was comparable with mean DLQI scores from other studies outside Nigeria carried out on normal populations.

i. Finlay and Khan 87 (1994 ) - 0.5

ii. Badia et al 89(1999 ) - 0.3

iii. Zachariae et al 90(2000 ) - 0.4

iv. Hachem et al 91(2002 ) - 0

30 patients with Alopecia age and sex matched with the normal population were also administered the DLQI. Mean DLQI for this group was calculated to be 8.83. This result being quite comparable with mean DLQI of 8.3 obtained by Williamson et al86.

4.4.3 Diagnosis of Alopecia

Laboratory investigations

Diagnosis of Alopecias was mostly clinical and laboratory investigations were requested for in some participants to aid

diagnosis. These included routine complete blood counts, thyroid screening, syphilis serology, punch biopsies, autoimmune screening, hormone profiles, serum levels of relevant micronutrients, radiological examinations among others carried out in the clinic for the various diagnoses.

Physical examination

Participants in this study also had a thorough clinical examination and the presence of skin lesions noted. The scalp was examined for pattern of involvement, estimated percentage area of involvement, presence of any hair abnormality and other scalp lesions. Other associated features like keloids, acne, obesity, cutaneous Lichen

Planus, Psoriasis, seborrheic dermatitis were noted.

Other means employed to aid diagnosis

1. A magnifying lens was employed to better characterize some

scalp lesions.

2. A light microscope where necessary was used to visualize scalp

scrapings and plucked hair.

The material scraped off onto plain white paper was neatly

wrapped and then transported to the laboratory for 30%

Potassium hydroxide (KOH) mount and direct examination as

well as culture on Saboraud’s agar.

3. Hair collections of shed scalp hair per day were requested for

in patients with suspected telogen effluvium as these patients

usually bring quite large collections of shed hair.

4. A hair pull test was done when needed to aid in diagnosis of

alopecia. A count greater than six was taken as abnormal.

These hairs were also inspected to know what phase of growth

they were in.

5. A trichogram was also employed where relevant and a telogen

count above 10-15% was regarded as abnormal.

6. Female pattern hair loss was checked for by comparing crown

part width to occipital part width. In female pattern hair loss,

the part width on the crown is wider compared with part width

on the occiput.

7. Scalp punch biopsy using a 4mm punch was undertaken for

lesions whose diagnoses were clinically unclear. The tissues

were fixed in 10% buffered formalin and sent for histology.

Where necessary these tissues were cultured for fungal and

bacterial elements.

4.4.4 Clinical severity of Alopecia

The severity of alopecia was classified based on percentage area involved into (0-10%) mild, (11-22%) moderate, (21-30%) moderately severe, (31-40%) severe and (>40%) extremely severe.

4.5 DATA ANALYSIS The generated data were collated and analyzed using Statistical

Package for the Social Sciences Software (SPSS) version 10.

Data from the alopecia patients and controls were collated and analyzed separately.

The findings were then compared as necessary to highlight any differences and probable relationships between variables of interest.

Frequency distribution tables and graphs were generated for categorical variables. Cross tabulations of variables were done within cases and between cases and controls.

The Chi–squared test, Student’s T test and Analysis of variance were employed to determine the statistical significance of the observed differences and probable associations between the variables studied among the cases and controls.

P–values less than 0.05 were accepted as being statistically significant.

CHAPTER FIVE

RESULTS

A. PATTERN OF ALOPECIA

5.1 Demographic data

The study period spanned from August 2006 to August 2007. During this time, a total of two thousand, eight hundred and forty four

(2,844) persons sought consultations for various dermatological conditions. Alopecia patients made up 4.6% of this number (Table I).

This number is sizeable and justifies a study on the effect of this condition on affected persons.

TABLE I: Top ten groups of skin disorders observed at study site.

Disease group Percentage

1. Dermatophyte infections 12.3

2. Papulosquamous eruptions 12.2

3. Contact dermatitis 7.5

4. Pruritus and urticaria 7.3

5. Pigmentary disorders 6.8

6. Atopic dermatitis 5.5

7. Parasitic infestations 5.2

8. Alopecia 4.6

9. Acne vulgaris 4.3

10. HIV/AIDS Associated disease 3.9

There were a total of 100 patients involved in this study. Of this number, 60(60%) were males and 40(40%) were females giving a male to female ratio of 1.5:1. (Figure 1).

Their ages ranged from 16 years to 61 years. The mean age was

33.65 ± 10.82 years. At the time of presentation alopecia was seen in 5(5%) patients below 20years of age, 68(68%) patients in the 21-

40 age group, 26(26%) patients in the 41-60 age group and 1 patient in the above 60 age group. (Figure II).

There were more males and females in the 21-40 years age group compared to the other groups. Figure III shows the age and sex distribution of the patients.

Sixty-six (66%) of patients had their alopecia starting between the ages of 21 and 40 years. An equal number of patients 17(17%) had their alopecia starting below 20 years of age and between 41 and

60 years of age. (Table II).

Table II: Age at onset, Sex and Clinical severity of alopecia.

(N=100,100%)

Sex

Clinical Age at Male Female Total

severity onset (%) (%) (%)

Mild Below 20 25 6 31

21-40 4 4 8

41-60 31 12 43

Moderate Below 20 13 7 20

21-40 2 3 5

41-60 18 13 31

Moderately Below 20 3 4 7

severe 21-40 1 1 2

41-60 5 8 13

Severe Below 20 2 2

21-40 3 1 4

Extremely Below 20 2 4 6

severe 21-40 2 2

41-60 3 6 9

The median age of the patients at the time of onset was 28years

(Age range, 6-58years).

Mean age of onset of males was 28.61 years and mean age of onset of females was 29.62 years.

Eighty five (85%) patients were presenting with the first episode of alopecia, only 1 (1%) patient had had more than 4 episodes of hair loss. Of the total number of patients, 61 (61%) experienced their first episode of hair loss within the first four decades of life, of which 5% occurred before the age of 20.

Alopecia was present for a mean duration of 30 months ± 71.7;

(range 0–312 months) before presentation.

5.2 Clinical Characteristics and Pattern of Alopecia

5.2.1 Pattern of involvement

All patients presented with alopecia of the scalp with a few having involvement of other body sites.

Ninety seven (97%) patients had only their scalp affected. Two (2%) had both scalp and eye brow alopecia and only 1 patient had involvement of all body sites.

At the time of first presentation, 95 (95%) patients had patchy alopecia, of this number 43(43%) had 0-10% area involvement

31(31%) had 11-20% involvement, 13(13%) had 21-30% area

involvement, 4(4%) had 31-40% involvement and another 4(4%) had

>40% involvement.

Five patients presented with diffuse alopecia. Of this number four

(4%) had >40% area involved and 1(1%) had generalized alopecia.

Severity of alopecia

Clinical severity of Alopecia was rated based on percentage scalp and body area involved. This ranged from mild, moderate, moderately severe, severe to extremely severe alopecia. (Figure IV).

Forty nine (49%) males presented with mild to moderate alopecia (0-

20% involvement) and 11(11%) presented with moderately severe to extremely severe alopecia (21->40% area involvement).

Twenty five (25%) of the female patients had mild to moderate alopecia and 15(15%) had moderately severe to extremely severe alopecia. (See Table II).

In general, there were more females with extensive alopecia.

Associated symptoms

Hair loss was asymptomatic in 30(30%) of patients 33(33%) patients had associated pruritus, pain in 23(23%) cases, tightness of the scalp in 3(3%) patients, “boils” in 5(5%) patients with keloid and dryness in 1(1%) patient each. (Figure V).

Associated disorders of skin appendages

Eleven (11%) patients had hair shaft abnormalities. These were exclamation mark hairs in 6(8%) patients. Tufted folliculitis, split hair ends and variable hair lengths were present in 1(1%) patient each.

Nail changes were observed in 17(17%) patients. They included longitudinal ridging () (11%), pitting (4%) and half and half nails (2%).

5.3 Associated diseases

Only 15(15%) patients reported a positive family history of hair loss.

In the course of reviewing the patients, some of them were diagnosed to have some medical conditions. Six (6%) had prolonged fever, 4% thyroid diseases and 8% related their hair loss to pregnancy.

Other co-existing medical conditions the patients had which were not associated with their alopecia were Asthma (2%), Diabetes mellitus (1%), systemic Lupus erythematosus (1%), HIV infection (1%) and scleroderma (1%).

Thirty three (33%) had other co-existing skin diseases (Table III).

Thirteen (13%) had these skin lesions related to their alopecia; DLE

(5%) scleroderma (3%) Psoriasis (3%), lichen planus (1%) and (1%). Twenty patients (20%) had skin lesions unrelated to their hair loss: seborrheic dermatitis (5%), Atopic dermatitis (3%),

Acne Vulgaris (3%), contact dermatitis (2%), exogenous ochronosis

(2%), Tinea manuum (2%), urticaria (1%), onychomycoses (1%) and

IgA dermatoses (1%).

Table III: Skin diseases coexisting with alopecia.

Skin diseases Number of

cases (%)

1 None 67

2 Discoid lupus 5

erythematosus

3 Scleroderma 3

4 Psoriasis 3

5 Seborrheic dermatitis 5

6 Atopic dermatitis 3

7 Acne vulgaris 3

8 Nickel dermatitis 1

9 Exogenous Ochronosis 2

10 Contact dermatitis 1

11 Lichen planus 1

12 Urticaria 1

13 Onychomycoses 1

14 Tinea manuum 2

15 Acne conglobata 1

16 ? IgA dermatoses 1

Drugs and substances used

Six (6%) patients gave a history of substances or drugs used prior to onset of their alopecia: hair relaxer (4%), antiretroviral drugs (1%) and razor blade (1%).

5.4 Clinical diagnosis of alopecia

Table IV shows the clinical diagnoses of the alopecia versus the gender of patients. Eighteen (18) different diagnoses were made in the course of the study. Keloid folliculitis (acne folliculitis nuchae and acne keloidalis nuchae) made up 28% of cases, Alopecia Areata

(15%), CCLE (14%), folliculitis decalvans (9%), lichen planopilaris

(6%) and dissecting folliculitis (5%). The above were the most common causes of alopecia.

Keloid folliculitis was the most frequent diagnosis and only one of the affected patients was female. The relationship between diagnosis and sex was statistically significant. (Χ2 = 70.28, p=0.0001).

Table IV: Clinical diagnoses of alopecia versus gender.

Diagnoses Sex Total

(%) Male (%) Female (%)

1 CCCA 1 1

2 CCLE 1 13 14

3 Traction alopecia 2 2

4 Acne folliculitis 4 4 nuchae

5 Alopecia areata 10 5 15

6 Lichen planopilaris 1 5 6

7 Scleroderma 3 3

8 Psoriasis 1 2 3

9 Folliculitis decalvans 8 1 9

10 Alopecia mucinosa 1 1

11 KFSD 2 2

12 Dissecting folliculitis 5 5

13 Male pattern 4 4 baldness

14 Acne keloidalis 23 1 24 nuchae

15 Chemical alopecia 4 4

16 Anagen effluvium 1 1

17 Pseudopelade of 1 1 Brocq 18 Trichotillomania 1 1

Total 60 40 100

Alopecia Areata was the second most frequent diagnosis with one of the patients presenting with alopecia universalis. This was followed by chronic cutaneous lupus erythematosus, folliculitis decalvans, lichen planopilaris and dissecting folliculitis.

Four (4%) males presented with male pattern hair loss, chemical

(relaxer) induced hair loss was also seen in 4(4%) patients who were all females.

Psoriasis and scleroderma were found in 3(3%) patients each.

Traction alopecia, keratosis follicularis spinulosa decalvans were seen in 2(2%) patient each whilst central centrifugal cicatricial alopecia, alopecia mucinosa, anagen effluvium and trichotillomania were found in 1(1%) patient each.

One (1%) patient remained without a definitive diagnosis even after several punch biopsies, thus suggesting a probable diagnosis of pseudopelade of Brocq.

5.5 Places of treatment

Of the total number of patients seen 65(65%) sought orthodox medical aid for the treatment of their hair loss, 33(33%) had first sought non-orthodox attention whilst 2(2%) patients declined to respond.

Of the 65 patients above, 44 had visited a general practitioner before presentation whilst 21 came first to the dermatologist.

Out of the other group of patients, who had sought non-orthodox means of treatment 22 had visited a chemist, 9 had tried tradomedical means and 2 had been to church. (Figure VI).

Figure VII: Alopecia Areata

Figure VIII: Central Centrifugal Cicatricial Alopecia

Figure IX: Chronic Cutaneous Lupus Erythematosus

Figure X: Dissecting Folliculitis

Figure XI: Acne Keloidalis Nuchae

Figure XII: Anagen effluvium

Figure XIII: Dada Hair in a Young Child

Figure XIV: Folliculitis decalvans with tufted folliculitis

Figure XV: Scleroderma

Figure XVI: Lichen Planopilaris

Figure XVII: Male Pattern Baldness 1

Figure XVIII: Male Pattern Baldness II

Figure XIX: Traction Alopecia

Figure XX: Lichen planopilaris. Band-like lymphohistiocytic infiltrate along the length of the hair follicle that obscures the junction between infundibular epithelium and perifollicular dermis. (Hematoxylin-eosin stain; original magnification 50×)

Figure XXI: Discoid lupus erythematosus. Epidermal atrophy, follicular horny plugs, vacuolar degeneration of the basal cell layer overlying a superficial and deep lymphohistiocytic dermal perivascular and perifollicular infiltrate. (Hematoxylin-eosin stain; original magnification 50×)

Figure XXII: Acne keloidalis nuchae. An infiltrate around the naked hair follicle, formed predominantly by neutrophils, a few plasma cells, lymphocytes, and occasional giant cells (hematoxylin and eosin, × 100 (a) , × 400 (b))

Figure XXIII: Non characterized pseudopelade (NCPB). Fibrosis of the superficial and deep dermis. Fibrotic tracts at sites of extinct hair follicles are also present. (Hematoxylin-eosin stain; original magnification 50×)

Figure XXIV: An anagen hair that has been plucked out: notice the soft, sticky tail.

Figure XXV: A normal telogen hair with a hard 'club' end, seen under a light microscope.

B. EFFECT OF ALOPECIA ON QUALITY OF LIFE

5.6 Socio demographic characteristics

5.6.1 Age and sex distribution

One hundred patients who presented with alopecia to the LUTH DOP clinic were studied. They were made up of 60(60%) males and

40(40%) females (See figure I). Their ages ranged from 16 years to

61 years. The mean age was 33.65 ± 10.82 years.

The control group were age and sex matched with the patients. They were also 60 (60%) males and 40 (40%) females (see figure 1). The age range was also 16-61 years (see figure II). The mean age for controls was also

33.65 - 10.82 years.

5.6.2 Level of literacy

The literacy levels of patients and controls are as shown in Table V.

Twelve (12%) of the patients had no formal education and 5(5%) of the controls had no formal education,

Eight (8%) of the patients stopped their education at the primary level and 7(7%) of the controls also stopped at this level. Twenty one

(21%) of the patients had secondary education and 20 (20%) of the controls also had secondary education. Fifty nine (59%) of the subjects attended tertiary institutions and 68 (68%) of the controls also had tertiary education.

TABLE V: Literacy Levels of Patients and Controls

Subjects Controls

Educational Males Females Total Males Females Total

Status % % % % % %

None 7 5 12 3 2 5

Primary 5 3 8 3 4 7

Secondary 16 5 21 13 7 20

Tertiary 32 27 59 33 35 68

Total 100 100

5.6.3 Occupation

The Employment status of the patient and controls is as shown in figure VII. For patients and controls, the proportion of employed persons were 61 (61%) and 63 (63%) respectively.

There were 21 (21%) students in the patient group and 29 (29%) in the controls group.

There were more unemployed patients (16) than controls (8).

5.6.4 Marital status

The marital status of patients and control is shown in figure VIII.

There were more singles in both the patient (54%) and control (59%) groups.

There were 44 (44%) married persons in the patient group and 39

(39%) in the control groups.

There were 1(1%) divorced and 1 (1%) widowed persons in both the patient and control groups.

The severity of alopecia was classified based on percentage area involved into mild (0-10%), moderate (11-22%), moderately severe

(21-30%), severe (31-40%) and extremely severe (>40%). Males

presented with 31% and 18% respectively of mild and moderate cases of alopecia. (See Table two (II)).

The proportions of single patients were 23%, 18%, 9% 2% and

Diagnosis No of Mean Mean Sum of anothe cases Age DLQI DLQI r 2% (%) Total

in Scores mild, moderate moderately severe, severe and extremely severe cases.

However, there was no significant statistical association between clinical severity and age

(f = 0.585, p>0.05), sex (f= 3.28, p>0.05) or marital status (f =

0.70, p>0.05).

5.7. Comparison of different diagnoses

Table VI shows the diagnosis, mean age distributions and the mean and sum of total DLQI scores for the patients and controls.

TABLE VI: DIAGNOSES, MEAN AGE AND MEAN AND SUM OF DLQI SCORES FOR

PATIENTS AND CONTROLS.

1 CCCA 1 32 10.0 10.0

2 CCLE 14 44 9.57 134.0

3 Traction alopecia 2 44 17.5 35.0

4 Acne folliculitis 4 29.3 3.5 14.0 nuchae

5 Alopecia areata 15 27.6 7.5 105.0

6 Lichen planopilaris 6 29.8 10.65 64.0

7 Scleroderma 3 38.7 3.3 10.0

8 Psoriasis 3 31.0 11.0 33.0

9 Folliculitis decalvans 9 31.1 3.3 30.0

1 Alopecia mucinosa 1 40.0 3.0 3.0 0

1 KFSD 2 39.0 9.5 19.0 1

1 Dissecting folliculitis 5 31.0 6.4 32.0 2

1 Male pattern baldness 4 32.8 1.5 6.0 3

1 Acne keloidalis 24 34.8 8.79 211.0 4 nuchae

1 Chemical alopecia 4 33.5 1.0 4.0 5

1 Anagen effluvium 1 48.0 7.0 7.0 6

1 Pseudopelade of Brocq 1 26.0 11.0 11.0 7

1 Trichotillomania 1 26.0 0.0 0.0

8

1 Controls 100 33.65 0.14 14.0

9

A total of eighteen (18) different diagnoses were made in the course of the study.

Keloid folliculitis (acne keloidalis nuchae and acne folliculitis nuchae) (28%), Alopecia Areata (15%), chronic cutaneous lupus erythematosus( CCLE) (14%), folliculitis decalvans (9%), lichen planopilaris (6%) and dissecting folliculitis (5%) were the most common causes of alopecia.

The Highest DLQl scores were obtained for keloid folliculitis, CCLE, alopecia areata and lichen planopilaris. The least scores were recorded in patients with trichotillomania, chemical induced hair loss and male pattern baldness (Table VI).

The total DLQl score was significantly higher for patients (mean

7.3±7.16, range 0-30), than for controls (mean 0.14±0.35, range 0-1)

(p=0.0001).

5.8. Impact on quality of life

The overall score of the DLQl ranged from 0-30 with a mean of 7.3 ±

7.16.

Of the total number of patients seen, only 27(27%) had no

impairment in their quality of life. Twenty nine (29%) recorded a

small effect on their life quality. Nineteen (19%), 18(18%) and

17(17%) patients had moderately, very large and extremely large

impairment of their quality of life.

The impact of alopecia on QOL of patients was also studied in

relation to the six domains (subscales) of the DLQI respectively.

The six subscales are symptoms and feelings, daily activities,

leisure, personal relationships, work/school and treatment.

The distribution of subscale scores are presented in Table VII.

TABLE VII: DISTRIBUTION OF SUBSCALE SCORES OF DLQI.

Subscale Mean + S. D

Symptoms and 2.66 + 1.90 feelings

Daily activities 1.38 + 1.82

Leisure 1.26 + 1.81

Personal 0.92 + 1.54 relationships

Work and school 0.58 + 1.04

Treatment 0.49 + 0.92

5.8.1 Symptoms and feelings

The overall mean symptoms and feeling score was 2.66 and 2.53,

2.32, 4.0, 1.25 and 3.11 respectively in mild, moderate, moderately

severe, severe and extremely severe cases.

Females had a higher mean score here than males (Χ2=8.604,

p>0.05)

Persons in the 21–40 age group had more affectation in this domain

(Χ2=17.63, p>0.05) and this was also the case for patients who had

their alopecia starting in this age group (Χ2=8.527, p>0.05).

Divorced patients had quite a high score of six (6) compared to

married persons score of 2.41 (Χ2=18.52, p>0.05).

The above differences though were not statistically significant.

5.8.2 Daily activities

Daily activities were not affected significantly by increasing disease severity (Χ2=15.371, p>0.05) and mean overall score here was 1.38.

Females were more affected in this domain. Persons above 60 years of life also had the most impairment here.

5.8.3 Leisure

Patients were minimally affected in this domain as overall mean score was 1.26.

There was also no significant association with clinical severity of alopecia (Χ2=17.095, p>0.05).

5.8.4 Work and School

Work and school life of patients was not significantly affected by the severity of their alopecia (Χ2=12.111, p>0.05), sex (Χ2=3.206, p>0.05) and age (Χ2=8.443, p>0.05). The overall mean score here was 0.58.

5.8.5 Personal relationships

There was a significant effect on QOL of patients in this subscale

(Χ2=146.24, p<0.05). Overall mean score here was 0.92.

5.8.6 Treatment

Here there was also no statistical significance between clinical severity and treatment (Χ2=8.20, p>0.05). Overall mean score here was 0.49.

C. INFLUENCE OF DEMOGRAPHIC AND CLINICAL CHARACTERISTICS

ON DLQL SCORES

5.9 The relationship between clinical, socio- demographic factors and

DLQL scores

The relationship between clinical, socio-demographic factors and

DLQl scores are shown in Table VIII.

Mean total DLQI score (8.50) was highest in the above 60 age group, followed by the 21-40 age group(8.25) and the 41-60 age group(5.36).

Patients who had their hair loss starting in their third to fourth decades of life had the highest mean score of 8.20 in this category.

Females had a higher mean disability score (8.08) than the males

(6.77).

Divorced persons had more impaired life quality than married persons.

Patients who had just primary education had the highest scores

(12.0) and those with no formal education had the least score of

3.92.

Students recorded the highest mean total DLQI score of 8.24.

There was no significant association between sex and DLQI scores

(t=-8.26, p>0.05). This was also true for employment (t=-8.63, p>0.05), marital status (t=-8.02, p>0.05) and literacy levels.

Interestingly, scores were not found to increase with increasing clinical severity of alopecia (Pearson’s correlation = -0.006). Mean total DLQI scores for mild, moderate, moderately severe, severe and extremely severe cases were 7.35, 6.29, 11.54, 1.75, and 6.78 respectively.

TABLE VIII: DLQI SCORES FOR CLINICAL AND SOCIO-DEMOGRAPHIC CHARACTERISTICS OF PATIENTS.

DLQI SCORES

NUMBER MEAN SUM

1 Clinical severity t=-23.76, p>0.05

Mild 43.00 7.35 316

Moderate 31.00 6.29 195

Moderately severe 13.00 11.54 150

Severe 4.00 1.75 7

Extremely severe 9.00 6.78 61

2 Employment status t=-45.56, p>0.05

Unemployed 16.00 7.50 120

Employed 61.00 7.03 429

Student 21.00 8.24 173

Retired 2.00 3.50 7

3 Education t=-16.59, p>0.05

None 12.00 3.92 47

primary 8.00 12.00 96

Secondary 21.00 6.52 137

Tertiary 59.00 7.61 449

4 Age group t=-30.84, p>0.05

Below 20 5 3.40 17

21-40 68 8.25 561

41-60 26 5.36 134

Above 60 1 8.50 17

5 Sex t=-12.19, p>0.05

Male 60 6.77 406

Female 40 8.08 323

CHAPTER SIX

DISCUSSION

A. PATTERN OF ALOPECIA

Alopecia is taken quite seriously by affected individuals and it is a

fairly frequent reason for consulting a dermatologist. However, not

many patients visit a specialist first, rather they get to the

dermatologist as a last resort. This was the case in this study and was also observed in another study92 carried out in Senegal.

6.1 Sociodemographic and clinical characteristics

Young adults made up the highest proportion of patients and most of them were males. One wonders if this is because they were more bothered about their conditions than females and so presented more. Some workers93 on alopecia areata in Singapore found out that the young male patients were actually more distressed about their disease than the females.

The median duration of alopecia in this study was found to be thirty (30) months ± 71.7; range 0–312 months. This is quite different from that recorded by Williamson and Gonzales 86 (median duration of hair loss =138 months ± 114; range 7-588). This difference in duration of hair loss may be because our patients presented earlier making one wonder if this is because they were more bothered than their western counterparts and so sought treatment earlier.

More than half of the patients presented with additional symptoms other than hair loss, most frequent of which was pruritus, this was also observed by an Nnoruka63 in southeastern Nigeria and Traore66 in Burkina Faso.

Fifteen (15%) patients gave a family history of hair loss.

One third of the patients on examination were found to have co- existing skin diseases which were associated with or even the cause of their alopecia. Surprisingly, it was the alopecia that made them present to the clinic and not the skin lesions.

6.2 Clinical diagnoses

Keloid folliculitis (acne folliculitis nuchae and acne keloidalis nuchae) which made up 28% of cases, Alopecia Areata (15%), CCLE

(14%), folliculitis decalvans (9%) lichen planopilaris (6%) and dissecting folliculitis (5%) were the most common causes of alopecia in this study.

The above pattern is quite different from results obtained by some authors66 in Burkina Faso, the American hair loss association and some workers at the Cleveland clinic (USA) 68.

The Burkina Faso authors66 found dermatophyte infection to be the most common cause of alopecia followed by Alopecia areata, Keloid folliculitis, androgenetic alopecia, traction alopecia, and cosmetic alopecia. The alluded reason for Tinea capitis being most prevalent was the inclusion of young subjects including school children in their study. Another author92 observed that Tinea capitis was found mainly in young people, mostly school children and they thought this trend could be explained by promiscuity! This though is a spurious association as T. capitis is not a sexually transmissible

infection. This present study did not include persons younger than

16 years of age and no patient presented with Tinea as a cause of hairloss. The result obtained in this study is quite different from the American pattern, in which most of the patients presented with androgenetic alopecia, followed by telogen effluvium and alopecia areata. They did not record any case of keloid folliculitis. This above differences may be explained by genetics and the fact that keloid folliculitis is almost unknown among Caucasians and it is thus a disease of the black race with kinky hair.

In this study and Traore et al’s66 study, alopecia areata was the second most frequent diagnosis.

Interestingly, androgenetic alopecia was high up in their list, being third, unlike in this study where only four patients presented with it. However, for the Americans it was their most prevalent diagnosis. In Nigeria today, many men about the age of 50 would consider keeping their hair very short – longer hair being considered as evidence of irresponsibility. This also offers a convenient excuse for masking receding and progressive hair loss from androgenic alopecia. This makes one wonder about the perception of baldness in the different societies. Could this be responsible for the disparities? Possibly, but this can only be confirmed with more research.

In this study, CCLE (14%) was quite prevalent but not so for Traore et al66 and the American study. In times past one would be forgiven if one considered CCLE to be a western disease but this is not the picture being painted by this study. It is possible that this may be the result of increased diagnosis due to the presence of trained specialists and improved laboratory services in Nigeria.

6.2.1 Keloid folliculitis

The cases of keloid folliculitis seen in this study were mostly males save for one female patient. Most of the male patients were young persons between the ages of 21and 40. This male predominance was also reported by Traore et al66 and Ngwanya94 in South Africa, though Ngwanya also had both males and females presenting with acne keloidalis nuchae.

This male predominance could be associated with the kinky hair structure of the African hair and the practice of closely cropping the hair, which is mostly done by men and especially in this age group. For some men, having their hair “skin cut” is actually a fashion fad.

In Nigeria today, few women wear their hair closely cut to the scalp. They mostly ‘relax’ their hair and ‘relaxed’ straightened hair will not behave like curled kinky hair. This may be why only one female presented with keloid folliculitis.

6.2.2 Alopecia areata

Alopecia areata was found to be more common in males with a male to female ratio of 2:1. This is quite different from the male to female ratio of 1:1.3 (a slight female preponderance) observed in the

Singapore study93. Alopecia areata was seen mainly in students and employed persons. This finding was also reported by Traore et al66.

The age of onset of alopecia areata (A.A) ranged from 14 years of age to 43 years. Most patients (85.8%) experienced their first episode of A.A in the first four decades of life. This is consistent with previous reports 27,95.

A strong family history of A.A (frequency of 20.40%) was reported in the western population27,96. Low frequencies (4.6%) of family history were noted in three Asian studies 93, 95, 97.

These workers postulated that the different genetic background of

Asians and Caucasians was responsible for this difference. In this study there was no family history in our subjects with A.A.

There have been few reports of an association between A.A and autoimmune disease. These are with thyroid disease and vitiligo93.

Tan et al93 observed a low frequency of 2.3% in association with thyroid diseases compared with others who reported frequencies of

8-28% 27, 96. No patient with A.A had any co-existing thyroid disease in this study.

The frequencies of associated vitiligo previously reported were 1.8% by an Indian group95, 4% by Muller and winkelmann27, 16% by

Cunliffe et al98 and 4.1% by Tan et al93. There was no associated vitiligo in this study.

Only one of our patients had associated Diabetes mellitus. Diabetes mellitus is said to occur more frequently in relatives of patients with AA rather than in AA patients themselves. This observation was also reflected in a previous report93.

6.2.3 Chronic cutaneous lupus erythematosus (CCLE)

It was interesting to note that after alopecia areata, the third most frequent diagnosis was CCLE. This is in keeping with Nnoruka’s63 findings, where in her case study, carried out in south eastern

Nigeria, 12 patients presented with CCLE though in her study it was also the most frequent cause of alopecia in women followed by alopecia areata. This is worthy of note because another author 66 working in Burkina Faso, reported only 1 patient out of 53 to have presented with CCLE in his study. This finding, however may be explained by differences in study location and methods of patient recruitment.

6.2.4 Folliculitis decalvans

Folliculitis decalvans was diagnosed only in males unlike in

Ngwanya’s study where he found it to be more common in women

than in men. This is in contrast to both this study and another previous study99.

Nnoruka63 also in her study which involved 39 women did not find a single case of folliculitis decalvans.

6.2.5 Others

Of all the patients who presented with lichen planopilaris only one, a female, had associated cutaneous lichen planus. There was a female preponderance in a ratio of 5:1.

Chemical (hair relaxer) induced alopecia and traction alopecia were seen in only women. Niang et al100 also reported this female preponderance.

Hair relaxants (especially the 1ye variants) in addition to the “hot comb” or “hair tongs” have been postulated to be the primary trigger leading to central centrifugal cicatricial alopecia (CCCA) in women63. They set off a process of inflammation, fibrosis and ultimately scarring. The only patient who presented with CCCA in this study was female.

B. EFFECT OF ALOPECIA ON QUALITY OF LIFE (Q0L)

Quality of life in dermatology has been measured for clinical, research, political and financial purposes 101.The diseases, which

have the potential to cause any cosmetic disfigurement like alopecia, have been reported to have a major impact on the Q0L of patients, many of whom feel stigmatized by their conditions 102.

This study sought to assess the impact of alopecia on the quality of life of patients and also to examine the effect of disease severity on the disability scores and it does provide evidence that alopecia negatively affects patients’ QOL. This result is consistent with those of other studies 85, 86.

6.3 Characteristics of study population

The age range of the recruited patients was 16-61 years. There was a preponderance of patients in the 21-40 age group. This finding is similar to that of 0zturkan et al103.

In this study, there was a male preponderance, with a 60% male population. This finding is different from that found in another study103. In their study they had a female population of 63%. Some other authors104 on the other hand, had an equal proportion of male and female subjects in their report.

Majority of the patients (59%) and controls (68%) had tertiary education as shown in Table V. Twelve (12%) of the patients and 5% of the controls had no formal education.

The high proportion of educated individuals suggests that these persons may be more conscious of the cosmetic effects of their alopecia and so seek medical intervention more.

There were more employed than unemployed persons in the patients and controls samples. This finding may be because of the site of study location.

The mean overall DLQ1 score was 7.3 ± 7.16 in this study. This score is slightly lower than that obtained in the pilot study (8.83).

This difference may be due to the small sample size (30) of the pilot study. Williamson et al86 in their study of alopecia which involved seventy (70) respondents, recorded a mean DLQI score of 8.3. The above results suggest that patients with Alopecia have impaired quality of life.

Other results obtained from other quality of life studies in other dermatologic conditions were Finlay and Khan (mean 7.3)89,

0zturkan et al103 (mean 7.61), Yazici et al104 (mean 5.80), Aghaei et al105 (Vitiligo; mean 7.05), Hahn et al 106 (Mean 5.80), Al-abadie et al107 (mean 4.82). These differences in scores can be attributed to the fact that the samples covered various diseases with different levels of severity.

6.4 Comparison of Different Diagnoses of Alopecia

Cosmetic disfigurements have been reported to have a major impact on the Q0L of patients many of whom feel stigmatized by their conditions102, 103,108.

Alopecia is quite a visible condition unlike some other dermatologic conditions which can be covered by clothing. The effect on the QOL has been shown in the overall index (DLQI) score of patients.

The highest DLQI score in this study were obtained for keloid folliculitis, alopecia areata, chronic cutaneous lupus erythematosus and lichen planopilaris. These conditions are associated with significant cosmetic disfigurement.

Male pattern baldness was one of the causes of alopecia which had the least scores. In trying to allude reasons for this an oral interview was conducted for some of the respondents. It was quite interesting to note that they felt male pattern baldness was a

‘normal’ process of growing old and nothing to be bothered about, however they were seeking treatment for it because they had access to a dermatologist. This reason may also be responsible for the low number of patients who presented with this condition.

In a study carried out by Lee et al109 in Korea, baldness was observed to have significant negative psychosocial effects, with balding men perceived as being older, less attractive, duller, less

confident and less potent. This opinion was held by the balding men themselves, others who were non-bald, and women.

6.5 Impact on quality of life

The overall score of the DLQI ranged from 0-30 with a mean score of

7.3 ±7.16. Patients in this study had varying degrees of impairment in their quality of life ranging from a small impairment to a moderate, very large and extremely large impairment.

6.5.1 Symptoms & Feeling

Questions 1and 2 of the DLQI which makes up the symptoms and feelings domain were found to have the highest scores in both males and females. This domain includes worry about thoughts and reactions of others to their hairloss. This finding is consistent with the result obtained in Ozturkcan’s 103 and Hahn’s106 studies.

The female patients were more affected in this domain than the male patients. This is similar to observations made by Jobanputra et al81.

Younger persons had more impairment in this subscale this finding was also reported by another study93. This was also true for divorced patients.

Patients with extremely severe alopecia were also mostly affected in this domain.

6.5.2 Daily activities

This study showed that a number of patients reported a reduction in their daily activities as evidenced by their scores in this subscale, though not as high as for the symptoms and feelings domain. Items in this subscale included going out of the house, choosing and buying clothes, going to the market and looking after homes and/or gardens.

This finding is similar to that observed by Al-mazeedi et al110.

Females also had more impairment in this domain than males.

6.5.3 Leisure

Some patients recorded some impairment in this domain suggesting a reduction in their leisure activities. These included sporting activities and making friends and meeting people. This observation was also made by Al- Mazeedi et al110.

6.5.4 Work and school

Very few patients in this study reported that their alopecia affected their work and schooling by preventing them from going to work and school or by being a problem at work or school.

Similar findings were reported by Al-Mazeedi et al110 and Ramsay and O Reagan 111.

6.5.5 Personal Relationships

Patients in this study had significant affectation of their Q0L in this domain. Items here included feelings of lack of understanding from others and sexual relations.

In the course of consultations with the patients, especially those who had experienced some impairment in their life quality, it was quite apparent from their narratives that they had gone through quite a lot on account of their hairloss. Some had been abandoned by prospective suitors and one patient in particular, even though her wedding was about two weeks away was yet to let her partner know that she had scarring alopecia from CCLE. This was because she was so sure he would abandon her as others had done previously.

The impact of hair loss on the patients was minimal in the area of their sexual activities. This is unlike what was observed in patients with psoriasis, who were found to have significant sexual difficulties 110,112.

6.5.6 Treatment

Most of the patients in this study did not find the treatment of their hair loss to be inconveniencing by making their homes messy or by taking up too much of their time. However, on oral interview quite a number of them complained that the cost of procuring their medications was too expensive for them.

C. INFLUENCE OF DEMOGRAPHIC AND CLINICAL CHARACTERISTICS

ON DLQI SCORES.

6.6 The relationship between clinical, socio- demographic factors and DLQL scores

The results of most Health Related Quality 0f Life studies 81,103 show that Q0L scores are worse in females than in males. This was corroborated by this study in which females were found to have a higher mean DLQI score than the males.

Some studies81, 93,110 have shown that the effect on the QOL increases with increasing severity of disease. This was also confirmed by a study 113 on effect of severe psoriasis on the quality of life. This study however, did not show the same trend of worsening DLQI scores with increasing severity of alopecia.

In view of all the above, authors have advocated a multidisciplinary approach in the management of dermatology patients81,110,114. This would involve the participation of psychiatrists and psychologists.

An early psychological evaluation of patients at risk will allow for early interventions and promote positive treatment outcomes and patient compliance with treatment112.

This study has shown that due to the visible aspects of skin lesions, especially alopecia and their potentially high psychological impact, the evaluation of quality of life in these conditions is a very useful complement to clinical practice and it provides an opportunity to fully optimize patient management and make it all encompassing.

6.7 LIMITATIONS OF THE STUDY

The study was carried out in the LUTH skin clinic thus making it a hospital based study which is not a fully accurate representation of what obtains in the larger society. Also, the study has not exhaustively investigated all the psycho-social factors which influence the impact of hair loss in our society because time required for such an inclusive

survey. However this study provides a platform for which other studies involving larger populations would be carried out.

CHAPTER SEVEN CONCLUSION AND RECOMMENDATIONS

CONCLUSION

This prospective, observational study with a case control design sought to determine the pattern of alopecia and the effect of alopecia on the quality of life of patients as compared to an age and sex matched control group of persons with no dermatologic or chronic medical conditions.

The study showed that:

1. Keloid folliculitis was the most frequent cause of alopecia

amongst male patients and CCLE was most frequent

amongst female patients.

2. Measurement of quality of life revealed that majority of

patients with Alopecia have a reduction of life quality.

3. Female patients had more impairment of their quality of life

than the male patients.

4. Increasing clinical severity of alopecia has no significant

impact on quality of life. Thus the presence of alopecia, no

matter the degree, negatively impacts the quality of life of

affected patients.

5. Disorders with the most significant disfigurement had the

highest scores and thus greater impairment of life quality in

affected individuals.

6. Awareness should be created amongst dermatologists on the

importance of Quality of Life in both clinical practice and

research.

7. More research is required to assess the perception of the

general population and affected individuals about male

pattern baldness.

8. More research is also required to assess the prevalence of

CCLE in Nigeria today with a view to evaluating possible

aetiologic aspects of the disease and other associated

factors.

RECOMMENDATIONS 1. Dermatologists should apply quality of life measurements in the

management of their patients, to help them assess and monitor

their progress and also objectively evaluate the overall impact of

treatments.

2. Dermatologists should bear in mind that their patients may

have underlying psychological disorders which may require

referral to a psychiatrist or psychologist.

3. Dermatologists should avail themselves of information and

receive training on psychopathology to enable them select

the optimal treatment approach to patients based on

improved knowledge of the relationship between

psychological problems and skin disease.

4. Further research is required to construct and validate

Nigerian questionnaires that would measure quality of life

for all the major dermatological disorders.

5. Therapies in the management of patients should be safe,

cheap, effective, rapid, acceptable and above all should

clearly demonstrate a positive influence on their quality of

life.

6. Quality of life measurements should be used to provide a

comparison with high profile systemic diseases in the

allocation of resources in medical specialties.

Demands on dermatologic services continue to increase and

in fact some authorities have argued that skin failure

should be rated with the failure of other organs as being

equally worthy of high quality care.

7. There should be increased collaboration between

dermatologists and psychiatrists in Nigeria. This

collaboration would need to take into cognizance though,

the varied socio-cultural characteristics of our environment.

8. Though the reforms in the Nigerian health sector are

laudable, more effort should be made to ensure that health

care services are both affordable and accessible to the

generality of the Nigerian populace.

REFERENCES

1. © 1993-2003. Microsoft Corporation. All rights reserved.

2. Houlberg M. ‘Social hair’: Yoruba hairstyles in South Western

Nigeria. In: The Anthropology of Clothing and Adornment.

Cordel JM and Schwarze RA editors. The Hague Mouton

Publishers.1979; P. 349-397.

3. Olumide YM; A pictorial self instructional manual on

common skin diseases. Ibadan, Nigeria, Heinemann, 1990.

4. Loussouarn G, Garcel A, Lozano I et al. Worldwide diversity of

hair curliness: a new method of assessment. Int J Dermatol

2007; 46(suppl 1):2-6

5. Olsen EA. Disorders of epidermal appendages and related

disorders. In: FitzPatrick’s Dermatology in General Medicine.

Freedberg I. M, Eisen A. Z, Wolf K, Auten KF, Goldsmith, Katz S.

I. McGraw-Hill 2003. PP 633-650.

6. Weidemeyer K, Schill W, Loser C. Diseases on hair follicles

leading to hair loss part 1: Non scarring Alopecias. Skin Med

2004; 3 (suppl 4): 209-214.

7. Hermes B, Pans R. Scar Forming alopecia. Comments on

classification, differential diagnosis and Pathobiology (in

German). Hautartz. 1998; 49: 462-472.

8. Randle V A, Ebling FJE: Seasonal changes in human hair

growth. Br J Dermatol 1991; 124:146.

9. Dawber RPR, Comaish S. Scarring electron microscopy of

normal and abnormal hair shafts. Arch Dermatol 1970;

101:316.

10. Whiting DA. Hair shaft defects, In: Disorders of hair growth:

Diagnosis and treatment, edited by E. A. Olsen. New York.

McGraw-Hill 2003.

11. Sinclair RD. et al. Handbook of Diseases of the Hair and scalp.

Oxford, Blackwell science, 1999; 161.

12. Ho M. et al. Pathogenesis in trichorrhexis invaginata (bamboo

hair). J. Invest Dermatol 83: 1:1981.

13. Gilchrist TC. A case of monilethrix with an unusual

distribution J. Cutan Genito-urinary Dis 16:151, 1998.

14. Korge BP et al. Identification of novel mutations in basic hair

keratins hHbl and hHb6 in monilethrix: implication for protein

structure and clinical phenotype. J. Invest. Dermatol 1999;

113:607.

15. Birch – Machin MA et al. Mapping of monilethrix to the type II

keratin gene cluster at chromosome 12q13 in three new

families, including one with variable expressivity Br J

Dermatol 1997; 137:39.

16. Mallon ME et al. Cheveux incoiffables – Diagnostic, Clinical and

hair microscopic findings and pathogenic studies. Br. J.

Dermatol 1994; 131:608.

17. Shelley WB, Shelley ED. Uncombable hair syndrome:

observation on response to biotin and occurrence in siblings

with ectodermal dysplasia. J. Am Acad Dermatol 1985; 13:97.

18. Solomon LM et al. Hereditary trichodysplasia. Maria Unna’s

hypotrichosis. J Invest Dermatol 1971; 57:389.

19. Cichon S et al. A distinct gene close to the hairless locus on

chromosome 8p underlies Maria Unna type hypotrichosis in a

German family. Br J. Dermatol 2000; 143:811.

20. Price VH. Structural anomalies of the hair shaft. In hair and

hair diseases, edited by CE. Orfanos, R. Happle, Berling,

Springer-Verlag, 1990, p363.

21. Price VH et al. Pseudopili annulati: An unusual variant of

normal hair. Arch Dermatol 1970; 102: 354.

22. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol

2002; 27:389-395.

23. Tosti A, Peluso AM, Misciali C, et al. Loose anagen hair. Arch

Dermatol 1997; 133: 1089-1093.

24. Chapalain V, Winter G, Langbein L. et al. Is the loose anagen

hair syndrome a keratin disorder? A clinical and molecular

study. Arch Dermatol 2002; 138: 501-506.

25. Safavi KH, Muller SA, Suman VJ et al. Incidence of alopecia

areata in Olmsted County, Minnesota, 1975 through 1989. Mayo

clinic Proc 1995; 70: 628-633.

26. Olsen EA et al. Alopecia areata investigational assessment

guidelines. J Am Acad Dermatol 1999; 40: 242.

27. Muller SA, Winkelman RK: Alopecia areata. An evaluation of

736 patients. Arch Dermatol 1963; 88: 290.

28. Paus R et al. Is alopecia areata an autoimmune response

against melanogenesis-related proteins exposed by abnormal

MHC class 1 expression in the anagen hair bulb? Yale J Biol

Med 1994; 66: 541.

29. Hordinsky MK: Alopecia areata. In disorders of Hair growth:

Diagnosis and treatment, edited by E. A Olsen. New York,

McGraw-Hill, 2003.

30. McElwee KJ, Tobin DJ, Bystryn JC, et al. Alopecia areata: an

autoimmune disease? Exp Dermatol 1999; 8:371-379.

31. McDonagh AJ, Tazi – Ahnini R. Epidemiology and genetics of

alopecia areata. Clin Exp Dermatol 2002; 27:405-409.

32. Olsen EA. Hair loss in childhood; in Disorders of Hair Growth:

Diagnosis and Treatment, edited by EA Olsen, New York,

McGraw-Hill, 2003.

33. Trakimas C. et al. Clinical and histologic findings in temporal

triangular alopecia. J Am Acad Dermatol 1994; 31:205.

34. Olsen EA: Pattern hair loss; In disorders of hair: Diagnosis and

treatment, edited by EA Olsen New York, McGraw-Hill, 2003.

35. Kaufman KD. Androgenic metabolism as it affects hair growth

in androgenetic alopecia. Dermatol Clin 1996; 14: 697.

36. Olsen EA. Female pattern hair loss. J. Am Acad Dermatol 2001;

45: 570.

37. Jamin C. Androgenetic alopecia (in French). Ann Dermatol

Venereol 2002; 27:373-382.

38. Thiedke CC. Alopecia in women. Am Fam Physician 2003;

67:1007-1014.

39. Kaufman KD. Androgens and Alopecia. Mol Cell Endrocrinol

2002; 198:89-95.

40. Carmina E, Labo RA. Treatment of hyperandrogenic alopecia in

women. Fertil Steril 2003; 79:91-93.

41. Mallari R, Sinclair RD. Shortness of breath: an uncommon side

effect of cyproterone acetate in the treatment of androgenetic

alopecia. Int J Dermatol 2002; 41:946-947.

42. Lam SM, Hempstead BR, Williams BF. A Philosophy and

strategy for surgical hair restoration: a 10-year experience.

Dermatol Surg 2002; 28:1035-1042.

43. Rothbaum BO, Ninan PT. The assessment of trichotillomania.

Behav Res Ther 1994; 32: 651.

44. Stein DJ et al. Trichotillomania and obsessive – compulsive

disorder. J Clin Psychiatry 1995; 56: 28.

45. Miller SA. Trichotillomania. A histopathologic study in sixty

six patients. J Am Acad Dermatol 1990; 23:56.

46. Mehregan AH. Trichotillomania: A clinicopathologic study.

Arch Dermatol 1970; 102:129.

47. Detwiler SP et al. Bubble hair: A case seen by over heating hair

dryer and reproducibility in normal hair with heat. J Am Acad

Dermatol 1994; 30:54.

48. Reda AM et al. Wooly hair nevus. J Am Acad Dermatol 1990;

22:377.

49. Esterly NB et al. Acquired progressive kinking of the hair. Arch

Dermatol 1989; 125: 813.

50. Cuozzo DM et al: Essential syphilitic alopecia revisited. J Am

Acad Dermatol 1995; 32: 840.

51. Jordan HF, Louw M. The moth-eaten alopecia of secondary

syphilis. Am J Dermatopathol 1995; 17: 158.

52. Bettencourt MLS, Olsen EA: Pityriasis amiantacea: A report of

two cases in adults. Cutis 1999; 64: 187.

53. Stenn K. et al. Hair follicle biology, the sebaceousgland and

scarring Alopecias. Arch Dermatol 135: 973.

54. Whiting DA: Cicatricial alopecia. A review of clinicopathologic

findings and treatment and a clinicopathological examination

of 358 cases using horizontal and vertical sections of scalp

biopsies. Clin Dermatol 2001; 19:211.

55. Templeton SF, Solomon AR: Scarring alopecia: A classification

based on microscopic criteria. J cutan pathol 1994; 21: 97.

56. Housman TS, Jorizzo JZ, McCarty MA et al. Low dose

thalidomide therapy for refractory cutaneous lesions of lupus

erythematous. Arch Dermatol. 2003; 139: 50-54.

57. Silvers DN, Katz BE, Young AM. Pseudopelade of Brocq is

lichen planopilaris: report of four cases that supports this

nosology. Cutis 1993; 51: 99-105.

58. Carmina E, Lobo RA. Treatment of hyper-androgenic alopecia

in women. Fertil Steril 2003; 79:91-95.

59. Bergfeld WF, Elston DM. Primary cicatricial alopecia (and other

causes of permanent alopecia) in Disorders of Hair Growth:

Diagnosis and Treatment, edited by EA Olsen. New York

McGraw-Hill, 2003.

60. Powell J, Dawber RP. Successful treatment regime for

folliculitis decalvans despite uncertainty of all aetiological

factors. Br J Dermatol 2001; 144: 428-429.

61. Brooke RC, Griffiths CE. Folliculitis decalvans. Clin Exp

Dermatol 2001; 26:120-122.

62. Sperling LC, Mezebish DS. . Med. Clin North Am.

1998; 82: 1155-1169.

63. Nnoruka EN. Hair loss: Is there a relationship with hair care

practices in Nigeria? Int J Dermatol Oct 2005; 44 (1): 13-7.

64. Ogunbiyi AO, Daramola OO, Alese OO. Prevalence of skin

diseases in Ibadan, Nigeria. Int J Dermatol Jan 2004; 43 (1):

31-36.

65. Nnoruka EN. Skin diseases in South East Nigeria: a current

perspective. Int J Dermatol Jan 2005; 44 (1): 29-33.

66. Traore A, Samadogo S, Bano F, Niamba P. Alopecia in

Consultations in the Dermatology Department at Burkina Faso:

Epidemiologic, Clinical and Etiologic Aspects. Int J Dermatol

2007; 46 (Suppl.1): 30-31.

67. McElwee KJ. Types of Hair loss. American Hair loss

Association. 2005.

68. Bergfeld WF, Mulinari-Brenner F. Hair disorders. The Cleveland

Clinic, Dec. 2003.

69. Fallowfield L. The quality of life: the missing measurement in

Health care. Human Horizon Series 1990 (Souvenir Press Ltd).

70. Halioua B, Beumont MG, Lunel F. Qualiy of life in

Dermatology. Int J Dermatol 2000; 39:801-806.

71. Picardi A, Abeni D. Stressful life events and skin diseases:

disentangling evidence from myth. Psychother psychosom

2001; 70:118-36.

72. Finlay AY. Quality of life assessments in dermatology. Semin

cutan Med Surg 1998; 17:291-6.

73. Sprangers MA, de Regt EB, Andries F, van Agt HM, Bijl RV, de

Boer JB, Foets M, Hoeymans N, Jacobs AE, Kempen GI, Miedema

HS, Tijhuis MA, de Haes HC. Which chronic conditions are

associated with better or poorer quality of life? J Clin

Epidemiol 2000; 53: 895-907.

74. Gupta MA, Gupta AK. Depression and suicidal ideation in

dermatology patients with acne, alopecia areata ,atopic

dermatitis and psoriasis. Br J Dermatol 1998; 139-846-850.

75. Van der Meeren HL, Van der Schaar MM, Van der Hurk CM. The

psychological impact of severe acne. Cutis 1985; 36: 84-6.

76. Wolf N. The beauty myth. New York Anchor/Double day, 1991.

77. Egele UT, Tauschke E. die alopezie: ein psychosomatisches

krankheitsbild. Psych Psychosom Med. Psych 1987; 37:31-5.

78. Nardi A. E. Social anxiety disorder has social and economic

burden. BMJ 2003; 327:1287.

79. Koblenzer C. S. Liaison dermatology. Int J Dermatol 1986; 6(25):28-

30.

80. Bamgboye E. A., Jegede R. O. Retrospective study of the pattern of

utilization of health services in a Nigeria University Hospital. African

Journal of Medical Science 1987; 16:27-32.

81. Jobanputra R, Bachmann M. The effect of skin diseases on

quality of life in patients from different social and ethnic

groups in Cape Town, South Africa. Int J Dermatol 2000; 39:

836-831.

82. Smith PG, Morrow RH. Methods for field Trials of Interventions

against tropical diseases. Oxford University Press. 1992; 49-51.

83. Alabi G. O. Trends in the pattern of skin diseases in Nigeria.

Nig Med J 1980; 10: 163-8.

84. Onayemi O, Isezuo SA, Njoku CH. Prevalence of different skin

conditions in an outpatients setting in North-western Nigeria.

Int J Dermatol Jan 2005; 44 (1): 7-11.

85. Fischer TM, Schmidts, Elsner P. S7 Hairdex – A tool for

evaluation of life quality in hair patients. European Hair resh

Soc. J Eur Acad Dermatol Venereol 15 (2): pp. 137-139.

86. Williamson D, Gonzalez M, Finlay AY. Quality of Life in

patients with hair loss. Brit J Dermatol 1997; 136:305-314.

87. Finlay AY, Khan GK. Dermatology Life Quality Index (DLQI) a

simple practical measure for routine clinical use. Clin Exp

Dermatol 1994; 19: 210-216.

88. Shikiar R, Bresnahan BW, Stone SP, Thompson C, Koo J,

Revicki DA. Validity and reliability of patient reported

outcomes used in psoriasis: results from two randomized

clinical trials. Health Qual Life Outcomes 2003; 1:53.

89. Badia X, Mascaro JM, Lozano R. Measuring health-related

quality of life in patients with mild to moderate eczema and

psoriasis: Clinical validity, reliability and sensitivity to change

of the DLQI. Brit J dermatol 1999; 141:698 -702.

90. Zachariae R, Zachariae C, Ibsen H et al. Dermatology Life

Quality Index: Data from Danish in-patients and out-patients.

Acta Derm Venereol 2000; 80:272-276.

91. Hachem JP, DePaepe K, Sterckx G et al. Evaluation of key

biographical and clinical parameters of skin barrier function

among hospital workers. Contact Dermatitis 2002: 46; 220-

223.

92. Kane A, Ndiage D, Niang SO et al. Tinea in Senegal: an

epidemiologic study. Int J Dermatol 2005; 44 (Suppl. I); 24-25.

93. Tan E, Tay Y, Goh C and Giam YC. The Pattern and Profile of

Alopecia Areata in Singapore – a Study of 219 Asians. Int J

Dermatol 2002; 41:748-753.

94. Ngwanya MR. Primary Cicatricial Alopecia. Int J Dermatol

2005; 44 (Suppl. 1): 18-21.

95. Sharma VK, Daun G, Kumar B. Profile of Alopecia Areata in

Northern India. Int J Dermatol 1996; 35:22-27.

96. Snellow WVR, Edwards JE, a questionnaire analysis of patients

and family. Int J Dermatol 1992; 31:186-189.

97. Sharma VK, Kumar B, Daun G.A Clinical Study of Childhood

Alopecia Areata in Chandigarh. Indian Pediatr Dermatol 1996;

13:372-377.

98. Cunliffe MJ, Hall R, Stevenson CJ, Weightman D. Alopecia

Areata, Thyroid Diseases and Autoimmunity. Br J Dermatol

1969; 81:877-881.

99. Olsen EA, BergFeld M, Cotsarelis G et al Summary of the North

American Hair Research Society (NAHRS) Sponsored Workshop

on Cicatrical Alopecia, Duke University Medical Centre,

February 10, 11, 2001. J AM Head Dermatol 2003; 18:103-110.

100. Niang S, Kane A, Dieng MT et al. Alopecia in Senegalese

Women. Int J Dermatol 2005; 44 (Suppl.1): 22-23.

101. Finlay AY. Quality of life measurement in dermatology: a

practical guide. Br J Dermatol 1997; 136: 305-314.

102. Jayaprakasam A, Darrey A, Osborne G, et al. Comparison of

assessments of severity and quality of life in cutaneous

disease. Clin Exp Dermatol 2002; 27:306-308.

103. Ozturkan S, Ermertcan AT, Eser E, Sahin ST. Cross validation

of the Turkish version of dermatology life quality index.

Int J Dermatol 2006; 45:1300-1307.

104. Yazici K, Baz k, Yazici AE, et all. Disease-specific quality of

life is associated with anxiety and depression in patients

with acne. J Eur Acad Dermatol Venereol 2004;18:435-439.

105. Aghaei S, Sodaifi M, Jafari P et al. DLQI scores in vitiligo:

reliability and validity of the Persian version. BMC Dermatol

2004; 4:8

106. Hahn HB, Melfi CA, Chuang TS, et al. Use of the Dermatology

life Quality index (DLQI) In a mid western US urban clinic. J

Am Acad Dermatol 2001; 45:44-48.

107. Kent G, Al-Abadie MSK. Factors affecting responses on

Dermatology life Quality index among Vitiligo sufferers. Clin

Exp Dermatol 1996;21:330-333.

108. Morgan M, McCreedy R, Simpson J et al. Dermatology

quality of life scales: a measurement of the impact of

skin diseases. Br J Dermatol 2003; 148:373-374.

109. Lee H, Ha S, Kim D, Kim J. Perception of men with

androgenetic alopecia by women and non balding men in

Korea: how the non bald regard the bald.

110. Al-Mazeed; K, El-shazly M, Al-Ajmi HS. Impact of psoriasis

on quality of life in Kuwait. Int J Dermatol 2006; 45:418-424.

111. Ramsay B, O‘Reagan MA. Survey of the social and

psychological effects of psoriasis. Br J Dermatol 1988;

118: 195-201.

112. Gupta MA, Gupta AK, Psoriasis and sex: a study of

moderately to severely affected patients. Int J Dermatol

1997; 36:259-262.

113. Finlay AY, Coles EC. The effect of severe psoriasis on the

quality of life in 369 patients. Br J Dermatol 1995; 132-244.

114. Weiss SC, Bergstrom KG, Weiss SA, et al. Quality of life

considerations in psoriasis treatment. Dermatol Nurs 2003;

15:120, 123-127.

APPENDIX I

QUESTIONNAIRE

The information obtained in this questionnaire shall be treated as strictly confidential

HOSPITAL NO:

INITIALS: DLQI Score

DIAGNOSIS:

SEX: M F

AGE (Yrs)

RELIGION: Christianity Islam Others

LEVEL OF EDUCATION: None 10 20 30

OCCUPATION: Employed Unemployed Student Retired

MARITAL STATUS: Single Married Divorced

Widowed

HOW OLD WERE YOU WHEN THE HAIR LOSS STARTED?

HOW MANY EPISODES OF HAIR LOSS HAVE YOU HAD?

1st 2nd 3rd >4th

ASSOCIATED SYMPTOMS

FAMILY HISTORY OF HAIR LOSS: Yes No

MEDICAL HISTORY Yes No

PROLONGED FEVER:

THYROID DISEASE:

VITILIGO:

PREGNANCY: OTHERS: Describe______

DRUGS OR SUBSTANCES USED JUST BEFORE HAIR LOSS STARTED______

______

DERMATOLOGY LIFE QUALITY INDEX The aim of this section is to measure how much your skin problem has affected your life OVER THE LAST WEEK. Please tick one box for each question.

1 Over the last week, how itchy, sore, painful or Very much stinging has your skin been? A lot

A little

Not at all

Very much 2. Over the last week, how embarrassed or self conscious have you been because of your skin? A lot

A little

Not at all

Very much 3. Over the last week, how much has your skin interfered with you going shopping or looking A lot after your home or garden? A little

Not at all Not relevant

Very much 4. Over the last week, how much has your skin influenced the clothes you wear? A lot

A little

Not at all Not relevant

Very much 5. Over the last week, how much has your skin affected any social or leisure activities? A lot

A little

Not at all Not relevant

Very much 6. Over the last week, how much has your skin made it difficult for you to do any sport? A lot

A little

Not at all

Not relevant

7 Over the last week, has your skin prevented you from working or studying?

Yes

No

A lot If “No” over the last week how much has your skin been a problem at work or studying? A little

Not at all

Very much 8. Over the last week, how much has your skin created problems with your partner or any of A lot your close friends or relatives A little

Not at all Not relevant

Very much 9. Over the last week, how much has your skin caused any sexual difficulties? A lot

A little

Not at all Not relevant

Very much 10. Over the last week, how much of a problem has the treatment for your skin been, for A lot example by making your home messy, or by taking up time?

A little

Not at all Not relevant

Please check you have answered EVERY question. Thank you.

©AY Finlay, GK Khan, April 1992.

[YORUBA TRANSLATION] OSUWON BI AILERA AWO ARA SE FA IDIWO SI IGBE AYE ALAFIA.

Idi ti a fi gbe iwe ibeere yi jade ni lati mo bi kokoro ti o yo si ara re ti se idiwo fun o lati bi ose kan sehin.

Jowo ko ami maaki yi  sinu apoti ti o wa niwaju ibeere kookan.

1 Lati bi ose kan seyin, bawo ni awo ara re se O yun mi yun o, da egbo, dun o, tabi ta o si? gidigan Pupo

Die Ko yun mi rara

Gidigan 2. Lati bi ose kan seyin, nje o nse akiyesi ara re Pupo nigba gbogbo tabi oju nti o nitori bi ara re se ri? Die rara

Gidigan 3. Lati bi ose kan seyin, nje bi ara re ti ri se idiwo fun o lati lo si oja, se itoju ile tabi ogba Pupo re? Die

Rara Ko ni nkankan se pelu re.

Gidigan 4. Lati bi ose kan seyin, nje bi ara re ti ri je ki o Pupo kiyesi iru aso ti iwo yi o wo?

Die

Rara Ko ni nkankan se pelu re.

Gidigan 5. Lati bi ose kan seyin, nje bi ara re ti ri se Pupo idiwo fun o lati jade lo si ipejo po awon

eniyan ati lati sin mi. Die

Rara Ko ni nkankan se pelu re.

6. Lati bi ose kan seyin, nje bi ara re ti ri je ki o Gidigan nira fun o lati se ere idaraya? Pupo

Die Rara

Ko ni nkankan

se pelu re.

7. Lati bi ose kan seyin, nje bi ara re ti ri se idiwo fun o lati si se tabi fun eko re? Beni

Beko

Ti idahun re ba je bee ko, bawo ni ara re se di Pupo ise tabi eko re lowo? Die Rara

Gidigan 8. Lati bi ose kan seyin, bawo ni bi awo ara re se Pupo ri se fa wahala laarin iwo ati oko tabi aya

re, awon ebi re tabi awon ore timo timo re? Die

Rara

Ko ni nkankan se pelu re.

Gidigan 9. Lati bi ose kan seyin, nje bi awo re ti ri se idiwo fun o nipa ibalopo? Pupo

Die

Rara Ko ni nkankan se pelu re.

Gidigan 10. Lati bi ose kan seyin, nje awo ara yi fun o ni Pupo iyonu fun apeere gba asiko re, d’oti ile re ati

na o lowo repete. Die

Rara

Ko ni nkankan se pelu re.

Jowo ri daju pe o dahun gbogbo ibeere won yi. E se.

©AY Finlay, GK Khan, April 1992.

EVERYDAY SPOKEN ‘NIGERIAN’ ENGLISH The purpose of this questionnaire is to know how much your skin problem has affected your life OVER THE LAST ONE WEEK. Please tick one box for each question.

Very much

1 Over the last week, how much has your skin A lot been itching you, paining you, stinging or biting you? A little

Not at all

Very much

2. Over the last week, how self conscious or A lot ashamed have you been because of the way your skin is? A little

Not at all

Very much

3. Over the last week, how much has your skin A lot problem affected your going to the market or

taking care of your house or compound? A little

Not at all

Does not apply

Very much

4. Over the last week, how much has your skin A lot problem determined the type of clothes you

wear? A little

Not at all

Does not apply

Very much

5. Over the last week, how much has your skin A lot problem affected your social outings and

activities? A little

Not at all Does not apply

Very much

6. Over the last week, how much has your skin A lot problem made it difficult for you to play any

sport? A little

Not at all

Does not apply

Yes 7 Over the last week, has your skin problem

prevented you from doing your job or school work? No

A lot

If your answer is “No”, over the last week how A little much has your skin problem hindered your job or school work? Not at all

Very much

8. Over the last week, how much has your skin A lot caused problems between you and your spouse

or boyfriend/girlfriend, or any of your relations or A little close friends? Not at all

Does not apply

Very much

9. Over the last week, how much has your skin A lot problem affected your `having fun’/`sleeping with’

your spouse/boyfriend/girlfriend? A little

Not at all

Does not apply

Very much

10. Over the last week, how much has the treatment A lot for your skin inconvenienced you, for example

by making your house messy, or by taking your A little time? Not at all

Does not apply

Please check you have answered EVERY question. Thank you.

©AY Finlay, GK Khan, April 1992.

WHEN DID YOU START GETTING BOTHERED ABOUT YOUR HAIR

LOSS? ______

WHERE DID YOU FIRST SEEK TREATMENT WHEN YOU NOTICED YOUR HAIR LOSS?

Orthodox

Dermatologist General Practitioner

Non-orthodox

Chemist church Tradomedical

PHYSICAL EXAMINATION

TO BE COMPLETED BY THE DOCTOR

AREAS OF INVOLVEMENT: Scalp

Brows Eyelashes Pubic hair Axilla

PATTERN OF SCALP INVOLVEMENT: Diffuse Patchy Ophiasis

% AREA OF SCALP INVOLVED:

0-10% 11-20% 21-30%

31-40% >40% 100%

HAIR SHAFT ABNORMALITY: Yes No

Describe______

______

SCALP, LESIONS: Yes No

Describe______

______

NAIL INVOLVEMENT: Yes No

Describe______

OTHER SKIN FINDINGS: Yes No

Describe______

______

INVESTIGATIONS

Skin scraping for mycology______

Skin biopsy______

Complete blood count______

______

Thyroid function tests ______

______

VDRL______

______

Bacteriology______

Others______

xiv