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Home , Alopecia areata, Alopecia totalis, Folliculitis, Folliculitis decalvans, Hair loss, Loose anagen syndrome

CPD Article

An approach to the diagnosis and management of patchy, non-scarring loss

Jordaan HF, MBChB, MMed(Derm) Professor, Department of , Faculty of Health Sciences University of Stellenbosch and Tygerberg Hospital

Correspondence to: Prof Francois Jordaan, e-mail: [email protected]

Abstract

This article presents a clinical approach to patchy, non-scarring and includes conditions like , trichotil- lomania, of the , syphilitic alopecia and traction . SA Fam Pract 2007;49(7): 26-29

Introduction Table II: Non- versus scarring hair loss Shedding of hair is termed effluvium or Non-scarring hair loss Scarring hair loss defluvium, and the resulting condition is Incidence common less common called alopecia (Greek: alópekia, [bald- /scaling/ -/+ + ness]). The normal scalp is adorned with pustulation approximately 100 000 . More than Atrophy - + 90% are in the growing phase (anagen). Loss of follicular - + Up to 100 hairs may normally be shed openings per day. Individuals are often aware of Tufted hair* - + and very concerned about subtle thin- Course regrowth is quite common no regrowth ning of their hair. Patients presenting Prognosis generally favourable generally unfavourable with hair loss are commonly encoun- * Tufted hair - more than one hair shaft emerge from a single follicular opening as a result of tered in clinical practice. The causes of abnormal follicular dynamics related to fibrosis. hair loss are outlined in Table I. Table I: Causes of hair loss Differences between scarring and non- persons may experience “going grey scarring hair loss are summarised in overnight”. Alopecia occurs in round or Scarring hair loss Table II. oval areas without any visible inflamma- Primary Five conditions frequently encoun- tion of the (Figure 1). associated • tered in clinics and presenting with There may be one, or several, discrete • erythematosus patchy, non-scarring hair loss, are alo- or confluent patches. Follicular open- • pecia areata, , dermato- ings are present. No atrophy or - • Follicular mucinosis associated phyte infection of the scalp, secondary ring occurs. The most common present- • , and traction folliculitis/alopecia. ing area is the scalp, but the , • Diffecting folliculitis , and may • Folliculitis keloidalis nuchae Secondary Alopecia areata also be involved. Alopecia areata tota- • Trauma Alopecia areata (AA) is an autoimmune lis (AAT) refers to total absence of ter- • Radiotherapy caused by interaction of T-lym- minal scalp hair (Figure 2) and alope- • Some dermatophyte • Primary neoplasia phocytes and follicular epithelium result- cia areata universalis (AAU) to total loss • Secondary neoplasia (metastasis) ing in progressive shrinkage of follicles of terminal body and scalp hair. Ophia- Non-scarring hair loss and loss of hair. In case of fulminant AA, sis is characterised by a bandlike pat- On an abnormal scalp • Figure 1: Alopecia areata. The scalp ap- Figure 2: . hair is • Seborrhoeic pears normal. (Figure courtesy of also sparse. (Figure courtesy of • Some dermatophyte infections Derm101.com) Derm101.com) • On a normal scalp Diffuse • Telogen hair loss • Anagen hair loss Patchy • Alopecia areata • Triangular alopecia • Trichotillomania • Secondary syphilis With a distinct pattern • Male pattern baldness • Female pattern baldness Other causes of hair loss • Hair shaft abnormalities • Congenital hypotrichosis •

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tern of hair loss over the periphery of the Table III: of trichotillotic hair loss and alopecia areata scalp. Hair loss usually develops grad- Alopecia areata Trichotillotic hair loss ually over weeks to months. Patches of Compulsive psychosomatic disorder AA can be stable and often show spon- Autoimmune disorder Females:males = 2:3 in children Mechanism Males = females, taneous regrowth over a period of sev- Females:males = 4:1 in adults Incidence Peak: second and fifth Children:adults = 7:1 peak two eral months; new patches may appear decades while others resolve. AA is asymptomat- to six years Sudden onset, no history of Insidious onset, history of hair pull- ic but individuals are usually very con- History cerned about the hair loss and possible hair pulling ing continued, progressive balding. Circumscribed, smooth, totally Ill-defined, uneven alopecia with Clinical fea- bald patch; residual exclama- broken hairs of different lengths: ex- Occasionally diagnostic, broken-off, tures tion hairs; loose marginal hairs clamation hairs and strong marginal stubbly hairs called exclamation point (in the active stage) hairs may be present hairs (distal ends are broader than Increased telogen hairs, lym- Increased catagen hairs; no inflam- phocytic infiltrate around ana- matory infiltrate; traumatised hair proximal ends) are present. With the Histopathology regrowth of hair, new hairs are fine, of- gen follicles; miniaturised folli- bulbs with haemorrhage; trichoma- cles; amelanotic hairs lacia (specific) ten white or grey. Microscopy of the skin pitting (dystrophic plate (irregularly eaten distal shows peribulbar , likened Nails changes) nail margins) to a “swarm of bees”, and miniaturisa- Psychological abnormality found tion of hair follicles. Underlying in 90%, with a triggering emotion- Obsessive-compulsive disorder The nails may show fine pitting (“ham- al common mered brass”) of the dorsal nail plate, Atopic and autoimmune Associations Atopic , anaemia mottled lunulae, trachyonychia (rough diseases nails) and onychomadesis (separation Good, except in certain groups of nail from matrix). Associated findings Prognosis (atopic, early onset, ophiatic and Fair in children, poor in adults include Hashimoto’s thyroiditis, , extensive forms) myasthenia gravis and Addison’s dis- Relapse rate 100% Recurrent in adults ease. Reassurance, , topical Reassurance, antidepressants, psy- Treatment immunotherapy chotherapy Differential diagnosis In the differential diagnosis, second- to wear a . Make-up applied to the Trichotillomania ary syphilis, grey-patch , eyebrows is helpful. Trichotillomania (TTM), first described trichotillomania, traction alopecia, early The first line of treatment is the appli- by Halopeau in 1889, is an obsessive- chronic cutaneous cation of a potent cream twice compulsive disorder, characterised and androgenetic alopecia should be daily for six weeks. If there is no im- by the irresistible urge to pull out hair. considered. The differences between provement, this treatment should be There is a sensation of relief after the trichotillomania and alopecia areata are terminated. Few and small spots of AA pulling episodes. The psychological outlined in Table III. can be treated with an intralesional ste- stimulus is satisfied by hair , roid. Tufted regrowth of hair common- but the resulting unsightly alopecia fuels Course ly results. the of the patient and results in a Spontaneous remission is common in Systemic glucocorticoids usually in- vicious cycle. patchy AA. Poor prognosis is associ- duce regrowth, but AA recurs on discon- Adult TTM is more frequently chronic ated with a number of factors (Table and is associated with more profound tinuation. The risks of long-term therapy IV). If AA occurs after , 80% of psychopathy. Adult TTM is more com- therefore rule out their use. Systemic cy- patients experience hair regrowth within mon in females (females:males 15:1). closporin induces regrowth, but AA re- a year. Recurrences of AA are, however, Childhood TTM is more common and curs when the drug is discontinued. Cy- frequent. also more common in females (females: closporin is costly and renal damage is males 4:1). TTM usually involves the Table IV: Factors indicative of poor prognosis troublesome. Induction of allergic con- tact dermatitis with nitrochlorobenzene, Figure 3: Trichotillomania. Hairs are thin • (bandlike pattern) dibutylester, or diphency- and of different lengths. (Figure • Alopecia areata totalis courtesy of Derm101.com) prone can be used successfully, but lo- • Alopecia areata universalis cal discomfort due to allergic contact • Onset < five years of age dermatitis, and the swelling of region- • Duration > five years of age al lymph nodes, poses a problem. Oral • PUVA (photochemotherapy) is variably Management effective, as high as 30%, and worth a No is currently available. Remis- trial in patients who are very distressed sion may be induced but the course is by the problem. The entire body must be not altered. Treatment for AA is gener- exposed since the therapy is believed to ally unsatisfactory. In many cases, the be a form of systemic immune suppres- most important factor in the manage- sion. PUVA treatment has many side ef- ment of the patient is psychological sup- fects, the most important being nausea, port from the dermatologist, family, and photosensitivity and the development of support groups. Individuals may prefer nonmelanoma skin .

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scalp, but sometimes the eyebrows or Figure 5: Dermatophyte infection of the imbiform pattern. Snail track ulcers are eyelashes are plucked. Manual domi- scalp. Multiple areas of hair loss commonly observed on the oral muco- nance is characteristic: left-sided with scarring. sa and flat, glistening condylomata lata develop in right-handed patients and are present at moist mucocutaneous vice versa. Lesions are ill-defined and junctions. Syphilitic alopecia is charac- the scalp surface is normal (Figure 3). terised by patches of hair loss on the The stubble of unevenly broken hairs is scalp. These patches show normal skin. highly characteristic. The residual stub- The pattern is typically described as ble hair has a normal colour and tex- moth-eaten (Figure 6). No particular pat- ture. Sometimes dystrophic “exclama- tern is observed. A clinical diagnosis of tion hairs” may also be found in TTM. secondary syphilis is confirmed by ap- The differences between AA and TTM propriate serological tests. A skin biop- are outlined in Table III. sy may be helpful. Treatment with peni- cillin is usually curative. Dermatophyte infection of the scalp Tinea capitis is most commonly caused diculosis should always be borne in Traction folliculitis/alopecia by Trichophyton violaceum of the spe- mind. Hair and scalp diseases induced by cies trichophyton. The infection is usu- The diagnosis of tinea capitis can of- traumatic hairstyling techniques, such ally spread from person to person. ten be established clinically, and can be as tightly drawn (Figure 7), are Infection by species of the genus mi- confirmed by microscopy of skin scrap- underappreciated. crosporum is less common. Microspo- ings or hair plucked from involved ar- rum infection is usually acquired from eas. Such samples can also be des- Figure 7: Traction alopecia. Traction follicu- litis is commonly associated. cats or dogs. patched for culture on Sabouraud’s The clinical presentation of this dermato- dextrose agar. A therapeutic trial of anti- phyte infection is variable, the common- fungal treatment remains an acceptable est being grey-patch tinea capitis. The alternative. number of lesions is variable. A single The treatment of choice is griseoful- may be present, but more com- vin 10 - 20 mg/kg per day, with a meal, monly one finds several lesions. Lesions for 6 to 8 weeks. Patients should be fol- show loss of hair and greyish, tightly lowed up to ensure adequate healing of packed, small scales (Figure 4). the infection. Regular use of a containing povidone-iodine decreases Figure 4: Dermatophyte infection of the the shedding of spores. scalp. Multiple areas of hair loss with scaling. Syphilitic alopecia (Secondary syphilis) A geometric pattern with the hair sec- Secondary syphilis, the stage of spiro- tioned into squares or bands is highly chaetemia, is characterised by constitu- characteristic. The hair in each square tional symptoms, variable organ involve- or band is pulled tightly to the centre ment, generalised lymphadeno-pathy, and then secured with a hair band. skin eruptions, mucosal lesions, muco- Maximum traction is produced round cutaneous lesions and hair loss. Skin the outer edges of the square or band eruptions include macular, papular, with less traction in the centre. The first papulosquamous, nodular and pustular variants. The skin is usually asymp- noticeable changes are faint erythema, tomatic and symmetrical. The palms some scaling and follicular mini pustules. and soles are commonly involved. In Subsequently, in the areas of maximum Yellow-patch tinea capitis is a relat- late stage secondary syphilis, lesions traction, follicle-based and pus- ed condition. Lesions are covered with often show an arciform, annular or cory- tules associated with alopecia become yellowish crusts caused by secondary evident. Hair loss and follicle-based Syphilitic alopecia. The scalp has . Tinea capitis may also be Figure 6: papules and pustules along the frontal a moth-eaten appearance, eye- scalp margin are common. The pustules -like and pustu- brow hair is absent and there is a are sterile. This form of hair loss is also lar. Black-dot tinea capitis is charac- rash on the cheek. common in persons wearing a terised by patches of alopecia studded or bangs. Other that can with black dots which represent broken- lead to traction folliculitis include hair off hair shafts packed with spores. Ab- twists worn by Sikh boys, chignons, hair scess-like lesions, e.g. kerion, and le- weaving and hair extensions. Traction sions displaying saucer-shaped scales folliculitis may be associated with hair (= scutulae) e.g. favus, are infrequent. casts. These casts encircle the hair Secondary pyoderma and cervical shaft, are yellowish white and are freely are often present. mobile. The units of pediculosis capi- Pyoderma may lead to scarring (Figure tis are firmly fastened and immobile. 5). When pyoderma of the scalp is ob- Continuous traction causes loosening served, tinea capitis, and pe- of the hair from the follicles resulting in

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i.e. folliculitis. If the traction continues, chronic inflammation ensues, which may lead to follicular atrophy with thinner, shorter hair. Initially the process is reversible, but follicular destruction, scarring and permanent hair loss may follow if traction persists. An associated posteriorposterior cervicalcervical lymphadenopathylymphadenopathy isis not uncommon.

See CPD Questionnaire, page 34

P This article has been peer reviewed

References 1. Shelleh HH, Khan SA, Al-Hatiti HS. Tricho- tillomania or alopecia areata? Int J Derma- tol 2006;45:1196-8. 2. Fox GN, Stausmire JM, Mehregan DR. Traction folliculitis: an underreported en- tity. Cutis 2007;79:26-30.

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ADVANCE trial: Treating Hypertension vs. Lowering : extending the benefi t?

Results from the largest ever study in Previous trials in type 2 diabetic pa- therapy and antiplatelet therapy. type 2 , the ADVANCE study, tients clearly demonstrated the benefit For the physician, ADVANCE will will have important clinical implica- of lowering blood pressure in these pa- show whether additional blood pres- tions for patients. Diabetes mellitus is tients. However, the Blood Pressure sure lowering with Coversyl Plus®, will emerging as one of the greatest threats target of 130/89 mmHg was never reduce mortality and the risk of the to the health of populations worldwide. reached in these trials, and blood pres- type 2 diabetic developing macro - and Epidemiological data from the Inter- sure treatment seen as intensive was in microvascular complications. These national Diabetes Federation puts the fact not intensive by today’s standards. results should ensure that blood pres- current number of patients with diabetes Therefore, the blood pressure lower- sure lowering in this patient group, with at 7,1 million in Africa. This number is ing arm of ADVANCE, with the use of an appropriately selected combination estimated to rise to 15 million in 2025. Coversyl Plus® (perindopril 4mg and of agents, gets the attention that it de- The current prevalence of diabetes in indapamide 1,25mg), aimed to begin serves. South Africa varies from 5-30% depend- lowering BP where previous trials have ing on region, age and ethnicity, and it ended by including type 2 diabetic FOR MORE INFORMATION AND RE- is well-known that these patients are at patients whatever their Blood Pressure SULTS VISIT: www.advance-trial.com increased risk for cardiovascular com- level (average starting blood pressure plications. Most diabetic patients are 145/81). These patients were included References: also hypertensive, and the presence of in order to demonstrate the benefit of 1. International Diabetes Federation. Executive Summary of the Diabetes Atlas. www.idf.org hypertension further increases the car- blood pressure lowering, as opposed 2. SEMDSA website. www.semdsa.org.za diovascular risk of diabetic patients. to only treating hypertension. Coversyl 3. Mancia G et al. Systolic and Diastolic Blood Plus® was chosen specifically for AD- Pressure Control in Antihypertensive Drug Tri- als. J Hyper 2002; 20:1461-1464 “People with diabetes have a two to four- VANCE, since perindopril has demon- 4. Chalmers J, “Treating Hypertension” or “Lower- fold greater risk of experiencing a car- strated 24 hour blood pressure control, ing Blood Pressure” Extending the Con- diovascular event compared to non-dia- and both perindopril and indapamide cept. Blood Pressure 2002; 11: 68-70 5. The ADVANCE Collaborative Group. Ratio- betics. However, despite this high risk, are glucose and lipid neutral. Added to nale and Design of the ADVANCE there is surprising little recent evidence this is the evidence that perindopril has Study: A Randomised Trial of Blood Pressure Lowering and Intensive Glucose Control in from randomised clinical trials on the role proven benefits beyond blood pressure High-Risk Individuals with Type 2 Diabetes of blood pressure lowering in the preven- lowering. Mellitus. J Hyper 2001; 19(suppl 4):S21-S28. tion of diabetic vascular disease”, points In ADVANCE, Coversyl Plus® was 6. The EUROPA Study. Lancet, 2003; 362:782- 788 out the ADVANCE study chairman John added to all existing therapy includ- 7. Myers et al Journal of Hypertension 2000 vol Chalmers from the George Institute. ing antihypertensives, lipid-lowering 18: 317-325

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