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An Approach to the Diagnosis and Management of Patchy, Non-Scarring Hair Loss

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An Approach to the Diagnosis and Management of Patchy, Non-Scarring Hair Loss CPD Article An approach to the diagnosis and management of patchy, non-scarring hair loss Jordaan HF, MBChB, MMed(Derm) Professor, Department of Dermatology, 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 hair loss and includes conditions like alopecia areata, trichotil- lomania, dermatophyte infection of the scalp, syphilitic alopecia and traction folliculitis. SA Fam Pract 2007;49(7): 26-29 Introduction Table II: Non-scarring hair loss 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- Erythema/scaling/ -/+ + ness]). The normal scalp is adorned with pustulation approximately 100 000 hairs. 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 skin (Figure 1). Lymphocyte associated • Lichen planus tered in clinics and presenting with There may be one, or several, discrete • Lupus erythematosus patchy, non-scarring hair loss, are alo- or confluent patches. Follicular open- • Pseudopelade of Brocq pecia areata, trichotillomania, dermato- ings are present. No atrophy or scar- • Follicular mucinosis Neutrophil associated phyte infection of the scalp, secondary ring occurs. The most common present- • Folliculitis decalvans syphilis, and traction folliculitis/alopecia. ing area is the scalp, but the eyebrows, • Diffecting folliculitis eyelashes, pubic hair and beard 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 disease caused by interaction of T-lym- minal scalp hair (Figure 2) and alope- • Some dermatophyte infections • 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 • Psoriasis Figure 1: Alopecia areata. The scalp ap- Figure 2: Alopecia totalis. Eyebrow hair is • Seborrhoeic dermatitis pears normal. (Figure courtesy of also sparse. (Figure courtesy of • Some dermatophyte infections Derm101.com) Derm101.com) • Traction alopecia 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 • Loose anagen syndrome 26 SA Fam Pract 2007:49(7) SA Fam Pract 2007:49(7) 27 CPD Article tern of hair loss over the periphery of the Table III: Differential diagnosis 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 Nail pitting (dystrophic plate Nail biting (irregularly eaten distal shows peribulbar lymphocytes, 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 psychology The nails may show fine pitting (“ham- al stress common mered brass”) of the dorsal nail plate, Atopic and autoimmune Associations Atopic diseases, 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, vitiligo, extensive forms) myasthenia gravis and Addison’s dis- Relapse rate 100% Recurrent in adults ease. Reassurance, steroids, topical Reassurance, antidepressants, psy- Treatment immunotherapy chotherapy Differential diagnosis In the differential diagnosis, second- to wear a wig. Make-up applied to the Trichotillomania ary syphilis, grey-patch tinea capitis, 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 lupus erythematosus cation of a potent steroid 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 plucking, roid. Tufted regrowth of hair common- but the resulting unsightly alopecia fuels Course ly results. the anxiety 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 puberty, 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 • Ophiasis (bandlike pattern) squaric acid 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 • Atopy PUVA (photochemotherapy) is variably Management effective, as high as 30%, and worth a No cure 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 cancer. 26 SA Fam Pract 2007:49(7) SA Fam Pract 2007:49(7) 27 CPD Article scalp, but sometimes the eyebrows or Figure 5:
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