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Why Am I Losing My Hair? a Differential Diagnosis

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Why Am I Losing My Hair? a Differential Diagnosis Why Am I Losing My Hair? A Differential Diagnosis As hair loss affects a large segment of our population, it is important for family physicians to be aware of the different causes, so patients can access treatment sooner. By Louis Weatherhead, BSc, MBBS, FRCPC air is a very important secondary This article will attempt to briefly out- H sexual characteristic in both men line these conditions. and women, and contributes greatly to the personal psyche. The sheer number of Androgenetic Alopecia hair cosmetics available attest to this, and thus, hair loss is often quite traumatic to This is, perhaps, the most common cause of many. hair loss occurring in many men, and some Why do people lose hair? There are women, who carry the genes responsible many causes, the most common of which for baldness. In susceptible people, certain are classified as follows: follicles in the fronto-vertical region of the 1. Androgenetic alopecia (AGA); scalp show end-organ sensitivity and pos- 2. Diffuse alopecia; sess an enzyme, 5 alpha reductase type II. 3. Alopecia areata (AA); This enzyme converts testosterone to dihy- 4. Cicatricial alopecia; drotestosterone (DHT), the active compo- 5. Traumatic alopecia; and nent, which acts on the susceptible follicles. 6. Miscellaneous causes of alopecia. This, in turn, causes progressive miniatur- The Canadian Journal of Diagnosis / July 2001 67 Hair Loss ization of the hair from normal terminal to Therapy for AGA vellous hairs, and then loss.1 Attempts to There is no true cure for AGA. Massage, classify hair loss have resulted in the modi- ultra violet light, shampoos and topical fied Hamilton Scale for men and the applications do not cure AGA.2 There are, Ludwig Scale for women (Figures 1 and 2). however, successes in restoration by med- As a rule of thumb, 20% of men in their ical and surgical means. 20s, 30% of men in their 30s, 40% in their 40s, etc., show evidence of AGA. Minoxidil This medication comes in a 2% and 5% solution. Its exact mechanism of action is unclear, but it is thought that it may act by stimulating the blood supply at the follicu- lar papillary level and by modulating follic- Dr. Weatherhead is clinical ular deoxyribonucleic acid (DNA). The associate professor, division effect is unpredictable and seems to show a of dermatology, University of Ottawa, Ottawa, Ontario. better response in women. In men, the best response seems to occur in those under 30 with non-extensive male pattern hair loss. The treatment requires a long-term commit- ment of six months minimum.1 68 The Canadian Journal of Diagnosis / July 2001 Hair Loss Figure 2. Ludwig scale for female-patterned androgenetic alopecia. Hair transplantation Figure 1. Modified Hamilton Scale for male-patterned androgenetic alopecia. This is a surgical procedure in which hair is taken from the inferior occipital area of the scalp as a donor strip. Finasteride This strip is then sec- Also known as This is primarily indicated for AGA in men tioned into follicular spot baldness, of Type I to Type IV pattern loss. unit grafts, which are Finasteride causes reversible inhibition of transplanted into alopecia areata Type II 5-alpha reductase enzyme. Eighty- recipient slits in the may affect up to five per cent of people using the medication bald scalp area. As the show reduction or cessation of further hair occipital scalp is not 1.7% of loss, and 66% of this population show var- effected by DHT, the Canadians by ied amounts of regrowth from mild to transplanted hairs sim- marked. A long-term commitment, a mini- ilarly will be unaffect- age 50. mum of six months, is required. Finasteride ed when placed in the recipient area and is not indicated in women of any age, and is will grow normally. The final result is actually contraindicated in women of child- dependent on the extent of hair loss and the bearing years due to the possibility of viril- total number of transplanted hairs. ization of the female fetus. Anyone pre- scribing this medication should be familiar Diffuse Alopecia with the product monograph and should counsel their patients as to the potential The most common cause of diffuse alopecia side-effects. is telogen effluvium.1,3 In the normal, The Canadian Journal of Diagnosis / July 2001 69 Hair Loss Figure 3. Alopecia areata. Figure 4. Folliculitis decalvans. young adult scalp, approximately 85% of day. The total duration may range from six follicles are in the anagen (growth) phase of to 18 months. Complete baldness rarely the hair cycle. occurs. Telogen effluvium describes the Although telogen effluvium is a sponta- increased shedding of telogen, the resting neously resolving condition, thyroid func- phase of the hair cycle, the hair having tion testing and serum ferritin levels should become a club hair and not growing fur- be obtained, because thyroid disease and ther). The increased shedding of these hairs low serum ferritin (value less than 40) may follows the acute precipitation of anagen play a role in prolongation of the problem. If follicles into telogen. This may occur due to these conditions are present, they should be multiple stress-related causes, such as: corrected. 1. Illness; 2. Post-operative state; Alopecia Areata 3. Medications; 4. Crash diets; Also known as spot baldness, AA is not 5. Emotional trauma; and uncommon and may affect up to 1.7% of 6. Post-partum state. Canadians by age 50. The etiology of AA is The only symptom of telogen effluvium unknown, although it is thought to be an is diffuse shedding of hair, which the patient autoimmune disorder, as helper T-cells are notices on pillows, brushes, combs and with commonly found in the lymphocytic infil- shampooing. The condition is triphasic. trate that exists around hair bulbs.4 Factors Phase 1 is accelerated hair loss; phase 2 is a implicated in the development of AA plateau phase with no more loss or gain; and include: phase 3 is a spontaneous resolution phase 1. Genetic considerations, as the role of whereby the amount of daily loss slowly re- human leukocyte antigen (HLA) class II turns to normal, less than 120 hairs lost per antigens DQ3, DR4 and DRW11 genes 70 The Canadian Journal of Diagnosis / July 2001 Hair Loss may increase susceptibility to AA;5 Table 1 2. Atopy may play a role in susceptibility CLASSIFICATION to development of AA; and OF CICATRICIAL ALOPECIA 3. Emotional stress often is linked to the development of AA. 1.Trauma How these factors influence or trigger a) Burns—thermal, chemical the onset of AA is, however, obscure in b) Radiation therapy/radiation nature.5 dermatitis c) Physical injuries Clinically, AA presents as a well circum- scribed, totally hairless patch. It is often 2. Infections noticed by chance by a hairdresser, parent a) Bacterial—follicular decalvans or friend, most commonly on the scalp (Figure 4), syphilis, cutaneous (Figure 3), although it may involve the eye- tuberculosis b) Fungal—inflammatory fungal brows, eyelashes or beard area. Exam- infections (kerion), favus ination at the periphery of the patch may c) Viral—Herpes zoster reveal the presence of hairs that taper to the 3. Neoplasms base (known as exclamation point hairs), a) Benign—epidermal nevi, cylindroma which suggest ongoing activity. b) Malignant—squamous cell In susceptible individuals, hair loss carcinoma, angiosarcomas, may extend to involve the loss of all scalp cutaneous metastases hair (alopecia totalis) and, in extreme 4. Inflammatory dermatoses cases, all scalp and body hair (alopecia a) Lupus erythematosus universalis). b) Lichen planopilaris (Figure 5) In AA, associated clinical changes may c) Sarcoidosis occur. Nail dystrophy may occur, varying d) Scleroderma/morphea e) Follicular mucinosis from fine pitting to marked ridging, trans- verse lines, thickening and splitting of the 5. Developmental disorders 6 nails. There also have been reports of a) Aplasia cutis cataracts occurring with AA. b) Facial hemiatrophy (Romberg’s syndrome) c) Epidermolysis bullosae Treatment of AA is varied. As the con- dition often resolves spontaneously within a year, patients can be followed. More commonly, topical or intralesional Cicatricial Alopecia steroids have been found to shorten this (Scarring Alopecia) clinical course. In persistent cases, immune modulation This develops as an end-stage condition, therapy using topical diphencyprone following a severe inflammatory process (DCP) or squaric acid dibutyl ester that causes permanent destruction of the (SADBE) have shown good response rates hair follicles. It may occur in a localized with good regrowth, even in cases of alop- area or be patchy and scattered throughout ecia totalis.5 the scalp. There are many causes of cicatri- The Canadian Journal of Diagnosis / July 2001 71 Hair Loss Figure 5. Lichen planopilaris. Photo courtesy of Merck Canada. Figure 6.Traction alopecia. Photo courtesy of Merck Canada. cial alopecia. It would be beyond the scope Clinically, the area of alopecia is mainly of this article to go into detail of all of these in one fronto-parietal area. It presents as an conditions and, as such, a classification of ill-defined patch, which shows hairs broken cicatricial alopecia is presented in Table 1. at varied lengths. Although this classification could be Trichotillomania also may be found in eye- more extensive, the conditions listed repre- lashes, eyebrows, moustache and beard areas. sent the more commonly found conditions This habit disorder is usually self-limited, leading to cicatricial (scarring) alopecia. however, if the problem is severe, patients should be managed with psychotherapy.7 Traumatic Alopecia Traction alopecia (cosmetic alopecia) The most common causes of traumatic alope- This variety of alopecia occurs as a result of cia are trichotillomania and traction alopecia. prolonged physical stresses imposed on the hair. There are two processes that account Trichotillomania for the patterns of hair loss seen.
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