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DIFFUSE AND ‘PATTERNED’ ALOPECIAS

Telogen effluvium

Etiology and pathogenesis

Telogen effluvium is a common, benign, and transient cause of hair loss, which occurs 2–3 months after a stressful event (Fig.28.7). Causes include chronic systemic diseases (e.g. liver failure, renal failure, and cancer), severe psychologic stress, surgery or anesthesia, crash dieting, acute physical stress (e.g. high fever and severe bleeding), and childbirth. The patient is typically a child or a woman either postpartum or aged from 30 to 60 years. Men are rarely affected.

Clinical

There is generally a history of rapid hair fall, but the hair and scalp generally look normal (the maximum proportion of hairs affected is 30–40%). The hair pull test is positive with more than approximately five hairs per pull. Microscopic examination shows excessive club hairs. Miniaturized hairs are not present.

    A chronic form is thought to occur and may be hard to distinguish from female androgenetic alopecia. In general, however, for female androgenetic alopecia, the onset is gradual and the patient usually in the second to fourth decade of life. The course is slow and progressive. The hair loss is worst over the frontoparietal scalp. There are many miniaturized hairs.

Differential diagnosis

The differential diagnosis of diffuse, extensive, acute, subtotal hair loss with noticeable hair fall includes the following.

    In addition, it may at times be difficult to exclude androgenetic alopecia. This is perhaps because there has been a degree of previously unrecognized androgenetic alopecia (there is no reason why telogen effluvium should not affect a scalp in which there is a background thinning), or may mean that the diagnosis is the chronic form of telogen effluvium.

    Blood tests (e.g. ferritin, thyroxine [T4], TSH, DHEAS, and free testosterone) may be required to exclude an ongoing organic cause that requires further therapy, and differential diagnosis from androgenetic alopecia may require scalp biopsy analyzed by horizontal sections.

Fig. 28.8 Anagen effluvium. Chemotherapy has severely disrupted the normally active hair root. Alopecia has resulted. The hair will regrow once the drugs are removed.

Treatment

Patient education and reassurance are needed. Increased hair loss correlates with regrowth of new hair. The patient can be reassured that the shed
hair is being replaced, and that progression to baldness does not occur (although an episode of telogen effluvium may occasionally ‘expose' a longer-term cause of hair thinning such as androgenetic alopecia).

Anagen effluvium

Slight or extensive, diffuse, non-scarring hair loss of the scalp may occur after a toxic insult to the growing hairs (i.e. those in the anagen phase). Cancer chemotherapeutic drugs are the most common offenders (Fig. 28.8).

Drug-induced alopecia

Other drug-induced mechanisms may also lead to alopecia. Non-scarring, diffuse hair thinning without scalp disease, weeks to months after starting the offending drug, is characteristic. Many drugs have been implicated, including anabolic steroids causing androgenetic alopecia in young women, and retinoids (e.g. isotretinoin, acitretin, and vitamin A). Note that retinoids can cause progressive kinking of the hair. The offending agent should be identified and eliminated.

Iron deficiency

Diffuse thinning of the scalp hair in a woman has been related to low iron. In the experience of the authors, anemia is usually not present. Recent or regular blood donation, heavy menstrual flow, and dietary deficiency are potential causes. An iron level, total iron-binding capacity (TIBC), and ferritin should be measured. The ferritin may be in the ‘normal' range, but evidence suggests that the low-normal range (e.g. <40ng/mL) is too low for some women. Some categorize this type of alopecia as a telogen effluvium. Of note, a recent study showed that the mean ferritin levels in patients with androgenetic alopecia (37ng/mL) and alopecia areata (25ng/mL) were statistically significantly lower than in normal individuals without hair loss. Further studies are needed to determine if iron supplementation aids hair regrowth in these populations.

    Ferrous sulfate replacement should be given. The ferritin should be maintained above 40ng/mL. Therapy should be extended over 6–12 months before efficacy is assessed.

Thyroid disease

Thin, fine hair is a feature of thyrotoxicosis. A diffuse, non-scarring alopecia may occur in hypothyroidism; the remaining hair may be dry and brittle. Other cutaneous manifestations of hypothyroidism include alopecia of the lateral eyebrows; non-pitting edema; and dry, coarse, cool, yellowish skin (Ch.12). The free T4 and TSH should be measured.

Androgenetic alopecia in women

Etiology and pathogenesis

Progressive loss of terminal hairs of the scalp in adults is a universal finding for both men and women (see discussion of anagen shortening and follicular miniaturization in the introduction). Significant loss is much less frequent in women, the age of onset is later, and the clinical pattern is different. However, some patients experience significant thinning in their mid adult years. There may or may not be a family history of such thinning, but a genetic predisposition is likely; this, and local follicular variation in hormone metabolism, may explain why most women, even with early-onset hair thinning, have normal circulating hormone levels.

    Occasionally, an abnormality of circulating hormones is the cause—investigations are briefly discussed in the differential diagnosis section—but most women with a significant androgen abnormality also have hirsutism (see earlier), which will determine relevant investigations. There is no overall correlation between androgen levels and the occurrence or severity of female androgenetic alopecia.

Fig. 28.9 Androgenetic alopecia in a woman. Note the thinning across the top, with preservation of the hairline.

Fig. 28.10 Androgenetic alopecia in a woman. Women with androgenetic alopecia rarely go bald, but the hair can become quite thin.

Clinical

Women who lose hair as they age characteristically develop thinning from the frontal hairline to the vertex, with preservation of the frontal margin of the hair (Figs 28.9 and 28.10). However, postmenopausal women may develop a receding hairline as part of female pattern androgenetic alopecia.

Differential diagnosis

The diagnosis is one of exclusion, especially in the early stages, and so all other causes of diffuse thinning must be ruled out (chronic telogen effluvium, iron deficiency, thyroid disease, and other hormonal abnormalities). DHEAS and total or free testosterone are good screens for endocrine abnormalities such as polycystic ovary disease or adrenal diseases (Figs 28.11 and 28.12). A positive screening examination should prompt referral of the patient to a specialist.

    If a hair pluck is performed from the affected area, there will be a reduced anagen:telogen ratio due to the reduced duration of anagen.

    The differential diagnosis is that in Table 28.1, but disorders such as central centrifugal cicatricial alopecia may also need to be considered.

    Differentiating androgenetic alopecia from chronic telogen effluvium or from diffuse alopecia areata may be particularly difficult, requiring scalp biopsy, and androgenetic alopecia may only be noticed as a problem when recovery from a different cause of hair fall is less complete than the patient anticipates.

Fig. 28.11 Endocrinologic abnormality. In this patient, the dehydroepiandrosterone sulfate (DHEAS) was 10 times the normal range.

Fig. 28.12 Male pattern alopecia occurring in a woman who presented with quite severe hirsutism of several months’ duration. This pattern of hair loss is strikingly different from the typical female androgenetic alopecia, and was due to an androgen-secreting tumor.

Treatment

Topical minoxidil 5% twice daily may be offered, although the patient should be informed of its general poor efficacy, the need for prolonged use, and the cost. Some have recommended giving an antiandrogen (e.g. spironolactone), because it will decrease DHT levels in the scalp, but good, controlled studies are lacking. Finasteride would appear logical but is contraindicated premenopausally and has been shown to be ineffective postmenopausally. The amount of estrogen in hormone replacement therapy is insufficient to influence the process.

Androgenetic alopecia in men

Etiology and pathogenesis

Androgenetic alopecia is a more scientific name for male pattern baldness. The process is one of miniaturization of the hair follicles, leading to hairs of progressively smaller diameter, weight, and lighter pigment. Ultimately, the affected hairs are completely lost.

Clinical

A young man in his twenties or thirties may become very distressed and seek medical help because of hair loss at the vertex and along the frontotemporal areas bilaterally (Fig.28.13). Individual hairs become smaller, and the hairline recedes. Later, the forehead seems to become taller, and finally, all terminal hair may be lost from the forehead to the vertex. Horizontal sectioning of biopsy specimens may be of diagnostic and predictive value. Extensive hair loss before age 30 and vertex baldness (but not frontal) has been associated with an increased risk for ischemic heart disease. Men younger than 55 years with severe baldness are fatter and are more likely to develop ischemic heart disease than those without hair loss.

Differential diagnosis

The diagnosis is usually obvious.

Treatment

Both minoxidil and finasteride can increase the size of miniaturized hairs anywhere on the scalp. Once an area becomes completely bald, neither of these medications will work. Topical minoxidil should be offered, but the patient should be informed of its low efficacy, the need for prolonged use, and the cost. The 5% solution is recommended and is available over the counter in the USA. It has greatest benefit within 4–6 months and then the improvement is maintained provided treatment is continued. Stopping the minoxidil leads to a return to where the patient would have been without treatment. Finasteride (1 mg per day) is an oral medication that has reasonable efficacy in one-third to a half of patients. Improved hair count is seen over at least 12 months. Alternatives, such as a hairpiece or hair transplantation, should be discussed.

Fig. 28.13 Androgenetic alopecia in a man. Note the bitemporal recession and thinning of the vertex.

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.