Hair Loss
Hair Loss, in medical term is called Alopecia.
Alopecia may be described as the lack of hair in areas where it normally grows. The most noticeable area in which alopecia develops is the scalp, but a loss of body hair may also occur. Patients may seek medical care for what is perceived as excessive hair loss even when alopecia is not present. Whether the problem is genetically induced male-pattern baldness or alopecia resulting from systemic illness, the primary care physician may be the first one to whom the problem is presented and must be able to offer the patient a rational approach to diagnosis and treatment.
Hair is a product of keratinocytes in the hair bulb. The hair shaft is made of hard keratin. Synthesis results from mitoses of cells within the hair matrix. The growth of hair is cyclical, the length of the cycle varying with the location. Scalp hair grows from 3 to 10 years, involutes over 3 months, and rests for another 3 months. In healthy young persons, about 85% to 90% of all scalp hairs are in anagen, the phase of active growth. Most of the remainder are in telogen, the resting phase of the hair cycle. The number of hairs on the scalp is estimated to be 100,000. If 10% to 15% are assumed to be in the telogen phase, then an average daily loss of 100 hairs in telogen is expected.
Hairs that grow for long periods and rest briefly are the most susceptible to interruptions of the growth cycle, and variations in the ratio of growth phase to resting phase are most noticeable. The longer the growth period, the longer the hair. Scalp hair grows at the rate of approximately 0.25 mm daily, but various factors can affect the rate.
The primary pathogenic mechanisms of hair loss are destruction of the hair matrix by physical agents and by infectious or immunologically mediated inflammation. Hair loss may occur when hair growth slows secondary to metabolic diseases or the administration of antimetabolites or other drugs. Physiologic alterations may also produce hair loss by altering the relation between the growing and resting phases of hair follicles. During pregnancy, fewer hairs are shed, so that fewer telogen hairs are produced. After parturition, the percentage of telogen hairs increases, and hair is lost. The process is diffuse and short-lived. This alteration in the ratio of resting hairs to the total may also develop secondary to pharmacologic changes induced by oral contraceptives. Destructive pathogenic mechanisms often produce scarring alopecia, whereas systemic illnesses and drugs usually result in nonscarring alopecia.
Alopecia can be divided into two categories, scarring (cicatricial) and nonscarring (noncicatricial). In the latter, the hair follicles are retained and the process is potentially reversible. In the scarring type, follicles are destroyed and hair never regrows. A few conditions that begin as nonscarring alopecia may later develop into scarring alopecia as a result of chronicity.
Scarring Alopecia. An inflammatory response to injury is often present. Forms of physical trauma, such as burns, radiation, injury, and chronic traction, are commonly responsible. Traction alopecia usually results from braiding or the use of tight hair rollers. The pattern of hair loss depends on the styling. The process is initially reversible but progresses to a scarring phase with chronicity. The use of hot combs in combination with petrolatum to straighten hair may result in inflammation with consequent fibrosis and hair loss. Infections—whether bacterial (resulting in deep cellulitis), fungal (Trichophyton schoenleinii), or viral (e.g., recurrent herpes simplex or herpes zoster)—produce inflammatory change and alopecia. Dermatologic processes such as discoid lupus erythematosus, scleroderma, lichen planus, cutaneous neoplasms, and granulomas may produce scarring alopecia, as can factitious conditions and neurotic excoriations.
Nonscarring Alopecia. Most often, alopecia is nonscarring, with male- and female-pattern baldness accounting for most cases. Male-pattern baldness (androgenetic alopecia) is symmetric, usually beginning in the frontoparietal scalp. Its development is related to age, genetic predisposition, and the presence of androgenic hormones. The inheritance is probably dominant, with incomplete penetrance. The process is permanent, with pigmented scalp hairs replaced by fine, unpigmented vellus hairs.
The presence of male-pattern hair loss in a female patient should provoke concern about androgen excess, manifested by hirsutism in mild cases and virilization in more serious cases. Polycystic ovary disease and hyperprolactinemia are common causes of mild androgen excess and hirsutism. Frank virilization occurs with androgen-producing ovarian and adrenal tumors. Dihydrotestosterone inhibits the growth of scalp hair while it stimulates the growth of facial hair and promotes a male pattern of pubic hair growth. Laboratory investigation reveals increased levels of free testosterone, sulfated dehydroepiandrosterone (DHEA), or both.
The mechanisms of female-pattern baldness are similar to those of male-pattern baldness, but female-pattern baldness is more diffuse; usually, the central and frontal areas are affected, without complete baldness. Age, family tendency, and androgenic hormones are important factors. Postpartum alopecia resolves within 18 months, but about half of women feel they have less hair after childbirth than they did before pregnancy.
Nonscarring alopecia often is associated with systemic disease, a metabolic abnormality, or the use of certain medications. Alopecia areata, a condition of unknown cause in which hair is rapidly lost, usually in circular patterns, is probably the second most common form of nonscarring alopecia. Alopecia totalis is the loss of all scalp hair, and in alopecia universalis, facial and body hair are lost as well. The course of alopecia areata is unpredictable. Some persons have one episode, in which the development of one or several bald spots is followed by spontaneous regrowth. In others, new areas of baldness may develop, and they become totally bald. Onset before puberty is associated with a poorer prognosis. Most investigators believe that an autoimmune mechanism is involved and that an association with other autoimmune diseases exists.
Alopecia may follow infectious diseases that produce a high, persistent fever, such as typhoid or pneumonia. Secondary syphilis, superficial folliculitis, and tinea capitis also may produce nonscarring alopecia. Commonly used medications that can cause alopecia include b-blockers, tricyclic antidepressants, anticonvulsants, warfarin anticoagulants, allopurinol, antithyroid drugs, quinine, verapamil, indomethacin, sulfasalazine, haloperidol, and vitamin A in excessive doses. Antineoplastic agents such as 5-fluorouracil, paclitaxel, cyclophosphamide, and methotrexate predictably produce hair loss. Oral contraceptives, hyperandrogenism, and pregnancy are known to interfere with the relation between resting and growing hairs and cause hair loss.
Diffuse hair thinning may occur in thyroid disease and iron deficiency. Less commonly, hypopituitarism and parathyroid disease produce hair loss. Alopecia is a manifestation of connective tissue diseases, notably systemic lupus erythematosus and dermatomyositis. Occasionally, hair loss is self-induced, a condition known as trichotillomania. Such patients may not be aware that they are plucking hairs, and the condition may indicate significant psychiatric disturbance.
Hair Breakage. Hair loss must be differentiated from hair breakage, which results from physical or chemical stress to the shaft. The term proximal trichorrhexis is sometimes used to describe hair breakage within the first centimeter from the scalp, whereas breakage beyond this point is called distal trichorrhexis. Hair straightening can cause proximal trichorrhexis. Patients often recognize distal breakage as split ends; such breakage may be accelerated by exposure to sunshine or swimming in chlorinated pools.