Alopecia Areata
Alopecia areata consists of sharply localized patches of sudden hair loss unaccompanied by any visible evidence of scalp disease. Usually, the patches are completely devoid of hair, but sometimes a few spared, normal hairs are present. Less often, some “broken off” hairs are scattered throughout the bald areas. These presumably occur because of mild cyclic exacerbations of the disease that lead to hair shaft fragility but not complete cessation of protein growth.
Typical lesions are 2 to 3 cm in diameter. Often only a single lesion is present, but careful examination may reveal two or three additional lesions in other areas of the scalp. In more severe cases, multiple, larger patches of hair loss are present, and in rare instances, total hair loss (alopecia totalis) occurs. Alopecia areata typically affects the scalp but occasionally involves the eyebrows, eyelashes, beard area, axillae, and pubis. When all sites are involved the process is called alopecia universalis.
The disease can occur at any age, but it is most commonly found in late childhood and in the early teens. A family history of similar hair loss is found about 25% of the time. Women are affected more often than men. Fingernail changes, especially pitting, occur in 20% of patients.
A few patients with numerous large patches of alopecia eventually obtain complete regrowth, but most go through years of dynamic equilibrium in which new patches develop as quickly as old patches regrow. A most unfortunate few patients develop total alopecia. The outlook for complete regrowth in these individuals is extremely poor. Patients with alopecia areata who have obtained complete remission have about a 25% chance of developing one or more subsequent episodes later in life.
The pathophysiology of alopecia areata involves a lymphocytic attack on growing (anagen) hair follicles. This results in an abrupt, synchronized switch of these follicles to the resting (telogen) phase. Recent evidence suggests that the follicles pass through the telogen phase but become arrested just as they enter the anagen phase. The switch from normally growing hair to the telogen phase is marked by the spontaneous loss (or easy removal) of the telogen, or club, hairs.
The actual cause of alopecia areata is unknown. Genetic factors are probably important, since a significant proportion of patients have a family history of the same disease. There is also considerable evidence pointing toward an autoimmune etiology. Patients are rather likely to have autoantibodies directed against thyroid cells, parietal cells, adrenal cortex cells, or intracellular proteins. Vitiligo and autoimmune thyroid disease are seen with increased frequency in patients with alopecia areata. There is also a higher-than-expected incidence of atopy in patients and their families. The significance of this finding is uncertain, but it is known that there are changes in skin-related cell-mediated immune response in atopics.
Emotional factors probably also play a role, although it is often difficult to decide whether those present are a cause or a result of the disease. When stress is a prominent, early causative factor, it may act through a triggering process, even as it does in initiation of autoimmune Graves’ disease.
Therapy, if it is to be attempted at all, should begin with the use of high-potency topical steroids; enhancement of the steroid effect can be obtained with nighttime shower cap occlusion. The success of this approach is unpredictable, but at the least it does buy time during which spontaneous remission sometimes occurs. If this approach fails, the intralesional injection of steroids can be attempted. Such injections frequently lead to sprouts of new hair growth, but tissue atrophy and eventual reloss from injected sites limit the acceptability of such treatment. In desperate cases, administration of systemic steroids can be considered. It is often possible to induce hair growth with systemic steroids, but unfortunately, growth is not sustained when therapy is switched to alternate days or is discontinued.
Three alternative treatment programs are worth considering. First, 2% minoxidil solution (Rogaine) can be applied several times daily. Second, the photosensitizing agent Oxsoralen can be applied topically or may be given orally. This is followed by exposure to ultraviolet light in the INA spectrum (PUVA therapy), which, in turn, induces a mild erythema.
Finally, patients can be sensitized to certain chemicals, such as dinitrochlorobenzene. Reapplication of the chemical to the bald areas at a later date causes induction of a (mild) contact dermatitis. The mechanisms through which these three therapies act are unknown, though the latter two are thought to be “immuno stimulating.”
The results with all three approaches are similar. About 25% of patients experience a cosmetically satisfying response, another 25% obtain very limited regrowth, and 50% do not respond at all.
Trichotillomania
Some children, when under significant psychic stress or as part of a habit, chronically pull, twist, or rub a localized patch of hair. The configuration of these patches is often strikingly angular in shape. No scalp disease is present, but invariably all of the hairs within the patch have fractured distal ends. Most of these broken hairs are about 1 cm long, since broken hairs must grow out to this length before they can be once again manipulated. Trichotillomania may be a form of obsessive-compulsive disorder. Treatment requires counseling and sometimes the use of psychopharmacologic agents.
Secondary syphilis. Patients with long-standing secondary syphilis often develop a peculiar pattern of patchy, “moth eaten” alopecia. The large number of patches, their small size, and their indistinct margins help to separate this condition from that of alopecia arcata. The hair loss is transient; regrowth occurs following adequate antibiotic therapy.
Pseudopelade. Pseudopelade represents the end stage of the inflammatory scalp diseases known as folliculitis decalvans and lichen planopilaris. Both of these conditions involve a noninfectious folliculitis with eventual scarring fibrosis of the involved follicles. The clinical appearance of pseudopelade consists of multiple small (1- to 2-cm) white patches totally devoid of hair. Coalescence of the central small patches may result in larger central area of baldness. The morphology suggests alopecia arcata, but as the process is scarring, no hair regrowth is possible.
Telogen Effluvium
Telogen effluvium is a dihlse type of alopecia that occurs when numerous but scattered hair follicles simultaneously change from the growth (anagen) phase to the resting (telogen) phase of the hair growth cycle. This may be compared to the situation in alopecia areata where a similar switch to telogen phase occurs in a tightly localized area. This similarity has led some clinicians to view idiopathic telogen effluvium as a type of diffuse alopecia areata. At the microscopic level, however, the two processes differ, inasmuch as the shift to telogen is accompanied by perifollicular inflammation in alopecia areata, whereas no inflammation occurs in telogen effluvium.
Patients who seek medical attention for diffuse hair loss of the telogen effluvium type seldom have much alopecia visible to the examiner. Proof of increased hair loss is easily obtained, however, by gently tugging at random tufts of hair. One or more telogen hairs will be removed with each tug in patients with telogen effluvium. Only an occasional loose hair will be found in people with normal hair growth. Alternately, the magnitude of the hair loss can be determined by asking the patient to save and count individual hairs found on the pillow, in the hairbrush, and in the basin or bathtub.
Most patients with telogen effluvium will report the loss of approximately 400 hairs/day. This number is 4 to 5 times greater than would be expected from people with normal hair growth.
Telogen effluvium is seen more commonly in women than in men. Moreover, telogen effluvium is frequently found in the postpartum state and following the discontinuation or oral contraceptive pills. These observations suggest that hormonal factors play a role in pathogenesis. The process is also seen, however, following episodes of physiologic stress (high fever, myocardial infarction, cerebral vascular accidents, ect.) and in association with psychologic stress, indicating that other unknown factors may also be important.
Patients with telogen effluvium rarely if ever progress to clinically significant baldness. Most instances of telogen diffluvium resolve spontaneously over a 6- to 12-month period. No effective treatment is recognized.
Male and Female Pattern Baldness
Both men and women may develop diffuse and patterned hair loss as they age. In men the loss is most noticeable at the vertex and in the hitemporal regions. In women the loss is more diffuse or is restricted to the vertex. Pattern loss may be seen as early as the third decade in men but is rarely apparent prior to the fifth decade in women.
Genetic factors are important in the pathogenesis of pattern loss. Both the degree of loss and the age at which it starts seem determined by familial patterns. Hormonal factors are likewise important, since men castrated at a young age do not develop pattern loss, regardless of genetic factors, until or unless supplemental testosterone is administered. The hormonal aspect of pattern loss in women is much less clear, although the usual delay in onset until after menopause suggests the possibility that estrogens are protective.
In general, there is a correlation between the age at which onset begins and the severity of eventual loss. Hair loss, regardless of how early it begins, however, is not linear with time. Individuals may go through short periods of intense loss followed by longer plateau periods of relative stability.
Topically applied 2% minoxidil (Rogaine) does result in a limited degree of regrowth during the first year or two of application. In addition, there may be a longer term protective effect wherein continual use retards the rate of hair loss.
Cosmetic improvement in pattern loss may be obtained through the use of small hair transplants taken from the lateral margins of the scalp where hair growth remains active. Scalp reduction techniques, used in conjunction with transplants, may reduce the number of transplants needed. Aesthetic success with these surgical techniques is highly variable and depends to a great deal on the skill and experience of the operator.
Hypothyroidism
Diffuse hair loss not associated with scalp disease is occasionally seen in women with moderate to severe hypothyroidism. The mechanism through which this occurs is unknown, but it is not likely related to serum levels of thyroid hormone, since replacement, while preventing further loss, fails to reverse the process.
Tags:alopecia areata, autoimmune graves disease, baldness, Dermatology Diagnosis, hair follicles, hair loss scalf disease
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