Adrenal steroid-genetic activity in subjects with alopecia totalis or subtotalis diffuse alopecia and alopecia areata.
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Direct immunofluroescence studies were performed on hairy and alopecic areas of scalp in patients with alopecia areata, alopecia totalis and male pattern alopecia. Abnormal deposits of C3 and occasionally of IgG and IgM were found in 92% of 12 patients with alopecia areata and in 21% of patients with male pattern alopecia. No abnormalities were seen in 4 patients with alopecia totalis. In both alopecia areata and male pattern alopecia, the deposits were most common along the basement zone of the inferior segment of hair follicles and occurred with equal frequency in alopecic and normal scalp. These observations suggest that immune factors may play a role in the pathogenesis of alopecia areata.
A psychological study on fifteen children with diverse etiologies of hair loss, viz., alopecia areata, alopecia totalis and trichotillomania was conducted in order to assess the degree of underlying psychodynamics in children with hair loss. The results confirm the relationship of the underlying emotional disturbance to the hair loss. Further, it appears that the more severe the psychopathology of the individual, the greater is the hair loss and/or the clinical manifestation of trichotillomania.
Thirty-one patients suffering from alopecia totalis and fourteen patients with idiopathic diffuse alopecia were examined for evidence of an endocrinopathy and their sera screened for organ-specific auto-antibodies. The results were compared with matched control groups of dermatological patients and a random group of dermatological patients. There was no statistically significant difference in the groups and the results were similar to those found in the general population.
We report three cases of alopecia areata occurring around central, pigmented nevi. The histologic appearance of the central nevus was that of the halo nevus. Removal of the nevus did not appear to alter the natural course of the alopecia. Histochemical studies showed a substantial increase of acid mucopolysaccharides in the dermis in each case.
We have previously demonstrated regrowth of hair in scalp skin grafts taken from patients with alopecia areata (AA) and alopecia universalis (AU) following engraftment on to nude mice. This present study was to determine whether serum from patients with AA and AU, has a role in the process of hair loss and the role of antibodies and complement. Forty mice were grafted with transplants obtained from seven patients. One group of the grafted mice was given patients' serum and another group normal serum. The mice were treated topically with cyclosporin (CyA), or olive oil. Hair growth was noted in most grafts and intravenous injections of serum did not prevent or inhibit this process. Immunofluorescence studies before grafting showed deposition of immunoglobulins and complement in hair follicles in both normal and affected scalp skin, but a more striking deposition was noted in the affected skin. Deposition of immunoreactants after grafting was observed only after the injection of serum from the patients but not with normal serum. Thus the sera from patients with AA or AU, when injected into nude mice with hair transplants from the scalp skin of patients with these disorders, does not alter the hair growth despite deposition of immunoreactants around the hair follicles.
In this study 8 patients with alopecia due to chronic discoid lupus erythematosus (CDLE), 10 patients with traumatic alopecia (TA), and 12 patients with male pattern baldness (MPB) were treated with the punch graft method (PGM). Stastistical evaluations of the results and factors influencing the results were careied out. The mean survival rate of hairs was 72% in CDLE, 97% in TA, and 104% in MPB. The mean number of hairs in a 4 mm graft before transplantation in 30 patients and 752 grafts was found to be 18.2. This is far more than the number reported in previous publications concerning PGM owing probably to the difficulties of counting several hairs simultaneously emerging from the same pilary canal when the hair is cut to a length of 1--2mm preoperatively. For this purpose the author has developed a special photographical magnifying system. The number of hairs surviving transplantation in MPB in a 4 mm graft was about 19 hairs per graft, which is superior to previous reports. This is possibly due to some modifications of the procedure made by the author. In a control series done with the same technique as that often seen in the literature, about 50% inferior results were obtained. These results were however similar to those reported in the literature. Consequently the modifications of the procedure have been successful. Only one article with a series of 12 patients with TA treated with PGM was found in the literature. The hair survival results of the author exeeded the reported results by about 100%. The size, hardness, and elevation of the scars of the donor holes were checked statistically after various treatments. It was found that the diameter of the scar is the same regardless of type of treatment but that a signifcantly greater risk of hard and elevated scars is taken if the bald grafts are put back in the donor holes. No complications were seen in this series. PGM is a safe method that gives good hair survival results on transplanted hairs in MPB and TA, but the results vary in CDLE. In spite of the good results with PGM the author emphasizes that, although the therory of the method is simple, both the preoperative judement and the performance with its practical difficulties and many cosmetic problems is complex and requires a lot of psychological insight, practice and experience before correct preoperative judgement and a maximally good cosmetic result can be achieved.
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BACKGROUND: A small percentage of patients with alopecia areata have connective diseases such as systemic lupus erythematosus, discoid lupus erythematosus, rheumatoid arthritis, and scleroderma. Lupus erythematosus is associated with a number of different types of alopecia, but the incidence of alopecia areata in lupus erythematosus has not been examined. OBSERVATIONS: Of our cohort of 39 patients with lupus erythematosus, alopecia areata developed in 10% (four patients), in contrast to 0.42% of general dermatologic patients. Biopsy specimens of alopecia areata lesions in each of our patients showed continuous granular deposition of IgG at the dermoepidermal junction, a finding usually found in only a minority of alopecia areata cases. Intralesional injections of corticosteroids were effective treatment. CONCLUSIONS: The incidence of alopecia areata in patients with lupus erythematosus is increased. Recognition of this form of alopecia allows for specific therapy with intralesional corticosteroids.
Postoperative alopecia is a minor complication of surgery but a cosmetic disaster to the patient. Over a 3 year period, 60 cases of occipital alopecia were discovered in patients following open-heart surgery and 5 cases on other surgical services. In contrast to previous reports, 29 patients had alopecia one year later, presumed to be permanent. Extensive operations, with prolonged recovery and elective overnight mechanical ventilation, were common to all. Retrospective analysis and prospective studies clearly demonstrated that localized scalp pressure was the cause of the alopecia and that the duration of pressure determined the extent of the damage. Moving the patient's head at regular intervals during operation and recovery eliminated the alopecia. The type of head rest used did not modify the development of alopecia. Electrical injury and the use of heparin, hypothermia, electrocautery, or hypotension were eliminated as possible causes. Conclusive evidence correlating periperative events with the formation of pressure sores in man has not been previously reported.
Recently, interleukin 1 (IL-1) was shown to protect rats from ARA-C-induced alopecia. The present study was designed to investigate the effect of combination rHu-IL-1 and ARA-C on transplantable chloroleukemia (C51) and at the same time evaluate the protective effect of IL-1 on the ARA-C-induced alopecia in the rat model. In vitro, IL-1 had no direct effect on growth, viability or differentiation of C51 cells, neither did IL-1 protect the C51 cells from ARA-C cytotoxicity. In vivo, the combination treatment of ARA-C + IL-1 aborted the development of transplanted chloroleukemia in 100% of rats, vs 60%, 10% and 0% survival for rats treated with IL-1, ARA-C and buffer respectively. All rates treated with ARA-C alone developed complete body alopecia. In contrast, none of the rats treated with combination IL-1 and ARA-C combination developed alopecia. Thus, IL-1 demonstrated a double beneficial effect, synergism with ARA-C against the leukemic cells on the one hand, and protection from ARA-C-induced alopecia, on the other.
Eight hundred patients with alopecia areata (AA) responded to a detailed questionnaire that was compiled, distributed, and analyzed by Help Alopecia International Research, Inc. (HAIR). Among those responding, 28% were men and 72% were women. Fifty percent had localized alopecia, 30% had alopecia totalis, and 20% had alopecia universalis. Forty-eight percent developed their initial onset before the age of 20. A very strong family history of 42% was found. There were 333 additional family members with AA. Many patients and relatives had concurrent atopic diseases (seasonal rhinitis, bronchial asthma, and atopic dermatitis). Associated autoimmune diseases including vitiligo, thyroid disease, and collagen vascular disease in patients and relatives appeared consistent with previous reports. Insulin dependent diabetes mellitus (IDDM) was not increased in patients but greatly increased in relatives. Additional analysis suggests a genetic association between the two diseases where expression of AA may prevent the development of IDDM.
Alopecia areata occurs more often in Down's syndrome than would be expected by chance, sixty cases being found among 1000 patients with this syndrome compared with one case among 1000 subnormal controls. Because alopecia areata is associated with some organ-specific autoimmune disease and thyroid antibodies are often found in Down's syndrome sera from affected patients were examined for the presence of fluorescent autoantibodies. Antibodies against thyroid components tended to be present in female mongols with alopecia areata in comparison with females in a normal population but not in male mongols. Futhermore, eight out of 23 female mongols (35%) with alopecia areata had antibodies against thyroid components compared with two out of 23 female mongols (9%) without alopecia areata.
Symptomatic hair loss and alopecia were seen in psoriatic lesions of the scalp in 47 patients. Remarkably, in 66% of the cases it was an inaugural manifestation, and in 36% the scalp was exclusively involved. Therefore 34% of the patients presented with a primary manifestation of isolated scalp psoriasis. Hair loss varied in intensity from protracted to moderate and massive (36% in tufts). It presented as acute (51%), chronic (36%) or chronic recurrent (13%). Thirteen patients (28%) became aware of the hair loss with the beginning of therapy. The alopecia was found to be circumscribed in 75% of the cases and diffuse in 25%. In 2 cases psoriatic alopecia also manifested itself at sites other than the scalp. The telogen count was found to be increased up to 25-86% in the florid stage. Examinations under the light microscope showed a patchy perifollicular lymphohistiocytic infiltrate in the upper and middle dermis with adnexotropia in several cases. This infiltrate can alter the follicle epithelium and may lead to a granulomatous foreign-body reaction with destruction of the hair follicle. After topical antipsoriatic treatment, most of the reexamined patients showed complete hair regrowth, while 5 developed a residual scarring. Therefore, in the patient with circumscribed or diffuse symptomatic alopecia, with or without scarring, psoriatic alopecia should be considered.
We have previously reported that several biological agents, when given simultaneously with cytosine arabinoside or cytoxan, will protect from cytosine arabinoside-induced but not from cytoxan-induced alopecia. In the present study we used the secosteroid 1,25-dihydroxyvitamin D3 in a different timing schedule to protect from chemotherapy-induced alopecia. In three separate experiments, 0.2 microgram of topical, 1,25-dihydroxyvitamin D3 protected rats from alopecia induced by etoposide, cytoxan, and an Adriamycin-cytoxan combination. In another experiment, 0.1 microgram protected rats from etoposide-induced alopecia at the site of application. 1,25-Dihydroxyvitamin D3 may offer a new and exciting approach to the prevention of chemotherapy-induced alopecia.
We report an unusual case of verrucal alopecia occurring on the vertex scalp of a black woman, which was presumed to be secondary to use of a thioglycolate permanent wave preparation. We describe the clinical and histologic features of this chemical and traumatic alopecia as well as that of frontotemporal chronic traction alopecia resulting from use of sponge rollers. Common hair care practices are a frequent cause of alopecia in black women. Familiarity with these hair practices will aid in the accurate diagnosis, prevention, and proper management of this problem. The evaluation, causes, and differential diagnosis of alopecia in a black woman are discussed.
Although it is clear from the foregoing that some of the drugs and chemicals used to treat severe alopecia areata are efficacious to some degree, it is impossible to draw any meaningful comparisons among the data outlined in Tables 1 and 2. Virtually all of the studies were designed differently. Differences in chronicity and extent of disease as well as history of previous treatment resistance may significantly affect efficacy data even as two investigators compare the same drug. Drug-induced hair regrowth in alopecia areata may be very slow; a cosmetic response may take 1 to 2 years to achieve. Efficacy determinations made at shorter intervals may, therefore, not reflect true therapeutic potential. Efficacy end points vary significantly and need to be standardized. From a practical standpoint, scalp hair coverage that is deemed by the patient to be cosmetically acceptable seems to be a reasonable efficacy end point to report. Maintenance of cosmetic effect with continued treatment and/or following discontinuation of treatment also is useful to document. Table 3 outlines my approach to therapy of alopecia areata. Topical treatments often must be used for as long as 3 months before evidence of regrowth can be seen. In my experience with severe disease, if topical treatments cannot control a flare or induce regrowth, then the patient will often require either lengthy or frequent courses of systemic steroids. In my experience, prednisone doses as low as 20 mg/d may be associated with aseptic neurosis of the hip or severe gastrointestinal bleeding. Severe alopecia areata is a disease for which all therapies are, at best, palliative and, at worst, potentially harmful to patients who are usually otherwise very healthy. The psychosocial significance of this disease is enormous. The insights shared by a long-time sufferer of the disease mirror those expressed by the many patients with whom I have worked during the past 12 years. Three key elements to effectively treat the patient are (1) to help the patient understand the disease; (2) to encourage the patient to share his or her feelings with the physician, family, friends, and other sufferers of the disease; and (3) to help the patient to maintain a sense of hope for future scientific knowledge and treatment of the disease. With a thorough knowledge of the potential benefits and risks of each treatment or combination treatment, the physician with the patient's understanding and cooperation may then embark on what may be in severe cases a lengthy and sometimes unproductive therapeutic process.