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PubMed2002

Analysis of the expression of cutaneous lymphocyte-associated antigen on the peripheral blood and cutaneous lymphocytes of alopecia areata patients.

Alopecia areata has been reported to be accompanied by abnormal autoimmune dysfunction. We examined the expression of cutaneous lymphocyte-associated antigen (CLA), which is a skin-specific lymphocyte homing receptor, in the peripheral blood lymphocytes and skin of patients with alopecia areata. In the patients' peripheral blood, the percentage of CLA-positive CD4+ or CD8+ lymphocytes, was significantly higher than that of normal controls. The patients with severe or progressive alopecia areata showed a much higher CLA-positivity compared to patients recovering from the disease. A chronological study showed that the percentage of CLA-positive peripheral blood lymphocytes, CD4 + or CD8 + lymphocytes decreased in parallel with the patients' good clinical course. The CLA-positivity in peripheral blood lymphocytes, CD4+ or CD8+ lymphocytes of patients with alopecia areata who did not respond to oral corticosteroid therapy remained higher than in those who responded well to the treatment. In the affected scalp skin, many infiltrating lymphocytes around the hair follicles, which were CD4+ or CD8+ lymphocytes, expressed CLA. These findings suggest that the CLA-positivity correlates with clinical activity and that CLA-positive CD4+ or CD8+ lymphocytes may play an important role in alopecia areata.

Adolescent↗
PubMed2001

Effect of adenovirus-mediated expression of Sonic hedgehog gene on hair regrowth in mice with chemotherapy-induced alopecia.

BACKGROUND: The Sonic hedgehog (Shh) gene is involved in the initiation of hair growth. We have shown that localized, transient, enhanced expression of the Shh gene in mouse skin mediated by an adenovirus (AdShh) vector accelerates initiation of the anagen (i.e., growth) phase of hair follicle development. Because hair regrowth in chemotherapy-induced alopecia is associated with follicle cell proliferation and active melanogenesis similar to that observed in the anagen phase of normal hair growth, we examined whether AdShh-mediated Shh expression would accelerate hair regrowth in the skin of mice with chemotherapy-induced alopecia. METHODS: After establishment of cyclophosphamide-induced alopecia, in either 3- or 7-week-old mice, AdShh or a control vector (AdNull) was delivered to dorsal skin by intradermal injection. Hair regrowth and melanogenesis were assessed by histology and gross morphology. Fisher's exact test was used to compare differences in outcomes between AdShh-treated and control (AdNull-treated or not injected with any vector [naive]) mice. All statistical tests were two-sided. RESULTS: Northern blot analysis confirmed enhanced Shh expression after AdShh administration in 7-week-old mice. Two weeks after AdShh administration, the injection site (all of five mice) showed large, anagen-phase hair follicles with a normal distribution of melanin. In contrast, both skin treated with AdNull (all of five mice) and skin from naive mice (all of five mice) showed dystrophic hair follicles with irregular distribution of melanin (P<.001 in both comparisons). Gross morphologic observations confirmed that AdShh-treated mice, but not naive mice or AdNull-treated mice, showed skin darkening at the injection site indicative of entry into anagen phase (P<.001 in both comparisons). AdShh treatment of 3-week-old mice with cyclophosphamide-induced alopecia was followed by accelerated hair follicle recovery (19 of 22 mice); such recovery was not observed at this rate in AdNull-treated or naive skin (P<.001 for both comparisons). CONCLUSION: Localized, transient, enhanced expression of Shh gene in skin, mediated by an adenovirus vector, might be a future strategy to accelerate hair follicle regrowth after chemotherapy-induced alopecia.

Adenoviridae↗
PubMed1991

Cell degeneration in alopecia areata. An ultrastructural study.

The morphology and prevalence of different forms of cell degeneration in hair follicles in acute alopecia areata were investigated. In addition to apoptosis and necrosis, a third morphological pattern of cell degeneration, dark-cell transformation, was evident. Fifteen patients with untreated acute alopecia areata and three normal adults without hair loss were studied. Electron microscopy revealed that although apoptosis of outer root sheath keratinocytes produces normal hair follicle involution (catagen), increased levels of apoptosis, necrosis, and dark-cell formation appear to be related to the pathology of alopecia areata. Although cell degeneration was generally restricted to keratinocytes of the lower follicle, melanocytes, Langerhans' and dermal papilla cells were also affected. Keratinocytic degeneration may affect layers of matrix cells in alopecia areata, unlike the apoptosis of scattered outer root sheath cells in normal catagen. The extent of cell death suggests a pathological rather than a physiological event in alopecia areata.

Acute Disease↗
PubMed1985

Expression of HLA-DR by anagen hair follicles in alopecia areata.

The expression of HLA-DR within hair follicles in alopecia areata was studied using an immunoperoxidase method. Scalp biopsies were taken from 12 patients with alopecia areata and from 6 normal control subjects. Frozen sections were stained with a panel of 4 anti-HLA-DR monoclonal antibodies, Leu 2, Leu 3, Leu 4, and T6 antibodies. The expression of DR in normal hair follicles and in most anagen follicles from nonlesional alopecia skin was confined to dendritic cells which were sparse below the level of the arrector pilorum insertion. Of the 37 anagen follicles examined in lesional skin, 25 displayed staining for DR on epithelial cells in the precortical matrix and presumptive cortex. Six follicles showed DR staining in other epithelial compartments, the lower bulb matrix, inner root sheath, and outer root sheath. Infiltration of the hair bulb matrix by T cells was seen in the majority of follicles where epithelial cells were DR+. The aberrant expression of DR antigens by hair follicle epithelium provides direct evidence that immune mechanisms are operating in the pathogenesis of alopecia areata. In a previous study of alopecia areata we found evidence of cell injury confined to the precortical matrix and presumptive cortex in lesional anagen follicles. The relative restriction of epithelial DR expression to the same site suggests that this region of the follicle is of fundamental importance in the disease process.

Alopecia Areata↗
PubMed1994

Severity of alopecia areata is associated with a polymorphism in the interleukin-1 receptor antagonist gene.

One of the most potent pro-inflammatory mediators is the early-acting cytokine interleukin-1. Its actions are regulated by a structurally related anti-inflammatory cytokine known as the interleukin-1 receptor antagonist. We have previously characterized a DNA polymorphism in this gene (IL-1rn) and have found associations between allele 2 and several chronic inflammatory diseases. In the present study, we tested the frequency of allele 2 of the IL-1rn gene in 90 patients with alopecia areata compared with 261 healthy controls. There was a significant association between allele 2 of the polymorphism and the severity of alopecia areata. The frequency of allele 2 increased from 24.1% in the control population to 25.9% in patchy alopecia areata, 36.1% in alopecia totalis, and 47.2% in alopecia universalis (p = 0.005). This severity association is similar to that found in other epithelial-related diseases, including inflammatory bowel disease, lichen sclerosus, and systemic lupus erythematosus.

Alleles↗
PubMed2005

Two mouse mutations mapped to chromosome 11 with differing morphologies but similar progressive inflammatory alopecia.

Alopecia is a common dermatological condition in humans and other mammals. Here, we present two similar but histologically distinct mouse models of scarring alopecia. Both mutant lines were generated using random genome-wide N-ethyl-N-nitrosourea mutagenesis, and both harbor dominant mutations on chromosome 11. In both mutants, there is an early onset of alopecia that progresses to nearly complete pelage hair loss in both males and females by 20 weeks of age. Histologically, there is an increased dermal cellularity due to inflammatory cell infiltration at 7-10 days of age. By 3 weeks of age, the epidermis is acanthotic and the dermis is approximately twice as thick as in control mice due to a substantial, mostly mononuclear, inflammatory cell infiltrate. This infiltrate becomes more perifollicular by 4-5 weeks of age but is localized differently in the two mutants. In alopecia 1 (Alo-1), the perifollicular infiltrate is confined to the portion of the follicle within the dermis, whereas in Alo-2, the infiltrate extends the full length of the follicle. Expression of major histocompatibility complex (MHC) class I on the follicular epithelium in the two mutants is much greater than that in non-mutants. Furthermore, MHC class I expression is localized differently in the two mutant lines and mirrors the pattern of the inflammatory infiltrate. Despite these differences, the clinical progression of alopecia is identical in both mutants. The early onset of the disease, predictable progression, and differences in inflammatory cell localization between the two mutants make these mice particularly useful models for inflammatory hair loss and autoimmune diseases in general.

Alopecia↗
PubMed1999

Evaluation of thyroid function in north Indians with alopecia areata: response to intravenous injection of 100 micrograms thyrotropin releasing hormone (TRH).

There is a lack of agreement on the overall prevalence of thyroid disease and thyroid function abnormalities in alopecia areata. Only one study is available from the Indian subcontinent. All patients with alopecia areata attending a dermatology outpatient clinic between 1983 and 1997 were screened for the presence of clinical thyroid disease. Sixty-two consecutive patients during the year 1994 were evaluated in detail for thyroid functions by measuring T3, T4, TSH levels and testing for antithyroid and antimicrosomal antibodies. Twenty-two patients randomly selected from the above-mentioned sixty two were studied for TSH response to intravenous injection of 100 micrograms TRH at -20, 0 and 20, 60, and 120 minutes after TRH injection. Thyroid disease was clinically evident in 16 (0.85%) of the 1700 patients with alopecia areata seen over the last fifteen years. All sixty-two patients evaluated for thyroid functions were clinically euthyroid. Seven (11.3%) out of these 62 patients had abnormal thyroid hormone levels. Antithyroid and antimicrosomal antibodies were found in five patients; all five had abnormalities in thyroid function. TSH response to TRH was suggestive of hypothyroidism in 4 (18%) of the 22 patients studied. Manifest thyroid disease is infrequently associated with alopecia areata. Abnormalities in thyroid functional status were more frequent; they were found in 7 (11.3%) out of 62 patients. TSH response to intravenous TRH was abnormal in an even higher proportion [4 (18%) out of 22 patients]. There was no apparent correlation with duration or type of alopecia areata.

Adolescent↗
PubMed2002

Seventeen cases of alopecia areata: combination of SADBE topical immunotherapy with other therapies.

Topical immunotherapy is effective for severe alopecia areata. However, there are patients with alopecia areata refractory to topical immunotherapy alone. We tried SADBE (squaric acid dibutylester) topical immunotherapy combined with topical dry ice cryotherapy, carpronium chloride (a parasympathetic nerve stimulant) and/or oral cepharanthin (a biscoclaur alkaloid) in alopecia areata refractory to topical SADBE. Seventeen patients with alopecia areata (3 multiple, 3 ophiasis, 5 totalis and 6 universalis) were treated with SADBE in our department in 1999 to 2001. In 3 cases (2 multiple and 1 universalis) out of the 17 cases, cosmetically acceptable regrowth of hair was observed in several months with topical SADBE alone. In the other 14 cases, the SADBE therapy alone for several months (mean: 6.9 months) resulted in no or poor regrowth of hair. However, with subsequent combination therapy of topical SADBE for several months (mean: 7.6 months), satisfactory regrowth of hair was observed in 6 of the 14 cases. Our cases indicate that combination therapy of topical SADBE with other therapies can be a choice for alopecia areata which is refractory to topical SADBE therapy alone.

Adjuvants, Immunologic↗
PubMed1995

PUVA treatment of alopecia areata partialis, totalis and universalis: audit of 10 years' experience at St John's Institute of Dermatology.

Our 10-year experience with PUVA treatment for alopecia areata, partialis, totalis and universalis was retrospectively reviewed using charts and follow-up questionnaires for 70 patients at St John's Institute of Dermatology. In all cases, several previous therapies were judged to be unsatisfactory prior to starting PUVA, and many cases were already deemed clinically refractory prior to referral for PUVA. If cases of vellus hair growth are excluded, and those who lost their PUVA-induced regrowth rapidly on follow-up, the effective success rate was at best 6.3% for alopecia areata partialis, 12.5% for alopecia areata totalis and 13.3% for alopecia areata universalis. We affirm that PUVA is generally not an effective treatment for alopecia areata.

Adolescent↗
PubMed1992

Profile of alopecia areata: a questionnaire analysis of patient and family.

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↗
PubMed1994

Prevalence of thyroid diseases in patients with alopecia areata.

BACKGROUND: The prevalence of thyroid disease in patients with alopecia areata previously reported varied from 0 to 28%. These thyroid diseases, include Hashimoto's thyroiditis, Graves' disease, simple goiter, and others. METHODS: The prevalence of thyroid diseases was determined in 152 consecutive patients with alopecia areata who presented to the dermatology clinic. A complete history was taken and a physical examination was performed. Thyroxine, triiodothyronine, thyroid-stimulating hormone, and microsomal antibody levels were measured in every patient. The control group consisted of 152 age- and sex-matched volunteers who had skin diseases other than alopecia areata or autoimmune disorders. RESULTS: Among 152 patients, age 10-59 years, four cases (2.6%) had a small simple goiter. Microsomal antibodies were detected in seven other patients (4.6%) with titers ranging from 1:100 to 1:1600. None of these seven patients had signs or symptoms of thyroid disease. Five cases (3.3%) of the control group had positive microsomal antibody tests with titers ranging from 1:100 to 1:400. The prevalence of positive microsomal antibodies in the alopecia areata group was not statistically different from the control group (chi 2 = 0.347, DF = 1, P = 0.5558). CONCLUSIONS: Among 152 patients with alopecia areata, 4.6% of patients had microsomal antibodies and 2.6% had a small simple goiter. Thus the prevalence of thyroid disease among these patients was 7.2%. The prevalence of positive microsomal antibodies in 4.6% of the patients was not statistically different from that of the control group.

Adolescent↗
PubMed1995

Antismooth muscle and antiparietal cell antibodies in Indians with alopecia areata.

BACKGROUND: Alopecia areata is suspected to be an autoimmune disease. We studied 104 consecutive patients with alopecia areata for the presence of autoantibodies and associated autoimmune diseases. METHODS: A detailed history and examination was carried out in all patients to look for associated atopy, diabetes mellitus, hypertension, rheumatoid arthritis, vitiligo, lupus erythematosus, and thyroid disorders, etc. in the patients or their family members. Venous blood for estimation of fasting and postprandial blood glucose was collected in 30 patients, especially in those with family history of diabetes mellitus. Antimitochondrial (AMA), antismooth muscle (SMA), antinuclear antibodies (ANA), antiparietal cell antibody (PCA), and antibody against thyroid microsome (TMA) were detected employing indirect immunofluorescence on a composite section of rat liver, stomach, kidney, and human thyroid. Skin biopsy was processed for direct immunofluorescence by a conventional technique. RESULTS: Disseminated discoid lupus erythematosus, lichen planus, urticaria, psoriasis, and seronegative spondylarthritis were associated with alopecia areata in one case each. Antismooth-muscle-antibodies and PCA were found in 36 (34.6%) and 44 (42.3%) patients respectively, followed by TMA in 8 (7.7%), AMA in 6 (5.7%), antithyroglobulin antibodies in 3 (2.8%), and ANA in 2 (1.9%) patients. The incidence of SMA was higher in men with alopecia areata (P < 0.001). Direct immunofluorescence carried out in 24 patients did not reveal significant findings, except for occasional immunoglobulin deposits around hair follicles and blood vessels. CONCLUSION: Alopecia areata in India is associated more often with antismooth muscle and antiparietal cell antibodies.

Adult↗
PubMed1998

Myasthenia gravis with alopecia totalis.

Myasthenia gravis was diagnosed on the basis of a positive Tensilon test in a 4-year-old male child with alopecia totalis. His scalp hair and eyebrows had began to disappear at the age of 10 months. No other physical abnormalities such as motor paralysis, were seen except for left ptosis and alopecia totalis. His serum titer of anti-acetylcholine receptor antibody was elevated. No immune system abnormalities (C3, C4, CH50, C-reactive protein, antinuclear antibody or lymphocyte function disorders) were detected. Although alopecia areata and alopecia totalis are sometimes present in adults with autoimmune diseases and myasthenia gravis, this association is rare in children. The present case represents the youngest patient with myasthenia gravis associated with alopecia totalis.

Alopecia↗
PubMed1994

Prevalence of nail abnormalities in children with alopecia areata.

We assessed the prevalence of nail abnormalities in 272 children with alopecia areata who were seen in our department during an eight-year period. Of these, 126 (46%; 50 girls, 76 boys) had nail abnormalities that were related to alopecia areata. Nail pitting was detected in 92 patients, including 37 with alopecia totalis or alopecia universalis. Three patients experienced an onychomadesis of all 20 nails during the acute onset of alopecia areata universalis. Thirty-two (11.7%) had nail thinning and severe nail plate surface abnormalities that were consistent with a diagnosis of trachyonychia.

Adolescent↗
PubMed1995

Congenital triangular alopecia (Brauer nevus).

Congenital triangular alopecia is manifested at 3 to 5 years of age by unilateral or, less frequently, bilateral patches of alopecia in the frontotemporal region. At this age the differential diagnosis is important, particularly as regards alopecia areata. Only about 47 cases have been reported, probably because the lesion is benign and nonprogressive. In 6200 patients seen in index visits, we found 7 with triangular alopecia, a frequency of 0.11%. We believe that males do not require treatment because of the later development of androgenic alopecia, but in women, surgical treatment is successful.

Adolescent↗
PubMed1995

Seasonal flank alopecia in affenpinschers.

Two intact, distantly related, female affenpinschers, belonging to a breeder, were referred in March 1993 for the investigation of bilateral, symmetrical flank alopecia in one bitch and bilateral, symmetrical flank, dorsum and tail alopecia in the other; the alopecia occurred from November to May and January to May, respectively. During that period the bitches were kept in a conservatory without artificial heating or lighting. The owner reported that the mother of one bitch had had bilateral, symmetrical flank alopecia during one winter when kept in the conservatory, but was normal the following winter when kept in the house. Three other females and a male exhibited the same clinical signs when kept in the conservatory during the winter. Seasonal flank alopecia has not previously been reported in affenpinschers.

Alopecia↗
PubMed1975

Alopecia areata, autoimmunity, and Down's syndrome.

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.

Adolescent↗
PubMed2005

Alopecia areata universalis sparing nevus flammeus.

Alopecia areata is a common form of nonscarring hair disorder of unclear etiology. Cases with alopecia areata sparing congenital melanocytic nevi have been described. It is explained by the Renbök phenomenon or inverse Köbner phenomenon, which refers to normal hair growth in the psoriatic lesions observed in patients with psoriasis and alopecia areata. We report a 30-year-old man presenting with rapidly progressing alopecia areata universalis, which spared a large nevus flammeus on the left parietal scalp. Our case gives further evidence to the notion that nevus as genetic mosaic may show genetically determined resistance to alopecia areata.

Adult↗