alopecia/phosphatase

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Protein tyrosine phosphatase nonreceptor type 22 gene polymorphism in alopecia areata: Does it have an association with disease severity?

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Alopecia areata is a condition involving hair loss from certain or all areas of the body. It has been considered as an immune-mediated disease, characterized by the infiltration of CD4+ and CD8+ lymphocytes in the hair follicles.The study aimed to assess

Alkaline phosphatase in alopecia areata.

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Male pattern alopecia a histopathologic and histochemical study.

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Three hundred and forty-seven tissue specimens were studied from 23 patients with male pattern alopecia. Characteristic features of pattern alopecia included: the presence of miniature or vellus follicles; a marked enlargement of the sebaceous glands and arrectores pilorum muscles; the presence of

Epidemiologic and genetic characteristics of alopecia areata (part 2).

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Alopecia areata (AA) is hypothesized to be an organ-specific autoimmune disease mediated by T cells to the hair follicles. Despite the fact that most cases of AA are sporadic, there is an accumulation of evidence that AA is a complex multigenetic trait with components of inherited predisposition. In

Factors Associated with Severity of Alopecia Areata.

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BACKGROUND Alopecia areata is the most common cause of localized, nonscarring alopecia. Unfortunately, there are few data regarding clinical features and epidemiology of alopecia areata in Korean patients, and its clinical course and treatment response rates are unpredictable. OBJECTIVE This study

Hair bundle defects and loss of function in the vestibular end organs of mice lacking the receptor-like inositol lipid phosphatase PTPRQ.

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Recent studies have shown that mutations in PTPRQ, a gene encoding a receptor-like inositol lipid phosphatase, cause recessive, nonsyndromic, hereditary hearing loss with associated vestibular dysfunction. Although null mutations in Ptprq cause the loss of high-frequency auditory hair cells and

The R620W polymorphism in PTPN22 confers general susceptibility for the development of alopecia areata.

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BACKGROUND The functional R620W (c.1858C>T) variant of the protein tyrosine phosphatase nonreceptor 22 gene (PTPN22) has been associated with a variety of autoimmune disorders. A recent study has suggested that R620W also contributes to the severe form of alopecia areata (AA). OBJECTIVE We sought to

PTPN22 profile indicates a novel risk group in Alopecia areata.

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Alopecia areata (AA) is a genetically determined autoimmune hair loss disorder. A polymorphism in protein tyrosine phosphatase N22 (PTPN22), which normally suppresses T-cell proliferation, has been associated with human autoimmune disease, including AA in European populations. PTPN22 genotype

Association between PTPN22 C1858T polymorphism and alopecia areata risk.

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Alopecia areata (AA) is a skin condition in which hair is lost from certain or all areas of the body. This condition has been described as an immune-mediated complex genetic disease, characterized by the presence of lymphocytes that are directed to the hair follicles in the anagen phase. The gene

Hair follicle morphogenesis and epidermal homeostasis in we/we wal/wal mice with postnatal alopecia.

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Mice with skin and hair follicle (HF) defects are common models of human skin disorders. A mutant strain with the we/we wal/wal genotype develops alopecia. We found the hair shaft structure in the pelage of mutant mice to have significant defects. Although these mice lose their hair at 21 days, a

Generalized trichoepitheliomas with alopecia and myasthenia gravis: clinicopathologic and immunohistochemical study and comparison with classic and desmoplastic trichoepithelioma.

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We report on a patient with a syndrome characterized by smooth facial papules and nodules; alopecia of the eyebrows, eyelashes, and most body hair; mild alopecia of scalp hair; possibly hypohidrosis; and myasthenia gravis. The clinical, histologic, and immunohistochemical findings are compared with

Vitamin D-Dependent Rickets Type II with Alopecia: A Rare Case Report.

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Vitamin D-dependent rickets type II is a rare hereditary disorder. It occurs due to mutations in the gene chr. 12q12-q14, which codes for vitamin D receptor. End-organ resistance to 1,25-(OH)2 vitamin D3 and alopecia in severe cases are the characteristic features. We report a case of a 4-year-old

Enteral calcium infusion used successfully as treatment for a patient with hereditary vitamin D resistant rickets (HVDRR) without alopecia: a novel mutation.

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BACKGROUND We report a novel mutation in a case of hereditary vitamin D resistant rickets (HVDRR) without alopecia and successful management of this condition with the intravenous formulation of calcium chloride delivered via gastric tube. METHODS A 22 month old male (length -3.4 SDS; weight -2.1

A novel mutation in helix 12 of the vitamin D receptor impairs coactivator interaction and causes hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia.

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Hereditary vitamin D-resistant rickets (HVDRR) is a genetic disorder most often caused by mutations in the vitamin D receptor (VDR). The patient in this study exhibited the typical clinical features of HVDRR with early onset rickets, hypocalcemia, secondary hyperparathyroidism, and elevated serum

Effectiveness of scalp cooling in reducing alopecia caused by epirubicin treatment of advanced breast cancer.

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The value of scalp cooling in the prevention of alopecia was investigated in 32 patients with advanced breast cancer who were given a mean of four courses of 40-80 mg/m2 of epirubicin. None of the 15 patients free from liver metastases who received scalp cooling required a wig, whereas four of eight

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Herbal & Natural Medicine

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