alopecia areata/phosphatase

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

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

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

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

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

The expression of T6 antigen within hair follicles in alopecia areata was studied using the APAAP technique (alkaline phosphatase monoclonal anti-alkaline phosphatase method). Scalp biopsies were taken from 15 subjects with alopecia areata, nine in an active stage and 6 in a stationary stage of the

For unknown reasons, the pilosebaceous unit displays prominent alkaline phosphatase (AP) activity, and alterations in AP activity are seen in alopecia areata. The role of AP in hair biology and pathology has been obscured by contradictory reports on the localization and activity of AP during the

Alopecia areata is an acquired hair loss disorder resulting from an immunologically- mediated attack on hair follicles and autoimmunity may play a part in its pathogenesis. The non-synonymous C1858T substitution in the PTPN22 gene, which encodes lymphoid protein tyrosine phosphatase, has been shown

BACKGROUND Alopecia areata (AA) is a T cell-mediated autoimmune disease that causes inflammation around anagen-phase hair follicles. Insufficient levels of vitamin D have been implicated in a variety of autoimmune diseases. OBJECTIVE To investigate the status of serum 25-hydroxyvitamin D (25(OH)D)

Hereditary vitamin D-resistant rickets type or vitamin D-dependent rickets type II is a genetically determined and rare autosomal recessive disorder, most often caused by mutations in the vitamin D receptor gene. It usually presents with rachitic changes not responsive to vitamin D treatment and the

Cyclosporin A (CsA), a cyclic endecapeptide, is a T cell-specific immunosuppressant and is successfully used in the field of organ transplantation. Another T cell-specific immunosuppressant, FK506, a more recently discovered macrolide antibiotic, is effective against graft rejection at much lower

The authors examined 2 groups of patients treated in the Department of Dermatology in Lublin: I--acne phlegmonosa patients, II--alopecia areata patients. In the I group the zinc content was examined in hair using the atomic absorption spectrophotometry method (ASA). The results obtained with this