Phenomena observed are analyzed using Bouguer’s law. (C) 2010 American Institute of Physics. [doi:10.1063/1.3327236]“
“Disease-modifying antirheumatic drugs (DMARDs) improve the disability and slow the progression of the joint damage in rheumatoid arthritis (RA). However, a large proportion of patients experience inefficacy by the end of 2 years. This loss of
efficacy may be due to expression of multidrug resistance (MDR) proteins on lymphocytes. The objective is to study the expression of MDR protein on the peripheral blood CH5424802 solubility dmso lymphocytes in patients with RA and correlate it with the disease status and response to treatment. Twenty-eight patients were enrolled. Expression of MDR-1 by flow cytometry was carried out on lymphocytes at baseline and after 4 months of therapy. This expression was correlated with disease activity scores (DAS 28). There
were 25 females with mean age of 48.13 years and median disease duration of 48 months. Eighteen patients were DMARD naive and ten were refractory to DMARD (methotrexate). The percentage of cells expressing MDR-1 in the DMARD-naive (p < 0.O5) and DMARD-refractory (p < 0.05) groups were significantly higher than the healthy controls at the baseline. The relative fluorescence intensity was significantly higher in the DMARD-refractory group (p < 0.05) as compared to the DMARD-naive group. After 4 months of therapy, there was significant improvement in the D value (p < 0.01) in the DMARD-naive group (treated with methotrexate only) and DMARD-refractory group Epacadostat solubility dmso (p < 0.05). A significant correlation (r = 0.563) between the DAS 28 scores and the D value (p = 0.003) was observed. Expression of MDR-1 in RA correlated with disease activity status and improved with DMARD therapy. It is not related to the refractoriness to therapy with methotrexate.”
reactive perforating dermatosis is characterized by umbilicated erythematous papules and plaques with firmly adherent crusts. Histopathological examination shows a typical cup-shaped ulceration in the epidermis containing cellular debris and collagen. There is transepidermal check details elimination of degenerated material with basophilic collagen bundles. The etiology and pathogenesis of acquired reactive perforating dermatosis are unclear. Metabolic disorders and malignancies are associated with this dermatosis. Associated pruritus is regarded as a key pathogenic factor. Constant scratching may cause a repetitive trauma to the skin. This pathogenesis may involve a genetic predisposition. The trauma may lead to degeneration of the collagen bundles. Treatment of acquired reactive perforating dermatosis follows a multimodal approach. Apart from the treating any underlying disease, treatment of pruritus is a major goal. Systemic steroids and retinoids, as well as UVB phototherapy are well-established treatment options. Some patients may also benefit from oral allopurinol.