Decreases In CRP Research Articles

Myeloperoxidase-antineutrophil cytoplasmic antibody-related crescentic glomerulonephritis after treatment for clinically amyopathic dermatomyositis: a coincidental combination or not?

A 60-year-old Japanese man exhibited rapidly progressive glomerulonephritis 10years after receiving prednisolone therapy for clinically amyopathic dermatomyositis (CADM). Upon admission, there were no signs of dermatomyositis. Laboratory analyses revealed the presence of myeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA) at 1,280 EU in the absence of anti-glomerular basement membrane antibody and anti-melanoma differentiation-associated gene 5 antibodies, which are typically expressed in CADM. A renal biopsy demonstrated that 14 of 29 glomeruli showed global sclerosis, and the remaining 15 glomeruli exhibited fibrotic and fibrocellular crescent formation without immunoglobulin and complement. Following treatment with 500mg/day methylprednisolone pulse therapy for 3days, the patient was started on 30mg/day of prednisolone orally. On the third day of hospitalization, we began hemodialysis for uremia and anuria with three treatments of plasma exchange starting on the tenth hospital day. Unfortunately, the patient's renal function did not recover, despite decreases in CRP and MPO-ANCA levels to the normal range. This case is the first English language report of MPO-ANCA-related crescentic glomerulonephritis in a patient who had recovered from CADM.

Relation of Improvement in Endothelium-Dependent Flow-Mediated Vasodilation After Rosiglitazone to Changes in Asymmetric Dimethylarginine, Endothelin-1, and C-Reactive Protein in Nondiabetic Patients With the Metabolic Syndrome

The mechanisms by which thiazolidinediones exert beneficial effects on the endothelium are still not clear. We examined the effects of rosiglitazone on the plasma markers of metabolic control (glucose, insulin, adiponectin, resistin, and lipid profiles), markers of inflammation (high-sensitivity C-reactive protein [CRP], interleukin-6, soluble CD40 ligand, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1), and markers of vasoreactivity (asymmetric dimethylarginine [ADMA] and endothelin-1) and analyzed the relations between changes in endothelium-dependent flow-mediated dilation of the brachial artery and changes in these markers to elucidate their roles in mediating the vascular protective effects of rosiglitazone. Of 70 nondiabetic patients who met a modified National Cholesterol Education Program definition of the metabolic syndrome, 35 were randomized to receive rosiglitazone (4 mg/day) and 35 to receive placebo for 8 weeks. At study end, treatment with rosiglitazone had significantly reduced plasma insulin (-25%, p = 0.004) and resistin (-16%, p <0.001), increased adiponectin (164%, p <0.001), low-density lipoprotein cholesterol (16%, p = 0.005), and apolipoprotein-B (14%, p = 0.003), and decreased CRP (-30%, p = 0.005), soluble CD40 ligand (-20%, p = 0.014), ADMA (-16%, p <0.001), and endothelin-1 (-11%, p <0.001) concentrations and systolic and diastolic blood pressures. Rosiglitazone treatment significantly improved flow-mediated dilation (p <0.001) and nitroglycerin-induced vasodilation (p = 0.001) of the right brachial artery. On multivariate analysis, changes in ADMA, endothelin-1, and CRP were independent predictors of improved endothelial reactivity with rosiglitazone. In conclusion, we have, for the first time, demonstrated the independent associations between the improvement in flow-mediated dilation and reductions in ADMA, endothelin-1, and CRP after 8 weeks of treatment with rosiglitazone in nondiabetic patients with the metabolic syndrome. These findings suggest that decreases in ADMA, endothelin-1, and CRP may serve as possible mechanisms for the improvement in endothelial function conferred by rosiglitazone treatment.