Co-existing proteinase 3-antineutrophil cytoplasmic antibody-associated vasculitis with immunoglobulin A nephropathy

No abstract available.

Clinical application of anti-proteinase 3 capture ELISA in diagnosis of Wegener's granulomatosis / 临床检验杂志

Objective To investige the sensitivity and specificity of anti-proteinase 3 (PR3) capture ELISA in diagnosis of Wegener's granulomatosis (WG),and the correlation between the capture ELISA and indirect immunofluorescence assay (IIF).Methods Anti-PR3 antibody and anti-neutrophil cytoplasmic antibody (cANCA) in sera from 72 patients with WG,206 healthy blood donors and 24 patients with autoimmune diseases were detected by classic ELISA,capture ELISA and IIF.Results The sensitivities of classic ELISA and capture ELISA for detection of anti-PR3 in WG diagnosis were 73.6% and 87.5% respectively.The specificities of both the ELISAs were identical (100%).Detection of anti-PR3 by ELISA or IIF alone led to the serological hit rate of 87.5% and 84.7% for WG respectively,but the combination of capture ELISA and IIF increase the hit rate up to 91.6%.Conclusions The sensitivity of anti-PR3 capture ELISA as well as its correlation with IIF is prior to classic anti-PR3 ELISA.The combined detection of anti-PR3 capture ELISA and IIF may increase the diagnosis rate of clinically suspected WG.

Effect of Camostat Mesylate on Chemical Compositions of Bile and Crystallization in Gallbladder Stone Patients

BACKGROUND: It has been well demonstrated that trypsin inhibitor can stimulate the secretion of cholecystokinin. Camostat mesylate (C20H22N4O5 CH3SO3H) is a synthetic trypsin inhibitor. We demonstrated the effect of camostat mesylate on the chemical composition of bile and the crystallization in gallbladder-stone patients. METHODS: Gallbladder bile sample from 22 patients with GB stones were analyzed. In 11 patients, camostat mesylate (Foy-pan ) was administered orally in a dosage of 600 mg per day for more than 5 days, and the results of the bile analysis were compared to those of 11 controls. RESULTS: The total protein concentration in the camostat group was lower than that in control group (0.21+/-0.10 vs 0.24+/-0.06 g/dl) but the difference was not significant (p=0.41). The total bile acid concentration in the camostat group was significantly lower than that in the control group (5.47+/-1.56 vs 6.85+/-1.32 g/dl, p=0.04). The concentrations of cholesterol and phospholipid were lower in the camostat group (0.35 +/- 0.19 vs 0.44 +/- 0.11 g/dl, 2.10 +/- 1.19 vs 2.92 +/- 0.93, respectively), but the differences were not statistically significant (p=0.20, p=0.09, respectively). The total lipid concentration which reflects the concentrated magnitude of the bile, was significantly lower in the camostat group (7.93 +/- 2.87 vs 10.20 +/- 2.01 g/dl, p=0.04). The cholesterol saturation index didn't demonstrate a significant difference between the two groups (1.06 +/- 0.27 vs 0.95 +/- 0.31, p=0.38). Crystallization in the bile from cholesterol stone patients, was observed every day for 7 days. Crystallizations was less frequent in the camostat group, but the difference was not statistically significant (1/6 vs 4/8, p=0.39). DISIDA (disofenin iminediacetate) scans were performed in 3 healthy volunteers to observe the changes in the radioactivities and the volumes of the gallbladders before and after the administrations of camostat. The peak radioactivities, the transittime to the peak radioactivity, and the gallbladder volume at the peak radioactivity in the scan after the administration of camostat were lower than in the corresponding values before the administration. CONCLUSIONS: Camostat mesylate lowers the concentration of all bile components. We assume that the effects of Camostat mesylate are mediated by CCK, which enhances gallbladder motility and limits the concentrating function of the gallbladder.