Sequential US can determine disease progression in patients with early RA. Such data may allow the clinician to treat RA patients earlier in the hope of preventing joint damage.
Gouty arthritis is uncommon in SLE; it occurs primarily in patients with long-standing SLE and nephritis. Worsening renal function usually preceded gout attacks, but SLE disease activity was minimal. Crystal-induced arthritis should be included in the differential diagnosis of a lupus patient presenting with acute inflammatory arthritis because the long-term treatment of the two conditions differs substantially.
Dose-response curves for the effect of continuous intravenous infusion of histamine on the gastric acid secretion was obtained in nine healthy volunteers of Indian origin. Each subject was studied with 5 doses (20, 40, 60, 80, and 100 μg/kg/h) of histamine acid phosphate administered for 3 h, on separate days, in random fashion. The plateau of secretion occurred in the 2nd h of infusion. The analysis of variance revealed that acid output significantly increased with increasing dose of histamine; the increase in acid output was significant at all dose levels except between 80 and 100 μg/kg/h. The analysis of data using dose of histamine independent of body weight gave a poorer fit to the regression line than that obtained with histamine dose on the basis of body weight, suggesting that dose of histamine should be administered on the basis of body weight. The estimate of calculated Vmax and the dose of histamine producing a response 50% of Vmax or (Km) by the three different transformations of the Michaelis-Menten equation gave somewhat different values for both these constants. All these were slightly different from direct estimation of Vmax and Km with analysis of curvilinear regression. The linear transformation using the plot of Cs/v versus Cs gave the best results. The double reciprocal plot underestimated both the constants. The value of Km in Indian subjects was almost six times the value in Western subjects, indicating the relative insensitivity of the parietal cells to histamine in our subjects.
Metiamide was given orally in one dose of 200 mg in 23 sutdies in patients with duodenal ulcer, 4 in the basal state, 11 during histamine infusion, and 8 before insulin hypoglycemia stimulation. In the latter 8 patients insulin was given at another time without metiamide. In 17 studies acid secretion was suppressed by metiamide--up to 75% in the basal state, 53% after histamine, and 80% after insulin. Pepsin secretion was reduced to the same extent as H+ in the histamine studies but not in the basal (57%) or insulin (44%) studies, so that in the latter pepsin/acid ratios were 3-fold greater than in controls. Blood levels of metiamide were measured in 17 studies. In 10 out of 11 who showed inhibition of 40% or more, peak blood levels of metiamide were 0.45 mug/ml to 1.25 mug/ml. In 5 of 6 who did not show inhibition, blood levels were 0.05-0.4 mug/ml; in the sixth it was 0.8 mug/ml. Therefore a critical blood level for suppression of basal or stimulated secretion appears to be approximately 0.45 mug/ml.
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