Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in Japan.

BACKGROUND: The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients. MATERIALS AND METHODS: Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 x 10(9) L(-1) were defined as idiopathic thrombocytopenic purpura responders. RESULTS: Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 x 10(9) L(-1) in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori-negative patients experienced the same improvement (P = 0.015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0.015). CONCLUSIONS: Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity.

Takayasu's arteritis associated with ulcerative colitis; genetic factors in this association.

Both ulcerative colitis and Takayasu's arteritis are though to be organ-specific immune-mediated inflammatory diseases. We present the rare case of a 23-year-old woman with a 4-year history of ulcerative colitis who developed Takayasu's arteritis one month after giving birth. She was found to carry the human leukocyte antigens (HLA)-B52 and DR2, which were previously noted to be associated with these inflammatory conditions in the Japanese population. The pathogenic relevance of this haplotype to the concomitant development of these two conditions is discussed.

Studies on duodenal cyclic AMP content content in pancreatic disease after administration of pancreozymin and secretin.

Cyclic AMP (cAMP) output in the duodenal contents of 11 normal subjects, 18 patients with chronic pancreatitis, six convalescing from acute pancreatitis and five with pancreatic carcinoma was measured after a single dose of pancreozymin and secretin. The technic was indirect, utilizing recovery of duodenal contents by the Dreiling tube rather than direct measurements of fluid that was not contaminated by bile. In all patients groups, cAMP output reached a peak after this stimulation with a concomitant increase of bicarbonate and amylase outputs. A significantly decreased cAMP output was observed in all pancreatic disease groups compared to the normal group. Patients with chronic pancreatitis showed a slightly decreased cAMP output, considerably decreased bicarbonate output and normal amylase output. In acute pancreatitis cAMP output was reduced with normal bicarbonate and amylase outputs. In pancreatic carcinoma cAMP decreased significantly, bicarbonate output was moderately reduced and amylase output was normal. cAMP output in all groups studied did not correlate with either bicarbonate output or amylase output.

Serum secretory component level in myeloma patients with disorders of the secretory surface.

Secretory component (SC) in myeloma serum was measured by a double antibody radioimmunoassay. It was elevated in patients with IgA myeloma and the highest level was observed in a patient with macroglobulinemia. The presence of disorders of secretory surface in myeloma patients slightly but not significantly elevated the serum SC concentration. A significant correlation between serum SC and IgG is demonstrated, but not between serum SC and IgA. Over the whole patient groups, serum SC is significantly related to serum IgM but not when patients with macroglobulinemia are excluded from the calculation. Serum SC is present as SC-IgM in macroglobulinemia and SC-IgM and SC-IgA in IgA myeloma.

Studies on circulating immune complexes of the liver diseases. 5. Anti-DNA antibodies and C1q binding activity.

Anti-dsDNA and anti-ssDNA antibodies, rheumatoid factors, HBsAg and C1q binding activity were determined in sera of patients with various liver diseases. Anti-dsDNA were only slightly increased in chronic aggressive hepatitis, activity severe and liver cirrhosis. A moderate elevation of anti-dsDNA was detected in possible lupoid hepatitis and it was highly increased in lupoid hepatitis as well as systemic lupus erythematosus. Non-specific elevation of anti-ssDNA titers were observed in all of the liver disease groups. In patients with increased anti-dsDNA titers, C1q binding activity and titers for rheumatoid factor and HBsAg tended to increase. According to reactivity of their sera to DNA, patients with liver disease could be divided in 4 groups: 1. high responders to dsDNA (lupoid hepatitis), 2. moderate responders to dsDNA (possible lupoid hepatitis or lupoid-like liver disease), 3. low responders (only positive for ssDNA), and 4. non-responders.

Studies on circulating immune complexes of the liver disease. 3. Conditions for Clq binding assay and low molecular weight Clq reactants.

Assay conditions for Clq binding activity (ClqBA) of aggregated human gamma globulin and pathologic sera were studied. The Clq component of complement was isolated by precipitation method and effectively radioiodinated using lactoperoxidase without loss of binding activity. The assay method was reproducible and the binding activity of normal sera was 5.0 +/- 2.4% (mean +/- S.D.). Amount of 125I-Clq, in the range of 50--1000 ng per assay tube, did not influence the binding activity. Competitive inhibition of intrinsic Clq was very limited. Sample sera for the determination can be stored at --20 degrees C and freezing-throwing of the sera did not increase ClqBA. In normal sera, the existence of solubilizer of Clq-reactant-complex or inhibitor of Clq-reactant binding working at 37 degrees C is suggested. For the low molecular weight reactants in pathologic sera reacting with Clq at 4 degrees C, following substances are proposed: 1. abnormal IgG, 2. hapten-IgG complexes or 3. anionic substances.

Studies on circulating immune complexes of the liver disease. 4. Clq binding activity.

Serum Clq binding activity (ClqBA) is increased in diabetes mellitus with liver injury, carcinoma of gastrointestinal tract with metastatic liver and chronic liver disease (CLD). Significant elevations of ClqBA level are observed in the order of liver cirrhosis, chronic aggressive hepatitis and chronic persistent hepatitis. In CLD there are significant correlations between ClqBA and gamma-globulin, rheumatoid factor, anti-DNA-antibody, CH50, C3, C4, C3-activator and HBsAg.

Studies on secretory component in digestive disease. IV. Levels of serum secretory component in liver disease.

The levels of serum secretory component (SC), immunoglobulins, rheumatoid factor, HBs-antigen and HBs-antibody were determined in patients with liver disease, especially chronic liver disease. In chronic liver disease, decreases in serum SC were accompanied by increases in the titer of rheumatoid factor. Patients with chronic liver disease and HBs-antigen or HBs-antibody had decreased levels of serum SC compared to seronegative patients. There was no correlation between the levels of serum SC and immunoglobulin in patients with chronic liver disease.

Studies on circulating soluble immune complexes of the liver disease. 2. Serum inhibitory activity of polyclonal rheumatoid factor binding to IgG-sepharose.

Circulating immune complexes were tested in the liver disease by measuring polyclonal rheumatoid factor (pRF) inhibition activity. The test is based on the inhibition of 125I-pRF binding to IgG-p-azobenzamidoethyl Sepharose 6B. Normal levels of the test were less than 23%. The inhibition activity in sera with liver disease was found to correlate with severity of the disease, as defined by histological criteria. There were correlations of the activity with serum gamma-globulin concentration, seropositivities for rheumatoid factor and hepatitis B antigen.

Studies on circulating soluble immune complexes of the liver disease. 1. Inhibition assay of polyclonal rheumatoid factor binding to IgG-sepharose.

Polyclonal rheumatoid factor (pRF) was isolated from sera seropositive for RF and it was radioiodinated with lactoperoxidase method. Using the 125I-pRF and IgG-p-azobenzamidoethyl Sepharose 6B, a competitive inhibition radioassay for detecting immune complexes is described. The assay can be performed in 90 min utilizing 10 microliter of serum with good reproducibility and endogenous RF in test serum did not interfere the reaction. The test can detect complexes nearly to 8s and as low as 0.1 microgram/ml of aggregated human IgG. Decomplementation by heating test sera is unnecessary. The assay was performed at 4 degrees C but less inhibition activity was obtained when it was carried out at 24 degrees C.