Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD). The Rabeprazole Study Group.

Rabeprazole, a new proton pump inhibitor, was studied in patients with acid-peptic-related diseases (duodenal ulcer, gastric ulcer, GERD) in three placebo-controlled, double-blind, randomized clinical trials. Men and women over the age of 18 were enrolled if the presence of an active duodenal or gastric ulcer or erosive or ulcerative esophagitis was confirmed on upper gastrointestinal endoscopy. Patients were randomly allocated to either placebo or rabeprazole 20 mg or 40 mg in the duodenal and gastric ulcer protocols or to placebo or rabeprazole 10 mg, 20 mg, or 40 mg in the GERD protocol. All doses of rabeprazole in all three studies were statistically significantly superior to placebo in healing acid-related lesions. There were no treatment differences between the rabeprazole doses in healing active peptic lesions. The incidence of positive [13C]urea breath test for H. pylori was 53% in patients with duodenal or gastric ulcers. H. pylori status was not effected by treatment with rabeprazole.

Large-cell anaplastic (Ki-1-positive) lymphoma complicated by disseminated intravascular coagulation.

Large-cell anaplastic lymphoma (Ki-1-positive lymphoma) was first described as a type of large-cell lymphoma that has morphologic, enzymatic, and immunologic similarities to malignant histiocytosis. To date, an association between Ki-1-positive lymphoma and disseminated intravascular coagulation has not been described, but cases of malignant histiocytosis with disseminated intravascular coagulation have been reported. We report a case of anaplastic, Ki-1-positive, large-cell lymphoma complicated by clinical and laboratory evidence of disseminated intravascular coagulation with histologic evidence of vascular invasion and fibrin thrombi.

Angiocentric immunoproliferative lesion (lymphomatoid granulomatosis). A cytogenetic, immunophenotypic, and genotypic study.

We report the occurrence of a cytogenetically abnormal clone 46,XX,t(1;6)(p35;q23),t(1;9;19)(q23;p24;q13) in the spleen of a 23-year-old woman with a three-year history of angiocentric immunoproliferative lesion (AIL) (lymphomatoid granulomatosis). The skin, lungs, spleen, liver and, focally, bone marrow were involved by atypical lymphohistiocytic infiltrates. Immunophenotypic study of the spleen showed that 46% of the cells displayed a helper/inducer T-cell phenotype. However, analysis of DNA isolated from the spleen failed to show clonal T-cell receptor beta-chain gene, T-cell receptor gamma-chain gene, or immunoglobulin heavy chain gene and light chain gene rearrangements. The finding of a cytogenetically abnormal clone supports the concept that angiocentric immunoproliferative lesion is a neoplastic process.

Hypertriglyceridemia and lipid inclusions in a case of Philadelphia chromosome-positive, acute nonlymphocytic leukemia.

We report a case of a 71-year-old female patient with an unusual morphological variant of Philadelphia chromosome-positive, acute nonlymphocytic leukemia. The myeloblasts exhibited an extreme degree of lipid vacuolization and the serum exhibited hyperlipidemia. The initial serum triglyceride level was 756 mg/dL. There were 26,000 white blood cells per cubic millimeter with 19% myeloblasts. The bone marrow contained greater than 80% myeloblasts that were myeloperoxidase- and chloracetate esterase-positive and typed positive for OKM1 and Leu 1 myeloid cellular markers. At remission, the lipid inclusions disappeared and the serum triglyceride levels returned to normal. Both abnormalities recurred at relapse. The cause of the hyperlipidemia and lipid inclusions was most likely an acquired hyperlipoproteinemia and secondary absorption of lipids into the malignant cells.

Histocompatibility antigens in progressive systemic sclerosis (scleroderma).

A study was undertaken to determine the distribution of major histocompatibility (HLA) antigens in progressive systemic sclerosis (PSS) (scleroderma). A total of 106 patients with PSS and 208 normal controls were tested for the presence of 18 different HLA antigens by the microcytotoxicity technique. These patients were equally divided between patients with classical diffuse scleroderma (53 patients) and those with the CREST syndrome variant of the disease (53 patients). When the P values were multiplied by 18, to correct for the number of antigens studied, no significant alteration in the frequency of any HLA antigen was found for the entire group of scleroderma patients or for either of the two subpopulations.