Pancreatitis associated with ondansetron.
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Biomedical subjects
Publications and source records attributed to J J Alberti-Flor.
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We report the case of a 26-yr-old patient with fulminant liver failure and acute hemorrhagic pancreatitis secondary to the use of trimethoprim-sulfamethoxazole (Bactrim DS). Our patient presented with skin rash and decreased C3 and C4 levels, which we believed was due to a hypersensitivity reaction secondary to the sulfonamide component (sulfamethoxazole). To our knowledge, this is the first case reported in which sulfamethoxazole-trimethoprim has been implicated as a cause of fulminant liver failure and acute hemorrhagic pancreatitis simultaneously, and emphasizes the need of discontinuing this medication as soon as there is evidence of liver and pancreatic dysfunction.
Pseudomembranous colitis is characterized by inflammatory plaques and pseudomembranes on the colonic mucosa. The disorder most commonly occurs after the use of antibiotics, which allow overgrowth of Clostridium difficile, a spore-forming, gram-positive rod that produces a toxin. Overgrowth of Staphylococcus aureus can also produce pseudomembranous colitis. In rare cases, pseudomembranous colitis is not associated with antibiotic use. When C. difficile is present, vancomycin or metronidazole usually produces a prompt response. In idiopathic cases, surgery may be required.
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A 16-years-old male with a history of Job's syndrome and a recent diagnosis of Crohn's disease was admitted to the hospital because of abdominal pain, nonbloody diarrhea, weakness, and fever. Due to failure to respond to medical therapy it was decided that an operation was indicated, and resection of the terminal ileum and right colon was performed. Cecum and ileum were inflamed, and pathologic studies revealed the presence of budding yeasts which on special stain were diagnostic of Histoplasma species. Successful management was accomplished with oral ketoconazole.
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The concentration of immunoglobulins and immune complexes was determined in the serum and bile of four patients with primary sclerosing cholangitis, only one of whom had chronic ulcerative colitis, and in four postcholecystectomy control patients. The result of the immunoglobulin studies demonstrated increased serum levels of IgM in primary sclerosing cholangitis as compared to control patients. The IgG, IgA, and IgM in bile were all significantly elevated as compared to controls (p = 0.02). Immune complexes in bile and serum were also determined in both groups by the C1q and conglutinin binding assays. Immune complexes in bile were elevated in three of four of the patients with primary sclerosing cholangitis. These findings further characterize primary sclerosing cholangitis in terms of biliary immunoglobulins and immune complexes but do not resolve whether these changes are an epiphenomenon or reflect a primary role of immunoglobulins and immune complexes in the pathogenesis of this disorder.
A 65-yr-old man who developed sudden respiratory arrest was found to have a long, smooth, esophageal filling defect on esophagogram. Endoscopy eventually proved this to be a large esophageal polypoid lesion that had arisen in the hypopharynx and extended to the midesophagus. He was successfully treated with a lateral pharyngotomy and excision of the hypopharyngeal polyp.
A 40-year-old man with a history of insulin-dependent diabetes mellitus was admitted to the hospital because of jaundice and pruritus. During his evaluation the diagnosis of primary sclerosing cholangitis and "microscopic" ulcerative colitis were established. Massive intraabdominal lymphadenopathy was discovered on CT scan and histological examination eventually proved this to be follicular hyperplasia. The case herein reported documents the association of primary sclerosing cholangitis with diabetes mellitus and ulcerative colitis as well as reporting the occurrence of massive intraabdominal lymphadenopathy.
A 59-yr-old man was admitted to the hospital for evaluation of right upper quadrant pain, anorexia, weight loss, and low-grade fever of 2-mo duration. During his evaluation, an abnormal liver ultrasound and computed tomography scan demonstrated what proved to be an avascular hepatic lesion. At surgery, the diagnosis of malignant fibrous histiocytoma was established. We present herein our findings of what we believe to be the first reported study of malignant fibrous histiocytoma of the liver.
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