Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We are reporting a forty-seven year old female who had three attacks of acute pancreatitis after having; eaten bananas. She was treated with a light diet and intravenous fluids during each of her admissions. The treatment concluded with the disappearance of clinical symptoms such as epigastralgia, nausea, vomiting and diarrhea within a few days. In addition, elevated serum and urine amylase levels returned to normal values in parallel with the clinical symptoms. The data during her three attacks of acute pancreatitis were as follows: serum total IgE level = 644 IU/mL, specific IgE to bananas = 2.18 UA/ml. No remarkable abnormalities were present in sonography, computed tomography, magnetic resonance imaging of the abdomen, and magnetic resonance cholangiopancreatography. Endoscopic examination of the upper digestive tract showed the ampulla of Vater swollen and edematous, thus a biopsy was performed. Toluidine blue staining and immunohistochemical staining against human mast cell tryptase with the biopsy specimens showed mast cells accumulating in mucosa and submucosa. By avoiding consumption of bananas, she has not suffered from any additional attacks of pancreatitis since the third attack in the last thirty-four months up to this day of December 10, 2004.
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PMID:Acute pancreatitis possibly caused by allergy to bananas. 1626 61

A 46-year-old woman was admitted to the hospital with complaints of chronic diarrhoea, vomiting and severe muscle weakness. Clinical examination showed a lethargic, malnourished, dehydrated patient with ascites and bilateral leg oedema. Laboratory evaluation revealed mild normochromic normocytic anaemia and severe hypoproteinaemia with hypoalbuminaemia. Upper gastrointestinal endoscopy showed a thickened, friable duodenal mucosa with multiple erosions. Colonoscopy revealed nodular, pseudopolypoid lesions with patchy erosions in the left hemicolon. Haematoxylin-eosin stained sections from biopsies of endoscopically abnormal bowel segments showed multi-focal aggregates of large, histiocyte-like cells with abundant pale cytoplasm in the lamina propria. These cells were negative on PAS, Ziehl-Neelsen, Giemsa and toluidine blue stains. Their immunophenotype was CD68 (+), c-kit/CD117 (+) and mast cell tryptase (+), which is consistent with mast cells. A trephine biopsy showed diffuse replacement of the bone marrow by atypical, monomorphic, frequently spindle-shaped mast cells. No associated haematopoietic malignancy was detected. The final diagnosis was aggressive systemic mastocytosis with involvement of the gastrointestinal tract complicated by protein-losing enteropathy. This association has not been reported previously. The patient has been treated with prednisolone and interferon-alpha and has since recovered.
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PMID:Aggressive systemic mastocytosis complicated by protein-losing enteropathy. 1684 41

Systemic mastocytosis is an uncommon condition characterized by abnormal proliferation of mast cells in one or more organ. The specific D816V KIT mutation is present in most cases. Gastrointestinal symptoms occur commonly but histologic characterization of gastrointestinal involvement is incomplete. The purpose of this study was (1) to describe the clinicopathologic features in five patients with systemic mastocytosis involving the gastrointestinal tract and (2) to determine whether gastrointestinal involvement is associated with the usual D816V mutation or a different mutation. Clinical details were obtained from the hospital of origin or referring pathologist. Histologic features were documented in slides stained with hematoxylin and eosin, mast cell tryptase and CD117. Molecular analysis for the D816V KIT mutation was performed on formalin-fixed paraffin-embedded sections. Symptoms included diarrhea/loose stools (n=5), abdominal pain (n=4), vomiting (n=3) and weight loss (n=3). Other findings included cutaneous lesions of mastocytosis (n=4), malabsorption (n=2), hypoalbuminemia (n=2) and constitutional growth delay (n=1). Sites of gastrointestinal involvement included the colon (n=5), duodenum (n=3) and terminal ileum (n=3). Endoscopic/gross findings included mucosal nodularity (n=4), erosions (n=2) and loss of mucosal folds (n=2). In three patients the endoscopic appearance was considered consistent with inflammatory bowel disease. All cases showed increased mast cell infiltration of the lamina propria, confirmed by immunohistochemistry for mast cell tryptase and CD117. In two cases, mast cells had abundant clear cytoplasmic resembling histiocytes. Marked eosinophil infiltrates were present in four patients, in one patient leading to confusion with eosinophilic colitis. Architectural distortion was noted in three cases. The D816V KIT mutation was present in all four cases tested. In conclusion, gastrointestinal involvement by systemic mastocytosis is characterized by a spectrum of morphologic features that can be mistaken for inflammatory bowel disease, eosinophilic colitis or histiocytic infiltrates. Systemic mastocytosis involving the gastrointestinal tract is associated with the usual D816V KIT mutation.
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PMID:Systemic mastocytosis involving the gastrointestinal tract: clinicopathologic and molecular study of five cases. 1893 52

A 53 year old woman presented with abnormal liver function tests and subsequently developed intermittent abdominal pain, vomiting and diarrhoea. There were no rash or anaphylactoid reactions. Endoscopic biopsies showed excessive density of eosinophils and immunohistochemical staining for tryptase revealed a florid mast cell infiltrate. A diagnosis of systemic mastocytosis was made by bone marrow biopsy. Systemic mastocytosis is a rare myeloid neoplasm often associated with gastrointestinal symptoms due usually to mediator release but may rarely represent organ infiltration. While endoscopic and routine biopsy appearances are non-specific, suggestive features should lead to staining for mast cell tryptase or CD 117. However, diagnose generally requires bone marrow biopsy. The prognosis in the majority of patients is good and supportive management only is required. For patients with aggressive disease, cytoreductive therapy may be needed.
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PMID:Systemic mastocytosis: a gastroenterological perspective. 2883 23