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)

Wolman's disease is a rare inherited disorder of lipid metabolism in which large amounts of triglycerides and cholesteryl esters accumulate in the visceral organs. The main clinical features of the infantile form of the disease are failure to thrive, vomiting and diarrhoea, hepatosplenomegaly and radiological evidence of calcification of the adrenals. We were able to follow the course of this disease in a female turkish infant. It was first admitted because of a transient swelling within the right angle of mandible, subfebrile temperatures and abdominal distension as well as vomiting at the age of three days. After symptomatic treatment she was discharged home without a specific diagnosis. At the age of 4.5 months she was readmitted with severe hepatosplenomegaly, hypochromic anemia and fever of unknown origin. Calcifications of the adrenals and lymphocytic vacuoles led to the diagnosis of Wolman's disease. Deficiency of acid lipase activity in leucocytes could establish this diagnosis.
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PMID:[Wolman's disease in an infant]. 232 17

Experimental reports have proved that bile acids damage the gastric mucosa. Moreover it is now accepted that duodenogastric reflux occurs in 20-30% of cholecystectomized persons. The Authors, with the purpose of defining a correlation between gastric mucosa damage by duodeno-gastric reflux and postcholecystectomy syndrome have taken into consideration two groups of 14 patients each. To the first group belonged cholecystectomized patients, who had episodic, often postprandial pain, constant heart burn, with associated vomiting and Hypochromic anemia. To the second group belonged asymptomatic patients with previous cholecystectomy. All these patients were endoscoped (EGDS), and their endoscopic biopsy specimens were surveyed. 99Tc HIDA cholescintigraphy was performed in all the groups of patients, after endoscopy. In 85% of symptomatic patients we found, during endoscopy, reflux of bile into the stomach with associated reddish and inflammatory change of antral mucosa vs. 7.14% of the control group. Atrophic chronic gastritis was found in 71.43% of endoscopic biopsy specimens of Symptomatic vs. 14.28% of asymptomatic patients. Superficial chronic gastritis was found in 28.57% of symptomatic vs. 50% of asymptomatic patients. At last we found active atrophic or superficial antral gastritis (Whitehead) in 90% of symptomatic patients vs. 0% of asymptomatic people. The Authors conclude that there is a positive correlation between duodenogastric reflux and postcholecystectomy syndrome when biliary reflux is correlated with an histological finding of antral active chronic gastritis.
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PMID:[Correlation between post-cholecystectomy syndrome and biliary reflux gastritis. Endoscopic study]. 269 12

A 9-year-old Bedlington Terrier was evaluated because of weight loss, inappetence, and hematemesis. Copper storage disease had been diagnosed previously on the basis of high hepatic copper concentration. Treatment had included dietary copper restriction and administration of trientine for chelation of copper. A CBC revealed microcytic hypochromic anemia. High serum activities of liver enzymes, high bile acid concentrations, and low BUN and albumin concentrations were detected. Vomiting resolved temporarily with treatment, but the clinicopathologic abnormalities persisted. Results of transcolonic portal scintigraphy suggested an abnormal shunt fraction. Results of liver biopsy and copper quantification revealed glycogen accumulation and extremely low hepatic copper concentration. Serum and hair copper concentrations were also low. Chelation and dietary copper restriction were tapered and discontinued. Clinical signs and all clinicopathologic abnormalities improved during a period of several months.
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PMID:Iatrogenic copper deficiency associated with long-term copper chelation for treatment of copper storage disease in a Bedlington Terrier. 1139 71

Seventeen client-owned dogs diagnosed with spirocercosis-associated esophageal sarcomas were retrospectively reviewed. The most common clinical signs noticed were vomiting and/or regurgitation (94%), lethargy and depression (59%), pyrexia and anorexia (41% each). Leukocytosis (82%) and microcytic hypochromic anemia (30%) were the most common hematological abnormalities. Caudal thoracic masses were demonstrated on survey radiographs of 13/15 of the dogs and thoracic spondylitis was detected in 12/15 dogs. Spirocerca lupi eggs were detected in 2/8 patients and worms were demonstrated on 1/11 at necropsy. Ten cases underwent surgical attempt to remove the tumors. In six of them partial esophagectomy (PE) was performed and all of them survived the immediate postoperative hospitalization. Five of the cases that underwent PE also received chemotherapy after surgery (doxorubicin (Adriamycin, Upjohn)) with an average survival time of 267 days. The histopathological results of the esophageal tumors were osteosarcoma (9), fibrosarcoma (5) and undifferentiated sarcoma (1). In areas endemic to spirocercosis, regurgitation or vomiting in dogs and microcytic hypochromic anemia and neutrophilia warrant ruling out esophageal sarcomas. Proper surgical treatment could prolong the dogs' lifespan for months, and improve their quality of life.
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PMID:Spirocercosis-associated esophageal sarcomas in dogs. A retrospective study of 17 cases (1997-2003). 1474 80

We report the case of a 7-month-old child who presented with regression of milestones, seizures, altered sensorium, and vomiting. An elder sibling had died of similar complaints. Lead encephalopathy was considered because of presence of microcytic hypochromic anemia and dense metaphyseal bands on wrist radiogram. Magnetic resonance imaging (MRI) of the brain revealed diffuse dysmyelination involving both periventricular and subcortical white matter. Such diffuse changes have not been described previously. The child's father was operating an illicit lead-acid battery manufacturing unit at home. The child was subjected to chelation therapy, which was accompanied by environmental exposure source modification. He showed significant improvement. Our case highlights the importance of taking a detailed occupational history and considering lead poisoning in the differential diagnosis of encephalopathy of unidentifiable cause.
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PMID:Lead encephalopathy in an infant mimicking a neurometabolic disorder. 1963 32

Plummer-Vinson syndrome (PVS) is a rare entity characterized by upper esophageal webs and iron deficiency anemia. We report a case of PVS whose esophageal web was rapidly improved by iron therapy. A 77-year-old woman was admitted to our hospital with complaints of dysphagia, vomiting, shortness of breath and weight loss for 1 month. Physical examination revealed conjunctival pallor, koilonychia, angular cheilitis and smooth tongue, and laboratory findings were consistent with microcytic hypochromic anemia with iron deficiency. Gastrointestinal endoscopy and barium-swallow esophagography detected a web that prevented passage of the endoscope into the upper portion of the esophagus. The patient received oral iron therapy daily; the hemoglobin concentration rose to 8.9 g/dl and the complaints of dysphagia were dramatically improved after 2 weeks, with improvement of luminal stenosis confirmed by gastrointestinal endoscopy and barium-swallow esophagography. The PVS described in this report had a distinct clinical course, showing very rapid improvement of dysphagia and esophageal web after 2 weeks of oral iron therapy.
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PMID:A case of plummer-vinson syndrome showing rapid improvement of Dysphagia and esophageal web after two weeks of iron therapy. 2502 78

Idiopathic pulmonary hemosiderosis is a potentially fatal disease that results from episodes of alveolar hemorrhage of unknown origin. The clinical spectrum is varied, and anemia may constitute the only manifestation of illness, preceding other signs and symptoms by several months. We present the case of a 4 year-old child presenting with fever, vomiting and prostration, associated with pallor. He had microcytic and hypochromic anemia refractory to iron therapy. Gastrointestinal bleeding was ruled out after negative extensive etiological investigation. Subsequently, pulmonary infiltrates suggestive of alveolar hemorrhage were observed in the chest radiography. The cytological exam of the bronchoalveolar lavage showed hemosiderin-laden macrophages. After the etiological study, the diagnosis of idiopathic pulmonary hemosiderosis was made by exclusion. He was initiated on corticosteroid therapy, later associated to an immunosuppressive agent, with subsequent correction of anemia and of the radiological pattern. The patient is currently asymptomatic.
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PMID:Severe iron-deficiency anemia as initial manifestation of pulmonary hemosiderosis in a child. 3051 70