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)

A 32-year-old male had suffered from persistent dull epigastric pain, constipation, postprandial vomiting, and body-weight loss for 2 months. An abdominal computed tomography (CT) scan showed thickening of the proximal jejunal wall. He was also referred to our center for an fluoro-2-deoxy-D-glucose-positron emission tomography (FDG-PET) scan because his tumor marker CA19-9 was above 800 ng/mL and malignancy was suspected. The PET scan showed an FDG-avid lesion over the upper left abdomen. Endoscopy of the small intestine revealed focal thickening of the mucosal fold and skip ulcer lesions in the jejunum. Culture from the biopsy tissue proved the diagnosis of Mycobacterium tuberculosis infection. No evidence of pulmonary tuberculosis was detected during further evaluation.
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PMID:Jejunal tuberculosis: incidental finding on an FDG-PET scan. 1657 May 67

We report a rare case of symptomatic hypoglycemia in a patient with intra-abdominal recurrence of a previously resected gastrointestinal stromal tumor (GIST). The patient is a 65-year-old woman who underwent resection of a large abdominal mass arising from the stomach, histologically diagnosed as a high-grade leiomyosarcoma. She was lost to follow up. Five years later, the mass recurred; core biopsy demonstrated a CD 117-positive, spindle-cell tumor, consistent with a GIST. She was placed on Gleevec, as there was evidence of multifocal disease, but imaging revealed only mild improvement. Subsequently, her clinical status deteriorated, and she was hospitalized for dehydration, vomiting, and mental status changes. Her blood glucose on admission was 22 mg/dL, and a dextrose infusion (50%) was necessary to maintain adequate blood glucose levels. Measurements of insulin, proinsulin, c-peptide, beta-hydroxybutyrate, and thyroid-stimulating hormone were normal, as were cosyntropin stimulation and glucagon response tests. Suspicions arose for tumor-secreted insulin-like factor. She underwent resection of the dominant 44-cm recurrence, with immediate rebound hyperglycemia, followed by complete normalization of her blood glucose levels. She was discharged on postoperative Day 5 without symptoms or insulin, and is alive with disease at 20 months. Paraneoplastic syndromes occur in only 15 per cent of patients with known malignancies (e.g., lung cancer and metastatic carcinoid), and are rarely reported in the setting of GIST. Hypoglycemia is most often observed in presence of insulinoma and only isolated case reports in GIST patients exist. Overexpression of insulin-like growth factor II is thought to be the mechanism of action. Supportive management and palliative resection or debulking is recommended when possible.
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PMID:Hypoglycemia in the setting of advanced gastrointestinal stromal tumor. 1721 25

It was reported that there was a case of severe malaria patient with jaundice who presented with arrhythmia (premature ventricular contraction) while getting quinine infusion was reported. A man, 25 years old, was admitted to hospital with high fever, chill, vomiting, jaundice. The patient was fully conscious, blood pressure 120/80 mmHg, pulse rate 100 x/minute, regular. On admission, laboratory examination showed Plasmodium falciparum (++++), total bilirubin 8.25 mg/dL, conjugated bilirubin 4.36 mg/dL, unconjugated bilirubin 3.89 mg/dL, potassium 3.52 meq/L Patient was diagnosed as severe malaria with jaundice and got quinine infusion in dextrose 5% 500 mg/8 hour. On the second day the patient had vomitus, diarrhea, tinnitus, loss of hearing. After 30 hours of quinine infusion the patient felt palpitation and electrocardiography (ECG) recording showed premature ventricular contraction (PVC) > 5 x/minute, trigemini, constant type--sinoatrial block, positive U wave. He was treated with lidocaine 50 mg intravenously followed by infusion 1500 mg in dextrose 5%/24 hour and potassium aspartate tablet. Quinine infusion was discontinued and changed with sulfate quinine tablets. Three hours later the patient felt better, the frequency of PVC reduced to 4 - 5 x/minute and on the third day ECG was normal, potassium level was 3.34 meq/L. He was discharged on 7th day in good condition. Quinine, like quinidine, is a chincona alkaloid that has anti-arrhythmic property, although it also pro-arrhythmic that can cause various arrhythmias, including severe arrhythmia such as multiple PVC. Administration of parenteral quinine must be done carefully and with good observation because of its pro-arrhythmic effect, especially in older patients who have heart diseases or patients with electrolyte disorder (hypokalemia) which frequently occurs due to vomiting and or diarrhea in malaria cases.
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PMID:Quinine-induced arrhythmia in a patient with severe malaria. 1729 7

Uzarigenin-glucoside-canaroside (UGC) is a steroid glycoside isolated from the leaves of ISOPLEXIS CHALCANTHA whose pharmacological properties have not been so far studied. In this paper the effect of UGC on isolated auricle of rabbits, urinary excretion of rats, isolated jejunum of rabbits, (86)Rb (+) uptake by erythrocytes as well as its emetic effect in pigeons are presented, using digoxin as standard. The pharmacological activity of UGC was similar to that of digoxin, UGC possessing, however, a lesser vomiting action.
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PMID:Pharmacological study of uzarigenin-glucoside-canaroside. 1734 69

Classical galactosemia is an autosomal recessive disorder caused by a deficiency of the enzyme galactose-1-phosphate uridyltransferase. Undoubtedly, some of the short term complications are linked to the toxic effects of the accumulated abnormal metabolites (galactose-1-phosphate and galactitol). However, the physiopathology of neonatal liver failure remains unclear. We report the case of a 7-week-old girl who was first diagnosed with liver failure, hypoprotidaemia, ascites and generalized edemas. High citrulline (293 micromol/L), on initial plasma amino acid, suggested the diagnosis of citrin deficiency. As the citric acid cycle intermediates were non-detectable (oxoglutarate, succinate and citrate), a cataplerotic state was suspected. As a result, citrate (as an anaplerotic treatment) induced a clear improvement in her liver function. Four weeks later, this patient was switched to a galactose-free formula (as recommended in citrin deficiency with galactosemia) and her pathological status returned to normal. Citrin deficiency was later ruled out by molecular biology studies; then we reintroduced a galactose-containing formula which re-evoked rapidly vomiting, galactose aversion and hepatic cytolysis and the diagnosis of classical galactosemia was established. Our case clearly shows that cataplerosis could play a role in the pathophysiology of the neonatal liver disease observed in classical galactosemia.
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PMID:Evidence of cataplerosis in a patient with neonatal classical galactosemia presenting as citrin deficiency. 1864 Jul 39

Hereditary galactosemia is a biochemical genetic disease due to a deficiency of galactose-1-phosphate uridyltransferase (GALT) enzyme activity (OMIM 606999). Acute manifestations occur in the neonatal period and are, with rare exceptions, related to lactose ingestion. They include poor feeding and growth, emesis, jaundice, liver disease, bleeding diathesis, anemia, renal tubulopathy, cataracts, encephalopathy and death from E. coli sepsis. Chronic manifestations, which also develop in prospectively treated patients, involve (a) the brain, resulting in delayed language acquisition, speech defects, and learning problems, and (b) the ovary, in the majority of females, producing hypergonadotropic hypogonadism. The serum FSH level is elevated in infancy/early childhood in many, but not all patients with a severe phenotype. There are few reports of patients with classic galactosemia having undergone pregnancy, labor, and delivery. The pathologic findings in the ovary, including a persistence of primordial follicles and streak gonads, have been variable. The etiology of primary ovarian insufficiency (POI) in galactosemia is unknown. Clinical surveillance includes screening for abnormalities in ovarian function at an early age. Treatment consists of estrogen/progesterone supplementation at the appropriate age. Reduced BMD has been reported. Future research is needed (1) to delineate the mechanisms behind reduced ovarian function in these young women; (2) to determine the timing of the lesion: prenatal, postnatal, and both pre- and postnatal; (3) to determine whether elevated galactose-1-phosphate is both necessary and sufficient to induce primary ovarian insufficiency; and (4) to understand the mechanism(s) behind the reduced BMD seen in children and adolescents with galactosemia.
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PMID:Galactosemia and amenorrhea in the adolescent. 1857 15

Fungal peritonitis is a relatively uncommon complication of peritoneal dialysis that contributes significantly to morbidity, drop out from the continuous ambulatory peritoneal dialysis (CAPD) program, and mortality. Candida sake infections were rarely published in literature. We present the first case of peritonitis due to C. sake. A 41-year-old man was admitted to our hospital with abdominal pain, nausea, vomiting, fever, weakness. Abdominal ultrasonography demonstrated a fistula tract, which has an opening at inferolateral of the umbilicus extending 5 cm from the skin into the abdominal cavity with a foreign body (11 x 10 mm length) inside the fistula. The foreign body was removed by surgery being apparently a part of a previously inserted peritoneal catheter. Postoperative specimens revealed polymorph leucocytes and yeast cells in Gram stain, and culture on Sabouraud dextrose agar (SDA) yielded a growth of a fungus, subsequently identified as C. sake with Api ID 32C. Fluconazole (200 mg/day) therapy was started. He recovered after two weeks of therapy. In conclusion, C. sake, a rare type of Candida species, should be considered as a probable peritoneal pathogen in patients with multiple episodes of bacterial peritonitis, previous broad-spectrum antibiotic therapy and diabetes mellitus.
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PMID:First case of continuous ambulatory peritoneal dialysis peritonitis due to Candida sake. 1862 71

Cyclic vomiting syndrome (CVS) is a disorder noted for its unique intensity of vomiting, repeated emergency department visits and hospitalizations, and reduced quality of life. It is often misdiagnosed due to the unappreciated pattern of recurrence and lack of confirmatory testing. Because no accepted approach to management has been established, the task force was charged to develop a report on diagnosis and treatment of CVS based upon a review of the medical literature and expert opinion. The key issues addressed were the diagnostic criteria, the appropriate evaluation, the prophylactic therapy, and the therapy of acute attacks. The recommended diagnostic approach is to avoid "shotgun" testing and instead to use a strategy of targeted testing that varies with the presence of 4 red flags: abdominal signs (eg, bilious vomiting, tenderness), triggering events (eg, fasting, high protein meal), abnormal neurological examination (eg, altered mental status, papilledema), and progressive worsening or a changing pattern of vomiting episodes. Therapeutic recommendations include lifestyle changes, prophylactic therapy (eg, cyproheptadine in children 5 years or younger and amitriptyline for those older than 5), and acute therapy (eg, 5-hydroxytryptamine receptor agonists, termed triptans herein, as abortive therapy, and 10% dextrose and ondansetron for those requiring intravenous hydration). This document represents the official recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition for the diagnosis and treatment of CVS in children and adolescents.
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PMID:North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition consensus statement on the diagnosis and management of cyclic vomiting syndrome. 1872 40

Acute gastroenteritis is a common reason for children to seek health care. Among the potential complications of acute gastroenteritis, the most common is dehydration. For mild to moderate dehydration, treatment options include oral and intravenous rehydration. Outpatient treatment failure for either method, when it occurs, is often due to persistent nausea and vomiting. Some authorities have suggested that the early administration of dextrose to patients receiving intravenous rehydration may help terminate vomiting and result in fewer outpatient treatment failures. The purpose of this report was to review the evidence supporting the effectiveness of early intravenous dextrose administration in the outpatient management of dehydration in children with acute gastroenteritis.
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PMID:Rehydration: role for early use of intravenous dextrose. 1914 16

Alcoholic ketoacidosis is an acute metabolic acidosis that typically occurs in people who chronically abuse alcohol and have a recent history of binge drinking, little or no food intake and persistent vomiting. Alcoholic ketoacidosis is a result of starvation with glycogen depletion and counter-regulatory hormone production, a raised nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) ratio related to the metabolism of ethanol, and volume depletion resulting in ketogenesis. Alcoholic ketoacidosis is characterized by elevated serum ketone levels and a high anion gap. Once the diagnosis of alcoholic ketoacidosis is made, the mainstay of treatment is hydration with 5% dextrose in normal saline. With timely and aggressive intervention, the prognosis for a patient with alcoholic ketoacidosis is good.
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PMID:[Alcoholic ketoacidosis]. 1929 98


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