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 12-year old boy suffered episodes of vomiting, lethargy, and hypoglycaemia from the age of 1 year. Adhering to a vegetarian diet caused an increase in frequency and severity of the attacks. It was found that he was suffering from systemic carnitine deficiency that responded promptly to treatment with L-carnitine.
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PMID:Systemic carnitine deficiency exacerbated by a strict vegetarian diet. 670 71

Three cases of diencephalic syndrome, associated with brain tumors, are reported in this paper. Case 1. A 2-2/12-year old boy was initially admitted to our hospital because of failure to thrive which began at the age of three months. Physical examination revealed emaciation (weight, 7.8 kg), irritability and pallor without anemia. Horizontal nystagmus was seen. Laboratory studies were normal except for abnormally high plasma growth hormone (p-GH) which was incompletely suppressed by hyperglycemia (induced by glucose) and was not elevated by hypoglycemia (induced by insulin). A low grade astrocytoma of the optic nerve compression the hypothalamus was partially removed. After the operation followed by irradiation, p-GH returned to normal both in its basal level and in its reaction to insulin loading, then his gain of weight was accelerated. He was readmitted, however, at the age of 6 8/12 years with headache and vomiting. Since subtotal removal of the recurrent tumor and irradiation, preoperative symptoms have disappeared up to the present (7 9/12 years old). Case 2. A 3-9/12-year old girl was initially admitted because of failure to thrive since the age of 2 years. Examination on admission revealed emaciation (10.5 kg), irritability and right hemiparesis. Laboratory studies were normal except for high serum cholesterol (290 mg/dl). (p-HG was not measured) The patient had been well after the subtotal removal of the hypothalamic astrocytoma except occasional headache until the age of 6 years. She was readmitted at the age of 9 years with progressive emaciation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diencephalic syndrome--report of three cases]. 671 44

Liver disease may cause a variety of clinical signs, including depression, anorexia, weakness, weight loss, vomiting, diarrhea, fever, abdominal pain, jaundice, ascites and CNS signs. Treatment is aimed at eliminating the cause, providing supportive care, and preventing secondary complications. Rest facilitates liver regeneration. Hypokalemia, respiratory alkalosis and hypoglycemia may complicate liver disease. Fluids should be given IV rather than SC to severely dehydrated animals. Preferred solutions include Ringer's and half-strength saline with 2.5% dextrose. Solutions containing lactate should not be used. Dietary management includes feeding adequate amounts of protein of high biologic value, carbohydrates, fat, vitamins and minerals.
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PMID:Management of liver disease in dogs and cats. 672 30

It has been five years since the original report indicating that intragastric feedings could reverse most of the clinical and metabolic abnormalities present in patients with type I glycogen storage disease. We have now treated seven patients with nocturnal intragastric feedings for five years. All patients have shown marked improvement in blood chemical values (urate, lactate, triglyceride, cholesterol) as well as linear growth. The only serious complication has been symptomatic hypoglycemia and acidosis resulting from acute gastroenteritis and vomiting. Results indicate that nocturnal intragastric feeding is a practical, safe, and effective form of long-term treatment for patients with type I glycogen storage disease.
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PMID:Type I glycogen storage disease: five years of management with nocturnal intragastric feeding. 676 11

Analyses of 23 fatal instances of hepatic injury in patients taking valproic acid reveals that all but three were less than 20 years old, and all but four had been taking the drugs for more than 1 month. Convulsions, facial edema, lassitude, and vomiting were prominent clinical features. Hypoglycemia was recorded in six patients. Rash and eosinophilia were not seen. Values for transaminases were modestly elevated in most patients. Most levels of SGOT were below 500 IU, and SGPT levels were below 200 IU. Livers showed microvesicular steatosis in most patients, usually accompanies by necrosis. Four patients had cirrhosis. Overt valproic acid-induced hepatic injury appears to be rare and hence, by definition, idiosyncratic. That it may be an idiosyncratic exaggeration of a much more frequent phenomenon is suggested by the higher incidence of seemingly trivial injury. The idiosyncrasy appears to be metabolic rather than immunologic, and the available information leads to the plausible hypothesis that a metabolite is responsible for the microvesicular steatosis seen in most fatal cases. The steatosis resembles that of Reye's syndrome and Jamaican vomiting sickness, and there is reason to believe that the metabolite responsible for the steatosis resembles the agent responsible for Jamaican vomiting sickness. A different metabolite is presumably responsible for the necrosis seen in many of the cases.
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PMID:Valproate-induced hepatic injury: analyses of 23 fatal cases. 681 94

The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements along with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld unless life-threatening acidemia is present or expected. Lastly, alcohol need not be detected on admission to make the diagnosis of this metabolic disturbance. However, when present, it could contribute directly to the lactic, acetic and B-hydroxybutyric acidoses. With respect to the theoretical constraints on ethanol metabolism, it appears that "overproduction" of NADH in the liver is best averted by converting ethanol to B-hydroxybutyric acid.
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PMID:Metabolic acidosis in the alcoholic: a pathophysiologic approach. 682

A boy, aged 7 months, of consanguineous parents presented with an acute onset of vomiting, fever, nonketotic hypoglycemia and acidosis and died from cardiac arrest after ventricular fibrillation. He had hepatomegaly and echocardiographically a non-obstructive cardiomyopathy. Autopsy was not allowed. After birth the child had suffered from a severe respiratory distress syndrome, transient metabolic acidosis and had a sweaty feet odour. Later on, development was retarded with a severe muscular hypotonia. Post mortem, numerous unusual organic acids were found in high concentrations in urine, e.g. dicarbonic acids, 2-hydroxyisobutyric, isovaleric, 3-hydroxyisovaleric acid, N-acyl glycines, isovalerylglutamic acid and sarcosine. This pattern indicated deficiencies of several acyl-Co A dehydrogenases in the metabolism of leucine, isoleucine, valine, lysine, short-chain fatty acids and sarcosine. This could be confirmed using cultured skin fibroblasts which were shown to degrade the corresponding labeled substrates insufficiently to 14CO2. It is assumed that the functional multiple acyl-Co A dehydrogenation deficiency is caused by a deficiency of a common link in the electron transfer system of these dehydrogenases which is inherited autosomal recessively in this family. Among the 12 patients reported, 7 died within the first 5 days of age.
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PMID:Multiple acyl-Co A dehydrogenation deficiency (MADD) in a boy with nonketotic hypoglycemia, hepatomegaly, muscle hypotonia and cardiomyopathy. Detection of N-isovalerylglutamic acid and its monoamide. 686 97

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

We observed eight infants with hereditary fructose intolerance which had been diagnosed by the fructose tolerance test and an aldolase assay on biopsied liver. None of these had been diagnosed before their admission to our department. The most frequent symptoms were vomiting and failure to thrive. All the patients had hepatomegaly. Laboratory findings were indicative of disturbed hepatic function. Hypoglycemia was found in only 3 out of 8 patients. The course was lethal in 2 patients; the 6 survivors are doing well following a fructose-free diet. The importance of practising paediatricians having the detailed nutritional history of the patient and precise knowledge of infant food formulae is stressed. The danger of using fructose continuing solutions for infusion therapy is pointed out. We also report a case of F-1,6-diphosphatase deficiency.
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PMID:[Clinical heterogeneity in fructose intolerance]. 717 Jan 90


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