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 previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

Medium-chain acyl-CoA dehydrogenase deficiency is a recently described inborn error of metabolism characterized by episodes of coma and hypoketotic hypoglycaemia in response to prolonged fasting. Secondary carnitine deficiency has been documented in these patients as well as the excretion in the urine of medium-chain-length acyl carnitine esters, such as octanoylcarnitine. Based on the potential toxicity of medium-chain fatty acid metabolites and the beneficial responses of patients with other inborn errors of metabolism and secondary carnitine deficiency, oral carnitine has been proposed as treatment for children with medium-chain acyl-CoA dehydrogenase deficiency. We report the results of carefully monitored fasting challenges of an infant with this deficiency both before and after 3 months of oral carnitine therapy. Carnitine supplementation failed to prevent lethargy, vomiting, hypoglycaemia and accumulation of free fatty acids in response to fasting despite normalization of plasma carnitine levels and a marked increase in urinary excretion of acyl-carnitine esters. Potentially toxic medium-chain fatty acids accumulated in the plasma in spite of therapy. Based on this study of one patient, we stress that avoidance of fasting and prompt institution of glucose supplementation in situations when oral intake is interrupted remain the mainstays of therapy for medium-chain acyl-CoA dehydrogenase deficient patients.
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PMID:Medium-chain acyl-CoA dehydrogenase deficiency: metabolic effects and therapeutic efficacy of long-term L-carnitine supplementation. 250 71

Corticotrophin (ACTH) deficiency is an important cause of a potentially lethal form of adrenocortical failure. Difficulties can arise in making the diagnosis, especially when secretion of other pituitary trophic hormones is normal. Presenting features of seven patients with ACTH deficiency, in whom the diagnosis was difficult for a variety of reasons, are reported and discussed. Two patients had a normal cortisol response to synthetic ACTH. The possibility of ACTH deficiency should be considered in any patient presenting with weight loss, vomiting, muscular fatigue and stiffness, hyponatraemia or hypoglycaemia.
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PMID:ACTH deficiency: problems in recognition and diagnosis. 254 52

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

With the development of sensitive and specific radio-immunoassays to measure the low circulating concentrations of vasopressin there has been a quantum leap in our understanding of the physiological processes involved in the regulation of its secretion. The results of Verney's pioneering studies in dogs led to the concept of 'osmoreceptors'. It is now appreciated that osmoregulation of vasopressin release is of principal importance in the maintenance of water balance. Functional characteristics of the osmoregulatory system have been defined clearly by independent laboratories, and more recently the physiological influences that can subtly alter this very finely controlled system have been described. Non-osmotic factors that release vasopressin have been recognized for many years. Secretion of vasopressin in response to haemodynamic influences has been characterized, and significant hypotension and/or hypovolaemia are potent stimuli to hormone release. Other non-osmotic factors--nausea/emesis, hypoglycaemia--may play important roles in disturbances of water balance. Vasopressin should not, however, be regarded as a stress hormone, since recent careful studies in a variety of species indicate that secretion is not enhanced following a series of different noxious stimuli.
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PMID:Regulation of vasopressin secretion. 269 40

Two male infants with hyperpigmentation, vomiting, lethargy and weight loss were reported. Hypoglycemia, hyponatremia, hypochloremia, hyperkalemia and metabolic acidosis were suggestive diagnosis of salt losing adrenocortical insufficiency. The absence of ambiguous genitalia, low 24 hour urinary 17 KS and pregnanetriol excretion precluded congenital adrenal hyperplasia. Low basal levels of plasma aldosterone and cortisol and low 24 hour urinary 17 OHCS excretion with disability to increase their corticosteroid secretions after ACTH stimulation as well as furosemide and theophylline infusions were supportive for the diagnosis of congenital adrenal hypoplasia. The definitive diagnosis was confirmed by ultrasonogram and computerized tomography. Family histories suggested X-linked recessive inheritance in these reported cases. Evidence of progressive postnatal adrenocortical degeneration was documented by progressive deterioration of adrenocortical functions beginning from mineralocorticoid to total corticosteroid deficiencies. The increased brain serotonin synthesis as the associated pathology of X-linked congenital adrenal hypoplasia was proposed on the basis of elevated basal plasma GH and PRL levels in the reported cases, taken together with an incidence of congenital LH deficiency and persistent ACTH hypersecretion in corticosteroid treated patients reported elsewhere.
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PMID:X-linked congenital adrenal hypoplasia: proposal pathogenesis. 273 38

Since skeletal muscle is an important source of precursor for gluconeogenesis, it would not be surprising if carbohydrate metabolism was altered in some muscle disorders. We report a 7-10/12-year-old white male with congenital muscular dystrophy whose recurrent episodes of vomiting and dehydration were due to fasting hypoglycemia. He was found to have a blood glucose of 21 mg/dl with an episode of vomiting and dehydration. Diagnostic fasting replicated the symptoms and hypoglycemia. Associated laboratory findings included hypoalaninemia, ketonemia, and acidosis. With use of frequent feedings, there were no further episodes over 1-9/12 years of observation. To our knowledge this is the first report of hypoglycemia complicating muscular dystrophy. However, hypoglycemia may not be diagnosed because of the nonspecific nature of the symptoms. Hypoglycemia should be considered when children with reduced muscle mass develop otherwise unexplained vomiting.
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PMID:Hypoglycemia in a child with congenital muscular dystrophy. 292 68

A 39 year old woman was admitted to a maternity unit at 34 weeks' gestation with nausea, vomiting, and jaundice. Her condition deteriorated, and she was transferred to hospital, deeply unconscious and hypotensive. The diagnosis of acute fatty liver of pregnancy was initially suggested by the typical history of prodromal malaise and vomiting and the rapid onset of hepatic encephalopathy with profound hypoglycaemia and only small increases in transaminase activities. Computed tomography was performed: there was no enlargement of the liver or spleen, but the attenuation value over the liver indicated appreciable fatty infiltration of the liver, establishing the diagnosis of acute fatty liver of pregnancy. Computed tomography is of value in the diagnosis of liver disease of late pregnancy, and this technique may become the method of choice for the investigation of acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy and diagnosis by computed tomography. 308 Jan 42

Four infants had noninfectious intractable diarrhea, vomiting, anasarca, hepatomegaly, hypoglycemia, and malnutrition within the first 3 months of life. Their parents originated from the same Northeastern part of Quebec, and consanguinity was found in two kindreds. Diarrhea was secretory in three infants (mean stool volume 87 ml/kg/day, Na+ 108 mEq/L, Cl- 85 mEq/L). Hypoalbuminemia (mean 2.0 gm/dl), present in all infants, appeared to be secondary to a protein-losing enteropathy, which was documented in two infants. Histologic examination of the upper small intestine showed only mild to moderate villous atrophy. The remarkable findings were those of cystic dilation of the crypts and acute inflammation of crypts and lamina propria, all of which were most prominent in the colon and terminal ileum; the changes were progressive over time. Mild lymphangiectasia was found in all of the patients. Congenital hepatic fibrosis, present in all, was associated in one patient with a nonfunctional multicystic kidney. Prolonged total parenteral nutrition, intravenously administered albumin, antisecretory agents, and antibiotics were unsuccessful in controlling the disease. Although a total colectomy was followed by a temporary decrease in stool output and normalization of serum albumin concentration in one infant, the patients died between 4 and 21 months of age.
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PMID:Secretory diarrhea with protein-losing enteropathy, enterocolitis cystica superficialis, intestinal lymphangiectasia, and congenital hepatic fibrosis: a new syndrome. 308 May 72

A 59-year-old woman with metastatic breast carcinoma presented with weight loss, vomiting, and polyuria. Basal endocrine testing revealed low levels of thyroxine, cortisol, and gonadotropins, and the presence of diabetes insipidus. Direct stimulation of the pituitary with hypophysiotropic hormones indicated intact pituitary reserve. Insulin-induced hypoglycemia, however, failed to increase plasma cortisol or growth hormone levels significantly. On computed tomographic scanning, a lesion was found in the area of the hypothalamus. Thus, a functional abnormality of the hypothalamic-pituitary axis causing clinically significant hypothalamic hypopituitarism was not clearly apparent following administration of hypothalamic releasing factors but was demonstrable with indirect stimulation via insulin-induced hypoglycemia. Insulin-induced hypoglycemia remains an important diagnostic test in the evaluation of hypopituitarism.
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PMID:Hypophysiotropic hormone testing in a patient with hypothalamic hypopituitarism. 308 91


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