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

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
 ...
PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.
 ...
PMID:Glycerol intolerance in a child with intermittent hypoglycemia. 16 54

Twin male infant siblings who presented in Harrow, UK, with a Reye's-like syndrome associated with profound hypoglycaemia, vomiting, diarrhoea, coma and death in one child, with dicarboxylic aciduria, and similarities to Jamacian vomiting sickness (hypoglycin toxicity) have been shown to excrete large amounts of a previously unrecorded urinary organic acid. This has been identified as 5-hydroxyhexanoic acid by gas chromatography mass spectrometry using a synthesized standard. Concentrations observed were 340 and 330 mg g-1 creatinine in the two patients. The metabolic precursor of the urinary acid is suggested to be hex-4-enoic acid, a probable chemical toxin closely related to the active organic acid metabolite of hypoglycin. The possibility of omega - 1 oxidation of hexanoic acid to 5-hydroxyhexanoic acid in these and other patients with dicarbocylic aciduris is also discussed.
 ...
PMID:Identification of 5-hydroxyhexanoic acid in the urine of twin siblings with a Reye's-like syndrome associated with dicarboxylic aciduria and hypoglycaemia and with similarities to Jamaican vomiting sickness. 57 58

Hypoglycin A(0.01--1.0 mmol/l) stimulated insulin release from pieces of rabbit pancreas in vitro in the presence or absence of extracellular glucose. The relevance of this finding to the hypoglycaemia of Jamaican vomiting sickness is discussed.
 ...
PMID:Hypoglycin stimulates insulin secretion. 59 Jun 55

A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.
 ...
PMID:[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia]. 66 98

The clinical picture of Reye's syndrome, characterized by an acute severe disease of brain and liver, initially has nonspecific generalized symptoms with cough, myalgia, and fever. The prognosis is poor. The disease starts with an infection, quickly followed by vomiting and loss of consciousness. In this phase the serum bilirubin is moderately raised, the transaminases markedly so. In addition to gastro-intestinal bleeding there may be hypoventilation, hypoglycaemia and seizures. Morbid anatomically there is a small-drop fatty infiltration of the liver and other organs with cerebral oedema. Aetiology and pathogenesis remain uncertain. Numerous therapeutic measures have been proposed.
 ...
PMID:[Reye's syndrome in adults (author's transl)]. 68 69

Twenty infants and young children with hereditary fructose intolerance (HFI) were admitted to hospital. None was diagnosed at admission. Referals were for vomiting of unknown aetiology (16X), pyloric stenosis or hiatus hernia (5X), toxic condition (3X), and hepatomegaly of unknown origin (5X). Feeding difficulties (20X), vomiting (18X), and failure to thrive (16X) were leading symptoms. The most frequent clinical findings were hepatomegaly (18X), pallor (14X), haemorrhages (13X). Ascites, oliguria, tachypnoea, fever, splenomegaly and rickets were less frequent. Laboratory findings were indicative of disturbed hepatic and renal tubular function and also of disturbed intermediary metabolism (hypokaliaemia, hypophosphataemia). However, hypoglycaemia was found in only 4 out of 15 patients tested. Differential diagnosis after hospital admission centered on metabolic disorders such as glycogenoses, galactosaemia, tyrosinosis, or Wilson's disease. Hepatitis, toxic hepatosis, liver tumour, intrauterine infection and sepsis were also considered. Eleven children had first ingested fructose within the first 6 weeks of life. The diagnosis was usually established only many weeks or months after first fructose intake and appearance of symptoms. This documents how difficult the diagnosis of this disease can be both in practice and in hospital. The course was severe in 11 children and lethal in 4. In only 5 patients was the course mild. The 16 survivors are doing well under fructose-exclusion diet. Irreversible visual impairment after intraocular haemorrhage occurred once. In each case HFI could have been suspected immediately, had a detailed nutritional history been taken. Practising paediatricians should know the composition of commonly used infant formulae. They should never prescribe sugared condensed milk for intractable vomiting prior to excluding HFI. Solution for intravenous infusion containing fructose and sorbitol are life-threatening for undiagnosed HFI patients.
 ...
PMID:Hereditary fructose intolerance in early childhood: a major diagnostic challenge. Survey of 20 symptomatic cases. 73

The urgent admission to hospital of diabetic patients is often precipitated by hypoglycaemia, by vomiting or by ketoacidosis following cessation insulin therapy. By the use of simple agents, such as glucagon, lemonade and quick-acting insulin, such episodes can usually be averted in the early stages by the diabetic, his family and his doctor. These preventive measures keep the diabetic at work or at school and out of hospital, but require the provision of a simple emergency kit.
 ...
PMID:The emergency management of the diabetic at home. 81 86

Adverse effects occurred in four youths after intravenous injection of an aqueous cannabis-seed tea, which was prepared by boiling the seeds. The effects were immediate and included nausea, vomiting, abdominal pain, watery diarrhea, chills, fever, hypovolemic shock, hypotension, and non-oligemic transitory renal failure. Other manifestations included persistent hypoglycemia, tachycardia, gastrointestinal bleeding, conjunctival hemorrhage, injury, jaundice, splenomegaly, leucocytosis, myalgia, arthralgia, motor weakness, and prostration. Ischemia was noted on electrocardiogram (EKG). All manifestations appeared to reverse within weeks, but these effects had been potentially fatal.
 ...
PMID:Adverse effects of intravenous cannabis tea. 87 75

In order to diagnose hereditary fructose intolerance up to now, there were only the dangerous fructose-load and the biochemical evidence of this metabolic defect from biopsies of liver, intestine or kidney. Since there are no screening tests nor tests for heterocygote carriers or prenatal diagnostic procedures, we tested a simple method to determine serum activities of the two enzymes concerned in this defect (fructose-1-phosphate aldolase, fructose-1,6-diphosphate aldolase). Even in completely healthy children we could measure both activities in a good range. Children with known liver lesion caused other than HFI had significantly increased activities of both enzymes. In 4 cases with HFI we could not measure any activity of fructose-1-phosphate aldolase and a decreased activity of fructose-1,6-di-phosphate aldolase in serum, despite an apparently damaged liver. We propose to define those two serum activities in any case of an obscure liver lesion, frequent vomiting and postprandial hypoglycemia in early childhood, in order to exclude HFI or to demonstrate its possible presence.
 ...
PMID:[Diagnostic procedures in hereditary fructose intolerance (author's transl)]. 90 45


1 2 3 4 5 6 7 8 9 10 Next >>