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)

BACKGROUND. Exposure of pregnant women to angiotensin converting enzyme inhibitor may have side effects on the fetus or newborn, mainly oligoamnios and impaired renal function. CASE REPORT N zero 1. A 34 year-old woman was given enalapril from the onset of her pregnancy because of hypertension from the age of 18 years. Oligoamnios was diagnosed in the fetus on gestational week 28; enalapril was then replaced by nifedipine but this drug was badly tolerated so that the woman was again given enalapril 8 days later. The baby (1700 g) was born by cesarean section at gestational week 34 because of acute distress syndrome; he developed hypotension, anuria, generalized oedema and was placed in intensive care. Treatment included ventilation, sympathomimetic agents, and diuretics. An exchange-transfusion followed by peritoneal dialysis was performed a few hours later. Renal function returned to normal between the 3rd and 5th day. Unilateral kidney hypoplasia was diagnosed at the age of 2 years. CASE N zero 2. A 24 year-old woman was given enalapril at the third trimester of a twin pregnancy. Delivery was full term at 37 weeks. The first baby, a boy weighing 2610 g, suffered from hypoglycemia and vomiting followed by hypotension and oliguria that required exchange-transfusion and repeated peritoneal dialysis. This boy has developed moderate chronic renal failure and hypertension. The second baby, a girl weighing 2,165 g, suffered from respiratory distress syndrome followed by hypotension and oliguria, but her renal function returned to normal within a few days. CONCLUSIONS. The use of angiotension converting enzyme inhibitor by pregnant women places the fetus at severe risk: treatment with this type of drug should be stopped as soon as pregnancy is confirmed.
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PMID:[Fetal and neonatal effects of maternal treatment with angiotensin converting enzyme inhibitor]. 795 36

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

The scientific literature concerning alcohol intoxication is enormous. However, less is known of alcohol-induced disturbances in children and adolescents and most of those reports concern cases of hypoglycemia in children under five years of age. We studied the clinical status and chemistry, especially acid-base balance, in 36 young teenagers treated at hospital for alcohol intoxication. On physical examination 6 patients were somnolent, 18 were comatose and 12 were in deep coma. The impairment of consciousness was directly proportional to the blood ethanol concentration. Acidosis was a central finding, and it was caused by a combination of respiratory and metabolic factors (a high blood PCO2 and a low base excess; r = 0.97, p < 0.001); the finding of respiratory acidosis dominated. Base excess correlated negatively with beta-hydroxybutyrate and lactate, as expected. All the metabolic products measured--acetate, beta-hydroxybutyrate and lactate--were significantly elevated compared with the control patients. No hypoglycemia was found. Prior treatment with intravenous glucose decreased vomiting and normalized the serum lactate concentration and PO2. Hypokalemia was the most common abnormality in serum electrolytes. In four patients the rate of fall of blood ethanol concentration was 2.8-3.3 mmol/h (0.13-0.15 g/l-1 h-1) and the mean acetate concentration was 0.8 mmol/l (SE 0.3). Biochemical disturbances in young teenage alcohol intoxicants resemble those previously found in adults. The severe toxicity by ethanol, manifesting in coma, occurs in lower blood alcohol concentrations in children than in adults.
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PMID:Alcohol intoxication in hospitalized young teenagers. 824 77

To clarify the mechanism underlying abnormal vasopressin (AVP) secretion in glucocorticoid deficiency, we examined the response of AVP secretion to osmotic stimulus produced by 5% saline infusion and analyzed the possible causative factors in seven patients with hypoosmolal hyponatremia resulting from adrenal insufficiency. In all patients, urinary sodium excretion persisted with urine osmolality exceeding plasma osmolality, and plasma AVP levels relative to plasma osmolality were elevated. Blood urea nitrogen, plasma creatinine, and PRA ranged from low to normal. All patients had nausea or vomiting, three had hypotension, and two had hypoglycemia; however, the primary cause of increased AVP secretion was attributed to none of these stimuli. After 5% saline infusion, patterns of changes in plasma AVP levels in individual patients were variable: levels decreased with increasing plasma osmolality in two patients and remained unchanged in the other five patients. Despite hyponatremia and absence of hypovolemia, thirst was present in the five patients, who responded normally to questions. This abnormality in AVP secretion and thirst was corrected after glucocorticoid replacement with normalization of plasma sodium concentrations and osmolality. Thus, glucocorticoid deficiency in man results in a clinical picture almost indistinguishable from that of the syndrome of inappropriate secretion of antidiuretic hormone. Persistent AVP secretion in this pathological state is due to a loss of hypotonic suppression of the osmostat for AVP release, which may be occasioned primarily by glucocorticoid deficiency per se and aggravated secondarily by multiple nonosmotic stimuli including nausea, hypotension, and hypoglycemia.
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PMID:Hyponatremia and osmoregulation of thirst and vasopressin secretion in patients with adrenal insufficiency. 826 45

A 21-month-old infant developed coma with hypotonia during a viral infection. Acyl CoA dehydrogenase deficiency was diagnosed on the basis of results of the chromatographic study of organic acids performed on a urine specimen collected during the acute episode. However, other disorders of mitochondrial and fatty acid oxygenation can generate similar symptoms. Emphasis is put on the need for collecting urine specimens in patients who develop alterations in consciousness and hypoglycemia without ketonuria during prolonged fasting or repeated vomiting due to a viral infection. Urine chromatography can suggest which enzyme is defective, although the diagnosis should always be confirmed by a study of fatty acid oxygenation in lymphocytes or fibroblasts.
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PMID:[Deficiency in medium chain acyl coA dehydrogenase manifested as febrile coma]. 834 83

In the past 5 years we have discovered 8 boys and 3 girls who suffer from fructose-1,6-bisphosphatase deficiency. Although they all showed the typical symptoms of the deficiency such as frequent vomiting, hypoglycemia, lactic acidosis, and hepatomegaly, the age at diagnosis varied from 2 months to 4 years. All the boys revealed the deficient enzyme activity in leukocytes but none of the girls. The liver biopsy was investigated in six patients to confirm the diagnosis. These results suggest the existence of tissue-specific isoenzymes for fructose-1,6-bisphosphatase possibly with a different gene origin.
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PMID:Diagnosis of fructose-1,6-bisphosphatase deficiency using leukocytes: normal leukocyte enzyme activity in three female patients. 838 9

A lymphosarcoma originating from kidneys, which metastasized to the ovaries, oviducts, heart and pancreas, was pathologically diagnosed in a 3-year-old female Japanese dog (Shiba dog). Clinically, the dog exhibited vomiting, diarrhea, oliguria and abdominal enlargement, associated with hypoglycemia. Grossly, the kidneys were enlarged and neoplastic masses were also seen in the ovaries and heart. Histologically, a majority of glomeruli and renal tubules were obliterated due to diffuse invasion by tumor cells. There were no metastatic lesions in the mesenteric and tracheobronchial lymph nodes, spleen and bone marrow. Most of the tumor cells were small- to medium-sized lymphoid cells with a large nucleus and scanty cytoplasm.
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PMID:Bilateral renal lymphosarcoma in a dog. 839 50

Eight patients with persistent hyperinsulinemic hypoglycemia of infancy who were treated with octreotide without pancreatectomy are described. All had severe, early-onset disease that would have required partial pancreatectomy had octreotide not been available. Along with octreotide, frequent feedings and raw cornstarch at night were required by all. Octreotide was given in three or four daily subcutaneous injections in four patients and in a continuous subcutaneous infusion with an insulin infusion pump in four. All had mild, transient gastrointestinal symptoms (vomiting, abdominal distention, steatorrhea) after the start of therapy. Asymptomatic gallstones were found in 1 patient after 1 year of treatment. No other long-term untoward effects were noted, including no detrimental effect on psychomotor development. Growth was not affected in five of six patients treated for more than 6 months. In five patients, octreotide was discontinued after 9 months to 5 1/2 years; patients were given diazoxide instead, two required percutaneous gastrostomy, and one 5 1/2-year-old child required no further treatment. The remaining three patients (aged 5 to 9 months) are still being treated with octreotide. We conclude that, with the use of octreotide, pancreatectomy can be avoided in some patients. Particularly in light of our findings of a high incidence of diabetes years after partial pancreatectomy, and clinical improvement after months to years of octreotide treatment, we believe that aggressive medical therapy, when effective, is preferable to partial pancreatectomy.
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PMID:Persistent hyperinsulinemic hypoglycemia of infancy: long-term octreotide treatment without pancreatectomy. 841 May 9

Defects in mitochondrial beta-oxidation may result in severe metabolic crisis after metabolic stress. The combination of hypoketotic hypoglycaemia and concurrent collapse of mitochondrial metabolic function may be very similar to that in Reye syndrome. Chronic effects on cardiac and skeletal muscle may be seen in some patients with defective long-chain fatty acid oxidation. Less common symptoms include peripheral neuropathy, pigmentary retinopathy, and failure to thrive with recurrent diarrhoea or vomiting. Collectively, such disorders are relatively common and their association with sudden infant death leads to a considerable demand for laboratory investigation. Currently the laboratory methods available are not capable of dealing with this demand in a rational and cost-effective manner and it is necessary to have careful clinically- and pathologically-based selection procedures if a useful service is to result.
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PMID:Defects in mitochondrial fatty acid oxidation: clinical presentations and their role in sudden infant death. 844 23

We have carried out a retrospective study on 100 children in hospital in Marseilles, France with a diagnosis of Plasmodium falciparum malaria. On admission, the main clinical features were anaemia (90 cases), fever (83 cases, > 40 degrees C in 22 cases), hepatomegaly (44 cases), vomiting (29 cases), neurological signs (22 cases), thrombocytopenia (13 cases), hyperparasitaemia (6 cases), jaundice (4 cases), shock (1 case) and hypoglycaemia (1 case). Severe malaria, as defined by the World Health Organization Malaria Action Programme, was rare in our study (only 2 cases) and the prognosis was good (no death, no sequela). The search for neurological signs such as impaired consciousness, prostration or convulsions is an effective and simple way to diagnose potentially severe cases. In the presence of these signs, intravenous quinine treatment resulted in a shortened duration of fever (30 h instead of 63 h) and thereby avoided patients becoming worse. In children without neurological signs or persistent vomiting, oral therapy may be used even if there is high fever or hyperparasitaemia, but close surveillance is required. Patients treated with halofantrine or mefloquine had a shorter stay in hospital than those treated with chloroquine (mean = 4 d instead of 5.7 d). The resistance of some strains to chloroquine may explain this difference.
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PMID:Choice of therapy for imported cases of falciparum malaria in children: a retrospective study of 100 cases seen in Marseilles, France. 846 3


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