Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41-year-old woman with Gaucher's disease developed bone crises of both proximal tibiae and of her spine concurrent with a syndrome of severe gastroenteritis. Three to six months later the bilateral symmetrical pathologic collapse of both lateral tibial plateaus occurred. The unusual occurrence of multiple bone crises with the gastroenteritis suggests a common causative agent, possibly a severe viremia.
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PMID:Acute bilateral symmetrical pathologic fractures of the lateral tibial plateaus in a patient with Gaucher's disease. 92 29

Studied were the lesions in the parenchymal organs and the hormonal glands in 20 pigs spontaneously died as a result of feeding with 1-lysine that had been contaminated with bacteria. The gross changes consisted of the enlargement and dark red coloration of the liver, gastroenteritis, hyperemia and hemorrhages in the kidneys and heart, oedema of the lungs and the wall of the gall bladder. Histologically, in the acute cases the liver showed hyperemia, pericapillary oedema, and granular dystrophia; in the subacute cases there were toxic dystrophy with the activation of the reticulo-endothelial system and subserous oedema in the gall bladder. The kidneys presented hyperemia, hemorrhages, and decreased volume of the glomeruloses in the subacute course of the disease. In terms of their function the heart, lungs, and kidneys displayed hemodynamic disturbances, and in the thyroid there were histologically changes characteristic of a follicular collapse. It is believed that the morphologic changes in the viscera investigated were due not to the intake of lysine itself, but to the effect of toxins produced by the concomitant microflora and the toxic amins (metabolites of the amino acids).
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PMID:[Pathomorphological changes in a disease in swine caused by feeding bacterial-contaminated 1-lysine]. 123 54

An epidemy of fatal posterior weakness was observed in Norwegian dairy goats with a spontaneous character (high fever, collapse, death). Clinical, postmortem, and histopathological findings indicated gastroenteritis, liver damage (necrotic foci), soft kidneys, pneumonia, and depletion of liver glycogen in goats up to 4 months of age. In older animals there was a prevalence of muscle degeneration. Indigenous goats did not exhibit any mortality, whereas the mortality rate in male crosses Norwegian X Tanzanian was 100%, regardless of their age. In young goats, the existence of a high mortality infectious syndrome with enterotoxaemia and fever is suspected, whereas older goats were probably exposed to a non-infectious myodegeneration.
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PMID:An epidemic of fatal posterior paralysis and sudden death in goats: a case report. 277 60

Twenty-four fatal cases of echo 11 infection in the eleven years 1968-78 are presented. All were children, and could be divided into two groups according to age at death and clinical presentation. The first group comprised 12 babies who died aged between 5 and 11 days after a short illness characterised by collapse, acidosis, and bleeding. At necropsy there was evidence of disseminated intravascular coagulation with haemorrhage into many organs including the renal medulla, suprarenal glands, gastrointestinal tract, and central nervous system. Six cases showed hepatic necrosis which was massive in three. Virus was present in many tissues. Infection was probably acquired from the mothers at delivery in 3 cases. Low maternal neutralising antibody titres and prematurity were thought to be adverse factors in the outcome. The second group consisted of 12 children aged between 9 weeks and 4 years 10 months who died suddenly. Pathological findings included upper respiratory tract infection, pneumonia, encephalitis, and gastroenteritis. Six of this group had been classified as 'cot deaths'. The role of echo 11 in the death of some of these older children is unknown. This report shows the danger of echo 11 to neonates, especially if unprotected by maternal antibody.
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PMID:Fatal infection with echovirus 11. 719 96

A 25-year-old woman presented with a history of secondary amenorrhoea for the last 3 years, coinciding with her delivery. She delivered at home and had massive postpartum haemorrhage. She was brought in a state of circulatory collapse to the nearest teaching hospital, where she was resuscitated. She developed anaemia, septicaemia and extradural empyema. The complications were managed and the woman improved. Presently, she approached us for infertility. She was investigated and diagnosed with postpartum hypopituitarism, that is, Sheehan's syndrome. Her gonadotrophin levels, luteinising hormone/follicle-stimulating hormone, were normal, serum oestradiol was low and serum prolactin was also on the lower side. She had started with genital atrophy and was given three cycles of cyclic oestrogen +progesterone combination. Ovulation was induced. She conceived and her antenatal period was uneventful. She delivered a full-term baby vaginally. However, she had inadequate lactation after delivery and lost the baby at one-and-a-half months' age due to gastroenteritis.
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PMID:A ray of hope for a woman with Sheehan's syndrome. 2338 98

Hemolytic anemia (HA) of the newborn should be considered in cases of rapidly developing, severe, or persistent hyperbilirubinemia. Several causes of corpuscular hemolysis have been described, among which red blood cell enzyme defects are of particular concern. We report a rare case of red blood cell enzyme defect in a male infant, who presented during his first months of life with recurrent and isolated neonatal hemolysis. All main causes were ruled out. At 6.5 months of age, the patient presented with gastroenteritis requiring hospitalization; fortuitously, urine organic acid chromatography revealed a large peak of 5-oxoproline. Before the association between HA and 5-oxoprolinuria was noted, glutathione synthetase deficiency was suspected and confirmed by a low glutathione synthetase concentration and a collapse of glutathione synthetase activity in erythrocytes. Moreover, molecular diagnosis revealed 2 mutations in the glutathione synthetase gene: a previously reported missense mutation (c.[656A>G]; p.[Asp219Gly]) and a mutation not yet described in the binding site of the enzyme (c.[902T>C]; p.[Leu301Pro]). However, 15 days later, a control sample revealed no signs of 5-oxoprolinuria and the clinical history discovered administration of acetaminophen in the 48 hours before hospitalization. Thus, in this patient, acetaminophen exposure allowed the diagnosis of a mild form of glutathione synthetase deficiency, characterized by isolated HA. Early diagnosis is important because treatment with bicarbonate, vitamins C and E, and elimination of trigger factors are recommended to improve long-term outcomes. Glutathione synthetase deficiency should be screened for in cases of unexplained newborn HA.
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PMID:Recurrent Isolated Neonatal Hemolytic Anemia: Think About Glutathione Synthetase Deficiency. 2758 54