Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portosystemic shunt was diagnosed in a 6-month-old Quarter Horse filly with acute onset of apparent blindness and a 3-month history of depression, lethargy, and ataxia. Clinicopathologic test results indicated slightly high gamma-glutamyl transpeptidase activity and serum total bilirubin concentration. Sulfobromophthalein half time was prolonged, and plasma ammonia and serum bile acid concentrations were high as well. Histopathologic findings of percutaneous liver biopsy included widespread hepatocyte atrophy and numerous prominent small arterioles in the area of the portal triad. On the basis of history, clinical findings, and clinicopathologic abnormalities, a presumptive diagnosis of portosystemic vascular anomaly was made. To confirm the tentative diagnosis, nuclear hepatic scintigraphy and operative mesenteric portography were performed. Medical treatment was unsuccessful, and the foal was euthanatized. Portosystemic shunts have been described in dogs and cats, but few cases have been reported in large animal species. Other, more common causes of neurologic abnormalities in foals, such as trauma, vertebral body abscesses, brain abscesses, and meningitis, must be ruled out before portosystemic shunt is considered.
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PMID:Clinical and diagnostic features of portosystemic shunt in a foal. 335 82

A mouse mutant with glutathionuria was discovered by screening for amino acidurias in the progeny of ethylnitrosourea-mutagenized mice. Total glutathione concentration was increased in both blood and urine but decreased in liver homogenates from affected mice. Glutathionuric mice exhibited lethargy, severe growth failure, shortened life spans and infertility. gamma-Glutamyl transpeptidase activity was deficient in kidney homogenates of glutathionuric mice. The glutathionuric phenotype in these mice is inherited as an autosomal recessive trait. This mouse mutant will be a useful animal model for the study of gamma-glutamyl transpeptidase physiology and glutathione metabolism.
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PMID:Mice with genetic gamma-glutamyl transpeptidase deficiency exhibit glutathionuria, severe growth failure, reduced life spans, and infertility. 913 8

Following intravenous inoculation with horse blood-infected with the agent of human granulocytic ehrlichiosis (HGE) from a human fatality, two rhesus macaques (Macaca mulatta) exhibited pyrexia and lethargy on days 4-12 postinfection (PI). Hematology revealed neutropenia, thrombocytopenia, and anemia, with ehrlichial morulae in monocytes and neutrophils on days 4-12. Blood was polymerase chain reaction (PCR)-positive on days 4-12 and bone marrow was PCR-positive on day 11. There was a minor increase in gamma-glutamyl transpeptidase on day 12 and serum interferon-gamma levels increased by day 18. Seroconversion occurred on day 20 PI to a titer of 100 by day 22. Western blot bands characteristic of HGE included 25-, 44-, 80-, 94-, 105-, and 125-kD bands. There was generalized lymphohistiocytic infiltration in the liver, spleen, lymph nodes, and other tissues. The liver had focal hepatocyte apoptosis. There was HGE DNA (by PCR) only in the spleen. Comparable findings were not observed in a monkey that received uninfected horse blood as a control. This animal model of human disease is important for further studies of HGE diagnosis, management, and pathogenesis.
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PMID:A simian model of human granulocytic ehrlichiosis. 1040 32

gamma-glutamyl transpeptidase (gamma-GT) deficiency in GGT(enu1) mice is associated with glutathionemia, glutathionuria, growth retardation, infertility, lethargy, cataracts, and shortened life span. Total liver glutathione (GSH) content is significantly reduced in gamma-GT-deficient mice due to chronic excessive GSH loss. Oral supplementation of GGT(enu1) mice with L-2-oxothiazolidine-4-carboxylate (OTZ), a cysteine prodrug, led to partial restoration of liver GSH content. The growth, physical appearance, and behavior of gamma-GT-deficient mice were substantially improved following OTZ supplementation. Tissue GSH deficiency is the proximate cause of the phenotypic abnormalities associated with murine gamma-GT deficiency.
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PMID:L-2-oxothiazolidine-4-carboxylate supplementation in murine gamma-GT deficiency. 1275 58