Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the recovery stage of the hemolytic uremic syndrome in 2 cases an increase of serum levels of GOT, GPT, LDH, gammaGT, 5'ND and AP was noticed, without signs of a recurrence of the disease. In one patient also jaundice and hepatomegaly were found. The observations suggest a parenchymal damage of the liver.
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PMID:Liver damage in the hemolytic uremic syndrome. 3 33

The incidence of hemolytic uremic syndrome (HUS) has been increased for these several years. As the cause of HUS, verotoxin-producing E coli (VTEC) is very important. By our nationwide survey for five years from 1986 to 1990, 146 cases with HUS were compiled. Among 122 cases of HUS, 101 cases (82.8%) had good prognosis, 15 cases (12.3%) had renal or CNS residue. And death rate was 4.9% (6 cases). Clinical features were compared between the groups of good and poor prognosis. In the group of poor prognosis, impaired consciousness, convulsion and hypertension were significantly high. The data of biochemistry such as BUN, creatinine, GOT, GPT, C3, CH50 and CRP were significant between two groups. Demonstration of VTEC and positive serum antibody were seen in 60% among 35 cases. Dr Takeda of National Children's Hospital estimates that the incidence of hemolytic colitis is 1200 cases per year, and the occurrence of HUS is about 100 cases per year, among them 70% cases may be caused by VTEC.
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PMID:[The etiology and clinical features of hemolytic uremic syndrome]. 802 78

Streptococcus pneumoniae is an uncommon etiological organism in hemolytic uremic syndrome (HUS). Production of neuraminidase by S. pneumoniae results in exposure of red blood cell T-antigen, resulting in hemolysis, thrombocytopenia, and acute renal failure. Hepatic involvement in this form of HUS has not been described in the literature. We report in three children with S. pneumoniae-associated HUS the presence of severely elevated transaminases and conjugated hyperbilirubinemia. Increases in asparagine transaminase ranged from 11 to 46 times normal values and an increase in alanine transaminase ranged from 1.6 to 8 times normal. In all patients the rise in total bilirubin was 7-15 times normal. Biliary tree obstruction and viral causes for liver dysfunction were absent. Hepatocellular injury in S. pneumoniae-associated HUS likely results from mechanisms involved in sepsis and pneumonia-induced jaundice, combined with severely increased bilirubin production following massive hemolysis. The hepatic injury in all three patients resolved within 9, 5, and 10 days. Our experience suggests that an extensive evaluation including liver biopsy is not indicated.
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PMID:Hepatocellular injury in Streptococcus pneumoniae-associated hemolytic uremic syndrome in children. 874 6

Shiga toxin producing Escherichia coli (STEC) are noninvasive enteric pathogens that may cause hemorrhagic colitis (HC) and diarrhea-associated hemolytic uremic syndrome (D+ HUS). We hypothesized that development of D+ HUS is associated with increased serum procalcitonin (PCT) levels. PCT was measured by an immunoluminometric assay in 113 patients. Concentrations of PCT were different in normal controls, disease control groups (rotavirus enteritis, HC due to non-STEC pathogens, chronic renal failure), and children with uncomplicated O157:H7 HC or D+ HUS. Children with D+ HUS showed higher PCT levels than those with uncomplicated O157:H7 HC, and increased concentrations were noted in cases requiring peritoneal dialysis. Severely increased concentrations were observed in children with D+ HUS on d 5 or 6 after the onset of enteritis, whereas serial measurements in those with uncomplicated O157:H7 HC remained within the normal range throughout the first week of illness. PCT was correlated with serum concentrations of lipopolysaccharide (LPS)-binding protein and serum levels of alanine aminotransferase. Using two separate sets of real-time PCR primers, we were unable to detect elevated PCT mRNA transcripts in nonadherent undifferentiated (monocytic) or differentiated (macrophage-like) THP-1 cells stimulated with purified Shiga toxin-1 and/or LPS. Our data show that serum levels of PCT are associated with the severity of illness in children with D+ HUS. Further studies are needed to determine the role of PCT in the pathogenesis of thrombotic microangiopathy associated to childhood D+ HUS.
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PMID:Procalcitonin in children with Escherichia coli O157:H7 associated hemolytic uremic syndrome. 1654 33

Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy often caused by mutations in complement factor H (CFH), the main regulator of alternative complement pathway. Because CFH is produced mainly by the liver, combined liver-kidney transplantation is a reasonable option in treatment of patients with severe aHUS. We studied complement activation by monitoring activation markers during liver transplantation in two aHUS patients treated extensively with plasma exchange and nine other liver transplantation patients. After the reperfusion, a clear increase in all the activation markers except C4d was observed indicating that the activation occurs mainly through the alternative pathway. Concentration of SC5b-9 was higher in the hepatic than the portal vein indicating complement activation in the graft. Preoperatively and early during the operation, the aHUS patients showed highest C3d concentrations but otherwise their activation markers were similar to the other patients. In the other patients, correlation was found between perioperative SC5b-9 concentration and postoperative alanine aminotransferase and histological changes. This study explains why supply of normal CFH by extensive plasma exchange is beneficial before combined liver-kidney transplantation of aHUS patients. Also the results suggest that perioperative inhibition of the terminal complement cascade might be beneficial if enhanced complement activation is expected.
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PMID:Complement activation during liver transplantation-special emphasis on patients with atypical hemolytic uremic syndrome. 2181 16