Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reported case of probable superfecundation is apparently the most extensively tested of all published cases: More than 40 specificities of the HLA Loci A and B, 5 of the Locus C, Bf and GLO I, furthermore ABO, MNSs, DCcCwEe, K 1--6, Fya, Fyb, Jka, Jk5, Lu3, Hp, Gc, Gm 1, 2, 4, 5, 21, Km 1, C3, Tf including C-subtypes, Pi, Bg, ACP, PGM1 including the extended polymorphism by PAGIF, AK1, ADA, 6-PGD, EsD, GPT, GALT, CAII and Hb. A reciprocal exclusion for putative father 1 and putative father 2 to the twin 2 and the twin 1, respectively, has been reached in 7 blood group systems: HLA, MNSs, Lu, Hp, Tf, Bg and GPT. The random probability for the fatherhood of an unknown third man suitable for both twins is extremely low among whites (1 : 10(8)) or blacks (1 : 10(9)). The development of paternity investigations within the last two years, mainly basing on isoelectrofocusing techniques, is shortly reported. The following systems are preferably involved: PGM1 (4 common alleles), Gc (including 1F and 1S), Pi (3 common subspecificities of M), C6, Tf (3 common subspecificities of C), FUC, Apo E, C2.
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PMID:The efficacy of modern blood group genetics with regard to a case of probable superfecundation. 719 69

Linkage relations between pepsinogen Pg5 and 28 genetic marker loci have been analyzed in Norwegian families. No strong hint of linkage was found. Linkage to Pg5 in males has been ruled out below 25% recombination for HLA and GPT, below 20% recombination for Rh, PGM1, ACP, Gc, MNSs, PGM3, and Gm and Pi, below 15% recombination for Hp, below 10% recombination for Fy, ABO, C3 and Jk and below 4% for Kell, Tf, C6, Km and Le(Se). Possibilities of loose linkages include Pg5-C6 and Pg5-MNSs, both of which should be followed up.
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PMID:Genetic linkage relation to the pepsinogen Pg5 locus. 731 69

In a group of 276 consecutive liver transplants 8 primary graft nonfunctions were identified (2.9%). Recipients showed a progressive elevation of transferases (mean maximum value ALT: 5000 +/- 1892 U/l) and bilirubin (mean maximum value: 20 +/- 11.8 mg/dl) and a decrease in the percent prothrombin time (mean minimum value 26 +/- 13 min.) in the post-implantation survival time of the 8 grafts (range 1-5 days). No statistically significant differences were observed between mean cold and warm-ischemia times for these 8 donor organs and those of a control group of 92 consecutive grafts. All organs except one were ABO isogroup and all except another one displayed negative lymphocytotoxic crossmatch. Predominantly small-droplet hepatocytic vacuolization with no nuclear displacement was observed in plastic-embedded semithin sections of all post-primary nonfunction liver tissues (severe in 4 grafts, centri-mediozonal in 2, and centrolobular in 2). In 3 cases where fresh liver tissue was available the lipidic nature of the vacuoles was confirmed with electron microscopy and with frozen sections stained with Sudan III. Other microscopic lesions were also observed: spotty monocellular coagulative necroses, variable extension of zonal coagulative necroses and hemorrhages, cholestasis and minor mixed inflammatory infiltrate. Comparative microscopic study of these tissues with the protocol biopsy specimens obtained 2-4 hours after reperfusion demonstrated previous liver cell-vacuolization in only 3 cases. In conclusion, an acute progressive microvascular steatosis developed in this primary nonfunction series. No specific etiopathogenic factors were identified.
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PMID:A clinopathologic review of 8 liver graft primary nonfunctions. 759 May 68

This paper reports the clinical syndrome of fulminant hepatic failure (FHF) following liver transplantation. FHF was defined as the sudden onset of liver failure [encephalopathy and prolonged International Normalised Ratio (INR)] without arterial thrombosis in the setting of a liver allograft. FHf post-transplant was seen in 8/154 (5.2%) adult patients undergoing transplantation. These eight patients developed a clinical syndrome characterised by: (a) a rapid rise in ALT levels to above 1000 U/l (mean maximum 1600 U/l), (b) a sudden increase in the INR to above 5 (mean maximum 5.6), (c) the development of high fever, (d) the persistence of thrombocytopenia (mean nadir 40 x 10(9)/dl), (e) a progressive rise in the bilirubin (mean maximum 400 mumol/l) and (f) the development of hepatic encephalopathy. In seven cases this syndrome occurred following good initial graft function at day 6 post (mean)-transplant. In one case the above syndrome developed immediately after liver transplantation. Four of the eight patients developed multiorgan failure associated with systemic acidosis (mean pH 6.84). All of these patients died (mean day 11). Four patients developed systemic alkalosis. Two of these four patients underwent successful retransplantation (on days 12 and 13) and remain alive at a mean of 11 months post-transplant. Six of the eight patients received OKT3 therapy without any apparent affect on clinical outcome. Compared to control group of patients (n = 28), 8 versus 2/28 had a positive cross-match with donor lymphocytes (P = NS), 1/8 versus 7/28 were ABO-non-identical (P = NS), 3/8 versus 10/21 had total MHC mismatches (P = NS) and 5/7 versus 6/16 had UW ischemic times above 10 h (P = NS). No patients had main hepatic artery thrombosis on angiography although four patients had evidence of intrahepatic microthrombi or arterial necrosis at autopsy. In all cases the histology showed massive haemorrhagic necrosis. Three cases had evidence of veno-occlusive lesions whilst foam cell arteriopathy was seen in two cases. Immunofluorescence was performed in three cases. In two cases there was evidence of immunoglobulin, complement and fibrin deposition in blood vessels. In conclusion, we describe an uncommon clinical syndrome occurring post liver transplant. This syndrome represents humorally mediated allograft rejection but there seems to be no relationship with tissue matching (antibody, ABO, MHC) or donor ischaemic times. If recognised earlier in the absence of multiorgan failure, urgent retransplantation seems to be the only effective therapy.
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PMID:Fulminant hepatic failure post liver transplantation: clinical syndromes, correlations and outcomes. 788 47

In Greenland, and especially East Greenland (Tasiilaq), a common recessive disease, cholestasis familiaris groenlandica (CFG)/Byler-like disease, occurs in Eskimo children [1]. In a period from 1964-1991, at least 22 children out of about 2,121 newborns were born with this disease (gene frequency q = 0.102). Samples from 126 persons, from a large pedigree in East Greenland including 7 affected and from two families in West Greenland with a total of 3 affected children, have been collected for studying 45 polymorphic markers and for mapping the CFG disease. Polymorphisms and exclusion data were found for the following markers: A1BG, ABO, ACP1, AHSG, C1R, C6, FY, GC, GLO1, GPT, HP, ITIH1, JK, GYPA, GYPB, ORM, P1, PGM1, PI, PON, RH and TCN2. Small positive lod scores (Z < 1.5) were found to the following markers: ITIH1, JK and TCN2. The following markers were nonpolymorphic in this material: ADA, AK1, ALAD, APOA4, APOH, BF, C3, BCHE, CHE2, CO, ESD, FUCA2, F13A1, F13B, KEL, LE, FUT1, LU, PEPD, PGD, PGP, PLG, FUT2, SOD1 and TF.
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PMID:Linkage studies of cholestasis familiaris groenlandica/Byler-like disease with polymorphic protein and blood group markers. 834 70

Regional variation in the genetic constitution and genetic differentiation of three tribal populations (Koya, Lambadi, and Chenchu) of Andhra Pradesh, South India, was examined from the data of 27 polymorphic loci (9 blood groups, 13 red cell enzymes, and 5 serum proteins). Significant heterogeneity was observed among the three tribal groups at several loci (ABO, RH, P, ADA, PGM, ACP, ESD, PGD, GPT, HP, C3, and BF). Pairwise comparisons also showed significant genetic differences between the Koya and the Chenchu at seven loci, between the Koya and the Lambadi at nine loci, and between the Chenchu and the Lambadi at seven loci. Gene differentiation among the three tribes was sufficient to allow an overall excess of heterozygosity. The FIS estimates of each tribe showed positive values, but a great number of alleles showed negative FIS values, supporting varying degrees of gene flow and admixture with neighboring populations. The genetic differentiation and affinity of 14 tribal populations of Andhra Pradesh were further examined using published and unpublished data on 11 polymorphic genetic systems. Despite the genetic distinctions between two Chenchu samples and Koya and Koya-related tribes (Koya Dora and Konda Dora), geographic proximity seems to be an important determinant of affinity of the tribal populations of Andhra Pradesh. The extent of genetic diversity is high compared with previous reports from this state. No evidence from the present data indicates that selection had any appreciable effect on local differentiation, but the present analysis suggests that differences are more likely to be maintained by genetic drift, admixture, and inbreeding.
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PMID:Genetic study of the tribal populations of Andhra Pradesh, south India. 905 43

This study presents the results of an examination of 3 blood-group systems (ABO, Rhesus, and P1) and erythrocyte enzymes (ADA, AK, ALADH, PGD, SAHH, PGM1, PGM3, GPT, GOT, ACP, UMPK, ESD and GLO) in populations that reside in R. Macedonia. Four population samples from the Republic of Macedonia (129 Macedonians from Skopje, 98 Albanians from Skopje, 95 Aromanians from Krusevo, 102 Aromanians from Stip) were included in the study. A comparison of the obtained results with data from literature on other Balkan populations has been made. The results of the comparison of the studied alleles indicate relatively small genetic distances among the studied populations. The obtained dendrograms indicate a larger homogeneity in the large Balkan populations, and a manifest trend of separating the Aromanian population of the Stip region. A larger separation is characteristic in the Greek population of Thrace.
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PMID:Genetic polymorphism of blood groups and erythrocytes enzymes in population groups of the Republic of Macedonia. 1835 78

We present a case report of a posttransplant patient who had hepatotoxicity due to both tacrolimus and cyclosporine and cholestatic jaundice due to tacrolimus. The patient did not show sustained improvement in enzyme and bilirubin abnormalities after an initial change from tacrolimus to cyclosporine or with a change back to tacrolimus, but he ultimately showed improvement when the blood concentration of tacrolimus was lowered. A 56-year-old man with subacute fulminant hepatitis induced by acarbose was admitted to our hospital for living donor liver transplantation. The liver graft consisted of the left lobe from his ABO-identical son. The early posttransplant course was uneventful. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin improved initially, but the ALT and AST levels later increased. A liver biopsy suggested a presumptive diagnosis of drug reaction. All drugs were discontinued, the immunosuppressive agent was changed from tacrolimus to cyclosporine. After initial improvement, the ALT and AST levels increased again. Assuming a reaction to cyclosporine, we decreased the concentration of cyclosporine in the blood. The enzyme levels improved temporarily but again began to rise. We changed the immunosuppressive agent to tacrolimus, which resulted in improvements in the ALT and AST levels; however, the total bilirubin level increased. We interpreted this increase as tacrolimus-induced cholestasis; in response, we decreased the blood concentration of tacrolimus to between 3 and 5 ng/dL and added 1,000 mg of mycophenolate mofetil to the drug regimen. The patient recovered without further complications. Repeated liver biopsies throughout the hospital course suggested that the mild mononuclear cell infiltration observed in a few triads had not been caused by acute rejection but had possibly been drug-induced.
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PMID:Hepatotoxicity caused by both tacrolimus and cyclosporine after living donor liver transplantation. 1864 79

A safety issue has been noted in applying rituximab to renal transplant patients with HCV infection, as a hepatitis C virus (HCV) flare-up and lethal cholestatic hepatitis C occurred in a renal transplant patient treated with rituximab for lymphoproliferative disorder. As double-filtration plasmapheresis (DFPP) and cyclosporine were reported to reduce hepatitis C viremia, we performed ABO-incompatible renal transplantation in two patients with positive HCV RNA by using rituximab, DFPP and cyclosporine-based immunosuppressant. The HCV RNA level was 3.3 x 10(5) IU/mL for Case 1 and 1.2 x 10(3) IU/mL for Case 2 before DFPP. After DFPP and renal transplantation, Case 1 had stable ALT levels and a transient decrease in HCV RNA to 7.9 x 10(4) IU/mL at 1 month followed by a gradual increase to 7.6 x 10(6) at 12 months, but Case 2 had a dramatic and persistent elevation of HCV RNA to 7.7 x 10(6) from 1 week to 12 months accompanied by elevated ALT levels. The serum creatinine levels were 1.5 mg/dL for Case 1 and 1.9 mg/dL for Case 2 at 12 months. Although cholestatic hepatitis C did not occur in our patients, who received rituximab for ABO-incompatible renal transplantation, the antiviral effect of cyclosporine and DFPP did not seem evident.
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PMID:Application of rituximab to hepatitis C-positive, ABO-incompatible renal transplantation. 1956 40

ABO-incompatible living-donor liver transplantation (ABO-LDLT) is generally more difficult to perform than ABO-incompatible kidney transplantation. Despite introduction of rituximab, ABO-LDLT in non-responders is a still difficult issue. A 23-year-old woman with primary sclerosing cholangitis underwent LDLT. The recipient's blood type was 0(+) and the donor's was B(+). Rituximab was infused twice on preoperative day (POD) 14 and 7. Plasma exchange (PE) was performed on PODs 5, 3, 2, and 1. However, repeated PE failed to decrease the anti-B antibody titer. On the other hand, preoperative esophagogastroscopy revealed esophageal varices with red color sign. Therefore, simultaneous liver transplantation and Hassab operation were performed. The donor left lobe of the liver was orthotopically transplanted into the recipient following Hassab operation. Flow cytometry on the day of surgery showed that the frequencies of B cells (CD20+) and memory B cells (CD20+/CD27+) in the peripheral blood were 0.9% and 0.3%, respectively; flow cytometry of cells recovered from the spleen revealed that the frequencies of B cells and memory B cells were 2.5% and 2.4%, respectively. Acute cellular rejection occurred on POD 15, and was treated by steroid pulse therapy, leading to a decrease in the anti-B antibody titer. The liver was functioning well on POD 390 (AST 19, ALT 34). In non-responders to ABO-LDLT, anti-donor blood type antibody-producing cells remains in the spleen after the conventional preoperative regimen. Splenectomy is an option for ABO-LDLT non-responders.
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PMID:Discrepancy of B cell frequency between periphery and spleen after rituximab treatment in ABO-incompatible liver transplantation. 2463 32


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