PubMed · 4556874
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M Yamanaka. 1972. [Biliary stasis].. https://pubmed.ncbi.nlm.nih.gov/4556874/
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Parameters related to hepatic oxidative stress, cell injury, phagocytic activity, and liver histology were studied in control rats and in animals subjected to L-3,3',5-triiodothyronine (T3) and/or lindane administration. Hyperthyroidism elicited a calorigenic response and increased rates of hepatic O2 uptake, which were not modified by lindane treatment. T3 diminished serum lindane levels as well as those in the liver and adipose tissue, whereas lindane enhanced serum T3 levels in animals given T3. Compared with control rats, lindane significantly increased the rate of formation of thiobarbituric acid reactants (TBARS) by the liver, with no changes in either the reduced glutathione (GSH) content, the TBARS/GSH ratio as indicator of oxidative stress, or in the fractional rates of lactate dehydrogenase (LDH) and GSH efflux from perfused livers as integrity parameters. Hyperthyroidism induced GSH depletion in the liver, with a significant enhancement in the TBARS formation, the TBARS/GSH ratio, and in the fractional LDH and GSH efflux. These parameters were increased further by joint T3 and lindane administration in a magnitude exceeding the sum of the effects produced by the separate treatments. In addition, hyperthyroidism led to Kupffer cell hyperplasia and significant increases in serum glutamate oxalacetate transaminase (GOT) and in hepatic zymosan-induced chemiluminescence, while liver myeloperoxidase (MPO) activity was found unchanged, compared with controls. Rats treated with lindane presented normal liver histology, with no changes in biochemical parameters related to cell injury. The joint administration of T3 and lindane, however, elicited a marked elevation in serum GOT and glutamate pyruvate transaminase (GPT), concomitantly with extensive liver necrosis and the presence of granulomas containing lymphocytes, Kupffer cells and polymorphonuclear leukocytes (PMN). In this condition, hepatic zymosan-induced light emission and MPO activity were enhanced over control values. It is concluded that hyperthyroidism increases the susceptibility of the liver to the toxic effects of lindane, which seems to be accomplished by potentiation of the hepatic oxidative stress status. The latter effect may be conditioned by an enhanced phagocytic respiratory burst activity due to the observed Kupffer cell hyperplasia and PMN infiltration, in addition to the increased production of reactive oxygen species in parenchymal cells.
OBJECTIVE: To provide physicians and other transfusion medicine professionals with a current consensus on infectious disease testing for blood transfusions. PARTICIPANTS: A nonfederal, nonadvocate, 12-member consensus panel representing the fields of hematology, infectious disease, transfusion medicine, epidemiology, and biostatistics and a public representative. In addition, 23 experts in hematology, cardiology, transfusion medicine, infectious disease, and epidemiology presented data to the consensus panel and a conference audience of 450. EVIDENCE: The literature was searched through MEDLINE and an extensive bibliography of references was provided to the panel and the conference audience. Experts prepared abstracts with relevant citations from the literature. Scientific evidence was given precedence over clinical anecdotal experience. CONSENSUS: The panel, answering predefined consensus questions, developed their conclusions based on the scientific evidence presented in open forum and the scientific literature. CONSENSUS STATEMENT: The panel composed a draft statement that was read in its entirety and circulated to the experts and the audience for comment. Thereafter, the panel resolved conflicting recommendations and released a revised statement at the end of the conference. The panel finalized the revisions within a few weeks after the conference. CONCLUSIONS: The serum alanine aminotransferase test should be discontinued as a surrogate marker for blood donors likely to transmit posttransfusion non-A, non-B hepatitis infection since specific hepatitis C antibody testing has eliminated more than 85% of these cases. Antibody to hepatitis B core antigen testing should continue as it may prevent some cases of posttransfusion hepatitis B; it may also act as a surrogate marker for human immunodeficiency virus (HIV) infection in donors and may prevent a small number of cases of transfusion-transmitted HIV infection. Syphilis testing should continue until adequate data can determine its effect on the rarity of transfusion-transmitted syphilis. Vigilant public health surveillance is critical in responding to emerging infectious disease threats to the blood supply.
OBJECTIVE: To evaluate the risk of post-transfusion and postoperative non-A non-B hepatitis in Australia immediately before the introduction of screening for hepatitis C. DESIGN: Retrospective testing of blood samples from a prospective study of cardiac surgery patients. Samples were taken from transfusion recipients and non-transfused controls at regular intervals for 12 months after surgery during 1987-1989. For all donor, recipient and control samples, alanine aminotransferase (ALT) levels were measured and tests for antibody to hepatitis B (anti-HBc, anti-HBs) and, when available, to hepatitis C (anti-HCV) were performed. SETTING: Cardiac surgery units. PARTICIPANTS: Participants were included if they lived in the metropolitan area, and had not had a transfusion in the past year. MAIN OUTCOME MEASURES: Post-transfusion hepatitis (two consecutive samples showing raised ALT levels, > 90 IU/L with no other known cause); hepatitis C infection and carriage (antibody to hepatitis C). RESULTS: Post-transfusion hepatitis occurred in 1.1% of 736 recipients of blood not screened for hepatitis C (i.e., two cases per 1000 unscreened units given). No hepatitis occurred in 514 controls. Seven of the eight patients with post-transfusion hepatitis seroconverted to hepatitis C virus infection. Seven of the 26 anti-HCV-positive donations transmitted hepatitis C, six of these were positive by recombinant immunoblot assay (RIBA) (one by second generation testing only) and one was RIBA indeterminate. Nineteen were RIBA non-reactive; one transmitted hepatitis but the recipient did not develop anti-HCV, although hepatitis C RNA was detected in the donation. Serum ALT was raised in four of the six infective donations. CONCLUSIONS: Hepatitis C virus infection accounted for almost all cases of non-A non-B post-transfusion hepatitis. First generation anti-HCV tests detected about 85% of infective donations. Surrogate testing of donations by ALT or anti-HBc offers no additional advantage.