Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Authors consider the different opinions expressed about the HBsAg screening in blood donors and its usefulness in preventing post transfusional hepatitis B (PTHB). They report data on the incidence of such a disease, as observed in their transfusional experience during the last 5 years, with a comparison between results obtained after CEP and RIA screening systems. The Authors point out the results of their retrospective investigation: the transfusion blood with a low HBsAg titre showed to be more infectious than the blood with high titre. Consequently, it is necessary to use more sensitive methods for HBsAg screening and possibly to increase their sensitivity or to combine them with other methods fit to evidence further markers of virus B.
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PMID:Screening of HBsAg and post-transfusional hepatitis type B. 72 67

Sera from 22 patients with systemic lupus erythematosus (SLE) were examined for the presence of hepatitis B antigen (HBsAG) by a complement fixation (CF) test, by an immunoelectrophoretic method (counterelectrophoresis-CEP), and by radioimmunoassay (RIA). The sera from 8 patients gave positive results using CF. However, the same sera and sera from 28 additional SLE patients, when tested with CEP and RIA, were not shown to contain HBsAG.
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PMID:Hepatitis B antigen and systemic lupus erythematosus. False positive complement fixation due to anti-antibodies. 108 49

Transfusion of whole blood or blood components is the mainstay of treatment in patients with beta-thalassemia and hemophilia. Owing to the scarcity of reports regarding the frequency of transfusion-transmitted hepatitis virus infections in thalassemia patients, the frequency of such infections was studied in India in 40 multi-transfused thalassemia patients (26 males, 14 females; mean age 8.1 +or- 5.3 years, range 1-35) with no clinical or biochemical evidence of liver disease. The enzyme-linked immunosorbent assay (ELISA) technique (Abbott) was used for all tests. The patients had received an average of 80 units (range 10-250) of blood. A majority of these units had been screened for hepatitis B surface antigen (HBsAg) using RPHA. HBsAg antibodies were present in 18 (45%), antihepatitis C virus (HCV) in 7 (17.5%), and antihuman immunodeficiency virus in 1 (2.5%) case, respectively. Of 18 HBsAg positive patients, antidelta and anti-HCV antibodies were present in 3 and 4 patients, respectively; 1 patient had both the antibodies. 4 of 40 (10%) patients had evidence of both hepatitis B virus (HBV) and HCV infection. In a US study, the frequencies of HBsAg and anti-HBs positively among thalassemics were 4.5% and 43.5%, respectively. In contrast, 90% of hemophiliacs show serological evidence of HBV infection. Routine screening of blood donors by CEP or RPHA technique was started in the hospital blood bank 7 years ago. The sensitivity of these techniques is much lower than that of RIA and ELISA and a majority of the patients has received initial blood transfusions before HBsAg screening was started. The study indicated that more than 50% of multi-transfused thalassemia patients showed serological evidence of one or more HBV, HCV, HDV, and HIV infection. Thus, screening of blood units for HBV, HCV, and HIV infections to be used for thalassemic patients and vaccination of thalassemic patients against hepatitis B is imperative.
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PMID:Frequency of hepatitis B, C and D and human immunodeficiency virus infections in multi-transfused thalassemics. 142 37

The porphyrias are a group of disorders caused by deficient activity of the enzymes responsible for the biosynthesis of haem. The skin is one of the major organs involved in most of these diseases because the porphyrins which accumulate are phototoxic. The common cutaneous porphyrias are variegate porphyria, porphyria cutanea tarda, congenital erythropoietic porphyria and erythropoietic protoporphyria, each caused by a different enzyme deficiency causing a distinctive pattern of porphyrin accumulation and typical clinical features. The genes encoding these enzymes have all been cloned recently, enabling the genetic defects underlying these disorders to be elucidated. The factors triggering sporadic porphyria cutanea tarda in predisposed individuals are now becoming clear: hepatic iron overload is required to induce the hepatic enzyme defect and many patients are haemochromatosis gene carriers. Hepatitis B, C, and HIV virus infection also contribute to disease expression. In erythropoietic protoporphyria, up to 5% of patients develop liver failure. It is now clear that some of these patients suffer from a different recessively transmitted form of the disease: this finding may make it possible to identify these patients at an earlier stage. Gene therapy holds particular promise as a future therapy and has successfully been used to correct enzyme defects in vitro. Bone marrow transplantation has also been tried in patients with congenital erythropoietic porphyria. The joints are not involved by porphyria. However, some non-steroidal inflammatory drugs prescribed by rheumatologists have phototoxic properties similar to uroporphyrin. These drugs cause a syndrome clinically and histologically indistinguishable from porphyria cutanea tarda which is known as pseudoporphyria.
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PMID:Porphyria. From Sir Walter Raleigh to molecular biology. 1059 49