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

Twenty-seven patients suffering from congenital coagulation defects of the prothrombin complex factors were investigated: six had haemophilia B; 14, factor VII defect; four, factor X defect; and three, factor II defect. Nineteen patients (70.3%) had previously received plasma and/or clotting factors concentrates. Among these, markers of hepatitis B infection (HBV) were present in five cases (26.3%) and hepatitis C (HCV) antibodies were found in seven cases (36.8%). The HIV1 prevalence was similarly high. In fact, five patients (26.3%), previously infused with factor IX or prothrombin complex factors concentrates, developed HIV1 infection. No patient with factor VII deficiency became HIV1 positive, despite the administration of unheated factor VII concentrates and the consequent HBV and HCV contamination. In the HIV1 positive group, three patients showed a false positivity for HIV2 antibodies. Five years after seroconversion, three patients developed AIDS (stage IV) and died, one had persistent generalized lymphadenopathy (stage III), and one with post-hepatitis liver cirrhosis was asymptomatic (stage II) for HIV infection. The significant decrease in total white cells, T4 lymphocytes and platelet counts and increase of beta 2-microglobulin and neopterin levels confirmed the prognostic value of these markers for the progression of HIV1 disease. Only one HIV1 negative transfused patient developed anti-HTLV-I p19 antibodies.
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PMID:Prevalence of HIV infection in a cohort of patients with congenital coagulation defects of the prothrombin complex factors. 178 37

This study was conducted on 40 Egyptian children (21 males and 19 females) with various chronic liver diseases, selected from the out-patient Pediatric Hepatology Clinic of Ain Shams University Hospital. Their ages ranged from 1.5 to 13 years with a mean of 5.98 +/- 3.72 years. Twenty healthy children of comparable age and sex to the patients were chosen as controls. All children were subjected to detailed history taking, thorough clinical examination and laboratory investigations including full blood picture, urine and stool examination, liver function tests, prothrombin time and hepatitis B surface antigen in addition to sigmoidoscopy with rectal snip examination, abdominal ultrasonography and liver biopsy. Moreover, immunological investigations were done, that included estimation of the serum complement levels of C3 and C4 by using single radial immunodiffusion method, assessment of the phagocytic and intracellular killing activity of polymorphonuclear leucocytes by living Candida albicans uptake and detection of non organ specific autoantibodies in the serum by indirect immunofluorescence technique. This study showed that the serum level of C3 was increased and C4 was decreased significantly in patients with chronic liver disease, especially in chronic active hepatitis. Regarding phagocytosis, there was significant impairment of the neutrophil phagocytic function but not the intracellular lytic activity of candida albicans. This reduced phagocytic function was more pronounced in patients having chronic hepatitis and cirrhosis than in bilharzial and other cases. Serum autoantibodies; antinuclear and antimitochondrial antibodies were absent in the sera of both patients and controls, while antismooth muscle antibodies were found in the sera of 47.5% of patients with chronic liver diseases and non of the control sera. The highest incidence of these antibodies was present in HBs Ag negative patients with chronic active hepatitis (80%). We concluded that patients with chronic liver diseases have disturbed functions of both complement and phagocytic systems that may lead to increased susceptibility to recurrent infections. So, routine assessment of immunological status with early diagnosis and treatment of infections are important in the proper management of these patients. In addition, detection of serum auto-antibodies in these patients is helpful in the early diagnosis of auto-immune liver diseases.
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PMID:Some immunological aspects of chronic liver diseases in Egyptian children. 187 66

The effect of prostaglandins (PG) in patients with fulminant and subfulminant viral hepatitis was studied. Seventeen patients presented with FHF secondary to hepatitis A (N = 3), hepatitis B (N = 6) and non-A, non-B (NANB) hepatitis (N = 8). Fourteen of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation, the mean AST was 1844 +/- 1246 units/liter, bilirubin 232 +/- 135 mumol/liter, PT 34 +/- 18 and PTT 73 +/- 26 sec, and coagulation factors V and VII were 8 +/- 4 and 9 +/- 51%, respectively. Twelve of 17 patients responded to PGE1 rapidly, with a decrease in AST from 1540 +/- 833 to 188 +/- 324 units/liter, a decrease in prothrombin time from 27 +/- 7 sec to 12 +/- 1 sec, PTT from 61 +/- 10 sec to 31 +/- 2 sec, and an increase in factor V from 9 +/- 4% to 69 +/- 18% and factor VII from 11 +/- 5% to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT but improvement was observed upon retreatment. After four weeks of intravenous therapy, oral PGE2 was substituted. Two patients have recovered completely and remain in remission six and 12 months following cessation of therapy. Two additional patients continue in remission after two and six months of PGE2. No relapses have been seen in patients with hepatitis A virus (HAV) or hepatitis B virus (HBV) infection. Liver biopsies in the 12 surviving patients have returned to normal. These results suggest efficacy of PGE for FHF. Further investigation is warranted.
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PMID:Treatment of fulminant viral hepatic failure with prostaglandin E. A preliminary report. 190 42

The 5'-flanking sequence of the human prothrombin gene was isolated by screening a human liver phage library with a human prothrombin cDNA as a hybridization probe. A phage was identified that contained 3 kilobase pairs of DNA upstream of the initiator methionine codon. Primer extension studies showed that the major transcription initiation sites were located 23 and 36 base pairs upstream of the initiator codon. DNA sequences in the 5'-flanking region of the human prothrombin gene were then analyzed for cis-activating transcriptional activity by a transient expression system using the human growth hormone gene as the reporter gene. The chimeric expression vector was introduced into HepG2 cells, and secreted human growth hormone was monitored by using a radio-immunoassay. These studies showed that the 3-kilo-base pair fragment contained sequences that were sufficient for the initiation of transcription in HepG2 cells. Subsequent deletion studies showed that the 3-kilobase pair fragment contained two elements: a weak promoter in the region immediately upstream of the mRNA coding sequence and an enhancer located between nucleotides -860 and -940. The enhancer element was active at a distance and in either orientation. In addition, the enhancer was liver cell-specific and acted on heterologous promoters including the herpes simplex virus thymidine kinase promoter and the mouse metallothionein I promoter. Comparison of the nucleotide sequence of the enhancer with a DNA sequence data base showed the enhancer sequence to be unique. The enhancer sequence is flanked by an inverted repeat 5' CCTCCC 3' and contains a putative binding site for hepatic nuclear factor 1. Deoxyribonuclease I footprint analysis and linker scanning mutagenesis showed that the enhancer contains multiple protein binding motifs. Mutagenesis of the 3' boundary CCTCCC sequence eliminated the enhancer activity. Comparison with other liver genes showed the presence of the CCTCCC sequence in the hepatitis B virus enhancer, the alpha 1-antitrypsin promoter, and the fibrinogen beta-chain promoter, suggesting a functional role for this motif.
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PMID:Characterization of a novel liver-specific enhancer in the human prothrombin gene. 191 8

With virus hepatitis B (VHB) associated with acute hepatic insufficiency, precoma and coma, one third of the patients develop bacterial purulent inflammatory complications involving mainly biliary system and intestine. Attendant bacterial complications promoted rapid progression of hepatic coma seen commonly on day 1-10 of the disease. The diagnosis in relevant patients recognizing bacterial complications clinically should be based on alterations in the liver size, the presence of fever, elevated body temperature, relatively low decrease of prothrombin index and fibrinogen against leukocytosis with stab neutrophil shift. These symptoms call for introduction of antibacterial drugs.
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PMID:[Bacterial complications in acute hepatic failure in patients with hepatitis B]. 194 86

The treatment of plasma with organic solvent/detergent mixtures at the time of plasma collection or pooling could reduce the exposure of technical staff to infectious viruses and enhance the viral safety of the final product. Treatment of plasma for 4 hours with 2-percent tri(n-butyl)phosphate (TNBP) at 37 degrees C, with 1-percent TNBP and 1-percent polyoxyethylensorbitan monooleate (Tween 80) at 30 degrees C, or with 1-percent TNBP and 1-percent polyoxyethylene ethers, (Triton X-45) at 30 degrees C resulted in the rapid and complete inactivation of greater than or equal to 10(4) tissue culture-infectious doses (TCID50) of vesicular stomatitis and Sindbis viruses, which are used as surrogates. Treatment of plasma with TNBP and TNBP and Tween-80 was shown to inactivate greater than or equal to 10(4) TCID50 of human immunodeficiency virus. TNBP treatment of plasma contaminated with 10(6) chimpanzee-infectious doses (CID50) of hepatitis B virus and 10(5) CID50 of non-A,non-B hepatitis virus prevented the transmission of hepatitis to chimpanzees. Immediately after treatment of plasma with 2-percent TNBP, the recovery of factors VIII, IX, and V and antithrombin III was 80, 90, 40, and 100 percent, respectively. Recovery of all factors was greater than or equal to 90 percent after treatment with TNBP and detergent mixtures. Treated plasma was fractionated by standard techniques into antihemophilic factor and prothrombin complex concentrates, immune globulin, and albumin. Prior treatment with TNBP or TNBP and detergent did not affect the separations of desired proteins. Therefore, it appears possible to inactivate viruses in plasma before the execution of standard fractionation procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of tri(n-butyl)phosphate detergent mixtures to inactivate hepatitis viruses and human immunodeficiency virus in plasma and plasma's subsequent fractionation. 175 94

By means of staphylocoagulase, plasma des-gamma-carboxy prothrombin (DCP) was measured in 255 subjects. Of these, 59 were healthy controls, 100 had primary hepatocellular carcinoma (PHC), 33 had cirrhosis of the liver, 16 had hepatitis, 11 had metastatic carcinoma of the liver (MCL), and 36 subjects had previously been treated with anti-vitamin K drugs. The mean plasma DCP level in the healthy subjects was 3.02 VGH U/l. Of PHC patients 80% had DCP levels greater than 6 VGH U/l, which we regarded as probably abnormal. None of the patients with benign liver diseases (cirrhosis of liver or hepatitis) had DCP greater than 10 VGH U/l. Of the patients with MCL 54.54% had DCP greater than 6 VGH U/l. In our study DCP was found to be as sensitive a tumor marker as alpha-fetoprotein (AFP) in the diagnosis of PHC and was better in distinguishing PHC from benign liver disease. Of PHC patients 92% had at least one of the two tumor markers. Simultaneous determination of DCP and AFP should be applied in mass survey programs for detecting PHC, especially in countries with a high prevalence of hepatitis B virus infection.
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PMID:Application of des-gamma-carboxy prothrombin as a complementary tumor marker with alpha-fetoprotein in the diagnosis of hepatocellular carcinoma. 246 47

We have investigated up to the beginning of 1987 114 patients with congenital clotting disorders. 84 had received plasma and/or clotting factors concentrates. 18 out of 84 (21%) had leukopenia, thrombocytopenia, or both. 64 out of 84 (76%) had been infected by hepatitis B virus. The great majority of them (62 out 64) developed adequate immunity (anti Hbs antibodies). Despite this, 47 out 84 (57%) showed persistently elevated transaminases. 17 out of 84 (20%) had HIV-seropositivity. Among them, 7 are free of symptoms related to such a virus up to present time, 8 developed AIDS-related complex and 2 had the full-blown AIDS and died. Non significant difference in HIV seroconversion or its clinical manifestations was noted depending on the administration of factor VIII concentrates versus prothrombin complex concentrates. In contrast, plasma administration appeared to be associated with a lower risk of viral transmission. No abnormality was observed in patients who had never received haemoderivatives, except the presence of anti Hbs antibodies in 1 of them.
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PMID:The prevalence of AIDS, AIDS related complex and HIV seropositivity in a large population of patients with congenital clotting disorders. 246 53

One hundred and fifty-seven patients with alcoholic liver disease were studied. Hepatitis B surface antigen (HBsAg) was positive in 20.4% of the patients. Those who were positive for the HBsAg presented at an earlier age, had a lower albumin level, a higher globulin level, a more prolonged prothrombin time, were more likely to have features of cirrhosis in the liver biopsy, and were probably more likely to suffer from hepatic encephalopathy in the follow-up compared with those negative for HBsAg. The mortality of subjects was low both on admission and during follow-up. It is concluded that chronic alcoholism and hepatitis B virus infection act synergistically in producing more severe liver damage and causing cirrhosis at a younger age compared with chronic alcoholism alone. One possible reason for the low mortality of the patients might have been their relatively good nutritional status.
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PMID:Synergism of chronic alcoholism and hepatitis B infection in liver disease. 249 Dec 28

We reviewed the records of 83 patients who underwent 100 orthotopic liver transplantations in order to determine the following: (1) the methods to predict blood usage, (2) the consequences of an ABO-incompatible transplant, (3) the benefit of providing cytomegalovirus (CMV)-negative blood products to CMV-negative patients receiving a liver from a CMV-negative donor, (4) the association of donor anti-hepatitis B core antigens and subsequent hepatitis B, and (5) the prognostic consequences of rouleaux observed in pretransplant blood compatibility testing. Patient diagnosis, the presence of ascites, a preoperative prothrombin time greater than 15 seconds, and a multifactorial "risk category" were all predictive of intraoperative blood loss. A history of previous gastrointestinal bleeding or an operation that involved the right upper abdominal quadrant was not predictive of intraoperative blood loss. Although CMV infection is common after liver transplantation, the prophylactic use of CMV antibody-negative blood products in CMV-negative recipients receiving a liver from a CMV-negative donor in our series was not associated with postoperative CMV infection. The transplantation of a liver positive for anti-hepatitis B core antigen was associated with subsequent hepatitis B surface antigen seroconversion in two of four cases. Transplantation of an ABO-incompatible liver and the presence of rouleaux observed in pretransplant blood compatibility testing were both associated with a significantly higher mortality. A careful review of laboratory data and medical records of patients undergoing liver transplantation should enhance the ability to modify the approach to the allocation of limited blood resources and the care and management of these patients.
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PMID:Intraoperative blood loss and patient and graft survival in orthotopic liver transplantation: their relationship to clinical and laboratory data. 253 41


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