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)

Hepatitis B associated antigen (HB-Ag) may be observed in the serum in subjects either apparently healthy or exhibiting a number of disease symptoms. Its incidence among the Geneva voluntary blood donors is 0.48% with 54% exhibiting the surface antigen ad and 34% ay. While the HB-Ag positive blood donors appeared clinically healthy, minor pathology was found in the majority of them (thrombocytopenia, histological evidence of inflammatory foci, of persistent hepatitis and of chronic aggressive hepatitis). In 82 patients suffering from hepatitis B the same ad-ay type distribution of the HB-Ag has been found. In 11 out of 31 patients increased Clq binding suggests the presence of circulating complexes. Diminutions in the level of complement components also indicates participation of complement in the formation of immunocomplexes. In 2 out of 3 patients with Hb-Ag positive polyarteritis nodosa, the Clq binding test was also positive. The pathophysiologic implications of hepatitis B infection are discussed in connection with the authors and other findings. It appears that the main defense mechanism leading to elimination of the viruses within the hepatocytes lies in cell mediated immunity. Hepatitis would then represent the side reaction of this defense mechanism. Antibodies are probably useful in preventing the virus from entering the cell, but also in the course of the cell mediated defense mechanism (elimination of viral material liberated during the T-cell hepatocellular interaction). Immune complexes may be operative in certain extrahepatic manifestations such as arthralgia. Polyarteritis nodosa may result from local antibody interaction with antigen fixed within arterial walls.
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PMID:[Physiopathology of hepatitis B virus infection]. 24 Jan 99

The antibiotic vancomycin shares many similarities with ristocetin, an agent noted for its effects on platelets and plasma fibrinogen. Vancomycin did not aggregate platelets as ristocetin, but platelets were incorporated into precipitates induced by vancomycin. Fibrinogen and factor VIII were precipitated from plasma at low concentrations of vancomycin. The precipitated fibrinogen remained clottable. Hepatitis B surface antigen was selectively precipitated from serum and could be recovered from the precipitate. Rabbits receiving bolus intravenous injections of high doses of vancomycin developed hypofibrinogenemia and thrombocytopenia within minutes and often went on to die. Studies with 125I-vancomycin revealed little stable binding of the antibiotic to platelets or fibrinogen. A relationship is suggested between the potent protein precipitating effects and phlebitis at the infusion site commonly associated with vancomycin therapy.
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PMID:Effects of vancomycin on platelets, plasma proteins and hepatitis B surface antigen. 118 37

Twenty-one adult patients with chronic hepatitis B and active viral replication as indicated by positivity for hepatitis B e antigen and hepatitis B virus DNA, with increased DNA polymerase levels for more than 6 months, were entered into a prospective trial of low-dose recombinant human alpha-interferon therapy. All patients were treated with 5 million units of recombinant interferon alfa-2b given subcutaneously every other day for 12 weeks. During treatment, 18 patients (86%) showed a significant reduction of DNA polymerase levels (p less than or equal to 0.001), which reached normal values in ten (48%). After 10 months' mean follow up, seven patients (33%) were hepatitis B e antigen negative and five (24%) subsequently became positive for antibodies to e antigen. By 27 months, nine patients (43%) were both hepatitis B e antigen negative and e antibody positive. Only one patient became permanently negative for hepatitis B surface antigen. One patient relapsed during the second year of follow up. Side effects necessitated withdrawal of therapy in two patients: one due to worsening thrombocytopenia after two doses of interferon (data omitted from the study results) and one due to a local reaction at the injection sites. Our data indicate that small doses of recombinant interferon alfa-2b given during a 12-week period induce a significant reduction in viral replication and approximately triple the spontaneous seroconversion rate observed in patients with chronic hepatitis B.
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PMID:Prospective trial of recombinant leucocyte interferon in chronic hepatitis B: a long-term follow-up study. 207 69

We conducted a prospective, randomized trial to study the efficacy and tolerance of long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B. Ten patients were randomly assigned to a 6-month interferon regimen, and 10 patients were assigned to a 3-week interferon trial. Eleven patients (five assigned to long-term treatment and six to short-term treatment) did not complete interferon therapy: eight had either severe thrombocytopenia or neutropenia; one had pronounced fatigue in relationship to administration of interferon; one had spontaneous bacterial peritonitis and sepsis and died; and one had a massive fatal variceal hemorrhage during interferon therapy. Most of the serious hematologic complications occurred in patients with cirrhosis and hypersplenism. In one patient, seroconversion to hepatitis B virus DNA negativity occurred before the onset of treatment. Four of the five patients able to complete the 6-month interferon regimen and only one of four patients able to complete the 3-week trial had seroconversion to hepatitis B virus DNA negativity. Thus, we conclude that the therapeutic response was better among patients who were able to complete a 6-month interferon trial. In patients with cirrhosis and hypersplenism, development of either severe thrombocytopenia or leukopenia associated with interferon therapy precluded completion of treatment.
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PMID:Long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B: a prospective, randomized treatment trial. 221 80

In 1985 a mixture of red cells collected in citrate anticoagulant with plasma derived from heparinized blood was introduced in Amsterdam to perform exchange transfusions in newborns. This heparin mixture has physiological levels of electrolytes, calcium and glucose, can be delivered on short notice and carries a minimal risk of transmission of infectious diseases because all blood components are tested for hepatitis B antigen and antibodies against syphilis and the human immunodeficiency virus. Retrospectively we evaluated 54 children treated in 1986 and 1987 with exchange transfusions using this heparin mixture. An adequate decrease in bilirubin values when necessary was observed while neither changes in sodium, potassium, calcium or glucose values nor adverse effects on the pH value were recorded. However, a remarkable transient thrombocytopenia was found following exchange transfusion with a decrease of the platelet count to an average of 39% of the initial value.
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PMID:[The use of a mixture of citrated erythrocytes and heparin plasma for exchange transfusions]. 221 59

Gianotti-Crosti Syndrome, or papular acrodermatitis of childhood, represents a characteristic rash that is irregularly associated with hepatitis B infection. The authors report papular acrodermatitis in a 10-month-old child with leukopenia, thrombocytopenia, circulating lymphoblasts, and acute anicteric hepatitis B. Physical examination revealed a densely distributed papular rash on the patient's extremities and face and neck, but not on his trunk, buttocks, palms, or soles. Laboratory investigation revealed a normal bone marrow and positive hepatitis B serology. This case reinforces the fact that hematologic findings should not dissuade the work-up of papular acrodermatitis for hepatitis B or other less commonly associated viruses.
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PMID:Transient lymphoblastosis and thrombocytopenia in Gianotti-Crosti syndrome. 230 5

This review describes the transmission, clinical picture and immunological abnormalities of HIV infection in children in general, and the special problems of AIDS in African children. The review begins with a thorough introduction to the epidemiology of AIDS. Transmission to children generally involves vertical transmission by placental transfer or transmission of HIV via transfusion of blood and blood products, or by contaminated needles. Casual transfer is unknown, and only a few cases of transmission via breast milk are known. The clinical picture of HIV infection in infants and children differs from that in adults in 3 important aspects: earlier onset, different clinical presentation and existence of AIDS embryopathy. The average onset was 5 months of age. The most common symptoms in young children are chronic interstitial pneumonitis without demonstrable etiology, hepatomegaly, failure to thrive, adenopathy, diarrhea, oral or perineal thrush, eczema and thrombocytopenia. The common opportunistic infections are pneumocystis carinii pneumonia, cytomegalovirus, Epstein-Barr virus, Cryptosporidium diarrhea, pyogenic infections of the middle ear and gram-negative septicemia. Several infections seen in adult AIDS cases are rare in children: mycobacterium avium-intracellulare, toxoplasma gondii, hepatitis B, as well as Kaposi's sarcoma, malignant lymphoma and cardiac abnormalities. The AIDS embryopathy or HIV dysmorphic syndrome is characterized by immunological abnormalities, growth failure, and craniofacial dysmorphism, particularly microcephaly, prominent box-like forehead, hypertelorism, flattened nasal bridge, obliquity of the eyes, blue sclerae and patulous lips. AIDS in African children is extremely difficult to diagnose because of similarities between the presenting symptoms and those commonly seen in sick children there, many of whom are also immune compromised. Where serotesting is available, the picture is complicated by cross reaction between the test agents and some factor found in sera from malaria patients. Seropositivity in some areas is high, increased by the prevalence of transfusion and injection treatments. Diagnosis is made more difficult by lack of laboratory facilities and difficulties in follow-up for pediatric patients. The CDC definitions of AIDS and ARC, and the WHO/CDC definitions of AIDS are appended.
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PMID:Human immunodeficiency virus infection in childhood. 245 15

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

A total of 20 patients with histologically proven primary hepatocellular carcinoma (PHC) received mitoxantrone IV at a dose of 10-16 mg/m2 every 3 weeks. All patients had previous hepatitis B infection. None underwent remission after treatment; 2 had stable disease and 18 progressive disease. The median overall survival was 13 weeks (range, 1-59 weeks). There was no evidence of significant antitumor activity for mitoxantrone in our patients with PHC. Hematotoxicity occurred in 100% of the patients with grades 2-4 leukopenia, 89% of those with grades 1-4 anemia, and 26% of those with grades 2-3 thrombocytopenia. Cardiotoxicity occurred in 20% of the patients after 14-30 mg/m2 mitoxantrone; these included complete heart block with fatal outcome in one case, decreased ventricular ejection fraction in one, and sinus tachycardia in two. Nausea, vomiting, fever, diarrhea, and alopecia were mild and occurred in 15%-45% of the patients Therefore, patients with PHC following hepatitis B infection may be less tolerant to mitoxantrone, resulting in the apparent increase in toxicities.
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PMID:Phase II study of mitoxantrone in unresectable primary hepatocellular carcinoma following hepatitis B infection. 253 94

The hematotoxicity of benzene exposure has been well known for a century. Benzene causes leukocytopenia, thrombocytopenia, pancytopenia, etc. The clinical and hematologic picture of aplastic anemia resulting from benzene exposure is not different from classical aplastic anemia; in some cases, mild bilirubinemia, changes in osmotic fragility, increase in lactic dehydrogenase and fecal urobilinogen, and occasionally some neurological abnormalities are found. Electromicroscopic findings in some cases of aplastic anemia with benzene exposure were similar to those observed by light microscopy. Benzene hepatitis-aplastic anemia syndrome was observed in a technician with benzene exposure. Ten months after occurrence of hepatitis B, a severe aplastic anemia developed. The first epidemiologic study proving the leukemogenicity of benzene was performed between 1967 and 1973 to 1974 among shoe workers in Istanbul. The incidence of leukemia was 13.59 per 100,000, which is a significant increase over that of leukemia in the general population. Following the prohibition and discontinuation of the use of benzene in Istanbul, there was a striking decrease in the number of leukemic shoe workers in Istanbul. In 23.7% of our series, consisting of 59 leukemic patients with benzene exposure, there was a preceding pancytopenic period. Furthermore, a familial connection was found in 10.2% of them. The 89.8% of our series showed the findings of acute leukemia. The possible factors that may determine the types of leukemia in benzene toxicity are discussed. The possible role of benzene exposure is presented in the development of malignant lymphoma, multiple myeloma, and lung cancer.
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PMID:Hematotoxicity and carcinogenicity of benzene. 267 98


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