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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Institutionalized patients with Down syndrome and matched controls with other causes of mental retardation were tested by immune adherence hemagglutination for the presence of antibody to hepatitis A antigen (anti-HA). Altogether 75.1% (175 of 233) exhibited presence of anti-HA, with no differences by sex or age. Patients reactive for hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs) were reactive for anti-HA significantly more frequently than those with a negative reaction for these markers. In contrast to serologic markers of hepatitis type B, prevalence of anti-HA does not depend on the cause of mental retardation or on the age at primary infection. The rate of anti-HA positivity was found to be closely correlated with duration of institutionalization. The study confirmed that many closed institutions for the mentally retarded are hyperendemic for hepatitis type A and that formation of anti-HA is not greatly affected by either immune deficiency or immune immaturity.
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PMID:Antibody to hepatitis A antigen in institutionalized mentally retarded patients. 13 79

The prevalence of exposure to hepatitis A virus (HAV) increases with increasing age; decreases with increasing socioeconomic class; increases with increasing serologic evidence of prior hepatitis B virus (HBV) exposure but is much more common than HBV exposure; is independent of sex and race; varies in different parts of the world as a function of hygienic, developmental, and unrecognized geographic factors; and is not affected by immune deficiency or immaturity. Transmission of type A hepatitis is enhanced by poor personal hygiene such as that seen in institutions for the mentally retarded. On the other hand, there is no increased exposure to HAV among homosexuals, who have frequent and intimate contact with multiple sexual partners; among hemodialysis patients and staff; or among multiply transfused individuals, all of whom are at significantly increased risk of exposure to HBV. No epidemiologic evidence has confirmed the existence of viremic or intestinal carriers of HAV, and the virus is rarely, if ever, spread by parenteral mechanisms. Finally, HAV appears to play no role in chronic liver disease and a very minor role in fulminant hepatitis; however, HAV is responsible for a sizable proportion (approximately 20%--40%) of sporadic hepatitis among urban adults.
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PMID:Hepatitis A virus infection: new insights from seroepidemiologic studies. 20 11

Immunosuppression for renal transplantation is associated with the risk of severe overwhelming infection with ubiquitous but normally relatively harmless micro-organisms. In recent years a number of adult cases of fatal hepatitis due to herpes simplex virus (HSV) infection have been reported. Nearly always immune deficiency was a significant factor. A case of fatal HSV infection with hepatitis following transplantation is reported. The case failed to respond to infusion with the antiviral agent cytosine arabinoside. The presentation, diagnosis and treatment of HSV fulminant hepatitis is discussed.
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PMID:Systemic herpes simplex infection with fulminant hepatitis post-transplantation. 79 3

At least since the discovery of the acquired immune deficiency syndrome and the "human immune deficiency virus" (HIV) it has been widely accepted, that viruses infect lymphocytes (mainly especially CD 4 positive helper lymphocytes) and can also be responsible for their deletion. However, since the HIV can only be found in a small proportion of the dying lymphocytes, other viruses as well as other (nonviral) cytotoxic agents and mechanisms must be taken into consideration. The conception of involved autoimmune phenomena is being accepted increasingly. Storch's hypothesis put forward in 1975, of primary or secondary viral infection of lymphocytes as pathogenetical principle of autoimmune hepatitis (infected B- and T-lymphocytes stimulate directly or indirectly the antibody synthesis and also trigger abnormal cellular immune reactions) was confirmed. Teleologically regarded, in most cases it remains open if the demonstrable autoantibodies and immune cells are pathogenic, protective, or indifferent for the individual. Analogous to symbiosis and parasitism, this postulate can be extended to pathogenic viral infections. Assuming that the human organism is anxious to remain unharmed and, like viruses maintain its adaptability by a system of multiform control systems one can imagine, that the autoimmunity induced by and therefore directed primarily against viruses can be regarded as "physiological", thus representing a protective mechanism against disturbing exogenous and endogenous factors. It can be considered part of the "prophylaxien" (Holle, 1989). Likewise, in autoimmune hepatitis as well, new findings speak for a participation of several (various) viruses in its aetiopathogenesis. It is hypothesized, that so-called "autogenes" exist which lead to autoimmune disease (like oncogenes involved in the pathogenesis of malignancies).
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PMID:[Virus and autoimmune disease. An excursion exemplified by autoimmune hepatitis]. 156 9

Two hundred eleven HIV-seropositive patients with AIDS, AIDS-related complex, or a CD4+ cell count less than 200 x 10(6) were examined for the presence of hepatitis B virus markers during the course of their HIV infection (median follow-up of 18 months; range of 1 to 107 months). Anti-HBs was detected initially in 138 patients (65%). Sixteen patients (8%) were HBsAg positive at entry. Fourteen had chronic HBV infection of whom 12 initially were positive for HBeAg and HBV DNA; 11 remained positive during follow-up, whereas one seroconverted to anti-HBe and lost HBV DNA. Two patients with chronic HBV infection were initially negative for HBeAg and HBV DNA: one later had reactivated HBV replication and one cleared HBeAg following onset of hepatitis D infection. The last two HBsAg-positive patients had resolving acute HBV infection. Six of the 57 patients who initially were negative for HBV markers acquired HBV infection during follow-up. Four of these six patients developed chronic infection whereas two patients had acute subclinical resolving hepatitis. In addition, four patients became HBsAg positive with their last serum samples, possibly indicating reactivation of HBV infection following progressive immunological and clinical deterioration. None of the patients developed clinical symptoms that could be ascribed to HBV infection, and transaminase elevations were only sporadically recorded. It is concluded that acquisition of HBV infections is not infrequent in HIV-seropositive patients with immune deficiency. Furthermore, the course of both previously established chronic HBV infection and newly acquired HBV infection is modified in such patients, whereas reactivation of past HBV infection seems to be a rare event.
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PMID:High incidence of hepatitis B infection and evolution of chronic hepatitis B infection in patients with advanced HIV infection. 200 76

Prevention of EBV-associated lymphoproliferative diseases in immune deficient individuals is preferred; however, standard therapy for the B cell lymphomas has been successful. Chemotherapy must be given cautiously lest further immune compromise result in opportunistic infections. Recently, Acyclovir has decreased morbidity of patients with acute infectious mononucleosis in immune competent persons. In contrast, immunodeficient patients with X-linked lymphoproliferative (XLP) syndrome do not seem to respond favorably. Hence, a prospective study is underway using prophylactic immunoglobulin containing (EBV)-specific antibodies. The mortality rate is 85% following EBV infection in XLP due to fatal infectious mononucleosis associated with fulminant hepatitis and virus-associated hemophagocytic syndrome, acquired hypogammaglobulinemia or malignant B cell lymphoma. We can detect XLP by noting failure of switching from IgM to IgG antibody production on secondary challenge with bacteriophage phi X174. Also, linkage studies with the XLP locus using restriction fragment length polymorphisms are being done to detect affected males pre-EBV infection. Our rationale for prevention of phenotypes of XLP is based on observations that infants in tropical Africa and males with XLP do not develop EBV-induced diseases while neutralizing maternal antibodies are present. An EBV vaccine will be used, when available, in seronegative males with XLP. Prevention of acquired immune deficiency by screening blood for human immune deficiency virus, encouraging prudent life styles, development of specific immunosuppressive agents, development of new antiviral agents (i.e., DHPG), and identification of high risk seronegative patients offer possibilities for preventing life-threatening EBV-induced diseases.
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PMID:Prevention and treatment of Epstein-Barr virus (EBV)-associated lymphoproliferative diseases in immune deficient patients. 243 95

Intravenous immunoglobulin has been used for hypogammaglobulinaemic conditions treated at the Royal Children's Hospital, Melbourne since 1972. Fifty-four children have been treated. Nineteen have been males with congenital hypogammaglobulinaemia (including 12 with sex-linked agammaglobulinaemia and 5 with hypogammaglobulinaemia with IgM); 8 have had common variable immunodeficiency, and 11 have had severe combined immune deficiency. Intravenous immunoglobulin has also been used for some patients with transient hypogammaglobulinaemia, isolated IgG deficiency, isolated IgA deficiency and isolated IgM deficiency. Infusions are given four weekly at a dose of 5-7.5 ml/kg of a 6% preparation (300-450 mg/kg). At diagnosis, a loading dose is given of 10-15 ml/kg (600-900 mg/kg). Previous studies have demonstrated a half-life of 25 days. The median preinfusion IgG concentration for the 22 children receiving monthly infusions currently is 68 IU/ml. Hospitalisation rates for infective illness have been reduced with the use of intravenous gammaglobulin. No patients are known to have developed hepatitis. Reactions to infusions are experienced by 60% of patients. These have not been reduced significantly by the addition of 10% maltose, but have been lessened considerably by using intravenous methylprednisolone (1 mg/kg) before the commencement of infusion.
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PMID:The long term treatment of childhood hypogammaglobulinaemia in Melbourne with intravenous gammaglobulin, 1972-1985. 244 Jul 42

The data obtained point to the aggravation of virus hepatitis A time-course in case of a mixed pathology. This may be due to the state of a certain immune deficiency characteristic of parasitic diseases, including helminthiasis. It is also possible that immune deficiency is an inevitable condition for helminths' existance in the host. This suggestion is supported by the fact of helminthic invasion of virus hepatitis patients.
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PMID:[Clinical and immunological indicators in patient with viral hepatitis A combined with ascariasis]. 275 98

Although rare, side-effects have been associated with the administration of iv immune globulins (IVIG). While the clinical presentation may be similar, several different mechanisms account for these adverse reactions. There are those effects in the hypogammaglobulinaemic patient which are probably due to antigen-antibody interaction (so-called inflammatory reactions), those due to spontaneous activation of the complement system (possibly caused by IgG aggregates), those due to true hypersensitivity (for example, hypersensitivity to IgA), and those due to possible contaminants or even stabilizers or preservatives which might have been used. The incidence and nature of clinical side-effects seen in 37 patients who were treated with a native IVIG is shown. In addition, data are provided which support the absence of transmission of human immune deficiency virus in idiopathic thrombocytopenia (ITP) patients, and the agents of non-A, non-B hepatitis in 41 immune-deficient patients having periods of follow-up ranging up to 18 months. Finally, evidence of the inactivation of human immunodeficiency virus during the manufacturing procedure is provided.
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PMID:Clinical safety of intravenous immune globulin and freedom from transmission of viral disease. 290 25

Evidence for transmission of non-A non-B hepatitis (NANB) was sought in 41 patients with primary immune deficiency who were receiving human intravenous immune globulin (IGIV) over periods ranging from 6 to 15 months at a monthly dosage of 400 mg/kg body weight. One lot of a reduced and alkylated IGIV and three lots of a nonmodified preparation stabilized at pH 4.2 were used. No evidence of NANB was found, although transient elevations in serum glutamic pyruvic transaminase (alanine aminotransferase) were found in 6 of the patients. The possible causes of the elevated levels in these 6 patients are discussed.
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PMID:Non-A non-B hepatitis and the safety of intravenous immune globulin, pH 4.2: a retrospective survey. Preliminary communication. 312 1


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