Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kaposi's sarcoma developed in two lymphoma patients previously treated by chemotherapy and chemoirradiation. The histologic picture in the two cases showed a non-Hodgkin's lymphoma with multifocal epithelioid histiocytic reaction. Both patients had Hepatitis-B surface antigen and other infections due to herpes and streptococcus. The European Jewish origin of the two patients, the previous chemotherapy, and their infective state tend to support more the hypothesis of predisposing factors in the occurrence of Kaposi's sarcoma than a coincidental association.
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PMID:Kaposi's sarcoma in two lymphoma patients with hepatitis B and other infections. 674 10

Little is known from the literature about the epidemiology of non A - non B hepatitis (NANB/H) in childhood. Aim of this study was to assess the prevalence of NANB/H in a consecutive series of children with acute viral hepatitis hospitalized over an one year's period. Thirty children, 9 females, aged 3-12 years, were studied. Serial blood samples were tested for HBsAg, anti-HBs, anti-HBc, anti-HAV (Abbott RIA), anti-HAV-IgM (Absorption Staph. aureus protein A), anti-EBV (Immunofluorescence), anti-CMV, anti-Herpes s. virus (complement fixation). The diagnosis of NANB/H was based on the absence of these markers. Nineteen patients (63,3%) had type A, and 5 (16,6%), had type B hepatitis. One child showed antibodies anti-Herpes with rising titer and 5 (16.6%), 2 females, were considered suffering from NANB/H. None of these patients had been injected or haemotransfuded; all but one came from rural ambient and two from the same family. Two children had an anicteric course. The illness lasted less than 30 days in all but one, who showed three peaks of transaminases and recovered after 70 days. These data show a prevalence of NANB/H in childhood greater than that elsewhere reported, while the absence of injections suggests a way of infection other than parenteral.
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PMID:[Prevalence of non A - non B hepatitis in childhood (author's transl)]. 680 82

Most studies of sexually transmitted diseases in homosexual men have examined prevalence in clinic populations; for comparative purposes, we analyzed data from a survey of 4,329 gay men conducted in 1977. Among 4,212 respondents to the self-administered questionnaire, 66.8 per cent reported previous infection with pediculosis; 38.4 per cent, gonorrhea; 24.1 per cent, nonspecific urethritis; 18.1 per cent, venereal warts; 13.5 per cent, syphilis; 9.7 per cent, hepatitis; and 9.4 per cent, herpes. Number of different lifetime sexual partners best predicted histories of symphilis (r = .249), gonorrhea (r = .402), and the other diseases; frequency of checkups, years as a practicing homosexual, and furtive sexual activities were among the many other significant correlates of venereal infections. Respondents most often sought examinations from private physicians (39.4 per cent); those who visited gay clinics were examined most often and felt most positive about their medical care. Gay men who participated in the survey reported frequent infections with many of the same sexually transmitted diseases often seen in private medical practices, public VD clinics, and gay health centers. Since high rates of disease are related to large numbers of different partners, frequent exposures with anonymous contacts, and anal intercourse, we recommend frequent examinations for those whose life-styles include these characteristics.
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PMID:The gay report on sexually transmitted diseases. 689 4

Herpes simplex is a rare but usually fatal cause of acute hepatitis in adults. Most previously reported cases have occurred in debilitated or immunosuppressed patients. We report two additional fatal cases that occurred in renal transplant recipients. In case 1, there is evidence that the allograft may have been the initial nidus of infection. In case 2, dissemination from a genital infection occurred and failed to respond to vidarabine therapy that was started early in the clinical course. We also review the literature concerning previously reported cases of herpes hepatitis.
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PMID:Herpes simplex type 1 hepatitis in renal transplantation. 700 42

Two different subpopulations of IgG antibodies to nucleic acids may be demonstrated: (1) IgG directed against single-stranded (ss) nucleic acids: they are found in normal human serum and increased in sera in subacute sclerosing panencephalities, multiple sclerosis and in other neurological diseases. Absent from normal cerebrospinal fluid, they can be synthetized inside the central nervous system during these diseases. Their only common antigenic determinant seems to be the polymeric single-stranded structure. No correlation can be demonstrated between their increase in sera and their local synthesis (inside the central nervous system) and between these data and the clinical stage. These facts suggest a "non-specific" reaction and not a pathogenic mechanism. (2) IgG antibodies directed against double-stranded (ds) nucleic acids: they were detected in cerebrospinal fluid during 3 neurological diseases only, all of proved viral etiology: subacute sclerosing panencephalitis, herpes meningoencephalitis and B hepatitis polyradiculoneuritis. These antibodies are also synthetized inside the central nervous system, and are distinct from antibodies to ss nucleic acids. The mechanism of production and the signification of these antibodies remains unknown, and their scarcity in MS patients must be stressed.
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PMID:Serum and cerebrospinal fluid antibodies to single-stranded and double-stranded nucleic acids in neurological diseases. 711 9

The protection of mice against experimental infections with three different viruses (herpes simplex, vaccinia and mouse hepatitis) by Propionibacterium granulosum strain KP-45 and isolated cell walls was investigated. Pretreatment of NMRI mice with P. granulosum strain KP-45 3-7 days prior to HSV intranasal infection resulted in lowering of mortality rate (herpes encephalitis) from about 95% in controls to 15-30%. Pretreatment of NMRI mice prior to vaccinia virus infection also caused a significant decrease of the number of specific tail lesions. Infection of BALB/c mice with mouse hepatitis virus type 3 (MHV-3) resulted in development of acute infection with lethality in 4-6 days, while in fairly resistant C3H mice chronic infection manifested by loss of weight, uncoordination followed by paralysis and death in few months was observed. Pretreatment of BALB/c mice 3-7 days prior to MHV-3 infection lowered the mortality rate to about 25-30% while no effect was observed in animals injected with P. granulosum KP-45 on the day of virus inoculation. In chronic MHV-3 infections treatment with P. granulosum KP-45 was started 2 weeks after virus inoculation and was continued every 10 days. This resulted in a significant lowering of the number of paralysed mice and in a decrease of the mortality rate. Titre of MHV-3 recovered from livers of infected mice 4 months after virus inoculation was also significantly lower in animals treated with P. granulosum KP-45 or isolated cell walls.
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PMID:Protection and therapy of mice with acute and chronic experimental virus infections with propionibacterium granulosum kp-45. 722 26

After the official confirmation of psittacosis in a collection of psittacine birds a total of 40 of them died during treatment with tetracycline. 36 of them underwent post mortem examination. From 33 birds the causative herpesvirus of Pacheco's parrot disease (PPD) was isolated and/or a non-purulent hepatitis diagnosed, the latter a characteristic for PPD. The cause of the outbreak was assumed to be a latent herpesvirus infection of individual birds which was activated by various stress factors during the psittacosis treatment. The macroscopic and histologic lesions, the results of virological investigations and the in vitro effect of acyclovir on the multiplication of the isolated herpes virus are described.
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PMID:[A herpesvirus-caused enzootic--Pacheco's parrot disease--in a psittacine collection]. 771 52

More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not, per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.
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PMID:Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL. 774 57

Although infrequent, untreated neonatal herpes results in death in half the cases and neurologic sequelae in three quarters of the survivors. Neonatal infection is usually acquired from maternal genital herpes, which is asymptomatic or unrecognized in 60% to 80% of women. The greatest risk of neonatal infection occurs when the mother has primary genital herpes involving the cervix at delivery, and the infant is premature and delivered with instrumentation (eg, scalp electrodes). More than 80% of neonates with herpes will have typical herpetic lesions of the skin, eye, or mouth, and most of the remainder will have either encephalitis or a sepsis syndrome with pneumonitis and hepatitis and negative bacterial cultures. Because herpes can mimic other neonatal infections, laboratory diagnosis is important, using cultures of the virus from lesions, peripheral blood white cells, or CSF. Treatment with intravenous acyclovir does reduce mortality and neurologic sequelae, but outcome is still guarded in babies with disseminated disease or encephalitis. Prevention focuses on caesarean section in women with active lesions at the time of impending delivery and avoidance of postnatal exposure. Further studies are needed to determine whether maternal screening (eg, HSV-2 type specific antibodies and vaginal cultures in selected women at delivery) will be cost effective in preventing neonatal herpes.
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PMID:Herpes simplex virus infection of the fetus and newborn. 801 61

A 36 year old primigravid woman presented with a "flu-like" illness and premature labour, followed by severe pneumonitis and hepatitis in the late second trimester of pregnancy. Progressive deterioration obliged an elective delivery of twins, stillborn at 25 weeks of gestation. Herpes virus isolated from one placenta, but not from any fetal tissue, was the only indication of a systemic herpes simplex infection in which there were no mucocutaneous lesions seen before or during the illness. There was no history of herpes simplex infection and antibody studies were not helpful initially for a diagnosis that was confirmed in retrospect. Double staining for viral DNA and antigen showed that the virus was present in host monocytes.
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PMID:Acute herpes hepatitis in pregnancy. 802 9


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