Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a retrospective study of a 12-year period (1981-1992) liver histology was analyzed in 227 autopsied patients infected with the human immunodeficiency virus. Normal histology could only be documented in 29 patients (13%). In the majority of cases (56%) uncharacteristic changes were seen such as steatosis (34%), hemosiderosis (10%) or non-specific reactive hepatitis (7%). The finding of hepatic peliosis obtained in 4 patients was not associated with inflammatory liver changes, especially infections from Rochalimaea. Within a wide range of opportunistic infections recorded in 50 patients (22%), hepatitis caused by Cytomegalovirus (8%), Toxoplasma gondii (5%), Leishmania donovani (1%), Cryptococcus neoformans and Pneumocystis carinii (each 0.5%) was diagnosed. Among 16 cases (7%) of mycobacterial liver infections typical mycobacteria were found in two patients and atypical mycobacteria in 14 patients, respectively. In 23 patients (10%) chronic viral hepatitis, caused by HBV (7%) or HCV infections (3%), respectively, was observed. Hepatitis was typed as mild only in each 5 patients with HBV or HCV infection, whereas the remaining cases showed a transition towards cirrhosis. Two patients with HBV-associated cirrhosis developed hepatocellular carcinoma. The remaining 32 malignant liver tumors represented secondary neoplasms, including 13 cases of non-Hodgkin's lymphomas.
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PMID:[Liver changes in AIDS. Retrospective analysis of 227 autopsies of HIV-positive patients]. 964 44

This analysis evaluated the extent to which infections with selected blood-borne viruses, specifically infection with hepatitis B virus, hepatitis C virus, and/or the human immunodeficiency virus (HIV), continue to contribute to the morbidity of persons with hemophilia. The Georgia Hemophilia Surveillance System collected information on 336 state residents with hemophilia A or B who were followed by a physician in 1994. Data abstracted from medical records included information on demographics, sources of hemophilia care, clinical characteristics, joint range of motion measurements, hospitalization, and results of laboratory testing for hepatitis B, hepatitis C, and the human immunodeficiency virus. Prevalence of infection with one or more of these viruses was determined, and relationships with disease severity, bleeding frequency, and amount of clotting factor prescribed were explored. No child under the age of ten was positive for the human immunodeficiency virus; hepatitis infection was also uncommon in this age group, in contrast to the very high frequency of such infections among older subjects. There was a strong association between HIV positive status and infection with one of the hepatitis viruses. The likelihood of all types of viral infection increased with frequency of bleeding and with amount of clotting factor received. Efforts to prevent transmission of lipid-enveloped viruses via clotting factor have been extremely effective. However, currently infected hemophilia patients will likely experience significant morbidity and mortality due to chronic liver disease and AIDS-related complications.
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PMID:Viral infections among patients with hemophilia in the state of Georgia. 972 74

Mouse hepatitis virus type 3 (MHV3), a coronavirus, is an excellent animal model for the study of thymic and extrathymic T cell subpopulation disorders induced during the viral hepatitis. To understand local hepatic immune responses, the phenotypes of resident hepatic lymphocytes were determined and compared that of splenic and thymic T cell subpopulations during the acute viral hepatitis induced by MHV3 in susceptible C57BL/6 mice. Single positive (SP) CD4+ or CD8+ cells strongly increased in the liver. A specific cell population, the double positive (CD4+ C8+) cells, normally present in liver and thymic cell preparations, decreased in C57BL/6 mice following the viral infection. alpha beta-TcRintermediate T cells shifted toward alpha beta-TcRhigh T cells in the liver and thymus of infected mice, but not in their spleen. The specific alpha beta-TcRint or high lymphocytes occurring in the liver of MHV3-infected mice expressed higher levels of leukocyte function antigen-1 (LFA-1) and Pgp-1 (CD44) activation markers, suggesting that they were either activated or antigen-experienced during the viral infection. No significant changes in T cell subpopulations were detected in the spleen. These observations suggest that MHV3 infection could induce an early in situ stimulation of resident hepatic T cells, despite a peripheral immunodeficiency in the thymus and spleen.
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PMID:Intrahepatic alpha beta-TcRintermediate LFA-1high T cells are stimulated during mouse hepatitis viral infection. 978 18

Injection drug use (IDU) is one of the most significant risk factors for viral hepatitis (B, D and C) and human immunodeficiency virus (HIV) infection. However, there is little information about the risk of infection among non-injection drug users (non-IDUs). The present study was designed to perform several objectives: (a) to evaluate the prevalence of serological markers of hepatitis B, D, C virus and HIV in IDU and non-IDU patients; (b) to compare the prevalence of these markers between both groups; (c) to identify risk factors for HCV and HIV in this population; and (d) to correlate the presence of HCV and liver function. A total of 385 consecutive patients (122 IDUs and 263 non-IDUs), admitted to the Drug Dependency Treatment Unit at the Hospital Insular of Gran Canaria between 1993 to 1994, were included in the study. The serological markers of HBV, HDV, HCV and HIV were determined by ELISA and immunoblot methods. In all cases we also measured syphilis tests (RPR and FTAabs), serum aminotransferases and serum gammaglutamiltranspeptidase. Compared to the non-IDU, the IDU group presents a higher prevalence of antiHBc (55.0% vs. 20.7%, p < 0.0001), antiHCV (87.6% vs. 35.3%, p < 0.0001) and antiHIV (21.8% vs. 2.7%, p < 0.0001). There was no significant difference in RPR positivity (0.9% vs. 4.9%, p = 0.06). Delta infection was only detected in injection drug users, and the prevalence was low. Using logistic regression, the only risk factors associated with antiHCV positivity were injection drug addiction (OR: 9.2, 95% CI: 4.9-17.0) and antiHBc positivity (OR: 5.5, 95% CI: 3.0-9.9). Similarly, the associated risk factors for HIV were injection drug addiction (OR: 5.9, 95% CI: 2.3-15.0) and antiHBc positivity (OR: 3.8, 95% CI: 1.5-9.2). However, no correlation was found between antiHCV positive and antiHIV or between these markers and RPR positivity. Patients positive for antiHCV showed significant elevations in aspartate aminotransferase and alanine aminotransferase levels, when compared with patients negative for antiHCV: 65.0 vs. 39.2 U/l (p < 0.001) and 88.4 vs. 40.3 U/l (p < 0.001), respectively. We conclude that drug users have an elevated prevalence of HCV, HBV and HIV infection, even if drug use is only inhalated. On the other hand, the main risk factors associated with HCV and HIV are injection drug addiction and exposure to hepatitis B virus. Finally, in the study population, liver dysfunction is closely related to HCV infection.
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PMID:Prevalence of serologic markers of HBV, HDV, HCV and HIV in non-injection drug users compared to injection drug users in Gran Canaria, Spain. 979 22

Genetic diagnosis is a revolutionary method that makes possible simultaneous viral isolation (detection) and identification. The method is so specific, sensitive, and rapid (non-culture) that leads not only to the diagnosis of viral infection, but also to prediction of the chemotherapy, monitoring during the therapy, and judging the efficacy of the treatment. Moreover, it contributes to understanding the disease pathophysiology. The qualitative results are sufficient for diagnosis, but quantitative analysis is sometimes necessary for the prediction of the efficacy and monitoring during treatment. It occasionally requires the numbers of genomic expression, the number of DNA/RNA copies, and the detection of point mutations for drug resistance. Many emerging and re-emerging infectious diseases, such as AIDS and viral hepatitis, are induced by viral infection via blood. The main causative agents of blood-borne viral infection are hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), human T cell leukemia virus type 1 (HTLV1), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human parvovirus B19. They play main roles in viral hospital infection. The risk of them being transmitted by transfusion of screened blood is very low, but it is always possible that infection may occur in a window period even after extensive blood screening tests. Therefore, to shorten a window period, genetic examinations will be accepted for screening tests in the near future. Prioritization of genetic examinations is needed to select the adequate method and sampling. After examinations, false positive and false negative results have to be extensively read out whether due to contamination or inhibition by agent such as heparin and hemoglobin. The causative virus should be decided by carefully eliminating passenger viruses or latent viruses. Because genetic examinations are so useful but occasionally yield false positive and negative results, genetic diagnosis should be judged totally by combination with other examinations, clinical signs, and clinical symptoms.
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PMID:[The role of genetic diagnosis in clinics--from the choice of ordering until reading the data]. 1059 Jun 77

Oman is generally hot and dry, but the Salalah region in southern Dhofar province is relatively cool and rainy during the summer monsoon, and has a distinctive pattern of infection. Important, notifiable infections in Oman include tuberculosis, brucellosis (endemic in Dhofar), acute gastroenteritis, and viral hepatitis: 4.9% of the adults are seropositive for hepatitis B surface antigen and approximately 1.2% for hepatitis C virus. Infection with human immunodeficiency virus is uncommon, and leprosy, rabies, and Crimean-Congo hemorrhagic fever are rare. Between 1990 and 1998, the incidence of malaria, (>70% due to Plasmodium falciparum) decreased from 32,700 to 882 cases. Cutaneous and visceral leishmaniasis (caused by Leishmania tropica and L. infantum, respectively) and Bancroftian filariasis occur sporadically. Intestinal parasitism ranges from 17% to 42% in different populations. A solitary focus of schistosomiasis mansoni in Dhofar has been eradicated. There are major programs for the elimination of tuberculosis, leprosy, and malaria, and to control brucellosis, leishmaniasis, sexually transmitted diseases, trachoma, acute respiratory infection in children, and diarrheal diseases. The Expanded Program on Immunization was introduced in 1981: diphtheria, neonatal tetanus, and probably poliomyelitis have been eliminated.
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PMID:Infectious and tropical diseases in Oman: a review. 1067 71

The common clinical presentations of herpes simplex virus (HSV) and molluscum contagiosum (MC) are well known to dermatologists. However, folliculitis due to these viruses is an infrequently reported entity and might be considered a sign of immunosuppression [such as infection with human immunodeficiency virus, (HIV)], especially in cases of folliculitis due to MC. The purpose of this study was to describe the clinical and histopathological characteristics of viral folliculitis due to HSV and MC. We retrospectively collected all our cases with histologically proven folliculitis due to HSV and MC between 1994 and 1999. A total of seven patients aged 7-54 years was identified. Prior to establishment of the diagnosis of folliculitis due to HSV and MC, they were treated with topical antibiotics or topical steroids, without improvement. Tentative diagnoses were bacterial folliculitis, syringoma, perifollicular fibrosis, contact dermatitis or pseudolymphoma. Biopsy of the lesions revealed multiple molluscum bodies in the follicular epithelium with sparing of the epidermis in four patients, and ballooning degeneration and intranuclear viral inclusions in the follicular epithelium in the other three. Three patients had evidence of underlying immune suppression, such as pregnancy, chronic viral hepatitis B and nasopharyngeal carcinoma. One patient had suffered from epilepsy for 4 years. Testing for HIV by enzyme-linked immunosorbent assay was negative in the four patients in whom this was performed, and T-cell subsets were normal in the three patients in whom these were quantified. In cases of molluscum folliculitis treated with simple curettage, the lesions cleared without scarring or recurrence. In cases of herpetic folliculitis, the lesions improved with antihistamines or acyclovir. MC or HSV should be considered in cases that present with folliculitis-like dermatoses but which are refractory to anti-infective and anti-inflammatory treatment.
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PMID:Viral folliculitis on the face. 1073 72

As more and more infectious agents become targets for immunization programmes, the spectrum of adverse events linked to vaccines has been widening. Although some of these links are tenuous, relatively little is known about the immunopathogenesis of even the best characterized vaccine-associated adverse events (VAAEs). The range of possible use of active immunization is rapidly expanding to include vaccines against infectious diseases that require cellular responses to provide protection (e.g. tuberculosis, herpes viral infections), therapeutic vaccines for chronic infections (e.g. human immunodeficiency virus (HIV) infection, viral hepatitis B and C), and vaccines against non-infectious conditions (e.g. cancer, autoimmune diseases). Less virulent pathogens (e.g. varicella, rotavirus in the developed world) are also beginning to be targeted, and vaccine use is being justified in terms of societal and parental "costs" rather than in straightforward morbidity and mortality costs. In the developed world the paediatric immunization schedule is becoming crowded, with pressure to administer increasing numbers of antigens simultaneously in ever simpler forms (e.g. subcomponent, peptide, and DNA vaccines). This trend, while attractive in many ways, brings hypothetical risks (e.g. genetic restriction, narrowed shield of protection, and loss of randomness), which will need to be evaluated and monitored. The available epidemiological and laboratory tools to address the issues outlined above are somewhat limited. As immunological and genetic tools improve in the years ahead, it is likely that we shall be able to explain the immunopathogenesis of many VAAEs and perhaps even anticipate and avoid some of them. However, this will only happen if the human and financial resources needed for monitoring and studying vaccine safety stay in step with the accelerating pace of vaccine development. Failure to make such a commitment would put all immunization programmes at risk.
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PMID:Vaccine adverse events in the new millennium: is there reason for concern? 1074 92

Chemokines are implicated in the pathogenesis of alcoholic liver disease in humans and in experimental models of alcohol intoxication. The major sources of these chemokines are Kupffer cells which represent more than 80% of tissue macrophages in the body. Kupffer cells are highly responsive to the effects of ethanol, endotoxin and human immunodeficiency virus (HIV)-1 glycoprotein120. These agents, either independently or in combination, may exacerbate the production of chemokines. Chemokines are agents that are highly chemotactic to mononuclear cells and granulocytes. The levels of these chemokines in sera and tissue are elevated in patients with alcoholic hepatitis, alcoholic cirrhosis, diseased livers, viral hepatitis, and in experimental models of chronic alcohol intoxication. Alcohol-induced influx of endotoxin from the gut into the portal circulation is suggested to play an important role in the activation of Kupffer cells which leads to enhanced chemokine release. The up-regulation of chemokines during alcohol consumption is selective. During the early phase of alcoholic liver disease, C-X-C or alpha-chemokines predominate. This is also associated with neutrophilic infiltration of the liver. In the later stage, up-regulation of C-C or beta-chemokine production and migration of mononuclear cells into the liver are observed, and this may lead to liver cirrhosis. Selective up-regulation of chemokine synthesis and release may involve differential modulation of the transcription factors required for chemokine gene expression. Increased cytokine release following alcohol consumption may also regulate chemokine secretion in Kupffer cells via paracrine and autocrine mechanisms and vice versa. In addition, infection with HIV-1 may further compromise the liver to more damage. During HIV-1 infection, a pre-existing liver disease superimposed on chronic alcohol consumption may also exacerbate HIV-1 replication and lymphocytic infiltration in the liver, because of the ability of HIV-1 gp120 to stimulate chemokine production by Kupffer cells and stimulate migration of inflammatory leucocytes in the liver.
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PMID:Impact of alcohol on the ability of Kupffer cells to produce chemokines and its role in alcoholic liver disease. 1082 77

Increase awareness and publicity of human immunodeficiency virus (HIV) has fostered a heightened sense of concern regarding the transmission of infectious agents during sports and athletic competition. Although the potential risk is low, there are other unanswered questions and issues regarding infectious disease and sports. Viral hepatitis is a common infection and predominantly affects the young who are most likely to lead active lives and engage in both amateur and competitive sport-related activity. This article summarizes the common forms of viral hepatitis and the associated clinical syndromes. In addition, a review of the literature addressing the effect of exercise and the various states of liver disease is presented. Finally, I will address the question regarding participation and return to physical activity following acute viral hepatitis, as well as chronic hepatitis.
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PMID:Viral hepatitis and exercise. 1091 Feb 99


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