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)

alpha-Interferon (IFN alpha) blocks replication of human immunodeficiency virus (HIV)-1 in vitro by interfering with the release of mature virions. Clinical trials have addressed the in vivo effects of IFN alpha, both alone and in combination with other agents, in a variety of patients at all stages of HIV-1 infection. Patients with late stages of HIV-1 infection (CD4 counts under 100) show few positive results following treatment with IFN alpha. Patients with earlier stages of HIV infection, however, may benefit from treatment with this agent. Several clinical trials have demonstrated the activity of interferon in the treatment of patients with acquired immunodeficiency syndrome, Kaposi's sarcoma, and CD4 counts over 200. In these trials, response rates of approximately 40% have been reported, with the probability of response directly correlated with the level of CD4 cells. These antitumor effects have been associated with declines in the circulating levels of the HIV-1 core antigen p24. alpha-Interferon activity has also been studied in patients concomitantly receiving zidovudine. In these studies, neutropenia, reversible with the concomitant administration of granulocyte macrophage colony-stimulating factor, has been the most common dose-limiting toxicity. Both the antitumor and antiviral activities of combination therapy appear to be at least as good as those observed when single agents are used. Controlled clinical trials are currently under way to evaluate the role of interferon therapy, both alone and in combination with zidovudine, in patients with early HIV infection.
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PMID:The role of alpha-interferon in patients with human immunodeficiency virus infection. 194 29

A case of hypothyroidism that manifested as depression and deteriorating functional status and that ultimately resulted in the death of a 41-year-old patient with AIDS is described. Postmortem examination revealed destruction of the thyroid gland by Kaposi's sarcoma. Analysis of stored serum samples revealed that the patient had become profoundly hypothyroid during his terminal illness. Practitioners are reminded of the need to exclude metabolic causes when treating encephalopathy in patients infected with human immunodeficiency virus.
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PMID:Hypothyroidism due to destruction of the thyroid by Kaposi's sarcoma. 196 92

In the United States Kaposi's sarcoma is at least 20,000 times more common in persons with acquired immunodeficiency syndrome (AIDS) than in the general population and 300 times more common than in other immunosuppressed groups. Among persons with the acquired immunodeficiency syndrome (AIDS) reported to Centers for Disease Control by March 31, 1989, 15% (13,616) had Kaposi's sarcoma. Kaposi's sarcoma was commoner among those who had acquired the human immunodeficiency virus (HIV) by sexual contact than parenterally, the percentage with Kaposi's sarcoma ranging from 1% in men with haemophilia to 21% in homosexual or bisexual men. Women were more likely to have Kaposi's sarcoma if their partners were bisexual men rather than intravenous drug users. Kaposi's sarcoma risk was not consistently related to age or race but varied across the United States, being greatest in the areas that were the initial foci of the AIDS epidemic. Thus Kaposi's sarcoma in persons with AIDS may be caused by an as yet unidentified infectious agent, transmitted mainly by sexual contact.
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PMID:Kaposi's sarcoma among persons with AIDS: a sexually transmitted infection? 197 96

Biopsy samples from five acquired immune deficiency syndrome (AIDS)-Kaposi's sarcomas and one non-AIDS-associated Kaposi's sarcoma were assayed by in situ RNA hybridization onto paraformaldehyde-fixed, paraffin-embedded skin sections for the presence of two fibroblast growth factor gene transcripts, FGFB and FGF5. FGF5 gene expression was detected in the characteristic Kaposi's sarcoma spindle-shaped cells in the five samples from human immunodeficiency-positive (HIV+) patients. FGFB transcripts were detected in Kaposi's sarcoma cells as well as in epidermis of HIV- and HIV+ patients. These results complement the observations about growth factor gene expression done on Kaposi's sarcoma-derived cell lines, which thus appear to be representative of what happens in vivo. Furthermore, they demonstrate a contrasting expression pattern of FGF5 and FGFB genes, both involved in the growth factor pathogenic cascade leading to Kaposi's sarcoma.
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PMID:Fibroblast growth factor gene expression in AIDS-Kaposi's sarcoma detected by in situ hybridization. 198 71

Oral candidiasis, herpetic lesions, oral mucosal warts, human immunodeficiency virus-associated gingivitis and periodontitis, Kaposi's sarcoma, hairy leukoplakia, and non-Hodgkin's lymphoma are oral manifestations of infection by the human immunodeficiency virus. This paper will explain how to identify these lesions, their significance, and recommended treatments.
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PMID:Oral manifestations of human immunodeficiency virus infection. 199 2

A wide variety of pathologies afflicting the genitourinary tract can be displayed by patients infected with the human immunodeficiency virus (HIV), including both infective and neoplastic conditions. Treatment can often be offered for such conditions using a combination of therapeutic approaches. These conditions should be looked for specifically in patients with HIV infection as treatment may improve their quality of life. A case is presented of a testicular seminoma (appearing in association with an intracranial mass and Kaposi's sarcoma) in a male patient with the acquired immune deficiency syndrome (AIDS); he made a good response to orchiectomy and radiotherapy for his seminoma. A short review is also given of the range of HIV-associated genitourinary pathologies which have been described to date.
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PMID:Urological manifestations of HIV-related disease. A case of AIDS-associated testicular seminoma, Kaposi's sarcoma and possible intracranial lymphoma. 200 34

Infection with the human immunodeficiency virus (HIV) may cause a variety of oral lesions, such as candidiasis, periodontal disease, hairy leukoplakia, Kaposi's sarcoma and a number of miscellaneous lesions and conditions. One hundred HIV-infected patients, including AIDS patients, referred to a University Hospital in Amsterdam, were examined orally. Most patients were initially seen by the Department of Internal Medicine, the oral examination by a well-trained dentist being part of the routine screening of all HIV-infected patients. In 80 per cent of all patients one or more HIV-related lesions of the oral mucosa was recorded. In 6 per cent of those patients the oral lesion was the first manifestation of the HIV infection. Hairy leukoplakia was observed in 15 per cent of all patients. Candidiasis proved to be the most common oral disease. In patients with full-blown AIDS the pseudomembranous form of candidiasis was the most common one, while in HIV-infected patients the erythematous type prevailed. These results emphasize the role of the dentist in making an early diagnosis of HIV infection.
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PMID:Oral manifestations of AIDS: an overview. 200 36

We examined data from San Francisco and other areas participating in the Surveillance, Epidemiology, and End Results (SEER) Program to determine the effect of the human immunodeficiency virus (HIV) epidemic on cancer incidence between 1973 and 1987. In this period, non-Hodgkin's lymphoma incidence has increased over 10-fold and Kaposi's sarcoma incidence has increased over 5000-fold in single San Francisco men 20 to 49 years of age. Increases in non-Hodgkin's lymphoma have been restricted to high-grade and diffuse large-cell (intermediate-grade) histological types. With the exceptions of non-Hodgkin's lymphoma and Kaposi's sarcoma, no other tumor has significantly increased in incidence. During 1987, we estimate that HIV-seropositive men in San Francisco had a 0.47% risk of developing non-Hodgkin's lymphoma and a 1.6% risk of developing Kaposi's sarcoma. The relative risks for non-Hodgkin's lymphoma and Kaposi's sarcoma associated with HIV infection were 104 and 40,000, respectively. For 1987, HIV was associated with 14% of all reported cancers (except non-melanoma skin cancer) in men aged 20 to 49. We expect that 1,890 to 2,730 excess cases of non-Hodgkin's lymphoma and 6,490 to 8,320 excess cases of Kaposi's sarcoma will occur in the United States in 1990.
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PMID:Increasing incidence of cancers associated with the human immunodeficiency virus epidemic. 200 49

Involvement of the pancreas by human immunodeficiency virus (HIV) infection has not been adequately addressed and is the object of this review. I analyzed the English language literature, including single case reports of pancreatic involvement and larger series reporting detailed pathological findings of patients with HIV infection. Nonspecific pathological changes in the pancreas are frequently seen at autopsy of HIV-infected patients, but are not more common than in controls. Several types of infections (mainly cytomegalovirus, Cryptococcus neoformans, and Mycobacteria) and neoplasms (lymphoma and Kaposi's sarcoma) can involve the pancreas because they are usually disseminated. Although the serum amylase may be elevated, the patient remains asymptomatic. Occasional instances of severe and even fatal pancreatitis have been reported with HIV infections and attendant drug toxicity. Pentamidine has a predictable incidence of hypoglycemic episodes and 2',3'-dideoxyinosine provokes pancreatitis in a minority of treated patients. Such drug toxicity seems to deserve greater clinical concern than opportunistic infections or neoplasms.
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PMID:Pancreatic involvement in human immunodeficiency virus infection. 200 47

Of 4,073 reported patients diagnosed with AIDS from 1978 through 1983, 821 (20%) were not reported to be dead by January 1987. Of these apparent long-term survivors, 780 (95%) were reported from 14 states or from local areas where collaborating health departments conducted special follow-up investigations: 119 (15%) were found to be alive, 475 (61%) were dead, and 186 (24%) were lost to follow-up. Health departments obtained consent to collect additional clinical and laboratory information on 48 of the living patients. Six (13%) had no laboratory evidence specific for human immunodeficiency virus (HIV) infection (antibody, antigen, viral isolation, or polymerase chain reaction assay); 41 (85%) had a positive result on at least one test; and one was not tested. Of the 41 infected patients, 25 (61%) had Kaposi's sarcoma (KS) and two (5%) had Pneumocystis carinii pneumonia as the only AIDS-indicative disease; the remainder had multiple diseases. CD4+ cell counts were low (less than 30% of total T lymphocytes) by the time of enrollment in 34 (87%) of 39 patients tested. When enrolled survivors with KS were compared with KS patients who had died within 2 years after AIDS diagnosis, survivors were less likely to have had other diseases in addition to KS than were nonsurvivors (31% versus 51%). While overall mortality by 1987 for patients diagnosed in 1978-83 was high (92-96%), a small number have survived and were doing relatively well clinically, despite evidence of continued CD4+ cell depression.
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PMID:Characterization of long-term survivors of acquired immunodeficiency syndrome. The Long-term Survivor Collaborative Study Group. 200 73


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