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)

Advances in antiretroviral therapy and treatment or prophylaxis against opportunistic infection have resulted in prolongation of the survival of patients with acquired immunodeficiency syndrome (AIDS). Previous research has demonstrated an association between AIDS and risk of non-Hodgkin's lymphoma (NHL). In addition to the approximately 3% of individuals found to have NHL at the time of AIDS onset, others continue to develop NHL following AIDS diagnosis. Data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute demonstrated a sharply increasing incidence of NHL among men in the age range 20-49 years since 1983 in the United States. Based on new data on the risk of NHL following AIDS diagnosis, on estimates of improved survival following AIDS diagnosis, and on projections of future AIDS incidence, we considered four sets of assumptions and estimated the number of AIDS-related NHL cases in 1992 to be between 2900 and 9800. Three of these projections were higher than the estimate of 4700 cases obtained by linear extrapolation of SEER incidence trends. These projections of AIDS-related NHL incidence suggest that between 8% and 27% of all NHL cases that occur in the United States in 1992 will arise as a consequence of infection with the human immunodeficiency virus (HIV), imposing a substantial health care burden. More research into the pathogenesis of lymphoma and new approaches to antiretroviral and antilymphoma therapy will be necessary to prevent and treat this formidable complication of infection with HIV.
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PMID:Projections of the incidence of non-Hodgkin's lymphoma related to acquired immunodeficiency syndrome. 202 64

Respiratory infection with Pneumocystis carinii (PC) is the most frequent serious opportunistic infection in the clinical setting of acquired immunodeficiency syndrome (AIDS). The factors responsible for the predisposition of human immunodeficiency virus (HIV)-infected patients for PC infection are not fully understood. We postulated that changes in the alveolar lining material (ALM) could play a role in the pathogenesis of PC infection in AIDS. We have compared constituents of ALM in bronchoalveolar lavage fluid from normal, nonsmoking volunteers with that of HIV-infected patients with pneumonia. Using an ELISA, we found that surfactant protein A (SP-A) was markedly elevated in the pneumonia patients. Mean SP-A values for the normal nonsmoking individuals (n = 21) were 1.50 +/- 0.25 micrograms/ml (mean +/- SEM). SP-A levels in the HIV-infected patients (n = 22) were significantly elevated (p less than 0.01) with a mean of 5.23 +/- 0.54 micrograms/ml. This increase was greatest in the patients with more clinically severe pneumonia. The increase in SP-A did not appear to be pathogen-specific as it was also observed in cases of non-PC pneumonia. We also found that total protein levels were nearly five times higher in the HIV-infected pneumonia patients. These studies indicate that the protein component of the ALM is markedly different from normal in cases of HIV-associated PC and non-PC infection. Further investigation is needed to determine the mechanism of these alterations and their role, if any, in AIDS-related pneumonia.
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PMID:Increased recovery of surfactant protein A in AIDS-related pneumonia. 202 16

HIV infection results in the destruction of the thymus-dependent cellular immune system and death due to opportunistic infection and malignancy. Immunosuppressive influences (other sexually or blood-transmitted viruses, HIV-derived peptides, semen, poor nutrition, drugs, etc.) favor the progression of the disease. Although immunorestorative agents may be expected to delay progression of the disease, John Hadden argues that no agent has yet proven useful in reversing the immunodeficiency in full-blown AIDS. However, two thymomimetic drugs, isoprinosine and diethyldithiocarbamate, inhibit the development of infections in patients with pre-AIDS in large multicenter trials, and preliminary data from trials with two thymomimetic peptides, thymopentin and ImReg-1, in pre-AIDS patients are encouraging.
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PMID:Immunotherapy of human immunodeficiency virus infection. 205 87

Scurfy (sf) is a spontaneous, sex-linked, recessive mutation that maps to the extreme proximal portion of the X chromosome, about 2 centimorgans from sparse fur (spf). Hemizygotes for sf manifest several clinical disorders, evident at 14 days of age, including scaliness and crusting of the eyelids, ears, and tail, runting, reddening and swelling of the genital papilla, anemia, cachexia, and early death (average, 24 days). Our studies indicate that the phenotype of hemizygous scurfy is not, as has been suggested, a model for human X-linked ichthyosis, but appears to be a disease primarily affecting the lymphoreticular, and possibly the hematopoietic, systems. Gross lesions include marked splenomegaly, hepatomegaly, enlarged lymph nodes, and variable thickening of the ears. The characteristic histologic lesion is a lymphohistiocytic proliferation and infiltration of peripheral lymph nodes, spleen, liver, and skin. In routine hematoxylin and eosin-stained sections, these lesions efface lymph node architecture, thicken the dermis, and form nodular portal infiltrates in the liver. Scurfy lesions characteristically contain a population of large blastlike cells with round to oval nuclei, a vesicular chromatin pattern, and prominent single nucleoli. Mixed perivascular infiltrates of lymphocytes, macrophages, and granulocytes sometimes are found in kidney, heart, pancreas, lung, and mesenteries. There is excessive hematopoiesis in the liver and spleen. Cells expressing B220 or Thy-1 antigens localize to appropriate areas in the lymph nodes and spleen, but are rare in the portal infiltrates and are absent from the skin. There is a marked, polyclonal increase in serum IgG, severe Coombs'-positive anemia, and leukocytosis with atypical mononuclear cells. Scurfy mice are negative for antinuclear antibodies. Despite their morphologically aberrant lymphoreticular system, scurfy mice can exist in a conventional environment without evidence of opportunistic infection. Raising scurfy mice in a specific-pathogen-free environment does not alter disease expression. Thus, while our findings indicate that scurfy disease may be the result of immune dysfunction, it is not a classic immunodeficiency.
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PMID:X-linked lymphoreticular disease in the scurfy (sf) mutant mouse. 205 95

In 4 years (1984-1987), 183 bone marrow examinations were performed on 155 human immunodeficiency virus (HIV) antibody positive patients. One hundred and fifty three had category IV AIDS. One-third of the marrows yielded specific information. This included opportunistic infection, in particular Mycobacterium Avium Intracellulare Complex (MAI) (24%), malignancy (4%), consistent with ITP (9%) and iron deficiency (1%). In the remaining two thirds of the bone marrows the most frequent non-specific abnormalities were dyserythropoiesis, erythroid hypoplasia, reticuloendothelial iron block, granulomas, lymphoid aggregates, plasmacytosis and histiocytosis. Common peripheral blood findings were anemia, lymphopenia, anisocytosis, rouleaux and atypical lymphocytes. Peripheral blood and bone marrow examinations on 16 patients on AZT are included. These patients have more pronounced blood and bone marrow abnormalities. The causes of these abnormalities are multifactorial and include low T4 levels, severe viral and other infections and therapy with marrow toxic drugs.
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PMID:Peripheral blood and bone marrow findings in patients with acquired immune deficiency syndrome. 209 Oct 4

The histopathologic changes of bone marrow during infection with the human immunodeficiency virus type 1 (HIV-1) are described. Bone marrow biopsies from 73 patients at different stages of HIV-1 infection were studied. Indications for biopsy included peripheral blood abnormalities, suspicion of lymphoma, or search for specific pathogens. Common histopathological features, suggestive of HIV-1 infection but nonpathognomonic were hypercellularity (67%), myelodysplasia (86.1%), plasmacytosis (98.6%), lymphocytic infiltration (31.1%) and histiocytic infiltration with or without granulomata (13.7%). Increases in reticulin fibers (54.7%), and stainable iron deposits, vascular congestion and serous atrophy of fat were frequent features. Opportunistic infections and neoplastic complications were detected in 7 cases: pathogens were demonstrated in 4 cases (Mycobacterium avium intracellulare (MAI), Cryptococcus neoformans, Toxoplasma gondii and Leishmania) and lymphoma in 3 cases (1 Burkitt lymphoma and 2 Hodgkin's disease). Bone marrow hypoplasia is usually a terminal event in AIDS and may be iatrogenic.
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PMID:Bone marrow findings in HIV infection: a pathological study. 210 65

We describe the clinical and histologic features of non-Hodgkin's lymphoma in 26 patients with human immunodeficiency virus 1 (HIV) infection. These represent 10 per cent of AIDS cases recorded in the Bordeaux area. Mean age was 42. Contamination was mostly related to homosexuality (50 per cent) and blood transfusion (27 per cent) with 5 female cases. The initial presentation of lymphoma was extranodal (69 per cent). Lymphoma spread was diffuse (65 per cent), involving the bone marrow (38 per cent), lymph nodes (35 per cent), central nervous system (27 per cent), oral and digestive mucosae (23 per cent), liver (19 per cent) and genital tract (12 per cent). Histologic types were of intermediate or high grade malignancy (88 per cent) with 38 per cent large, non cleaved-cell (centroblastic) subtype. Median survival was 4 months. Lymphoma caused death in 65 per cent of patients and opportunistic infection in 18 per cent. Lymphoma was the first manifestation of HIV infection in 10 patients (38 per cent) and was responsible for AIDS in 14 (54 per cent). Diagnosis of lymphoma could be established at an early stage on extranodal biopsy. In these patients a prolonged disease-free survival was obtained after chemotherapy alone or associated with radiotherapy.
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PMID:[Non-Hodgkin's lymphoma associated with human immunodeficiency virus infection. Bordeaux experience with 26 cases]. 213 32

Preexistent feline leukemia virus (FeLV) infection greatly potentiated the severity of the transient primary and chronic secondary stages of feline immunodeficiency virus (FIV) infection. Of 10 FeLV-FIV carrier cats, 5 died of experimentally induced FIV infection, compared with 2 deaths in 10 cats infected only with FeLV and 1 death in 7 cats infected only with FIV. FIV-infected cats with preexistent FeLV infections developed severe depression, anorexia, fever, diarrhea, dehydration, weight loss, and leukopenia 4 to 6 weeks after infection and were moribund within 2 weeks of the onset of signs, whereas cats infected only with FIV developed much milder self-limiting gross and hematologic abnormalities. Pathologic findings in dually infected cats that died were similar to those observed previously in cats dying from uncomplicated primary FIV infection but were much more widespread and severe. Coinfection of asymptomatic FeLV carrier cats with FIV did not increase the levels of FeLV p27 antigen present in their blood over that seen in cats infected with FeLV alone. The amount of proviral FIV DNA was much higher, however, in dually infected cats than in cats infected only with FIV; there was a greater expression of FIV DNA in lymphoid tissues, where the genome was normally detected, and in nonlymphoid tissues, where FIV DNA was not usually found. Dually infedted cats that recovered from the primary stage of FIV infection remained more leukopenic than cats infected with FIV or FeLV alone, and their CD4+/CD8+ T-lymphocyte ratios were inverted. One of these cats developed what was considered to be an opportunistic infection. It was concluded, therefore, that a preexistent FeLV infection in some way enhanced the expression and spread of FIV in the body and increased the severity of both the resulting transient primary and chronic secondary stages of FIV infection. This study also demonstrated the usefulness of the FIV model in studying the role of incidental infectious diseases as cofactors for immunodeficiency-causing lentiviruses.
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PMID:Feline leukemia virus infection as a potentiating cofactor for the primary and secondary stages of experimentally induced feline immunodeficiency virus infection. 215 26

The acyclic purine nucleoside analogue 9-(2-phosphonomethoxyethyl)adenine [PMEA; formerly referred to as 9-(2-phosphonylmethoxyethyl)adenine] is a potent and selective inhibitor of human immunodeficiency virus replication in vitro and of Moloney murine sarcoma virus-induced tumor formation in mice. In the latter system PMEA has stronger antiretroviral potency and selectivity than 3'-azido-3'-thymidine (AZT). We have now investigated the effect of the drug in cats infected with the feline immunodeficiency virus (FIV). In vitro, PMEA was found to efficiently block FIV replication in feline thymocytes (50% effective dose, 0.6 microM). When administered to cats at doses of 20, 5, or 2 mg/kg per day, PMEA caused a dose-dependent suppression of FIV replication and virus-specific antibody production. Seropositive field cats with signs of opportunistic infection (gingivitis, stomatitis, and diarrhea) showed clinical improvement during PMEA therapy (5 mg/kg per day) and recurrence of the disease after treatment was discontinued. Thus, FIV infection in cats is an excellent model to test the efficacy of selective anti-human immunodeficiency virus agents in vivo.
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PMID:Suppression of feline immunodeficiency virus infection in vivo by 9-(2-phosphonomethoxyethyl)adenine. 215 2

Opportunistic infections ultimately occur in most patients infected with human immunodeficiency virus (HIV) and are responsible for 90% of deaths. Over the decade since the acquired immunodeficiency syndrome (AIDS) was first recognized, important advances have been made in reducing the morbidity and mortality of opportunistic infections in patients infected with HIV. These include an improved understanding of the relationship between immunologic parameters and infection, allowing the occurrence of infectious complications to be more predictable; development of prophylactic regimens and chronic suppressive regimens that are effective, well tolerated, and convenient; and emphasis on earlier diagnosis and therapeutic intervention of those infectious processes that are not prevented. These advances have allowed the quality and duration of patient survival to improve during this decade, but they can also be anticipated to alter the spectrum of clinical manifestations that health care providers are going to see during this epidemic's second decade.
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PMID:Problems in the management of opportunistic infections in patients infected with human immunodeficiency virus. 218 28


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