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)

Severe cellular immunosuppression developed in a 25-year-old man with hemophilia B who was infected with the human immunodeficiency virus (HIV). Four days after administration of sulfamethoxazole-trimethoprim (SMX-TMP) for prophylaxis against Pneumocystis carinii pneumonia (PCP), diffuse uptake of both lungs was confirmed on a 67Ga scintigram. Reticular shadows were also seen throughout both lung fields on a chest CT scan. These findings were compatible with PCP, according to the guidelines for presumptive diagnosis of the acquired immunodeficiency syndrome, published by the Centers for Disease Control and Prevention. The dose of SMX-TMP was increased, but interstitial pneumonitis worsened and was accompanied by fever, skin rash, and liver dysfunction, which are common in HIV-infected patients receiving SMX-TMP. No evidence of PCP or of any other opportunistic infection was found by bronchoalveolar lavage. Adverse reactions diminished after SMX-TMP administration was stopped. The 67Ga scintigram and chest CT findings also returned to normal. We concluded that the interstitial pneumonitis was induced by SMX-TMP. SMX-TMP is the first choice anti-PCP drug, but a high incidence of adverse reactions in patients with HIV infection has been reported. Therefore the possibility of SMX-TMP-related pulmonary toxicity must be considered in HIV-infected patients.
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PMID:[Sulfamethoxazole-trimethoprim-induced pneumonitis in a patient with hemophilia B who was infected with the human immunodeficiency virus]. 881 Jul 66

To assess the zoonotic potential of Encephalitozoon-like microsporidia, we isolated and cultivated spores from specimens of urine, respiratory secretions, and stool from six patients infected with human immunodeficiency virus and from nine rabbits. Because spores of Encephalitozoon-like species are indistinguishable by microscopy, we characterized the isolates by western blot analysis and by restriction enzyme analysis of the small subunit (SSU) rDNA after amplification by the polymerase chain reaction. We identified Septata intestinalis in one patient and Encephalitozoon hellem in two symptomatic patients. Encephalitozoon cuniculi was found in all rabbits and in three patients. One of these patients had clinical manifestations of infection with this parasite (severe interstitial pneumonitis). We observed abatement of symptoms and cessation of parasite excretion when these patients were treated with albendazole. Our findings suggest that E. cuniculi may be pathogenic in humans and that it is a zoonotic parasite.
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PMID:Immunologic and molecular characteristics of Encephalitozoon-like microsporidia isolated from humans and rabbits indicate that Encephalitozoon cuniculi is a zoonotic parasite. 885 78

Common variable immunodeficiency (CVID) is a primary immunodeficiency disorder characterized by decreased levels of circulating immunoglobulins (Ig) and increased susceptibility to infections. We describe the case of a girl, progressively developing CVID, whose first clinical manifestations were noninfectious diffuse pulmonary infiltrates and rapidly developing hilar and mediastinal lymphadenopathies causing a severe "superior vena caval syndrome". Histological evaluation of surgical samples showed follicular and paracortical hyperplasia of the lymph nodes and poorly organized, non-necrotizing, noninfectious, "reactive" granulomata in lymph nodes and pulmonary tissue. Daily treatment with azathioprine and prednisone induced resolution of the intrathoracic abnormalities but was associated with a progressive decrease of circulating IgG and IgA levels and natural killer (NK) lymphocytes that was not related to treatment. This case demonstrates that granulomatous inflammatory changes may be the first manifestations of common variable immunodeficiency, and that this disorder must be included in the differential diagnosis of lymphoid interstitial pneumonitis and of bilateral mediastinal lymph node enlargement leading to superior vena caval syndrome.
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PMID:Common variable immunodeficiency presenting in a girl as lung infiltrates and mediastinal adenopathies leading to severe "superior vena caval" syndrome. 888 Jan 19

Increasing numbers of children with human immunodeficiency virus (HIV) infection continue to be seen in the United States. Pulmonary infections constitute a major cause of morbidity and mortality in these children Pneumoncystis carinii pneumonia, pulmonary lymphoid hyperplasia/lymphoid interstitial pneumonitis, and bacterial pneumonias, all described in high frequency in the earliest cases of pediatric acquired immunodeficiency syndrome, remain the pulmonary diseases confronted most often. Other pathogens, such as Mycobacterium tuberculosis and respiratory virus infections are now being identified in increasing numbers in HIV-infected children. Advances in our understanding of these disease processes and their clinical manifestations have allowed development of a systematic approaches to the common problem of the HIV-infected child with fever, tachypnea, and hypoxemia and an abnormal chest radiograph. These approaches, coupled with improvements in available treatment options, have led to earlier diagnosis and improved survival. Prophylaxis strategies have been developed for the most serious pulmonary infections, especially P carinii pneumonia. However, lack of identification of infants and children at risk of HIV infection has limited their effectiveness. Pulmonary infections in HIV-infected children continue to take a high toll with regard to morbidity and mortality. Only with continued advances in primary therapy to slow progression of the underlying immunodeficiency and widespread use of available prophylactic guidelines will these be reduced.
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PMID:Human immunodeficiency-virus-related pulmonary infections in children. 888 75

Infection of sheep by visna-maedi virus causes an interstitial pneumonitis similar to that associated with human immunodeficiency virus type-1 (HIV-1). Visna-maedi virus infection of alveolar macrophages leads to their activation. In this study we determined whether an imbalance in oxidant-antioxidant activity may be involved in the pathogenesis of the disease. We investigated the spontaneous and phorbol myristate acetate (PMA)-induced release of hydrogen peroxide (H2O2), and the activities of superoxide dismutase and glutathione peroxidase in alveolar macrophages from lambs experimentally-infected with visna-maedi virus, and in ovine alveolar macrophages infected in vitro. Alveolar macrophages from lambs experimentally-infected in vivo exhibited normal spontaneous H2O2 release and had superoxide dismutase and glutathione peroxidase activities similar to those from control animals. In contrast, after in vitro stimulation with PMA the H2O2 production by macrophages from experimentally-infected lambs was significantly increased. Similarly, spontaneous and PMA-induced H2O2 production by in vitro infected macrophages was significantly increased as compared to controls. In conclusion, the increased capacity of alveolar macrophages infected with the human immunodeficiency virus type-1-related visna-maedi virus to release hydrogen peroxide on stimulation suggests an oxidant-antioxidant imbalance, which may contribute to the pathogenesis of the observed chronic interstitial pneumonitis.
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PMID:Oxidant-antioxidant imbalance in the experimental interstitial lung disease induced in sheep by visna-maedi virus. 890 54

In May 1995, a 52-year-old man complaining of fever and dyspnea was admitted to a hospital. Based on clinical and radiographic findings, hypersensitivity pneumonitis was suspected. Steroid pulse therapy was unsuccessful, and he was then transferred to our hospital. A chest X-ray film showed bilateral ground-glass shadows and a high-resolution CT scan showed cystic air spaces. The number of CD4-positive lymphocytes in peripheral blood was very low. A test for anti-human immunodeficiency virus antibody was positive and Pneumocystic carinii was found in bronchoalveolar lavage fluid. The acquired immunodeficiency syndrome and Pneumocystis carinii pneumonia were diagnosed. In this patient, the level of serum KL-6, a new marker of interstitial pneumonitis, was very high, and KL-6 was expressed on type II pneumocytes. The level of serum KL-6 may be useful as a marker of the activity of Pneumocystis carinii pneumonia.
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PMID:[Pneumocystis carinii pneumonia associated with high levels of serum KL-6]. 902 32

Limited information is available about the pathogenesis of acquired immune deficiency syndrome (AIDS)-associated idiopathic interstitial pneumonitis, a common noninfectious complication of human immunodeficiency virus (HIV) infection. Infection of C57B1/6 mice with LP-BM5 retrovirus, a murine model of AIDS, leads to development of a diffuse interstitial pneumonitis that displays many features of human AIDS-associated interstitial pneumonitis. To further characterize the cellular and molecular features of this lung disease, the temporal development of cellular infiltration, cytokine expression, and virus replication were evaluated in lung tissue of virus-infected mice. Persistent expression of viral RNA was detectable in lungs as early as 1 wk after infection. Infiltration of the lungs by CD4+ and CD8+ T cells, by IgG+ and IgA+ B cells, and by macrophages was observed by 4 wk after infection and continued through 8 wk of infection. Histologically, cellular infiltration was most pronounced in peribronchial and perivascular regions, whereas inflammation of alveolar septae and alveolar spaces was minimal. In contrast to normals, T cells from infected lungs were immunodeficient in that they failed to proliferate in response to the mitogen concanavalin A (ConA). However, evaluation of cytokine mRNA expression by interstitial lung lymphoid cells indicated that cells from infected lungs were chronically activated, in that elevated expression of interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) was observed throughout the course of infection. Similarly, expression by interstitial lung lymphoid cells of mRNA for the proinflammatory cytokine IL-1 and the fibrogenic cytokine transforming growth factor-beta (TGF-beta) was also increased following infection. These results indicate that retrovirus-induced immunodeficiency in mice is associated with infiltration and chronic activation of lymphoid cells in the lungs. Furthermore, simultaneous expression of IL-10, IFN-gamma, and TGF-beta suggests that cytokine-expressing cells in infected lungs may be unresponsive to inhibitory and antiinflammatory effects of IL-10 and/or TGF-beta, thus contributing to chronicity of inflammation in this disorder.
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PMID:Pulmonary lymphoid cell activation and cytokine expression in murine AIDS-associated interstitial pneumonitis. 903 22

Human immunodeficiency virus-infected patients occasionally exhibit alveolar septal wall thickening and decreases in gas diffusion capacity, but the mechanism underlying these abnormalities is unknown. The present study evaluated septal wall thickness and gas exchange properties in a murine model of the acquired immunodeficiency syndrome and determined whether there were alterations in lung lymphocyte deposition and activation that could contribute to changes in respiratory structure and function. Although alveolar septal wall thickness did not differ from control at 1, 2, and 4 wk postimmunosuppressive virus infection, at 8 wk after infection, septal wall thickness was substantially increased. Immunohistochemical evaluation at this time revealed marked increases in the septal wall deposition of fibronectin and collagen type IV. Pulmonary function tests on anesthetized mice with virus-induced septal wall thickening demonstrated that, although total lung capacity, compliance, and functional residual capacity were unaltered, diffusion capacity for carbon monoxide was significantly impaired. A diffuse nonspecific interstitial pneumonitis was present in lungs of immunodeficient mice, and flow cytometry indicated that both lymphocytes and macrophages were activated. Reverse transcriptase-polymerase chain reaction analysis of lung lymphocytes demonstrated enhanced mRNA expression for several cytokines known to affect lung structure. These results show that impaired gas exchange occurs in a murine model of acquired immunodeficiency syndrome and suggest that such alterations may be mediated by elaboration of cytokines from activated lung lymphocytes and macrophages.
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PMID:Pulmonary mechanical and immunologic dysfunction in a murine model of AIDS. 914 44

With changes in the demographics of human immunodeficiency virus (HIV) infection, women and children are becoming the fastest growing group of newly infected patients. With longer survival after HIV infection, more women infected with HIV are becoming pregnant. Pulmonary disease is one of the most common presenting conditions in an AIDS-defining illness. Pneumocystis carini pneumonia and tuberculosis are the most common disorders that herald the onset of AIDS. They are also the most frequently encountered HIV-related pulmonary complications during pregnancy. Others have been rarely reported during pregnancy and include fungal infections (Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitus), bacterial infections (Haemophilus influenzae and Streptococcus pneumoniae along with Pseudomona aeruginosa), viral infections (CMV), opportunistic neoplasms (Kaposi's sarcoma, lymphoma) and miscellaneous conditions peculiar to HIV-infected individuals (nonspecific interstitial pneumonitis, lymphoid interstitial pneumonitis, isolated pulmonary hypertension, and pulmonary edema secondary to cardiac disease or drug abuse). Most of the data regarding the pulmonary complications of HIV infection come from studies in nonpregnant patients. The extent to which pregnancy affects the course of respiratory disease in HIV infection and vice versa is not well documented. Clinical presentation is usually not altered by pregnancy. Except for minor modifications mainly related to potential fetal effects, the diagnostic work-up and management are similar to those in the nonpregnant patient. The most important effect of pregnancy on these conditions remains the delay in diagnosis and treatment. A high index of suspicion should, therefore, be maintained. In addition, most prophylactic measures recommended in nonpregnant HIV-infected individuals also apply to pregnant women.
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PMID:Human immunodeficiency virus (HIV)-related pulmonary complications in pregnancy. 929 23

Postmortem bronchoalveolar lavage of feline immunodeficiency virus-infected cats indicated an alveolitis process, and histological examination of their lungs confirmed the occurrence of alveolitis, parenchymatous lymphoplasmocytic infiltration and myomatosis. Similar lymphoid interstitial pneumonitis has been described in human and animal lentiviral diseases: lymphocytic interstitial pneumonitis in HIV-1-infected human beings, and maedi in sheep infected by the maedi-visna virus. Such lymphoid interstitial pneumonitis may thus be a common feature of lentiviral infections.
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PMID:Interstitial lung disease in feline immunodeficiency virus (FIV) infected cats. 930 May 50


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