Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The effectiveness and security of azidothymidine (AZT) in the treatment of patients with infection by the human immunodeficiency virus (HIV) and persistent generalized adenopathies (PGA), were assessed. Thirty six patients with HIV infection and PGA participate in the study. Eighteen were treated with AZT and the other 18 were included in the control group, since they did not accept the treatment. Both groups were homogeneous with respect to their clinical, immunological and virological characteristics. A common study protocol was used and the clinical, immunological and virological effectiveness was assessed. Lymphocyte subpopulations were quantified by flow cytometry, viral antigens were determined by sandwich-type ELISA and antibodies against viral proteins (anti-gp120, anti-gp160, anti-gp41, anti-gp24 and anti-p18) were detected by Western blot. Naranjo and Busto's algorithm was used for the causality of adverse effects. We did not observe any significant differences regarding the presence of infection and the evolution of AIDS in both groups. A positive response to thrombocytopenia was observed, more evident in patients under low doses of AZT. The small initial transitory improvement of the immunological parameters was not statistically significant. The viral antigen was not modified by the treatment. With respect to the behaviour of the several antibodies studied, no differences were observed. The initial doses of AZT had to be modified in 44% of patients due to their hematological toxicity, more frequent in the first stages of the treatment. In two patients, the treatment had to be finally discontinued due to severe neutropenia. 25% of patients showed mild to moderate gastrointestinal manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Azidothymidine in the treatment of patients with human immunodeficiency virus infection and persistent generalized adenopathies]. 146

Disseminated histoplasmosis (DH) is recognized as an opportunistic infection in patients with the human immunodeficiency virus (HIV), especially in regions where histoplasmosis is endemic. At the Kansas University Medical Center 148 patients were hospitalized with the diagnosis of AIDS from December 1983 to March 1991; 23 of these patients (16%) had disseminated histoplasmosis. The charts of these 23 patients were reviewed. Clinical signs and symptoms included fever (91%), cough (65%), and weight loss (48%). Splenomegaly, hepatomegaly, or lymphadenopathy was present in 52% of all patients. Anemia (39%), leukopenia (65%), and thrombocytopenia (52%) were common, and 22% had pancytopenia. Diagnosis was made by peripheral smear examinations (organisms visualized on 7 of 22 smears [32%]), blood cultures (positive for H capsulatum in 16 of 20 patients, [80%]), bone marrow cultures (positive in 14 of 15 patients, [93%]), and bone marrow aspirate and biopsy examinations (organisms seen on 18 of 21 stains, [86%]). The combination of these four tests revealed the diagnosis of DH in 23 of 23 patients (100%). Induction and maintenance amphotericin B therapy was given to all but 2 patients, and currently 8 of the 23 are alive. DH is a common opportunistic infection in AIDS patients from regions endemic for histoplasmosis. When DH is suspected, a peripheral smear examination, blood cultures, bone marrow cultures and bone marrow aspirate and biopsy should be done to make the diagnosis, since suppression of the disease is possible with appropriate therapy.
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PMID:Disseminated histoplasmosis in patients with AIDS. 147 Sep 57

In the majority of adult and pediatric patients with AIDS, hematologic abnormalities including leukopenia, anemia, and thrombocytopenia are commonly observed. In addition to these findings, changes in hematopoietic progenitor cells occur, including a reduction of multipotential-forming units, granulocyte-macrophages, macrophage as well as eosinophil colony-forming units, and bone marrow erythroid burst-forming units. This study examined alterations in human fetal liver hematopoiesis in 2nd trimester abortuses from human immunodeficiency virus (HIV)-seropositive women. The differentiation and growth potential of hematopoietic cells in vitro were monitored. Upon initial isolation, some populations of liver hematopoietic cells from abortuses of HIV-seropositive women were significantly decreased when compared to age-matched samples from fetuses of normal females including the percentage of early T cells [cluster of differentiation (CD)2], B cells (CD19), and early monocytes (CD14). A decrease in multipotent progenitors (CD34), myelomonocytes (CD33), and panleukocytes (CD45) was also observed. In contrast, after 21 d in culture, cells from HIV abortuses demonstrated an increase in the percentage of CD14 cells when stimulated with erythropoietin and granulocyte-monocyte colony-stimulating factor, as well as an increase in CD45 phenotype after exposure to granulocyte-monocyte colony-stimulating factor alone. These samples showed a persistence of erythropoietic elements (transferrin and CD36 phenotype) when compared to normal controls. No significant difference in the in vitro growth of hematopoietic progenitors (bone marrow erythroid burst-forming units, granulocyte-macrophage colony-forming units, and multipotential forming units) between these samples and normal controls was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in human fetal hematopoiesis are associated with maternal HIV infection. 150 4

We studied human megakaryocytes to determine if they both expressed and synthesized Fc gamma and CD4 membrane receptors. The strategy employed relied on demonstration of receptor protein and mRNA in megakaryocytes present in freshly made marrow smears, or in megakaryocytes isolated from aspirated normal bone marrow by counterflow centrifugal elutriation. Protein was detected immunochemically, whereas mRNA was detected either by in situ hybridization, or by reverse transcription, polymerase chain reaction (RT-PCR). Using these methods CD4 and Fc gamma RII protein and mRNA were detected in most megakaryocytes. Fc gamma RI and Fc gamma RIII protein was not detected in these cells. Megakaryocytes were also cultured with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) to determine the effect of this growth factor on Fc gamma RII expression. As has been noted in cells of the monocyte-macrophage lineage, exposure to rhGM-CSF resulted in a significant increase in the level of megakaryocyte Fc gamma RII mRNA and protein. These observations are significant because they provide a physiologic basis for known viral trophism displayed by megakaryocytes. They are also of interest because they suggest that alternative portals exist for entry of human immunodeficiency virus (HIV-1) into megakaryocytes and that such infection may play a role in acquired immunodeficiency syndrome (AIDS)-related thrombocytopenia.
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PMID:Expression of Fc gamma RII and CD4 receptors by normal human megakaryocytes. 153 89

A 33-year-old white homosexual man, infected with the human immunodeficiency virus, presented with acute anemia and thrombocytopenia not responsive to transfusions or to treatment with steroids and intravenous gamma-globulin. Hematologic workup was compatible with peripheral sequestration or loss of blood cells; however, there was no evidence of gastrointestinal or other sources of hemorrhage, and the only significant finding was a progressive liver enlargement. An abdominal computerized tomographic scan showed a massive homogeneous liver without focal lesions, a very small amount of ascites, and no retroperitoneal fluid collections. A transjugular liver biopsy specimen showed the cystic, blood-filled cavities characteristic of peliosis hepatis. Cavities varied in size, all contained pooled erythrocytes, and some had areas suggestive of thrombi in various stages of organization. Bacteria similar in morphology to those described in bacillary peliosis hepatis were seen in the peliotic spaces. The clinical picture began resolving shortly after treatment with zidovudine and ampicillin/sulbactam was started and had totally resolved 6 months after presentation. This case shows that bacillary peliosis hepatis is a reversible entity that may produce acute sequestration of blood in the liver.
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PMID:Bacillary peliosis hepatis as a cause of acute anemia in a patient with the acquired immunodeficiency syndrome. 153 98

The Wiskott-Aldrich syndrome (WAS) is an inherited disease involving defects of platelets (small size, severe thrombocytopenia due to accelerated destruction) and T lymphocytes (progressive immunodeficiency, lymphopenia). The best-characterized molecular defect is the deficiency and, in some cases, abnormal forms of the T-lymphocyte surface mucin molecule CD43; deficiency of the platelet surface mucin GPIb was observed previously in two of four patients. Neither of these defects is primary, since CD43 and GPIb are encoded by autosomal genes and the disease is X-linked. This study uses cellular biological approaches to explore the possibility that destruction of structurally defective WAS platelets, mimicked experimentally by sonication of normal platelets, plays a role by releasing protease and generating other cellular defects. We show that a protease of normal platelets, identified as Ca(2+)-dependent neutral protease (calpain), which is known to cleave platelet GPIb, also specifically cleaves CD43 on the surface of neighboring desialylated T lymphocytes. The identification of the CD43 cleaving protease was based on its requirement for Ca2+ and inhibition by leupeptin, but not by diisopropylfluorophosphate (DFP). The approximate site of CD43 cleavage was identified by the use of a rabbit antibody. Sensitivity of GPIb to calpain is shown to be sialylation-independent and that of CD43 to be sialylation-dependent, and these findings are explained in terms of molecular structures. These and previous findings are incorporated into a putative mechanism, which explains most of the defects in the WAS. The mechanism suggests that the primary defective molecule in the WAS is unlikely to be a surface glycoprotein, but rather a cytoplasmic molecule with a function in cytoskeletal interactions and/or calcium ion regulation and calpain activation.
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PMID:Effect of platelet calpain on normal T-lymphocyte CD43: hypothesis of events in the Wiskott-Aldrich syndrome. 155 70

Among 180 children infected with human immunodeficiency virus (HIV-1), 14 (8%) developed thrombocytopenia during the course of the disease and have been followed for an average period of 18.8 months. Eight of 14 patients had clinical signs of bleeding. Increased levels of anti-platelet IgG antibodies were detected in 86% of patients tested and did not correlate with severity of disease. Eight patients were treated initially with intravenous immunoglobulins (IVIG) and responded with a transient increase in the platelet count of at least 30 x 10(9)/L. Sustained remission could not be achieved in the patients treated with IVIG alone. Corticosteroids were used in 6 patients who became refractory to IVIG and resulted in sustained remission in only one patient. Spontaneous remission of thrombocytopenia occurred in one patient. Ten patients were treated with zidovudine (ZVD) for a period of 3-20 months. Sustained improvement in the platelet counts occurred in only three of the children treated with ZVD.
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PMID:Thrombocytopenia in children infected with human immunodeficiency virus: long-term follow-up and therapeutic considerations. 156 Mar 41

During 1983-1988, hospitalizations of patients with a diagnosis of human immunodeficiency virus (HIV) infection increased from 1.3 to 33.7 per 100,000 persons. We used the National Hospital Discharge Survey, which is based on a representative sample of discharges from nonfederal short-stay hospitals, to describe illnesses among hospitalized patients with HIV infection. Of 222,200 such hospitalizations during 1983-1988, most occurred among persons who were 25-44 years of age (79%), white (66%), and male (90%). Among men 25-44 years of age, HIV admissions increased from 8.5 to 148.6 per 100,000 persons during 1983-1988; among black men 25-44 years of age, HIV hospitalizations increased from 43.1 to 387.4 per 100,000 persons. Among women, hospitalizations increased 3.4-fold. Frequently listed illnesses in the Centers for Disease Control (CDC) AIDS case definition were Pneumocystis carinii pneumonia (30%), candidiasis (20%), and Kaposi's sarcoma (13%). Other frequently listed illnesses included infections (39%) such as pneumonia, sepsis, and urinary tract infections; blood dyscrasias (30%) such as anemia, thrombocytopenia, and agranulocytosis; metabolic (17%), gastrointestinal (16%), and respiratory disorders (12%); and drug abuse (9%). These data provide a minimum estimate of HIV hospitalizations because for some patients HIV infection may not be specified on the discharge record. HIV hospitalizations are increasing markedly and are associated with a broad spectrum of severe morbidity.
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PMID:Increasing impact of HIV infection on hospitalizations in the United States, 1983-1988. 156 Mar 47

Infection with the human immunodeficiency virus type 1 (HIV-1) results in a variety of pathological changes culminating in the acquired immune deficiency syndrome (AIDS). While most of these changes can readily be accounted for either by direct effects of HIV-1 on the immune system or by indirect effects of secondary infectious agents as a result of faulty immune surveillance, the direct cause for a number of disease states, including some neuropathies, myopathies, nephropathy, thrombocytopenia, wasting syndromes and increased incidence of cancers (primarily lymphoma) has remained an enigma. We have recently shown that the HIV-1 protease, a viral encoded enzyme necessary for virus maturation and infectivity, can cleave a variety of host cell cytoskeletal proteins in vitro. Potential substrates for the HIV-1 protease are found in all of the cell types affected in these unexplained diseases. Recent proposals suggest that elements of the cytoskeleton may play an important role in the regulation of large scale genetic regulation. We propose that some of the degenerative changes associated with infection by HIV-1 are a direct consequence of cleavage of host cell cytoskeletal proteins, which in turn may be responsible for the increased incidence of cancer in HIV-1 infected individuals as a result of the perturbation of the regulation of gene expression by cytoskeletal components.
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PMID:Potential role of the viral protease in human immunodeficiency virus type 1 associated pathogenesis. 158 3

Three cases of thrombotic thrombocytopenic purpura (TTP) and coexistent human immunodeficiency virus (HIV) infection are presented with a review of 15 cases reported in the literature. Of the 18 total patients, one-half presented with no symptoms of HIV infection while nine patients presented with symptomatic HIV disease before or simultaneous to the diagnosis. The presenting symptoms were similar to those with classic TTP and included fever in 75% and 40% with neurologic symptoms. Laboratory parameters reflected the microangiopathic hemolytic anemia typically seen in patients with TTP. The median hematocrit was 19.4%, while the median platelet count was 16,000/mm3. As with classic TTP, patients with HIV-related TTP only had mild renal dysfunction (median creatinine of 1.2 mg/dl, range 0.8-4.8 mg/dl). Plasma exchange produced clinical remission in a majority of the patients. Importantly, approximately one-third of the patients died prior to the initiation of therapy. We conclude that TTP is a rare but treatable condition in patients with HIV infection. A TTP diagnosis should be considered in patients with HIV infection who present with severe anemia and thrombocytopenia. Plasma exchange should be considered as initial therapy. The role of both antiplatelet therapy and aspirin is unknown.
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PMID:Thrombotic thrombocytopenic purpura in patients with human immunodeficiency virus infection: a report of three cases and review of the literature. 158 7


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