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)

A 7-year-old leukemic girl developed pancytopenia following chemotherapy and was given several transfusions of nonirradiated blood. Within 2 weeks she developed a maculopapular rash, fever, abnormal liver function, diarrhea, and wasting. She became septic and died 6 weeks later. Transfusion-associated graft-versus-host disease (GVHD) was suspected clinically. At autopsy, changes diagnostic of GVHD were present in the skin and liver. The remarkable feature of the case was the histopathology of the thymus, which was morphologically "dysplastic," i.e., minute, lymphoid depleted, devoid of a corticomedullary demarcation, and completely lacking in Hassall's corpuscles. These changes were virtually identical to those seen in the thymus of children with severe combined immunodeficiency disease (SCID). There was no evidence of preexisting immune deficiency. There is compelling experimental evidence that GVHD can produce changes in the thymus that are identical to those of "thymic dysplasia." These observations have led to the hypothesis that immunodeficiency associated with GVHD may stem, in part, from injury to thymic epithelium resulting in defective T cell maturation. As a corollary of this hypothesis, it has been suggested that the pathogenesis of some forms of SCID may involve GVHD-associated injury to the thymus by a maternal allograft acquired in utero. This report further documents thymic pathology in human GVHD and discusses these changes in the light of these ideas.
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PMID:Thymic involution with loss of Hassall's corpuscles mimicking thymic dysplasia in a child with transfusion-associated graft-versus-host disease. 186 63

Over the last 3 decades, epidemiologists and clinicians have identified a few clinical entities that appear to result when a viral infection and a chemical exposure overlap and interact. Ampicillin rash during infectious mononucleosis, Reye's syndrome following salicylate ingestion and certain viral infections, and the association of AIDS-related Kaposi's sarcoma with abuse of nitrite inhalants and infection due to human immunodeficiency virus are examples of such phenomena. Preclinical research provides additional evidence that viruses and chemicals may interact and produce illnesses in animals. We hypothesize that other virus-drug interactions may exist. Identifying such interactions may lead to a better understanding of the pathogenesis of currently baffling illnesses and may provide insights into ways of preventing and/or treating diseases that appear uncontrollable now.
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PMID:Adverse virus-drug interactions. 177 71

We observed 12 patients with acute human immunodeficiency virus type 1 (HIV-1) infection. The clinical syndrome was characterized by fever (all cases), generalized lymphadenopathy (11), arthralgias and myalgias (9), sore throat (9), rash (7), splenomegaly (6), and other less frequent signs and symptoms. All patients had a spontaneous resolution of their symptoms within 5-30 days. Anti-HIV-1 serum antibodies, as measured by enzyme immunoassay (EIA) at the onset of clinical illness, were negative in every patient. HIV antigen (p24), on the contrary, was detectable in nine cases. Western blot IgM and IgG analysis was serially performed: IgMs were positive in nine cases and IgGs in three. The CD4+/CD8+ ratio was low in all patients because CD8+ were remarkably increased and CD4+ slightly reduced. A laterocervical lymph nodes biopsy was performed in four patients. The morphological and immunohistological pattern of the acute HIV-1-related lymphadenopathy did not correspond to any of the typical ones. The envelope virus protein gp120/160 was found in interfollicular and follicular lymphocytes, in endothelial cells, and in interdigitating and dendritic reticulum cells. The p17 and p24 core virus proteins were mainly detected in endothelial, interdigitating, and dendritic reticulum cells, but in only a few lymphocytes. The follow-up suggests a rapid evolution to ARC and AIDS in patients showing an acute symptomatic HIV infection.
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PMID:Acute HIV-1 infection: clinical and biological study of 12 patients. 196 96

A rapidly enlarging left inguinal adenitis, with positive groove sign, and fever, chills, malaise, hypotension, headache, scarlatiniform rash, choleroid diarrhea, and proteinuria developed in an homosexual man who was positive for human immunodeficiency virus. The needle aspiration of the inguinal mass showed group A beta-hemolytic streptococci and the blood cultures were negative, suggesting group A streptococcal cellulitis-adenitis with toxic strep syndrome. Treatment with penicillin and surgical drainage was successful. Bacterial infections associated with defective humoral immunity appear to be common in patients with acquired immunodeficiency syndrome (AIDS), and some of these infections have a remarkable extensive and lethal evolution. Therefore streptococcal adenitis should be considered in any patient with AIDS or AIDS-related syndrome in whom rapidly enlarging inguinal nodes develop.
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PMID:Group A streptococcal cellulitis-adenitis in a patient with acquired immunodeficiency syndrome. 199 49

A hydroxynaphthoquinone compound (566C80) has been shown to be effective in the prevention and treatment of murine Pneumocystis carinii pneumonitis. In a phase I study, five cohorts of four human immunodeficiency virus-infected men received 100, 250, 750, 1500, and 3000 mg of the compound orally once daily for 12 days. A sixth cohort received 750 mg three times daily for 5 days, then twice daily for 16 days. Evaluation included clinical, hematologic, and biochemical studies and the pharmacokinetics of 566C80. The only drug-related adverse effect was a maculopapular rash in one patient that resolved without discontinuation of the drug. With the largest dosage tested (3000 mg) the following pharmacokinetic measures were achieved: maximum plasma concentration, 39 micrograms/ml; time to maximum plasma concentration, 8.0 h; area under plasma concentration-time curve at steady state, 1088 h.micrograms/ml; plasma half-life, 51 h; and total plasma clearance, 4.09 l/h. Compound 566C80 offers promise as a new drug class for P. carinii pneumonia.
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PMID:Safety and pharmacokinetics of 566C80, a hydroxynaphthoquinone with anti-Pneumocystis carinii activity: a phase I study in human immunodeficiency virus (HIV)-infected men. 201 Jun 37

Inflammatory muscle involvement during the course of human immunodeficiency virus (HIV) infection is described and guidelines are suggested for its differentiation from the myopathy associated with azidothymidine (AZT) therapy. Six patients infected with HIV presented with proximal muscle weakness, biochemical and electromyographic abnormalities consistent with myositis. One patient had a skin rash characteristic of dermatomyositis. Muscle biopsy findings demonstrated the presence of an inflammatory cell infiltrate and HIV-p24 antigen. All patients developed their clinical picture prior to AZT therapy and responded to steroids with or without coadministration of AZT.
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PMID:Characteristics and pathogenesis of myositis in human immunodeficiency virus infection--distinction from azidothymidine-induced myopathy. 204 82

Human immunodeficiency virus (HIV) infection of the esophagus has recently been implicated as a cause of giant esophageal ulcers in HIV-positive patients with odynophagia. The authors examined four patients in whom esophagograms (one single-contrast and three double-contrast studies) revealed giant, HIV-related ulcers indistinguishable from those of cytomegalovirus (CMV) esophagitis. All four patients had severe odynophagia, one had an associated maculopapular rash, and two became HIV-positive at approximately the time of clinical presentation. In all patients, biopsy samples, brushings, and cultures obtained with endoscopy were negative for CMV or herpes simplex. One patient had positive brushings for candidiasis, but this may have resulted from fungal superinfection of the ulcer. Two patients were treated with orally administered steroids, and all four had swift clinical improvement; symptoms disappeared during an average period of 8.3 days from presentation. HIV-related esophageal ulcers should be distinguished from CMV ulcers, so that appropriate treatment can be initiated in these patients.
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PMID:Giant, human immunodeficiency virus-related ulcers in the esophagus. 206 93

Six hemophilia patients previously seronegative for human immunodeficiency virus (HIV) seroconverted between September 1986 and September 1987. None had risk factors for HIV infection other than hemophilia. We compared the factor concentrates received by these patients with the concentrates received by 10 seronegative hemophilia patients. A statistically significant association was observed between seropositivity and the receipt of two lots of Factor VIII produced from the same plasma pool (odds ratio 77, p = 0.0014); five of the six case subjects but none of the control subjects had received concentrate from one of the two lots. Available evidence suggests that the sixth case subject had also received concentrate from an implicated lot. Symptoms including rash and fever were reported in five cases within 6 weeks after the implicated concentrate had been given. The implicated lots were produced from plasma from paid donors that had been screened and then heated at 60 degrees C for 30 hours in the lyophilized state. Subsequent to our investigation all concentrate produced by this process was removed from distribution.
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PMID:HIV transmission to patients with hemophilia by heat-treated, donor-screened factor concentrate. 211 26

We conducted a Phase I open-label trial of 2',3'-dideoxyinosine (ddI) for the treatment of the acquired immunodeficiency syndrome (AIDS) and severe AIDS-related complex. A single daily dose of ddI was administered orally to 34 patients (17 with AIDS and 17 with AIDS-related complex) for a median of 12 weeks (range, 2 to 56). We studied six dose levels from 1.6 to 30.4 mg per kilogram of body weight per day. Of the 17 patients previously treated with zidovudine, 13 had had hematologic side effects. The maximal tolerated dose of oral ddI was estimated to be 20.4 mg per kilogram per day. Pancreatitis and peripheral neuropathy were the major dose-limiting toxic effects. Other toxic effects included elevations in hepatic transaminase levels, abnormalities in cardiac conduction, rash, and asymptomatic elevations in serum urate levels and the creatine kinase fraction from skeletal muscle. Treatment with ddI was associated with an increase in the mean number of CD4 lymphocytes from 125 per cubic millimeter at base line to 182 per cubic millimeter after 10 weeks (P = 0.005). There were also increases after 12 weeks in the mean total lymphocyte count (from 0.8 to 1.2 x 10(9) per liter) and the mean hemoglobin level (from 12.9 to 14.1 g per deciliter) (both P less than 0.01). The amount of human immunodeficiency virus p24 antigen decreased by more than 50 percent in 14 of 19 patients with detectable antigen. No differences in response were observed between patients previously treated with zidovudine and those never treated with the drug. We conclude that ddI has antiretroviral activity in patients with AIDS or AIDS-related complex and that the toxicity of ddI differs from that of zidovudine. However, controlled trials are necessary to evaluate the efficacy of ddI.
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PMID:Once-daily administration of 2',3'-dideoxyinosine (ddI) in patients with the acquired immunodeficiency syndrome or AIDS-related complex. Results of a Phase I trial. 210 98

Fourteen patients with T-cell-derived leukemia and lymphoma underwent high-dose chemoradiotherapy and anti-T-cell monoclonal antibody-treated autologous bone marrow transplantation (ABMT). All patients were either in sensitive relapse or had adverse prognostic features, and five patients had a history of bone marrow involvement with disease. Patients received a median of 2 (1 to 3) prior chemotherapy regimens; 10 patients received local radiotherapy. After high-dose ablative therapy, greater than 500/mm3 granulocytes and greater than 20,000 untransfused platelets/mm3 were noted at a median of 23 (13 to 48) and 26 (15 to 43) days post-ABMT, respectively. Natural killer (NK) cells, T cells (predominantly T8+), and monocytes were noted within the first 1 to 2 months post-AMBT, as seen in other series. Disease-free survival was a median of 10.1 months, 5.9 months for patients with T acute lymphoblastic leukemia or lymphoblastic lymphoma and 25.6 months for patients with T non-Hodgkin's lymphoma (NHL). Toxicities were common and severe. Thirty-six percent of patients developed bacteremias early post-BMT. Late complications included a skin rash consistent with graft versus host disease; infections with Herpes zoster, hepatitis, and Pneumocystis carinii; and the development of Epstein-Barr virus associated lymphoproliferative syndrome. Our findings suggest that patients who have undergone T-depleted ABMT have a profound immunodeficiency not reflected in the phenotypic reconstitution of the T and NK cells. Characterization of the functional deficiency may facilitate the development of methods to reduce the long-term toxicity of AMBT in these patients.
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PMID:T-cell-depleted autologous bone marrow transplantation therapy: analysis of immune deficiency and late complications. 219 91


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