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)

Visceral leishmaniasis is an endemic infection in Mediterranean countries, where it has become a frequent complication of acquired immunodeficiency syndrome (AIDS). The incidence of visceral leishmaniasis is increasing in Spain due to human immunodeficiency virus (HIV)-related cases, but some aspects of its epidemiology, clinical features, and management remain unknown. In addition, no comparative clinical studies about the disease in HIV-infected and non-HIV-infected patients have been reported. During a 24-year period, 120 cases of visceral leishmaniasis were diagnosed at our institution and 80 (66%) were associated with HIV infection. The mean age at diagnosis was higher in HIV-infected that in non-HIV-infected patients (33.2 versus 23.2 yr; p = 0.002), but the male/female ratio was similar in both groups. The main risk factor for HIV infection was intravenous drug abuse (78.7%). The clinical presentation of leishmaniasis was similar in both groups, but HIV-infected patients had a lower frequency of splenomegaly than HIV-negative individuals (80.8% versus 97.4%; p = 0.02). HIV-infected patients had a greater frequency and degree of leukopenia, lymphocytopenia, and thrombocytopenia. Most of them were profoundly immunosuppressed (mean CD4+ lymphocyte count, 90 cells/mm3) at the time of diagnosis of leishmaniasis, and 53.7% had AIDS. The sensitivity of serologic studies for Leishmania was significantly lower in HIV-infected than in non-HIV-infected patients (50% versus 80%; p < 0.001), but the diagnostic yield of bone marrow aspirate (67.1% versus 79.4%) and bone marrow culture (62.9% versus 66.6%) was similar in both groups. After initial treatment, the response rate was significantly lower in HIV-infected than in non-HIV-infected individuals (54.8% versus 89.7%; p = 0.001). The relapse rate was 46.2% and 7.5%, respectively (p < 0.001). Secondary prophylaxis with antimonial compounds or amphotericin B seems to be useful in preventing relapses in HIV-infected patients. The mortality rate was higher (53.7% versus 7.5%; p < 0.001) and the median survival time shorter (25 versus > 160 mo; p < 0.001) in AIDS patients than in HIV-negative individuals. Although leishmaniasis could contribute to death in a significant number of HIV-infected patients, it was the main cause of death in only a few of them. The CD4+ lymphocyte count and the use of highly active antiretroviral therapy and secondary prophylaxis for leishmaniasis were the most significant prognostic factors for survival in AIDS patients. Visceral leishmaniasis behaves as an opportunistic infection in HIV-infected individuals and should be considered as an AIDS-defining disease.
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PMID:Visceral leishmaniasis in human immunodeficiency virus (HIV)-infected and non-HIV-infected patients. A comparative study. 1120 3

Early after seroconversion, macrophage-tropic human immunodeficiency virus type 1 (HIV-1) variants are predominantly found, even when a mixture of macrophage-tropic and non-macrophage-tropic variants was transmitted. For virus contracted by sexual transmission, this is presently explained by selection at the port of entry, where macrophages are infected and T cells are relatively rare. Here we explore an additional mechanism to explain the selection of macrophage-tropic variants in cases where the mucosa is bypassed during transmission, such as blood transfusion, needle-stick accidents, or intravenous drug abuse. With molecularly cloned primary isolates of HIV-1 in irradiated mice that had been reconstituted with a high dose of human peripheral blood mononuclear cells, we found that a macrophage-tropic HIV-1 clone escaped more efficiently from specific cytotoxic T-lymphocyte (CTL) pressure than its non-macrophage-tropic counterpart. We propose that CTLs favor the selective outgrowth of macrophage-tropic HIV-1 variants because infected macrophages are less susceptible to CTL activity than infected T cells.
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PMID:Macrophage tropism of human immunodeficiency virus type 1 facilitates in vivo escape from cytotoxic T-lymphocyte pressure. 1122 94

According to federal estimates, at least 500,000 of the 1 million Americans currently infected with the human immunodeficiency virus (HIV) are likely to develop acquired immunodeficiency syndrome (AIDS) by the year 2000. In Maryland, where 866 AIDS cases have been reported to date, at least 25,000 state residents are expected to develop AIDS by the year 2000. A disproportionate number of AIDS cases occur in the black population due to higher rates of intravenous drug abuse. Of those seeking an AIDS antibody test at Maryland's health department facilities, 24% of blacks compared with 7% of whites have tested positive for the HIV virus. Even among drug addicts, blacks appear to be more affected by the AIDS epidemic, presumably because of greater use of needle sharing. A 1966 Baltimore study found that 45% of black addicts compared with 9% of white addicts were infected with HIV. Over the next 10 years, an average of 6 persons is expected to die each day from AIDS in Maryland. Baltimore public health officials are expecting an explosion of AIDS cases in the years ahead among gay men, drug users, their sex partners, and their infants. The threat of AIDS is most appreciated by middle class suburban singles and college students, who are at a lower risk of contracting the disease. On the other hand, blacks and Hispanics in the inner city appear not to fully appreciate the threat of AIDS and have been less responsive to educational efforts.
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PMID:Truth about AIDS reaching those who least need it. 1228 13

Idiopathic collapsing glomerulopathy is an aggressive variant of focal segmental glomerulosclerosis (FSGS) seen primarily in adults. Its etiology is unknown. Nearly identical pathology is seen in association with nephrotic syndrome in human immunodeficiency virus type 1 (HIV-1)-infected patients, raising the possibility that viral infection plays a role in pathogenesis. This is supported by the recent discovery of parvovirus B19 DNA in some cases of idiopathic collapsing glomerulopathy. We report a case of collapsing glomerulopathy in a 16-year-old girl who presented with steroid-resistant nephrotic syndrome and pulmonary tuberculosis. In the absence of the usual associations (adult age group, African-American race, or history of intravenous drug abuse), infection is the sole known risk factor in this case. This lends support to the hypothesis that immune dysregulation due to infection per se, rather than infection by specific viral agents, may lead to collapsing glomerulopathy in susceptible individuals.
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PMID:Collapsing glomerulopathy in a 16-year-old girl with pulmonary tuberculosis: the role of systemic inflammatory mediators. 1517 56

In addition to its role in mineral metabolism, 1,25-dihydroxivitamin D3 (1,25(OH)2D3) also has immunomodulatory effects. Vitamin D receptor (VDR) mediates genomic actions of 1,25(OH)2D3, by acting as a transcription factor that modulates the expression of several 1,25(OH)2D3 response genes. Variations at the VDR locus have been associated with susceptibility and progression to several immune diseases. We investigated the association between rates of progression to acquired immunodeficiency syndrome (AIDS) and the Fok-I polymorphism, which is located at the initiation codon of the VDR gene. The study was performed with a cohort of 185 patients infected with human immunodeficiency virus type 1 (HIV-1): all belonged to the intravenous drug abuse risk group. Progression to AIDS was according to the Centers for Disease Control 1993 criterion (CDC-1993). In addition, a first drop in CD4 cell count to below 200 microL(-1) was considered as outcome. Patients who reached outcomes during follow-up were considered progressors. Non-progressors were those patients remaining outcome-free after a minimum follow-up of 8 years. Heterozygous at the Fok-I polymorphism were over-represented in the group of patients that progressed to AIDS CDC-1993 (50% of progressors versus 36% of non-progressors, P=0.061; risk ratio (RR)=1.38 (95% confidence interval (CI): 0.98-1.96)) and in the group of patients that showed a drop in CD4 cell count to below 200 microL(-1) (52% of progressors versus 36% of non-progressors, P=0.037; RR=1.44 (95% CI: 1.02-2.03)). Mean time to AIDS CDC-1993 was shorter for those with Ff genotype than for those with FF and ff genotypes (non-Ff genotype patients), (log rank test P=0.035; Cox hazard ratio (HR) for Ff versus non-Ff=1.53 (95% CI: 1.0-2.33), P=0.047). In addition the drop in CD4 cell count to below 200 microL(-1) was reached faster in Ff carriers than in non-Ff patients (log rank test P=0.015; HR for Ff versus non-Ff=1.77 (95% CI: 1.12-2.8), P=0.014). According to these results, HIV-1 seropositive patients carrying the Ff genotype could be considered prone to a faster progression to AIDS.
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PMID:Association between AIDS disease progression rates and the Fok-I polymorphism of the VDR gene in a cohort of HIV-1 seropositive patients. 1522 72

Peliosis is a pathological entity characterized by the gross appearance of multiple cyst-like, blood-filled cavities within parenchymatous organs. Peliosis has been related to several underlying debilitating illnesses such as tuberculosis, hematological malignancies, the acquired immunodeficiency syndrome (AIDS), and post-transplant immunodeficiency, as well as intravenous drug abuse, chronic alcoholism, and in conjunction with the intake of oral contraceptives or steroids. The classical pathoanatomical concept is based upon the opinion that peliosis exclusively develops in organs belonging to the mononuclear phagocytic system (liver, spleen, bone marrow, and lymph nodes). However, a paucity of studies indicates that other organs such as lungs, parathyroid glands, and kidneys may be affected too. Concerning the underlying pathogenetic mechanisms of onset and maintenance of peliosis, the morphological data obtained by different investigators suggest that there is more than one path of formal pathogenesis (e.g., congenital malformation of vessels manifesting under altered local intravascular pressure conditions, acquired vascular disorder triggered by toxic noxae, active proliferation of vessels corresponding to the benign end on the spectrum of neoplastic vascular lesions). In the liver, at gross inspection, the peliotic lesions give the cut sections a "swiss cheese" appearance. Microscopically, two different types of peliosis can be distinguished in the liver: (1) "parenchymal peliosis" consisting of irregular cavities that are neither lined by sinusoidal cells nor by fibrous tissue, and (2) "phlebectatic peliosis" characterized by regular, spherical cavities lined by endothelium and/or fibrosis. One of the differential diagnoses that most closely resembles peliosis hepatis is secondary hepatic congestion due to veno-occlusive disease or the Budd-Chiari syndrome. In the spleen, the peliotic lesions may be arranged sporadically, disseminated, or in clusters in an uneven distribution pattern. Histologically, the cavities show frequently well-demarcated margins that may appear focally lined by sinusoidal endothelium, or totally lack a clear cell lining. Differential diagnoses are hemangiomas and involvement of the spleen in hairy-cell leukaemia. Since the disease may culminate in spontaneous rupture of the affected organ and thus may mimic a violent death at autopsy, peliosis is far more than just another morphological curiosity. Awareness of peliosis at autopsy as well as an appreciation for the histopathological changes in less characteristic or advanced cases may become an important issue for both the forensic and clinical pathologist.
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PMID:Pathology of peliosis. 1573 6

Cholestasis in a patient with Hodgkin's disease is uncommon, and the causes of cholestasis are mainly direct tumor involvement of the liver, hepatotoxic effects of drugs, viral hepatitis, sepsis and opportunistic infections. Vanishing bile duct syndrome (VBDS) represents a very rare cause for cholestasis in this disease. We report here on a case of a 45-year-old man who developed VBDS during the complete remission stage of Hodgkin's lymphoma. There was no history of hepatitis or intravenous drug abuse, and the patient had negative results for hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. The serological studies for antinuclear antibodies, anti-mitochondrial antibodies and anti-smooth muscle antibodies were also negative. Liver biopsy disclosed the absence of interlobular bile ducts in 9 of 10 portal tracts without any active lymphocyte infiltration and there were no Reed-Sternberg cell in the liver. The patient's cholestasis was in remission and the serum bililrubin level was normalized after two months without treatment, but tumor recurrence was noted at multiple sites of the abdominal lymph nodes on follow-up abdomino-pelvic computed tomogram.
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PMID:[Spontaneous resolution of vanishing bile duct syndrome in Hodgkin's lymphoma]. 1598 Jun 75

The paper covers an investigation of 150 patients with infective endocarditis (IE), including 100 patients (aged 18 to 30 years old) with intravenous drug abuse as the main risk factor. This subgroup is characterized by an acute clinical course of IE, with tricuspid valve disorder in most cases and septic pulmonary embolism relapse in 72% of cases. Heart failure, multiple cardiac valvular disorder and focal lung destruction were found to be the main factors of unfavorable outcome. A relation between the size of vegetation on the heart valves and the mortality rate was established. At the same time, secondary immunodeficiency due to HIV-infection had no significant effect on the mortality rate in the group of drug addicts. More frequent cases of heart failure with systemic circulation embolism lead to higher hospital mortality in the group of patients with a subacute clinical course of IE. In elderly patients other concomitant pathology resulted in late IE detection and a high mortality rate.
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PMID:[Infective endocarditis: the features of its clinical course and the prognosis]. 1598 78

A 44-year-old diabetic man with isolated septic arthritis of the left acromioclavicular joint (A-C) caused by Staphylococcus aureus is described. He was admitted to the Department of Rheumatology with clinical symptoms of left shoulder arthritis and fever. Laboratory findings showed leukocytosis, elevated levels of erythrocyte sedimentation rate and C-reactive protein, all indicating septic arthritis. Blood culture was positive for Staphylococcus aureus. Left A-C joint x-ray and ultrasonography, and whole body scintigraphy with 99 mTc radiolabeled autologous leukocytes pointed to septic arthritis of the A-C joint. The patient was treated for six weeks with antibiotics successfully. Infection of the A-C joint is uncommon, even in conditions such as immunodeficiency, renal dialysis and intravenous drug abuse which are associated with unusual joint infections, and can be differentiated from shoulder joint infection, by maximal tenderness over the A-C joint on examination, and findings of A-C joint widening, effusion, and bony erosions on imaging studies.
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PMID:Septic acromioclavicular arthritis in a patient with diabetes mellitus. 1641 93

Human immunodeficiency virus (HIV) infection continues to rise in drug-abusing populations and causes a dementing illness in a subset of individuals. Factors contributing to the development of dementia in this population remain unknown. We found that HIV-infected individuals with the E4 allele of Apolipoprotein E (ApoE) or history of intravenous drug abuse had increased oxidative stress in the CNS. In vitro studies showed that HIV proteins, gp120 and Tat, Tat + morphine but not tumor necrosis factor-alpha (TNF-alpha), caused increased neurotoxicity in human neuronal cultures with ApoE4 allele. Microarray analysis showed a differential alteration of transcripts involved in energy metabolism in cultures of ApoE3 and 4 neurons upon treatment with Tat + morphine. This was confirmed using assays of mitochondrial function and exposure of the neurons to Tat + morphine. Using this in vitro model, we screened a number of novel antioxidants and found that only L-deprenyl and diosgenin protected against the neurotoxicity of Tat + morphine. Furthermore, Tat-induced oxidative stress impaired morphine metabolism which could also be prevented by diosgenin. In conclusion, opiate abusers with HIV infection and the ApoE4 allele may be at increased risk of developing dementia. L-deprenyl and a plant estrogen, diosgenin, may have therapeutic potential in this population.
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PMID:Increased vulnerability of ApoE4 neurons to HIV proteins and opiates: protection by diosgenin and L-deprenyl. 1669 50


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