Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection causes disturbances in lipid metabolism that may be mediated by cytokines. Therefore we studied plasma lipids, lipoproteins, triglyceride (TG) metabolism, and serum cytokines in three groups: patients with the acquired immunodeficiency syndrome (AIDS) without active secondary infection, patients with evidence of human immunodeficiency virus infection but without clinical AIDS (HIV+), and controls. Plasma TGs and FFA were increased in AIDS, while plasma cholesterol, high density lipoprotein (HDL) cholesterol, apolipoprotein-A-1 (Apo-A-1), low density lipoprotein (LDL) cholesterol, and Apo-B-100 levels were decreased. Increased TG levels in AIDS were primarily due to increases in very low density lipoprotein of normal composition; in addition, LDL and HDL were TG enriched. In HIV+, TGs and FFA were not increased, but total cholesterol, HDL cholesterol, Apo-A-1, and Apo-B-100 were significantly decreased. Interferon-alpha (IFN alpha) and C-reactive protein levels were increased in AIDS, but tumor necrosis factor and haptoglobin levels were not. There was a significant correlation between plasma TGs and IFN alpha levels (r = 0.477; P less than 0.01), but not between TGs and tumor necrosis factor, C-reactive protein, haptoglobin, or P-24 antigen. In addition, there was no relationship between circulating IFN alpha levels and plasma cholesterol, HDL cholesterol, Apo-A-1, LDL cholesterol, Apo-B-100, or FFA. TG clearance time and postheparin lipase were significantly decreased in AIDS and HIV+. There was a strong correlation between serum IFN alpha levels and TG clearance time in AIDS and HIV+ (r = 0.783; P less than 0.001). In summary, decreases in cholesterol and cholesterol containing lipoproteins (including HDL) in both AIDS and HIV+ precede the appearance of hypertriglyceridemia and are not related to IFN alpha or TG levels. Our data raise the possibility that with development of AIDS, subsequent increases in IFN alpha may contribute to increases in plasma TG levels in part by decreasing the clearance of TG.
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PMID:Lipids, lipoproteins, triglyceride clearance, and cytokines in human immunodeficiency virus infection and the acquired immunodeficiency syndrome. 137 35

A protein profile has been monitored during human immunodeficiency virus (HIV) infection. The investigation concerned 60 patients suffering from acquired immunodeficiency syndrome (AIDS), 24 asymptomatic HIV-antibody seropositive subjects and 22 healthy HIV-antibody seronegative, individuals voluntary blood donors. Data show that retinol-binding protein, thyroxin-binding prealbumin and beta 2-microglobulin are already modified in HIV infection (p less than 0.05) whereas the other protein alteration becomes apparent during AIDS. These studies demonstrate that severe, but progressive malnutrition occurs in patients with AIDS. On the other hand nutritional abnormalities can be shown to have a deleterious effect upon the disease course as revealed by increasing alpha-1-acid glycoprotein and C-reactive protein levels for 60 to 70% of patients.
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PMID:[Inflammatory reaction markers and nutritional markers in HIV infection]. 177 13

The data on the presence of factors blocking the reaction of E-rosette formation and leukocyte chemotaxis in the blood sera of patients with AIDS-related complex (ARC) and HIV-positive donors are presented. Most frequently the blocking of E-rosette formation coincided with the presence of a inhibiting effect on the migration capacity of leukocytes. This blocking activity was not linked with the presence of C-reactive protein in the circulation stream. The treatment of ARC patients with plasmapheresis and/or travolol was accompanied either by the disappearance of blocking activity or by the appearance of activity stimulating E-rosette formation.
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PMID:[Inhibitor factors in the serum of patients with the AIDS-related complex]. 186 28

The acute phase response induced by 19 episodes of Pneumocystis carinii pneumonia (PCP) was analysed in a retrospective study. There were 9 men and 1 woman with HIV, aged 25-45 years (mean 37.2) and 4 men and 4 women with other immunodeficiencies, aged 18-35 years (mean 26.2). The outcome of these two groups with PCP did not differ: in the HIV group 4 died and in the non-HIV group 2 died. In the HIV group, peak serum C-reactive protein (S-CRP) ranged 41-228 mg/l, mean 126 (77.3), and in the non-HIV group 19-290 mg/l, mean 105 (89.1) (NS). The patients with a fatal outcome had higher mean peak S-CRP: 186 (73.8) mg/l versus 85.3 (63.5) mg/l in the survivors (p = 0.007). The HIV infection itself did not increase the S-CRP concentration, which was normal before or after PCP in all 7 survivors of the 11 episodes. Thus, PCP induces a clear-cut S-CRP response, which may be used for monitoring the treatment and evaluating the prognosis of the patient.
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PMID:Acute phase response in Pneumocystis carinii pneumonia. 212 43

Liposomes were prepared from phospholipid formulations recognized or ignored by cells of the reticuloendothelial system (RES+ve or RES-ve, respectively). The ability of these liposomes to interact with CD4+ve cells in purified leukocyte fractions or in whole blood has been determined. RES+ve liposomes bound to monocytes in purified leukocyte fractions or in whole blood, but did not bind to lymphocytes. RES-ve liposomes did not bind to either monocytes or lymphocytes. The attachment of an anti-Leu3A (CD4) monoclonal antibody to the outer surface of RES-ve liposomes resulted in their interaction with both monocytes and lymphocytes. The binding was blocked by prior incubation of the leukocytes with free anti-Leu3A antibody. RES+ve liposomes were rapidly eliminated from the circulation of mice after intravenous injection, whereas RES-ve liposomes remained in the circulation for prolonged periods of time (half-life much greater than 5 h), even after incubation with the opsinizing acute-phase reactant, C-reactive protein. These results suggest that RES-ve liposomes possessing surface-bound anti-Leu3A may provide a means of targeting antiviral agents to those cells at risk from HIV infection.
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PMID:Immunoliposome targeting to CD4+ cells in human blood. 238 76

Hypoalbuminemia is the most powerful predictor of mortality in end-stage renal disease. Since protein-calorie malnutrition can decrease albumin synthesis it is assumed that hypoalbuminemia results principally from malnutrition in these patients, but albumin synthesis may also be decreased as part of the acute-phase response, and hypoalbuminemia can also result from redistribution of albumin pools or from albumin losses. We measured albumin synthesis, fractional catabolic rate, and distribution from the turnover of [125I] human albumin in six hemodialysis patients with plasma albumin less than 35 mg/ml and in six patients with plasma albumin greater than 40 mg/ml. Patients with liver disease, HIV, or other infection were excluded. Both groups were maintained with high-flux polysulfone dialyzers for more than three months. Kt/Vurea and PCR were measured during each dialysis (N = 12 to 18/patient). A four-day calorie and protein intake was determined by dietary history and long-term nutritional status was determined anthropometrically. Measured variables included serum urea, creatinine, transferrin, and the positive acute-phase proteins alpha 2- macroglobulin, C-reactive protein, ferritin, and IGF-1. Albumin synthesis was significantly reduced in the low albumin group. There were no differences in dietary intake, body composition, PCR, BUN, creatinine, or Kt/Vurea. Plasma albumin concentration correlated negatively with ferritin, C-reactive protein and alpha 2-macroglobulin. Albumin synthesis rate correlated negatively with both alpha 2-macroglobulin and Kt/Vurea. Both plasma albumin concentration and synthesis rate correlated positively with IGF-1, and both were independent of PCR and all other nutrition-related variables.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of hypoalbuminemia in hemodialysis patients. 756 20

Between June 1986 and October 1992, disseminated toxoplasmosis was diagnosed in 16 AIDS patients. 13 cases were diagnosed at autopsy where multiple organ involvement was documented in all 13. Three patients were diagnosed intra vitam. All 3 survived with appropriate treatment. Clinical features indicative of disseminated toxoplasmosis were: fever of unknown origin between 39 degrees and 40 degrees C in 16 cases, clinical signs suggestive of sepsis or septic shock in 15, with progression to multiorgan failure in 10, disseminated intravascular coagulopathy in 6, confusion, disorientation or apathy in 13 and lack of a systemic pneumocystis carinii prophylaxis in all 16. Typical laboratory markers were: CD4 cell counts below 100 x 10(6)/l in 16 cases, elevation of serum lactic dehydrogenase in 16 and creatine phosphokinase (in 4/6), normal or only slightly elevated C-reactive protein (in 9/11), positive Toxoplasma gondii IgG antibodies in 15/16 and negative IgM antibodies in all 16. Lesions indicative of cerebral toxoplasmosis were visualized on cranial computerized tomography in only 3/10 evaluated patients. In patients with advanced HIV infection presenting with a systemic illness, including the clinical and laboratory features described above, systemic Toxoplasma gondii infection must be included in the differential diagnosis. In these patients, specific and if warranted, invasive diagnostic procedures followed by early vigorous therapeutic intervention should be considered.
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PMID:Disseminated toxoplasmosis in AIDS patients--report of 16 cases. 778 18

The membrane-bound glycoprotein intercellular adhesion molecule 1 (ICAM-1) plays an important role for many cell-contact-dependent immune functions. A soluble, circulating form of ICAM-1 (cICAM-1) has been detected in the serum of healthy persons and increased concentrations in tumor patients have been reported. We measured serum levels of cICAM-1 in HIV-1-infected individuals with a recently developed ELISA. In contrast to HIV-seronegative controls (median value of 294 ng/ml, range of 185-408 ng/ml; n = 22), significantly elevated concentrations were detected in 76 HIV-1-infected persons (median of 487 ng/ml, range of 231-1,524 ng/ml; p < 0.0001). In HIV-1-infected individuals, cICAM-1 values did not correlate with the absolute number of CD4+ T cells or with disease progression according to the Walter Reed staging classification. Concentrations of cICAM-1 correlated with the serum concentrations of IL-6 (p = 0.0015; Spearman's rank correlation analysis) and with urinary neopterin (p = 0.005), but not with the C-reactive protein. Since there is evidence that cICAM-1 can interfere with immunological functions, the high amounts circulating in HIV-1-positive individuals could contribute to the disturbance of the immune system in HIV-1 infection.
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PMID:Elevated concentrations of circulating intercellular adhesion molecule 1 (ICAM-1) in HIV-1 infection. 809 41

A case report of a 28-year-old mother of two children with FUO is presented. Physical examination revealed an anemic and febrile woman, who lost 10 kg of weight during the past 3 months. Furthermore, two lymphatic nodes with diameters below 1 cm were detected at the neck and inguinal region. A search for origin of fever including evaluation of foci, malignancies and laboratory investigations was primarily unsuccessful. At day 7 after admission a pericardial murmur could be heard. Echocardiography revealed a pericardial effusion, which increased up to 4 cm during the following days, leading to hemodynamic impairment and asystole. Immediate CR was successful, pericardial effusion was aspirated. Looking for etiology of fever the presence of IgM-antibodies against toxoplasma gondii by an ELISA test was possible. Therefore, toxoplasmosis was diagnosed and a treatment-regimen comprising pyrimethamin and sulfadiazin was initiated. Because of the threat to life and very high titers of C-reactive protein, antibiotic therapy (imipenem) was given additionally. An immunologic impairment was excluded by normal ratio of CD4:CD8 of lymphocytes, normal HIV-test and a nonsuspicious Jamshidi-biopsy of the bone marrow. However, in week 9 after admission lymphatic node-tumors suddenly appeared at the neck and pulmonary hilus. After diagnostic exstirpation a malignant non-Hodgkin-lymphoma (T-cell-type) was diagnosed. It is concluded that in obscure pericardial effusion toxoplasmosis should be considered and that this manifestation may be a precursor of malignant non-Hodgkin-lymphoma.
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PMID:[Toxoplasmosis peri-myocarditis as initial manifestation of highly malignant non-Hodgkin's lymphoma]. 817 47

The acute phase C-reactive protein (CRP) was measured in serum of HIV-infected patients suffering from Pneumocystis carinii pneumonia (PCP) (32 patients), bacterial pneumonia (10 patients), and in 19 immunocompetent patients with bacterial pneumonia. The HIV-infected patients with bacterial pneumonia had a significantly lower CRP level than the immunocompetent patients (50% versus 95% had an s-CRP level > 80 mg/l). No significant difference was found in the CRP response to P. carinii or bacteria in HIV-infected patients with pneumonia due to these microorganisms (20% versus 50% had s-CRP > 80 mg/l). In the group of PCP patients, a significantly lower CRP level was found in those with CD4 positive lymphocyte counts below 50 x 10(6)/l. There was no correlation between the CRP response and the severity of the PCP as estimated by the degree of hypoxia. We conclude that the CRP level cannot be used to discriminate between PCP and bacterial pneumonia in HIV-infected patients.
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PMID:The C-reactive protein responses in HIV-infected patients with pneumonia. 836 26


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