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 paper is concerned with a study of a response of lymphocytic Fc receptors (FcR) to modulators regulating their expression (prostaglandins E2 and F2, 2 X 10(-9) M, isoproterenol 10(-5), 10(-6) M) as compared to changes in the lymphocyte membrane lipid composition of patients with obesity of II-III degree with a high blood cholesterol level up to 9-10 nmol/l. Two groups were distinguished among obese patients: "areactive" in which lymphocytic FcR did not respond to modulators, and "reactive" in which FcR responded at least to one of 4 utilized modulators. Research into the lipid spectrum of lymphocytic membranes revealed a significant decrease in the concentration of nonesterified fatty acids in membranes of "areactive" lymphocytes to 4 +/- 0.6% (against the normal level of 8.9 +/- 0.7%). In order to make up completely for immunodeficiency in obesity, lipotropic agents and food rich in polyunsaturated fatty acids could be recommended.
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PMID:[Changes in the lipid composition of the lymphocyte membranes and in the reactions of the lymphocytic Fc receptors in obesity]. 208 64

It has been shown that prolonged use of plasmapheresis with a 7-day interval in patients with hereditary hypercholesterolemia is potentially dangerous because of possible development of immunodeficiency. LDL plasmasorption and immunosorption produce a beneficial effect on the concentration of immunoglobulins. It is assumed that immunosorption permits the elimination not only of lipoproteins but also lipoprotein-containing immune complexes from the blood channel.
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PMID:[The effect of plasmapheresis and the plasmasorption and immunosorption of low-density lipoproteins on the humoral immunity function of patients with hereditary hypercholesterolemia]. 233 15

Previous studies have indicated that human immunodeficiency virus (HIV) is enclosed with a lipid envelope similar in composition to cell plasma membranes and to other viruses. Further, the fluidity, as measured by spin resonance spectroscopy, is low and the viral envelope is among the most highly ordered membranes analyzed. However, the relationship between viral envelope lipids and those of the host cell is not known. Here we demonstrate that the phospholipids within the envelopes of HIV-1RF and HIV-2-L are similar to each other but significantly different from their respective host cell surface membranes. Further, we demonstrate that the cholesterol-to-phospholipid molar ratio of the viral envelope is approximately 2.5 times that of the host cell surface membranes. Consistent with the elevated cholesterol-to-phospholipid molar ratio, the viral envelopes of HIV-1RF and HIV-2-L were shown to be 7.5% and 10.5% more ordered than the plasma membranes of their respective host cells. These data demonstrate that HIV-1 and HIV-2-L select specific lipid domains within the surface membrane of their host cells through which to emerge during viral maturation.
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PMID:Lipid composition and fluidity of the human immunodeficiency virus envelope and host cell plasma membranes. 838 72

The triad of human immunodeficiency virus (HIV) infection, nutritional status and immune function are intimately related, each factor having effects on the others. The dominant effect in this three-way relationship is the effect of HIV infection on nutritional status, an effect which, until the advent of potent anti-retroviral drugs, has been manifest primarily as wasting. Recently, more complex metabolic abnormalities have become apparent, particularly fat redistribution syndromes, hyperlipidaemia and hypercholesterolaemia. For the converse effect, the effect of nutritional state on HIV disease progression, there is good evidence that clinical outcome is poorer in individuals with compromised nutrition. However, the beneficial effects of nutritional support have been more difficult to demonstrate. For macronutrients, effective macronutrient supply improves survival in severely-malnourished individuals and may have beneficial effects in less-severely-affected individuals. Micronutrient deficiencies appear to be involved in modifying clinical HIV disease and may also be associated with enhanced mother-to-child transmission of virus, particularly in developing countries. Intervention trials in this setting are currently under way. In conclusion, the interaction of HIV infection and nutrition is of great importance not just because of the major impact that HIV infection has on nutritional state, but also because strategies to improve nutritional status, both quantitatively and qualitatively, may have a beneficial effect on the clinical and immunological course of the disease.
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PMID:Nutrition and immune function in human immunodeficiency virus infection. 1060 11

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

Human immunodeficiency virus (HIV) protease inhibitors are associated with several metabolic abnormalities including hypercholesterolemia and hypertriglyceridemia. Fenofibrate is a new lipid-lowering agent for adults with very high triglyceride levels that was administered to two HIV-positive patients who were taking protease inhibitors and developed hypertriglyceridemia. Starting dosages were 134 and 201 mg/day, and were increased to 268 mg/day in both patients. Triglyceride levels decreased from 1450 to 337 mg/dl (76.8%) and from 1985 to 322 mg/dl (83.8%), respectively, after 10 months of therapy. High-density lipoprotein levels increased in both patients.
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PMID:Use of fenofibrate in the management of protease inhibitor-associated lipid abnormalities. 1085 29

Recent reports of myocardial infarctions in young persons infected with human immunodeficiency virus (HIV) who are receiving protease inhibitor therapy have raised concerns about premature coronary artery disease in this population. Endothelial dysfunction, hypercoagulability, hypertriglyceridemia, and abnormal coronary artery pathology were in fact associated with HIV infection prior to the availability of protease inhibitor therapy. Newly recognized risk factors, such as insulin resistance, hypercholesterolemia, and fat redistribution syndrome, may exacerbate underlying atherosclerotic risk for patients receiving protease inhibitors. Data on the incidence of myocardial infarction among these patients are largely limited to case reports but are of concern. Pending the availability of further data, it is prudent to monitor these patients for hyperlipidemia and consider interventions to modify cardiac risk factors.
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PMID:Coronary artery disease and human immunodeficiency virus infection. 1101 31

We prospectively followed 20 consecutive patients with human immunodeficiency virus type 1 (HIV-1) with viral loads of <200 RNA copies/mL. These patients had been treated with 2 nucleoside reverse transcriptase inhibitors and > or =1 HIV-1 protease inhibitor for > or =3 months; they developed body changes consistent with lipodystrophy and requested they be switched from protease inhibitor to efavirenz. At baseline and every 3 months, we assessed the following: body mass index, waist-to-hip ratio, regional fat thickness (assessed by sonography), fasting total and high-density lipoprotein cholesterol, triglycerides, glucose, insulin, CD4(+) cells, and viral load. At baseline, hypertriglyceridemia (> or =200 mg/dL) was present in 17 (85%) patients, hypercholesterolemia (> or =200 mg/dL) in 14 (70%), and impaired fasting glucose (> or =110 mg/dL) in 8 (40%); CD4(+) T cells were 280x10(6) cells/L (range, 64-942x10(6) cells/L). HIV-1 RNA had been at <200 copies/mL for a median of 14 months (range, 3-24 months). Six months after switching to efavirenz, there was a reduction in triglyceride levels (a decrease of 31%; P=.03) and fasting insulin resistance index (a decrease of 28%; P=.03), but total and high-density lipoprotein cholesterol and glucose did not change. Waist-to-hip ratio decreased from 0.92 to 0.87 (P=.06). Subcutaneous fat thickness did not change. CD4(+) cells remained stable (363x10(6) cells/L; range, 102-741x10(6) cells/L; P=.65). Nineteen patients (95%) had HIV-1 RNA levels that remained at <200 copies/mL. Although CD4(+) response and viral suppression remained preserved after 6 months of switching from protease inhibitor to efavirenz, the benefits of this approach on the evolution of lipodystrophy were limited, and our findings do not support its routine recommendation to treat lipodystrophy.
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PMID:Impact of switching from human immunodeficiency virus type 1 protease inhibitors to efavirenz in successfully treated adults with lipodystrophy. 1107 62

We report a case of hypercholesterolemia that occurred 2 weeks after the start of highly active antiretroviral therapy following a needlestick exposure to human immunodeficiency virus (HIV) in an HIV-negative health care worker who was receiving thyroid replacement therapy. The elevated thyrotropic hormone level and hypercholesterolemia resolved after the antiretroviral therapy was stopped.
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PMID:Hypercholesterolemia in a health care worker receiving thyroxine after postexposure prophylaxis for human immunodeficiency virus infection. 1134 May 37

Four cases of human immunodeficiency virus (HIV)-infected patients who developed coronary heart disease (CHD) while under treatment with a protease inhibitor (PI) are described, and the epidemiologic and clinical features of 18 cases reported in the literature are analyzed. Cardiac manifestations mostly included myocardial infarctions. Smoking and hyperlipidemia were the most common risk factors for CHD, reported in 72 and 81% of the patients, respectively. Hypercholesterolemia was observed in 75% of the cases at the time of the cardiovascular event. Ninety percent of the patients with pretreatment normal lipid values experienced a rise in the plasma lipid levels during PI therapy. Although a definite relationship between the development of CHD and HIV PIs can not be made, this analysis suggests that PI-induced hyperlipidemia may play a role in accelerating coronary atherosclerosis in patients with concomitant risk factors. Evaluation and control of risk factors for CHD should be performed in each patient for whom treatment with a PI is indicated.
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PMID:Coronary heart disease associated with the use of human immunodeficiency virus (HIV)-1 protease inhibitors: report of four cases and review. 1159 16


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