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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess a possible association between antiretroviral treatment and paronychia, we conducted a retrospective cohort study of 288 human immunodeficiency virus-positive protease inhibitor recipients. Indinavir treatment-adjusted for age, sex, CD4 count, diabetes status and other antiretroviral drug exposures-was significantly associated with paronychia of the great toe (hazard ratio 4.7; 95% confidence interval 1.6-13.9).
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PMID:Paronychia in association with indinavir treatment. 1111 93

Cardiovascular disease (CVD) risk associated with fat redistribution seen among HIV-infected individuals remains unknown, but may be increased due to hyperlipidemia, hyperinsulinemia, increased visceral adiposity, and a prothrombotic state associated with these metabolic abnormalities. In this study we characterized plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (tPA) antigen levels, markers of fibrinolysis and increased CVD risk, in HIV lipodystrophic patients compared to controls. Furthermore, we investigated the effect of treatment with metformin on PAI-1 and tPA antigen levels in patients with HIV-associated fat redistribution. Eighty-six patients (age 43 +/- 1 yr, BMI 26.1 +/- 0.5 kg/m(2)) with HIV and fat redistribution were compared to 258 age- and BMI-matched subjects from the Framingham Offspring study. In addition, 25 HIV-infected patients with fat redistribution and fasting insulin >15 microU/mL [104 pmol/L] or impaired glucose tolerance, but without diabetes mellitus were enrolled in a placebo-controlled treatment study of metformin 500 mg twice daily. PAI-1 and tPA antigen levels were significantly increased in patients with HIV related fat redistribution compared to Framingham control subjects (46.1 +/- 4 vs 18.9 +/- 0.9 microg/L PAI-1, 16.6 +/- 0.8 vs. 8.0 +/- 0.3 microg/L tPA, P = 0.0001). Among patients with HIV infection, a multivariate regression analysis including age, sex, waist-to-hip ratio, BMI, smoking status, protease inhibitor use and insulin area under the curve (AUC), found gender and insulin AUC were significant predictors of tPA antigen. Twelve weeks of metformin treatment resulted in decreased tPA antigen levels (-1.9 +/- 1.4 vs +1.4 +/- 1.0 microg/L in the placebo-treated group P = 0.02). Similarly, metformin resulted in improvement in PAI-1 levels (-8.7 +/- 2.3 vs +1.7 +/- 2.9 microg/L, P = 0.03). Change in insulin AUC correlated significantly with change in tPA antigen (r = 0.43, P = 0.03). PAI-1 and tPA antigen, markers of impaired fibrinolysis and increased CVD risk, are increased in association with hyperinsulinemia in patients with HIV and fat redistribution. Metformin reduces PAI-1 and tPA antigen concentrations in these patients and may ultimately improve associated CVD risk.
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PMID:Increased PAI-1 and tPA antigen levels are reduced with metformin therapy in HIV-infected patients with fat redistribution and insulin resistance. 1115 71

This study investigated the usefulness of a new platelet aggregometer with a laser-scattering method for detection of heparin-induced small platelet aggregates in chronic hemodialysis patients. Using this device, small platelet aggregates (particle size 9--25 microm) were detectable, but these aggregates could not be detected using a conventional light transmittance aggregometer. The laser-scattering intensity of the small aggregates was increased with an increasing dosage of heparin as agonist. These aggregates were disaggregated by heparin neutralization with protamine sulfate. Induction of small platelet aggregates by heparin was inhibited by preincubation with nafamostat mesilate, a synthetic protease inhibitor, and cilostazol, a platelet phosphodiesterase inhibitor, but not by the therapeutic doses of aspirin or argatroban, a selective thrombin inhibitor. The dialysis patients with long-term heparin use could be divided into two groups: responders to heparin, who formed small aggregates with a scattering intensity over 0.51 x 10(5) V after addition of 0.5 IU/ml of heparin obtained from normal platelet-rich plasma without inductor, and nonresponders, who showed an intensity under 0.51 x 10(5) V. The rate of heparin responders among dialysis patients was significantly higher than the rate among normal subjects. Heparin-induced small aggregates were detected in 13 (36.1%) of 36 normal subjects with no history of heparin infusion and in 37 (62.7%) of 59 dialysis patients who received heparin anticoagulation during each dialysis session. Dialysis patients with coronary heart disease did not have a significantly higher rate of heparin responders than patients without complications. There was no significant difference in the positivity rate between cases complicated by diabetes and those without diabetes. In patients who had more than 2 episodes of thrombotic occlusions of an arteriovenous fistula, the rate of responders and the enhancement of scattering intensity of small aggregates by heparin were significantly increased compared with these in patients without occlusions during the preceding 2 years. Moreover, dialysis patients with a positive heparin response showed a marked increase in scattering intensity of small aggregates after heparin infusion in each dialysis session. Determination of the response to heparin prior to heparin use in dialysis patients with repeated thromboembolic complication may be useful in choosing anticoagulant regimens.
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PMID:Characteristics of heparin-induced platelet aggregates in chronic hemodialysis with long-term heparin use. 1125 32

The Food and Drug Administration (FDA) is warning AIDS physicians that there may be a slight risk of developing diabetes and hyperglycemia among patients receiving protease inhibitor therapy. The attack rate appears to be less than one percent and the FDA is not suggesting discontinuing using protease inhibitors. The text from the FDA Talk Paper describing the diabetes mellitus or hyperglycemia occurrences is included.
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PMID:Protease inhibitors: FDA warns doctors of diabetes risk. Food and Drug Administration. 1136

People who are using protease inhibitor therapies and are at risk for diabetes may develop hyperglycemia. All of the approved protease inhibitors have been implicated; however, discontinuation of the treatment has resolved the hyperglycemia. The role of protease inhibitors in hyperglycemia remains unclear, although the causes may include a patient's underlying risks and more frequent testing of a new drug. Frequent urination, thirst, and fatigue are among the symptoms that patients should report to their doctor and the Food and Drug Administration (FDA).
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PMID:Protease inhibitors and diabetes: a growing problem. 1136 47

Patients taking protease inhibitors are beginning to report a number of strange side effects that may be associated with the drugs, although that has not been conclusively proven. Side effects include new or exacerbated cases of diabetes or hyperglycemia, hemolytic anemia, spontaneous bleeding in hemophiliac patients, and changes in body composition. The first unusual symptoms were fatty deposits in the abdomen (Crix belly) and back (Buffalo humps), with wasting symptoms in the upper body. No hard data indicates that these symptoms are directly connected to protease inhibitor use. About 70 percent of all patients on protease inhibitors take Crixivan (indinavir). An Internet discussion group for patients to compare experiences with the drug is available.
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PMID:Protease inhibitor side effects take people by surprise. 1136 85

Reports of metabolic disorders, such as diabetes mellitus and hyperlipidemia, occurring during treatment with protease inhibitor (PI) regimens are prompting patients and providers to try to better understand the links between these disorders and antiretroviral treatments. The Food and Drug Administration (FDA) first reported PI-associated diabetes in June 1997. Diabetes mellitus can be managed by controlling diet and exercise, or by supplementing treatment with oral hypoglycemic drugs. Hypertriglyceridemia has also been associated with PI therapies, and is apparent even in patients experiencing good results from antiretroviral therapy. Treatment for hypertriglyceridemia encompasses monitoring diet and exercise, limiting alcohol, watching hypertension, and quitting smoking. Patients at higher risk for pancreatitis can consider using lipid-lowering drugs and fibric acid derivatives. Alterations in fat distribution have also been linked to PI use, particularly in the back of the neck and upper back, and abdominal area. Researchers have seen evidence of anomalous fat distribution in some patients prior to PI treatment. Management has not consistently been remedied by diet and exercise. Sustaining overall health, reducing blood lipids, and controlling risk factors for cardiovascular disease need to be implemented. Unless the abnormalities are severe and potentially harmful to the patient, it is not commonly recommended to change the PI treatment.
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PMID:Metabolic complications of antiretroviral therapies. 1136 97

Lipodystrophy has been reported by some as one of the side effects of protease inhibitor therapy. However, evidence of lipodystrophy occurring prior to protease therapy supports the premise that this phenomenon has unknown origins. Characteristics of this disorder are the redistribution of fat to unusual places in the body, such as under abdominal muscles or at the base of the neck. Theories are proposed to explain the causes of lipodystrophy, and some of the possible treatments are discussed. Other side effects of protease inhibitor therapy that have been observed are changes in triglycerides, higher cholesterol, diabetes, and high blood pressure. All of these have the potential to lead to heart disease.
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PMID:Therapy side effects update. 1136 37

Reports of success with protease inhibitor-based HAART are appearing at the same time as reports of puzzling metabolic effects. These effects include loss of peripheral subcutaneous fat, truncal obesity, hyperlipidemia, and frank diabetes. There is no consensus on how often these problems manifest themselves. Patients taking protease inhibitors (PIs) also appear to be at higher risk of developing coronary disease, although more study is needed. Another question explored is whether PI-related complications can be reversed.
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PMID:Metabolic complications of protease inhibitors: what have we learned so far? 1136 49

An ongoing study, the Women's Interagency HIV Study (WIHS), evaluated the rate of diabetes mellitus (DM) in their cohort of HIV-positive women. The study enrolled 2,000 HIV-positive and 500 HIV-negative women. The women who were divided into groups based on their experience with antiretrovirals, were followed at regular intervals for four years. The incidence of diabetes was highest among women taking protease inhibitors. Risk factors for developing diabetes tended to include protease inhibitor use, age, and baseline weight.
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PMID:Diabetes in women taking protease inhibitors. 1136 75


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