Treatment with protease inhibitors associated with peripheral insulin resistance and impaired oral glucose tolerance in HIV-1-infected patients

Walli, Ravi; Herfort, Oliver; Michl, Gerlinde M.; Demant, Thomas; Jäger, H.; Dieterle, C.; Bogner, Johannes R.; Landgraf, R; Goebel, F. D.

doi:10.1097/00002030-199815000-00001

Cited by 482 publications

(282 citation statements)

References 13 publications

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“…It is well known that in the HAART era many HIV-infected patients have developed associated comorbidities such as chronic liver disease, diabetes, cancer and cardiovascular disease [10,[22][23][24][25][26][27], and the present study shows that comorbidities are independently associated with mortality in this population. The prevalence and prognosis of comorbidities may vary according to the characteristics of HIV transmission and the type of comorbidities.…”

Section: Discussionsupporting

confidence: 57%

Trends in mortality and antibiotic resistance among HIV‐infected patients with invasive pneumococcal disease

Grau¹,

Ardanuy

Liñares

et al. 2009

HIV Medicine

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Objectives The aim of the study was to describe trends and risk factors for mortality and changes in antibiotic resistance, serotypes and clones among HIV‐infected patients with invasive pneumococcal disease (IPD). Methods A prospective study of 199 episodes of IPD occurring in a cohort of 4011 HIV‐infected patients was carried out. Predictors of mortality included clinical and microbiological data. The 7‐valent pneumococcal conjugate vaccine (PCV7) for children was introduced in late 2001. Time periods were classified for mortality studies as pre‐ (1986–1996), early (1997–2001) and late (2002–2007) highly active antiretroviral therapy (HAART) era, and for serotype studies as pre‐PCV7 (1986–2001) and PCV7 (2002–2007) era. Results Of 199 IPD episodes, 71 (36%) occurred in HIV‐infected patients with associated comorbidities (mainly liver cirrhosis; 52 of 71), which increased in recent years. The incidence of IPD decreased from the pre‐HAART era to the early HAART era and then remained stable in the late HAART era (24.1, 8.4 and 7.4 episodes per 1000 patient‐years, respectively). Rates of 30‐day mortality have risen over the three periods (8, 19 and 25%, respectively; P=0.017). In multiple logistic regression analysis, predictors of mortality were shock at presentation [odds ratio (OR) 7.01; 95% confidence interval (CI) 2.05–23.87] and associated comorbidities (OR 4.27; 95% CI 1.53–11.92). In the PCV7 era, IPD caused by non‐PCV7 serotypes increased, and resistance to betalactams decreased. The most frequent genotypes were Spain9V‐ST156, Spain23F‐ST81, ST8819F, Sweden1‐ST304 and Spain6B‐ST90. Conclusions In the late HAART era, the incidence of IPD has not significantly decreased. Mortality from IPD has risen in association with an increase in comorbidities such as liver cirrhosis. New vaccination strategies are needed to diminish the burden of IPD in the HIV‐infected population.

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Section: Discussionsupporting

confidence: 57%

Trends in mortality and antibiotic resistance among HIV‐infected patients with invasive pneumococcal disease

Grau¹,

Ardanuy

Liñares

et al. 2009

HIV Medicine

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“…Indeed, patients' longer survival following the introduction of cART may be considered as an additional risk for renal dysfunction, as long-term toxic events associated with the prolonged used of ART have been observed (e.g. metabolic alterations, diabetes, hypertension and cardiovascular events) [12][13][14]. It has been hypothesized that antiretroviral medications may have a direct effect in increasing the risk of renal dysfunction, and a variety of cART-related effects, including proteinuria, renal tubular damage, interstitial nephritis and overall declines in glomerular filtration rates, have been noted [15][16][17][18][19][20][21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of glomerular filtration rate in HIV-1-infected patients before and after combined antiretroviral therapy exposure*

et al. 2010

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The prevalence and factors associated with an increased risk of renal dysfunction in HIV-infected patients receiving or not receiving antiretroviral therapy (ART) have been poorly evaluated in observational settings. MethodsPatients in the ICONA Foundation cohort with at least two creatinine values available while still ART-naïve were enrolled in the study. A logistic regression analysis was performed to identify predictors of an estimated glomerular filtration rate (eGFR)o90 mL/min/1.73 m 2 at baseline. The incidence and predictors of a 420% reduction in eGFR from pre-combination ART (cART) levels (or a decrease from ! 90 to o90 mL/min/1.73 m 2 ) were evaluated by Poisson regression. ResultsA total of 1505 patients were included in the study; 363 (24%) had eGFRo90 mL/min/1.73 m 2 at baseline. Older patients [odds ratio (OR) 1.58 per 10 years older; Po0.00001], female patients (OR 2.41 vs. male patients; Po0.00001), those who had diabetes and/or hypertension (OR 2.36 vs. neither; Po0.03) and patients with higher baseline CD4 count (OR 1.06 per 100 cells/mL higher; Po0.03) showed a greater risk of eGFRo90 mL/min/1.73 m 2 . Ninety-six patients experienced an eGFR decrease of 420% from pre-cART levels (6.8 per 100 person-years). Older age [relative risk (RR) 1.41 per 10 years older; P 5 0.005], female gender (RR 2.25 vs. male; P 5 0.003) and current exposure to didanosine (ddI), tenofovir and protease inhibitors were the major determinants. ConclusionsWe observed a relatively high rate of mild renal dysfunction in the absence of ART. In addition to traditional risk factors such as older age and diabetes/hypertension, female gender and current use of ddI, tenofovir and protease inhibitors were associated with a greater risk of decreased renal function as measured by eGFR.Keywords: antiretroviral exposure, estimated glomerular filtration rate (eGFR), renal impairment [7][8][9][10][11], there are a number of other factors potentially influencing the onset of renal disorders through different mechanisms, whose prevalence may be different in an HIV-positive population compared with the general population. Indeed, patients' longer survival following the introduction of cART may be considered as an additional risk for renal dysfunction, as long-term toxic events associated with the prolonged used of ART have been observed (e.g. metabolic alterations, diabetes, hypertension and cardiovascular events) [12][13][14]. It has been hypothesized that antiretroviral medications may have a direct effect in increasing the risk of renal dysfunction, and a variety of cART-related effects, including proteinuria, renal tubular damage, interstitial nephritis and overall declines in glomerular filtration rates, have been noted [15][16][17][18][19][20][21][22][23].The potential role of tenofovir in renal toxicity is a current clinical research question. As a consequence of its tolerability, convenient dosing and efficacy, this nucleoside reverse transcriptase inhibitor (NRTI) has been widely used as a component of cART regimens. There are...

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“…In concert with this, increased serum glycerol and triglycerides were observed. Additionally, the patients demonstrated higher than normal insulin levels suggestive of insulin resistance (5,6). The degree of lipodystrophy in patients varies but has been reported to be greater than 80% in one study (5).…”

mentioning

confidence: 93%

The effects of protease inhibitors on basal and insulin-stimulated lipid metabolism, insulin binding, and signaling

Cammalleri

Germinario

2003

Journal of Lipid Research

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Treatment with protease inhibitors associated with peripheral insulin resistance and impaired oral glucose tolerance in HIV-1-infected patients

Cited by 482 publications

References 13 publications

Trends in mortality and antibiotic resistance among HIV‐infected patients with invasive pneumococcal disease

Trends in mortality and antibiotic resistance among HIV‐infected patients with invasive pneumococcal disease

Evaluation of glomerular filtration rate in HIV-1-infected patients before and after combined antiretroviral therapy exposure*

The effects of protease inhibitors on basal and insulin-stimulated lipid metabolism, insulin binding, and signaling

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