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1.  Increased Coronary Atherosclerotic Plaque Vulnerability by Coronary Computed Tomography Angiography in HIV-Infected Men 
AIDS (London, England)  2013;27(8):1263-1272.
PMCID: PMC3740057  PMID: 23324657
HIV; atherosclerosis; myocardial infarction; plaque; cardiovascular disease
2.  Increased Coronary Atherosclerosis and Immune Activation in HIV-1 Elite Controllers 
AIDS (London, England)  2012;26(18):2409-2412.
HIV-1 elite controllers (EC) spontaneously maintain suppressed levels of viremia, but exhibit significant immune activation. We investigated coronary atherosclerosis by coronary CT angiography (CTA) in: 1) EC, 2) non EC, chronically HIV-1 infected, ART-treated patients with undetectable viral load (“chronic HIV”), and 3) HIV-negative controls. Prevalence of atherosclerosis (78% vs. 42%, P<0.05) and markers of immune activation were increased in EC compared to HIV-negative controls. sCD163, a monocyte activation marker, was increased in EC compared to chronic HIV-1 (P<0.05) and compared to HIV-negative controls (P< 0.05). These data suggest a significant degree of coronary atherosclerosis and monocyte activation among EC.
PMCID: PMC3660105  PMID: 23032411
3.  Receptor activator of nuclear factor kappa β ligand (RANKL) and its relationship to coronary atherosclerosis in HIV patients 
HIV-infected individuals have an increased prevalence of coronary artery disease (CAD). Receptor activator of nuclear factor kappa β ligand (RANKL) and osteoprotegerin (OPG) have been postulated as mediators of vascular calcification. 78 HIV-infected men and 32 healthy controls without history of CAD were prospectively recruited to undergo cardiac computed tomography (CT) and CT angiography to assess coronary artery calcium and plaque burden. sRANKL was lower in HIV-infected individuals than controls (2.52 [1.08, 3.98] vs. 3.33 [2.44, 4.64] pg/ml, P=0.01, median [IQR] respectively). sRANKL was negatively associated with the number of coronary segments with plaque (Spearman ρ=−0.41, P<0.001) and Agatston calcium score (ρ=−0.30, P<0.01) in HIV-infected individuals even after adjusting for traditional cardiovascular risk factors.
PMCID: PMC3766949  PMID: 22842843
atherosclerosis; receptor activator of nuclear factor kappa β ligand; osteoprotegerin; coronary artery disease; HIV
4.  Arterial inflammation in patients with HIV 
Cardiovascular disease is increased in HIV patients, but the specific mechanisms are unknown.
To assess arterial wall inflammation in HIV, using 18fluorine-2-deoxy-D-glucose Positron Emission Tomography (18FDG-PET), in relationship to traditional and non-traditional risk markers, including sCD163, a marker of macrophage activation.
Design, Setting, and Participants
81 participants were investigated in a cross-sectional study from November 2009 to July 2011. 27 HIV-infected participants without known cardiac disease underwent cardiac 18FDG-PET and coronary CT imaging for coronary calcium (CAC). Two separate non-HIV control groups were compared. One control group (n=27) was matched to the HIV group for age, gender and Framingham Risk Score (FRS) and had no known atherosclerotic disease (FRS-Matched Controls). The second control group (n=27) was matched on gender and selected based on the presence of known atherosclerotic disease (Atherosclerotic Controls).
Main Outcome Measure
Arterial inflammation was prospectively determined as the ratio of FDG uptake in the arterial wall of the ascending aorta/blood background, as the target to background ratio (TBR).
HIV participants demonstrated well-controlled HIV disease (CD4 641±288 cells/mm3, HIV RNA <48 [<48, <48] copies/mL). All were receiving ART (duration 12±4 yrs). The mean Framingham Risk Score (FRS) was low in both HIV and FRS-Matched Controls (6.4 (4.8–8.0) vs. 6.6 (4.9–8.2), P=0.87). Arterial inflammation in the aorta (Aortic TBR) was higher in the HIV vs. FRS-Matched Control Participants (2.23 (2.07–2.40) vs. 1.89 (1.80–1.97), P<0.001), but was similar compared to Atherosclerotic Controls (2.23 (2.07–2.40) vs. 2.13 (2.03–2.23), P=0.29). Aortic TBR remained significantly higher in the HIV group vs. the FRS-Matched Controls after adjusting for traditional cardiovascular risk factors (P=0.002) and in stratified analyses among participants with undetectable viral load, zero calcium, FRS<10, and LDL< 100 mg/dL (2.59 mmol/L) (all P<0.01). Aortic TBR was associated with sCD163 (P=0.04) but not with CRP (P=0.65) or D-Dimer (P=0.08) among HIV-infected patients.
Persons infected with HIV, compared to non-infected controls with similar cardiac risk factors, had signs of increased arterial inflammation which was associated with circulating markers of macrophage activation.
PMCID: PMC3724172  PMID: 22820791
5.  The Biology of Atherosclerosis: General Paradigms and Distinct Pathogenic Mechanisms Among HIV-Infected Patients 
The Journal of Infectious Diseases  2012;205(Suppl 3):S368-S374.
Complications of atherosclerosis, including myocardial infarction and stroke, are the leading cause of death and disability worldwide. Recent data strongly implicate cardiovascular death as a contributor to mortality among patients with human immunodeficiency virus (HIV) infection, with evidence suggesting increased incidence of atherosclerosis among these patients. Therefore, greater understanding of atherosclerotic mechanisms and how these responses may be similar or distinct in HIV-infected patients is needed. Key concepts in atherosclerosis are reviewed, including the evidence that inflammation and abnormal metabolism are major drivers of atherosclerosis, and connected to the current literature regarding atherosclerosis in the context of HIV.
PMCID: PMC3349296  PMID: 22577210
6.  Increased Epicardial Adipose Tissue Volume in HIV-Infected Men and Relationships to Body Composition and Metabolic Parameters 
AIDS (London, England)  2010;24(13):2127-2130.
Epicardial fat accumulation may have important clinical consequences, yet little is known regarding this depot in HIV patients. We compared epicardial fat volume in 78 HIV-infected men and 32 HIV-negative controls. Epicardial fat volume was higher in HIV than control subjects (p=0.04). In HIV patients, epicardial fat volume was strongly associated with visceral adipose tissue area (VAT)(ρ = 0.76, p<0.0001), fasting glucose (ρ = 0.41, p=0.001) and insulin (ρ = 0.44, p=0.0003). Relationships with glucose and insulin remained significant controlling for age, race, BMI, adiponectin, VAT, and antiretroviral therapy. Epicardial fat may be an important fat depot in HIV-infected patients.
PMCID: PMC3620604  PMID: 20588167
HIV; epicardial fat; visceral fat; glucose; atherosclerosis
7.  Soluble CD163, a Novel Marker of Activated Macrophages, Is Elevated and Associated With Noncalcified Coronary Plaque in HIV-Infected Patients 
The Journal of Infectious Diseases  2011;204(8):1227-1236.
Background. Pro-inflammatory monocytes/macrophages may contribute to increased atherosclerosis in human immunodeficiency virus (HIV)–infected patients. We investigate—to our knowledge, for the first time—sCD163 and other markers of monocyte activation in relationship to atherosclerotic plaque in HIV-infected patients.
Methods. One hundred two HIV-infected and 41 HIV-seronegative men with equivalent cardiovascular risk factors and without history of coronary artery disease were prospectively recruited and underwent computed tomography coronary angiography.
Results. sCD163 levels and presence of plaque were significantly higher among antiretroviral-treated subjects with undetectable HIV RNA levels, compared with seronegative controls (1172 ± 646 vs. 883 ± 561 ng/mL [P = .02] for sCD163 and 61% vs. 39% [P = .03] for presence of plaque). After adjusting for age, race, lipids, blood pressure, glucose, smoking, sCD14, and HIV infection, sCD163 remained independently associated with noncalcified plaque (P = .008). Among HIV-infected patients, sCD163 was associated with coronary segments with noncalcified plaque (r = 0.21; P = .04), but not with calcium score. In contrast, markers of generalized inflammation, including C-reactive protein level, and D-dimer were not associated with sCD163 or plaque among HIV-infected patients.
Conclusions. sCD163, a monocyte/macrophage activation marker, is increased in association with noncalcified coronary plaque in men with chronic HIV infection and low or undetectable viremia. These data suggest a potentially important role of chronic monocyte/macrophage activation in the development of noncalcified vulnerable plaque.
Clinical Trial Registration. NCT00455793.
PMCID: PMC3203384  PMID: 21917896
8.  Increased Coronary Artery Calcium Score and Noncalcified Plaque among HIV-infected Men: Relationship to Metabolic Syndrome and Cardiac Risk Parameters 
In this study, the effects of traditional cardiac risk factors on coronary artery calcium (CAC) score and presence of plaque, including noncalcified plaque, measured by computed tomography coronary angiography, were compared among HIV-infected and non HIV-infected subjects, with respect to the presence of the metabolic syndrome (MS).
Design and methods
HIV-infected men recruited for the presence of the MS (HIV+MS, n=27) were compared to two control groups, HIV-infected men recruited without regard to metabolic criteria (HIV, n=87), and HIV-negative control men (C, n=40), also recruited without regard to any metabolic criterion.
All three groups were similar in age, demographic parameters, and smoking. MS was seen in 100% of the HIV+MS group, compared to 28% in the HIV-infected control group and 11% in the HIV-negative controls. HIV+MS subjects had higher mean CAC score than HIV-infected controls (72±25 vs. 30±8, P=0.04, HIV+MS vs. HIV) and HIV-negative controls (72±25 vs. 18±7; P=0.02, HIV+MS vs. C). With respect to CAC, only the HIV+MS group had increased CAC compared to non HIV. In contrast, both HIV groups demonstrated an increased prevalence of plaque [63% vs. 38%, P=0.04 (HIV+MS vs. C) and 59% vs. 38%, P=0.02, (HIV vs. C)] and increased number of noncalcified plaque segments compared to the HIV-negative group [1.26±0.31 vs. 0.45±0.16, P=0.01 (HIV+MS vs. C); 1.02±0.18 vs. 0.45±0.16, P=0.04 (HIV vs. C)]. Plaque and noncalcified plaque did not differ significantly between the HIV groups.
Metabolic abnormalities in HIV patients are specifically associated with increased coronary artery calcification, whereas HIV itself or other factors may be associated with the development of noncalcified lesions.
PMCID: PMC2974783  PMID: 20720497
Coronary artery calcification; metabolic syndrome; HIV
9.  Effects of Obesity, Body Composition, and Adiponectin on Carotid Intima-Media Thickness in Healthy Women 
Increased common carotid intima-media thickness (IMT) is predictive of coronary artery disease and stroke.
In this study, we investigated common carotid IMT by obesity category in a cohort of healthy women without previously known cardiovascular disease.
Design, Setting, Participants, and Main Outcome Measures
One hundred healthy women (aged 24-59 yr) from the general community enrolled in an observational study conducted at an academic medical center participated in the study. B-mode ultrasound imaging of the common carotid arteries was used to measure common carotid IMT in 99 subjects. Fat distribution was determined by computed tomography. Hormonal and inflammatory parameters related to cardiovascular disease and obesity were measured.
IMT was higher in obese [body mass index (BMI) ≥ 30 kg/m2], compared with overweight women (BMI ≥ 25 and < 30 kg/m2) [0.69 mm, interquartile range (IQR) 0.60-0.75 mm] vs. 0.62 mm [IQR 0.56-0.68 mm), P = 0.044] and in comparison with lean women (BMI < 25 kg/m2) [0.69 mm (IQR 0.60-0.75 mm) vs. 0.59 mm (IQR 0.54-0.67 mm), P = 0.016]. In multivariate modeling, age (beta = 0.0050 mm change in IMT per year of age, P = 0.003), smoking (beta = 0.0044 mm change in IMT per pack-year, P = 0.046), and sc abdominal adiposity (beta = 0.00026 mm change in IMT per square centimeter, P = 0.010) were positively associated with IMT, whereas adiponectin (beta =–0.0042 mm change in IMT per milligram per liter, P = 0.045) was negatively associated with IMT. Visceral adiposity (beta = 0.00048 mm change in IMT per square centimeter, P = 0.092) was not significantly associated with IMT after adjusting for age, race, smoking, sc abdominal adiposity, and adiponectin.
Obesity is associated with increased common carotid IMT in young and middle-aged women. Adiponectin and sc abdominal adiposity are associated with carotid IMT in this population.
PMCID: PMC3210448  PMID: 16522690
11.  Effects of TNF-α neutralization on adipocytokines and skeletal muscle adiposity in the metabolic syndrome 
In a prior study, we have shown that tumor necrosis factor (TNF)-α neutralization improves inflammatory markers and total adiponectin in patients with the metabolic syndrome, without improving insulin sensitivity. In this study, we sought to extend our understanding of the effects of TNF-α neutralization in this human model of obesity by investigating the responses of high-molecular-weight (HMW) adiponectin, resistin, leptin, and muscle adiposity to etanercept in patients with the metabolic syndrome. Fifty-six men and women with the metabolic syndrome enrolled in a double-blind randomized placebo-controlled trial. Circulating concentrations of total and HMW adiponectin, resistin, and leptin were determined at baseline and after 4 wk of treatment with etanercept. Muscle adiposity was measured by computed tomography (CT). Although etanercept increased total adiponectin concentration, the HMW form, which is thought to mediate insulin sensitivity, was unchanged. Thus the ratio of HMW to total adiponectin decreased following etanercept treatment compared with placebo (−0.03 ± 0.03 vs. 0.06 ± 0.03, P = 0.02). Resistin tended to decrease in the etanercept-treated group compared with placebo (−0.6 ± 0.7 vs. 1.2 ± 0.7 ng/ml, P = 0.06), whereas leptin was not altered. Etanercept decreased muscle attenuation on CT [−0.61 ± 0.64 Hounsfield units (HU) vs. 1.54 ± 0.77 HU in placebo, P = 0.04], suggesting an increase in muscle adiposity. Together, these results demonstrate that neutralization of TNF-α in obese humans results in differential effects on critical adipokines and body composition indexes. These findings may help to explain the lack of effect on insulin sensitivity and extend our knowledge of the biological effects of TNF-α neutralization in obesity.
PMCID: PMC3196534  PMID: 17374698
tumor necrosis factor-α; adiponectin; resistin; muscle adiposity; metabolic syndrome
12.  Dyslipidemia and lipid management in HIV-infected patients 
Purpose of review
Dyslipidemia is highly prevalent among patients living with chronic HIV infection and may confer increased risk of cardiovascular disease in this patient population. This review summarizes recent data investigating lipid abnormalities and its management in HIV-infected patients.
Recent findings
Studies in the last year have evaluated the effects of various lipid-lowering therapies not previously investigated in the HIV patient population. Rosuvastatin is a potent statin that appears to be well tolerated and effective in HIV-infected patients with hypercholesterolemia.
Dyslipidemia is common in HIV-infected individuals. Medical therapy of lipid disorders needs to take potential drug–drug interactions of lipid-lowering medications and antiretroviral agents into consideration.
PMCID: PMC3154840  PMID: 21297466
cardiovascular risk factors; HIV; lipids
13.  Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men 
AIDS (London, England)  2010;24(2):243-253.
The degree of subclinical coronary atherosclerosis in HIV-infected patients is unknown. We investigated the degree of subclinical atherosclerosis and the relationship of traditional and nontraditional risk factors to early atherosclerotic disease using coronary computed tomography angiography.
Design and methods
Seventy-eight HIV-infected men (age 46.5 ± 6.5 years and duration of HIV 13.5 ± 6.1 years, CD4 T lymphocytes 523 ± 282; 81% undetectable viral load), and 32 HIV-negative men (age 45.4 ± 7.2 years) with similar demographic and coronary artery disease (CAD) risk factors, without history or symptoms of CAD, were prospectively recruited. 64-slice multidetector row computed tomography coronary angiography was performed to determine prevalence of coronary atherosclerosis, coronary stenosis, and quantitative plaque burden.
HIV-infected men demonstrated higher prevalence of coronary atherosclerosis than non-HIV-infected men (59 vs. 34%; P = 0.02), higher coronary plaque volume [55.9 (0–207.7); median (IQR) vs. 0 (0–80.5) μl; P = 0.02], greater number of coronary segments with plaque [1 (0–3) vs. 0 (0–1) segments; P = 0.03], and higher prevalence of Agatston calcium score more than 0 (46 vs. 25%, P = 0.04), despite similar Framingham 10-year risk for myocardial infarction, family history of CAD, and smoking status. Among HIV-infected patients, Framingham score, total cholesterol, low-density lipoprotein, CD4/CD8 ratio, and monocyte chemoattractant protein 1 were significantly associated with plaque burden. Duration of HIV infection was significantly associated with plaque volume (P = 0.002) and segments with plaque (P = 0.0009) and these relationships remained significant after adjustment for age, traditional risk factors, or duration of antiretroviral therapy. A total of 6.5% (95% confidence interval 2–15%) of our study population demonstrated angiographic evidence of obstructive CAD (>70% luminal narrowing) as compared with 0% in controls.
Young, asymptomatic, HIV-infected men with long-standing HIV disease demonstrate an increased prevalence and degree of coronary atherosclerosis compared with non-HIV-infected patients. Both traditional and nontraditional risk factors contribute to atherosclerotic disease in HIV-infected patients.
PMCID: PMC3154841  PMID: 19996940
atherosclerosis; cardiovascular risk factors; coronary artery disease; coronary computed tomography angiography; HIV
14.  Increased Aldosterone Among HIV-Infected Women with Visceral Fat Accumulation 
AIDS (London, England)  2009;23(17):2366-2370.
Increased aldosterone has been associated with obesity and the metabolic syndrome in non HIV-infected patients, but aldosterone has not been investigated among HIV-infected patients with increased visceral adipose tissue (VAT). 24-hour urine aldosterone was assessed among age and BMI-matched HIV-infected women with increased VAT, HIV-infected women without increased VAT and healthy controls. 24-hour urine aldosterone was higher in HIV-infected women with increased VAT and was associated with systolic blood pressure, VAT, and hemoglobin A1c. Increased aldosterone may contribute to the detrimental effects of excess visceral adiposity on blood pressure and glucose homeostasis among HIV patients.
PMCID: PMC2921849  PMID: 19770620
Aldosterone; Lipodystrophy; HIV; Visceral Fat
15.  Relationship of peak growth hormone to cardiovascular parameters, waist circumference, lipids and glucose in HIV-infected patients and healthy adults 
Clinical endocrinology  2009;71(6):815-822.
Relative growth hormone (GH) deficiency is highly prevalent in patients with HIV. The purpose of this study was to investigate relationships of GH to metabolic and anthropometric parameters in HIV patients and non-HIV controls.
Peak GH and metabolic parameters were assessed in a cross-sectional study of 191 HIV patients and 62 age and BMI-matched healthy controls.
Peak GH was assessed by GHRH/arginine stimulation testing.
HIV patients demonstrated similar BMI, but increased waist circumference (WC) and reduced peak GH to GHRH/arginine compared with control subjects (12.4 [6.3, 24.8] vs. 21.3 [8.8, 34.5] μg/l, P=0.006, HIV vs. control). Among HIV and non-HIV groups, peak GH was inversely associated with WC (rho=−0.44, p<0.0001; rho=−0.63, p<0.0001)(HIV patients and controls, respectively), blood pressure (rho=−0.17, p=0.02; rho=−0.36, p=0.004), triglycerides (rho=−0.37, p<0.0001; rho=−0.43, p=0.001), glucose (rho=−0.34, p<0.0001; rho=−0.30, p=0.02), insulin (rho=−0.43, p<0.0001; rho=−0.60, p<0.0001) and CRP (rho=−0.29, p<0.0001; rho=−0.59, p<0.0001). Among HIV patients, the inverse association between peak GH and fasting glucose remained significant (β=−0.006mmol/l change in glucose per μg/l change in GH, p=0.004) controlling for age, gender, race, BMI, WC, protease inhibitor(PI) and nucleoside reverse transcriptase inhibitors(NRTI). Similarly, the inverse association between peak GH and triglycerides remained significant (β=−0.01mmol/l change in triglycerides per μg/l change in GH, p=0.02) controlling for age, gender, race, BMI, WC, PI and lipid-lowering medications. HIV men with peak GH<7.5μg/l demonstrated higher BMI, WC, SBP, triglycerides, glucose and CRP.
Reduced GH secretion is independently associated with dyslipidemia and higher glucose, among HIV patients with abdominal fat accumulation.
PMCID: PMC2889024  PMID: 19508594
16.  Decreased respiratory quotient in relation to resting energy expenditure in HIV-infected and non-infected subjects 
The purpose of this study was to evaluate the relationship of respiratory quotient (RQ), a surrogate marker of substrate oxidation, as well as body composition and dietary intake to resting energy expenditure (REE) among HIV-infected patients in the current era of HAART and among non HIV-infected control subjects. Resting energy expenditure (REE) is increased in HIV-infected patients, but little is known regarding the potential contribution of altered substrate metabolism, body composition and dietary intake to increased energy expenditure in this population. RQ, REE, body composition and dietary intake parameters were assessed in 283 HIV-infected patients and 146 community-derived HIV-negative controls that were evaluated for metabolic studies between 1998 and 2005. RQ was lower (0.83±0.00 vs. 0.85±0.01, P=0.005) whereas REE adjusted for fat free mass (FFM) was higher (31.8±0.3 vs. 29.8±0.3 kcal/d/kg, P=<0.0001) in HIV-infected compared to control subjects. In multivariate modeling among HIV-infected patients, including age, gender and parameters of immune function, FFM (beta=24.811334, P <0.0001), visceral adiposity (beta=0.7182746, P=0.008), and total body fat (beta=8.0506839, P=0.041) were positively associated with REE, whereas RQ was negatively associated with REE (beta= −528.4808, P=0.024). Overall r2=0.705, P<0.0001 for the model. In control subjects, by contrast, only visceral adiposity (beta = 1.0612073, P=0.004), total body fat (beta = 15.805547, P=0.010), and FFM (beta = 22.613005, P <0.0001) were significant predictors of REE, and there was no relationship with RQ. Overall r2=0.825, P<0.0001 for the model. These data suggest that alterations in substrate metabolism may contribute to increased REE in HIV-infected patients compared to control subjects.
PMCID: PMC2691476  PMID: 19375582
HIV; resting energy expenditure; lipid oxidation; substrate metabolism; RQ
17.  Low-Dose Physiological Growth Hormone in Patients With HIV and Abdominal Fat Accumulation 
Antiretroviral therapy can be associated with visceral adiposity and metabolic complications, increasing cardiovascular risk, and reduced growth hormone (GH) secretion may be a contributing factor.
To investigate the effects of low-dose physiological GH administration on body composition, glucose, and cardiovascular parameters in patients with human immunodeficiency virus (HIV) having abdominal fat accumulation and relative GH deficiency.
Design, Setting, and Patients
A randomized, double-blind, placebo-controlled trial of 56 patients with HIV, abdominal fat accumulation, and reduced GH secretion (peak GH <7.5 ng/mL) conducted at a US academic medical center between November 2003 and October 2007.
Patients were randomly assigned to receive either subcutaneous GH or matching placebo titrated to the upper quartile of normal insulinlike growth factor 1 (IGF-1) range for 18 months. Starting dose was 2 μg/kg/d and increased to maximum dose of 6 μg/kg/d (average dose, 0.33 mg/d).
Main Outcome Measures
Change in body composition assessed by computed tomographic scan and dual-energy x-ray absorptiometry. Secondary outcomes included glucose, IGF-1, blood pressure (BP), and lipids. Treatment effect was the difference in the change between GH and placebo groups, using all available data.
Fifty-five patients (26 with GH and 29 with placebo) were included in the safety analyses and 52 patients (25 with GH and 27 with placebo) were included in the efficacy analyses. Visceral adipose tissue area (treatment effect [last-value-carried-forward analysis {n=56}, -19 cm2; 95% confidence interval {CI}, -37 to -0.3 cm2], -19 cm2; 95% CI, -38 to -0.5 cm2; P=.049); trunk fat (-0.8 kg; 95% CI, -1.5 to -0.04 kg; P=.04); diastolic BP (-7 mm Hg; 95% CI, -11 to -2 mm Hg; P=.006); and triglycerides (-7 mg/dL, P=.002) improved but 2-hour glucose levels on glucose tolerance testing increased in the GH group vs the placebo group (treatment effect, 22 mg/dL; 95% CI, 6-37 mg/dL; P=.009). The IGF-1 levels increased (treatment effect, 129 ng/mL; 95% CI, 95-164 ng/mL; P<.001). Adverse events were not increased for GH vs placebo (23%; 95% CI, 9%-44% vs 28%; 95% CI, 13%-47%; P=.70).
In HIV-associated abdominal fat accumulation and relative GH deficiency, low-dose GH received for 18 months resulted in significantly reduced visceral fat and truncal obesity, triglycerides, and diastolic BP, but 2-hour glucose levels on glucose tolerance testing were increased.
PMCID: PMC2532757  PMID: 18677023

Results 1-17 (17)