Statin Efficacy Reduced in Vitamin D Deficient Patients on Antiretroviral Therapy
Researchers found that vitamin D deficiencies can modify the effect of rosuvastatin in patients with HIV.
Vitamin D supplementation in vitamin D-deficient patients with HIV may be effective in increasing the efficacy of certain statins, according to research published in the Journal of Acquired Immune Deficiency Syndromes.
Corrilynn O. Hileman, MD, assistant professor of medicine at Case Western Reserve School of Medicine in Cleveland, Ohio, and colleagues used linear modeling to assess the effect of rosuvastatin on plasma 25-hydroxyvitamin D (25[OH]D).
Investigators focused on a prespecified secondary endpoint for analyses (25[OH]D concentration) and aimed to evaluate the effect of rosuvastatin on 25(OH)D concentration over the course of 96 weeks and to determine whether baseline vitamin D levels modify the effects of rosuvastatin.
The SATURN-HIV trial (ClinicalTrials.gov identifier: NCT01218802) included 147 adults aged 18 years or older with HIV-1 infection who were stable and undergoing antiretroviral therapy (ART). Those with known coronary artery disease, diabetes, or another inflammatory condition were excluded. Those randomly assigned to receive rosuvastatin (n = 72) were prescribed 10 mg daily; 75 adults were in the placebo group. Twenty-eight participants withdrew or were lost to follow-up.
The following table shows baseline demographic and clinical characteristics of the 147 participants.
|Mean age||45.4 ± 9.9 years|
|Body Mass Index (BMI)||28.1 ± 6.5 m/kg2|
|Framingham risk score||5% ± 5% 10-year risk|
|Low-density lipoprotein cholesterol||94.4 ± 24.9 mg/dL|
|High-density lipoprotein cholesterol||48.6 ± 15.9 mg/dL|
|Triglyceride levels||151.4 ± 109.9 mg/dL|
|Mean current CD4+ cell count||640 ± 300 cells/mm3|
|Mean nadir CD4+ cell count||200 ± 146 cells/mm3|
|Mean ART duration||7.1 ± 5.2 years|
At baseline, mean and median plasma 25(OH)D concentrations were 18 ± 8.3 ng/mL and 16.1 (interquartile range, 11.7-22.2), respectively. Nearly 90% of participants (88.9%) had concentrations below 30 ng/mL; 23.1% were vitamin D insufficient, 53.1% were vitamin D deficient, and 13.6% were severely vitamin D deficient.
Over the course of 96 weeks, 25(OH)D stayed consistently low in both groups. A small but statistically significant decrease in 25(OH)D level was noted between baseline and week 28 in the rosuvastatin group (mean absolute change, −2.6 ± 8.2 ng/mL [P <.01] in rosuvastatin vs +1.0 ± 8.5 ng/mL [P =.51] in placebo; P =.02 between both groups).
Analyses of low-density lipoprotein cholesterol showed that at each point in time (0-24 weeks, 0-48 weeks, and 0-96 weeks), participants with 25(OH)D concentrations greater than or equal to 20 ng/mL at baseline experienced a greater sustained decrease in low-density lipoprotein cholesterol than those considered vitamin D deficient.
For each outcome assessed, "the beneficial effects of rosuvastatin were either not apparent or attenuated in participants with 25(OH)D <20 ng/ml," the researchers noted.
"[V]itamin D status modifies the effect of rosuvastatin on several outcomes that differentiated between groups in the SATURN-HIV study including changes in [low-density lipoprotein cholesterol]," the researchers concluded. "Because vitamin D deficiency is common in HIV, further study is needed to see if vitamin D supplementation concurrent with statin administration improves outcomes in this subgroup."
Dr Hileman has served on a medical advisory board for Gilead Sciences. Dr McComsey has received research grants from BMS, Gilead Sciences, Merck, and GlaxoSmithKline, and has served as a consultant to BMS, Viiv/GlaxoSmithKline, ICON, and Gilead. Study drugs were provided by AstraZeneca.
Hileman CO, Tangpricha V, Sattar A, McComsey GA. Baseline vitamin D deficiency decreases the effectiveness of statins in HIV-infected adults on antiretroviral therapy [published online December 29, 2016]. J Aquir Immune Defic Syndr. doi: 10.1097/QAI.0000000000001281