isotretinoin and Atherosclerosis

We aimed to reveal the relationship of serum uric acid (SUA) with monocyte-high-density lipoprotein ratio (MHR) and other inflammatory markers in acne patients before and after isotretinoin treatment. In this way, we can try to shed light on the relationship between isotretinoin treatment and atherosclerosis.. Two hundred twenty-four acne patients who administered isotretinoin (0.5-1 mg/kg/day) were enrolled in the study. In the pretreatment phase and 3 months after treatment, MHR, SUA, mean platelet volume, neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio, monocyte-lymphocyte ratio, serum triglyceride, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) levels of the patients were analyzed.. Compared to the pretreatment phase, three months after treatment, there was a statistically decrease in neutrophil count and an increase in lymphocyte count (p: 0.002, p: 0.011, respectively). Accordingly, there was a statistically significant decrease in NLR (p: 0.001). It was noteworthy that MHR and SUA levels increased significantly (p: 0.042, p: 0.010, respectively) and there was a positive correlation between SUA level and MHR (r: 0.212, p: 0.012). Serum total cholesterol, LDL, and triglyceride levels increased and HDL levels decreased significantly after treatment (p: 0.001).. This study contributes to the comprehension of the relationship between isotretinoin treatment and atherosclerosis, which has been frequently reported in the literature. It was thought that the isotretinoin-induced SUA increase might be related to dyslipidemia. Isotretinoin may initiate the atherosclerotic process in vascular endothelial and smooth muscles, with SUA increase and HDL decrease. An increase in MHR is also an inflammatory marker indicating this process.

Topics: Acne Vulgaris; Atherosclerosis; Cholesterol, HDL; Humans; Isotretinoin; Lipoproteins, HDL; Monocytes; Uric Acid

Studies conducted on isotretinoin have shown that it may indirectly lead to atherosclerosis. The objective of this study was to determine the effect of systemic isotretinoin on subclinical atherosclerosis. The present study included 63 patients with acne vulgaris who had used isotretinoin for 6 months. Glucose, insulin, and homeostatic model assessment of insulin resistance levels; body mass index; waist circumference; blood pressure; lipid profile; and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), high-sensitivity C-reactive protein, and oxidized low-density lipoprotein (Ox-LDL) levels were compared in the patients at the initiation and discontinuation of the treatment. At the discontinuation of the treatment, LOX-1 and Ox-LDL levels showed a significant increase (P < .001 and P = .040, respectively). Differences in waist circumference were positively correlated with an increase in LOX-1 levels (r = .274; P = .030). Isotretinoin causes an increase in the levels of subclinical atherosclerosis markers. Although the present study sample size was small, we believe that caution should be exercised considering the risk of atherosclerosis during isotretinoin use in men with high waist circumference and cardiovascular risk factors; further studies are warranted in this regard.

Topics: Acne Vulgaris; Atherosclerosis; Humans; Isotretinoin; Lipids; Male; Scavenger Receptors, Class E