Background: Diabetic dyslipidemia has specifics that differ from dyslipidemia in patients without
diabetes, which contributes to accelerated atherosclerosis equally as dysglycemia. The aim of this study was to
deduce the interdependence of diabetic dyslipidemia and cardiovascular diseases (CVD), therapeutic strategies
and the risk of diabetes development with statin therapy.
Method: We conducted a literature review of English articles through PubMed, PubMed Central and Cochrane,
on the role of diabetic dyslipidemia in atherosclerosis, the antilipemic treatment with statins, and the role of statin
therapy in newly developed diabetes, by using key words: atherosclerosis, diabetes mellitus, diabetic dyslipidemia,
CVD, statins, nicotinic acid, fibrates, PCSK9 inhibitors.
Results: hyperglycemia and dyslipidemia cannot be treated separately in patients with diabetes. It seems that
dyslipidemia plays one of the key roles in the development of atherosclerosis. High levels of TG, decreased levels
of HDL-C and increased levels of small dense LDL- C particles in the systemic circulation are the most specific
attributes of diabetic dyslipidemia, all of which originate from an inflated flux of free fatty acids occurring due to
the preceding resistance to insulin, and exacerbated by elevated levels of inflammatory adipokines. Statins are a
fundamental treatment for diabetic dyslipidemia, both for dyslipidemia and for CVD prevention. The use of statin
treatment with high intensity is endorsed for all diabetes-and-CVD patients, while a moderate - intensity treatment
can be applied to patients with diabetes, having additional risk factors for CVD. Statins alone are thought to
possess a small, although of statistical significance, risk of incident diabetes, outweighed by their benefits.
Conclusion: As important as hyperglycemia and glycoregulation are in CVD development in patients with diabetes,
diabetic dyslipidemia plays an even more important role. Statins remain the cornerstone of antilipemic treatment
in diabetic dyslipidemia, and their protective effects in CVD progression overcome the risk of statin- associated