0,56 CME

Dislipidemia diabetik: Pendekatan

Pembicara: Dr. Suhas Gopal Erande

Anggota Akademik RSSDI Konsultan Dokter Senior, Rumah Sakit Akshay, Pune

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Keterangan

Diabetic dyslipidemia refers to the characteristic lipid abnormalities often seen in individuals with diabetes, including elevated triglycerides, low HDL cholesterol, and increased small dense LDL particles. Approaches to managing diabetic dyslipidemia involve a combination of lifestyle modifications, glycemic control, and targeted lipid-lowering therapies to reduce cardiovascular risk in diabetic patients. Encouraging a balanced diet, regular exercise, and weight management are essential for improving lipid profiles in diabetic patients. Emphasize a diet rich in whole grains, fruits, vegetables, and healthy fats while limiting saturated and trans fats, refined sugars, and processed foods. Emphasize a diet rich in whole grains, fruits, vegetables, and healthy fats while limiting saturated and trans fats, refined sugars, and processed foods. Fibrates can help lower triglycerides and increase HDL cholesterol levels in diabetic patients with high triglyceride levels. medication can be added to statin therapy to further lower LDL cholesterol levels by inhibiting cholesterol absorption in the intestines. These supplements can help lower triglycerides, although their effect on cardiovascular outcomes is still under investigation. These medications can help lower LDL cholesterol levels by binding to bile acids in the intestines.

Ringkasan

  • Diabetes, particularly type 2, is characterized by insulin resistance in skeletal muscle, adipocytes, and hepatocytes, leading to lipolysis rather than lipogenesis in adipocytes. This results in an increased influx of free fatty acids into the liver, causing beta-oxidation, gluconeogenesis, and hepatic steatosis, now termed metabolically associated steatotic liver disease (MASLD). Excess triglycerides are generated in the hepatocyte, assembled into VLDL, and released into circulation.
  • The metabolism of VLDL leads to the formation of VLDL1 and VLDL2, ultimately producing LDL cholesterol and triglyceride-enriched LDL cholesterol. This latter form is acted upon by hepatic lipids and CETP, creating small, dense LDL, which is particularly atherogenic. Understanding this pathophysiology is crucial for appreciating diabetic dyslipidemia.
  • Various anti-diabetic drugs, like metformin, pioglitazone, sulfonylureas, gliptins, GLP-1 receptor agonists, and insulins, can influence triglyceride, HDL, and LDL levels. Metformin generally reduces LDL, while pioglitazone may increase LDL, but it's less atherogenic. Some gliptins and GLP-1 receptor agonists have been shown to reduce LDL.
  • The 2023 American Association of Clinical Endocrinologists guidelines emphasize assessing a complete lipid panel and implementing lifestyle interventions (dietary fiber, healthy fats, reduced saturated fats, physical activity, and weight control). The baseline risk of atherosclerotic cardiovascular disease (ASCVD) should be estimated to determine LDL targets.
  • LDL targets vary based on ASCVD risk: less than 100 for moderate risk, less than 70 for high risk, and less than 55 for very high risk. Triglyceride levels above 500 require separate consideration to prevent pancreatitis. Risk assessment tools like the American College of Cardiology/American Heart Association ASCVD risk calculator are recommended.
  • Statins remain the cornerstone of diabetic dyslipidemia management, with high-intensity statins (atorvastatin 40-80mg, rosuvastatin 20-40mg) capable of lowering LDL by more than 50%. Screening for dyslipidemia is essential in all type 2 diabetics, and in type 1 diabetics starting at age 12 or earlier if there's a family history.
  • Fasting lipid profiles are preferred for accurate triglyceride measurements, especially in patients with insulin resistance. Non-fasting profiles are more convenient, but fasting is recommended if triglycerides are above 440. Non-HDL cholesterol should be routinely calculated as a co-primary target.
  • Coronary artery calcium (CAC) scores can aid in ASCVD risk assessment and treatment decisions. Treatment involves pharmacotherapy (statins, ezetimibe, PCSK9 inhibitors) alongside dietary modifications: limiting carbohydrates to 50-60% of total calories, prioritizing low glycemic index carbohydrates, and increasing fiber intake to at least 40 grams.
  • LDL is a direct cause of ASCVD, and reducing LDL levels is key to reducing cardiovascular events. The clinical benefit is proportional to the absolute reduction in LDL, regardless of the drug used. Bempedoic acid is a newer option, particularly for statin-intolerant patients.
  • In children with type 1 diabetes, management focuses on lifestyle interventions, glycemic control, and weight loss. In chronic kidney disease patients, guidelines are less clear-cut and the risk-benefit must be carefully considered on a case-by-case basis. Pomegranate may offer some lipid-lowering benefits in dialysis patients when drug options are limited.

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