Treatment of severe hypertriglyceridemia — case study

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Background: Severe hypertriglyceridemia (sHTG) is defined as a triglyceride (TG) concentration of ≥ 500–1000 mg/dL. Triglyceride levels ≥ 1770 mg/dL increase the risk of acute pancreatitis (AP), which is associated with a poorer prognosis than AP of other etiologies. A TG concentration ≥ 885 mg/dL is indicative of chylomicronemia, which is mainly caused by familial chylomicronemia syndrome (FCS) and multifactorial chylomicronemia syndrome (MCS). The treatment of chylomicronemia differs according to its etiology. Case report: A patient with a TG concentration of 12,950 mg/dL was transferred from another hospital to undergo lipoprotein apheresis. Lipid-lowering therapy consisting of rosuvastatin, fenofibrate, enoxaparin, ezetimibe, and a continuous intravenous insulin infusion with 5% glucose was initiated. Apolipoprotein B was measured, and lipoprotein electrophoresis was performed. Genetic testing for FCS and APOE variants was also undertaken. The patient’s medical history revealed several secondary risk factors for hypertriglyceridemia, including overweight, excessive alcohol consumption (2–4 beers daily), psoriasis, and a diet high in saturated and trans fatty acids as well as simple sugars. Pharmacological treatment combined with the temporary cessation of food intake reduced the TG concentration to 4933 mg/dL. Following lipoprotein apheresis and the introduction of a low-fat diet (10–15% of energy from fat), together with the elimination of alcohol, simple sugars, and refined grains, the TG concentration decreased to 329 mg/dL. Based on the presence of secondary risk factors, the response to pharmacological and dietary treatment, laboratory findings, and FCS risk assessment scores, FCS was considered unlikely. As MCS was considered the more probable diagnosis, the recommended total fat intake was increased to 20–30% of energy intake, with continued emphasis on controlling dietary fat composition, reducing body weight, and maintaining restrictions on alcohol and carbohydrate intake. Treatment with rosuvastatin, fenofibrate, ezetimibe, and omega-3 fatty acid supplementation was continued. During outpatient follow-up, the TG concentration was 232 mg/dL one week after hospital discharge and 108 mg/dL after three months. Conclusions: Identifying the etiology of severe hypertriglyceridemia is essential for selecting appropriate pharmacological and dietary treatment.

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