Differential diagnosis of unconjugated hyperbilirubinemiadetected after coronary artery stenting

Abstract

Introduction. An increase in bilirubin and liver enzyme activity may be one of the side effects of statin therapy, often occurring in patients after AMI and coronary artery stenting, or in high and very high risk individuals on high and moderate intensity statin therapy. The frequency of occurrence of increased transaminases and bilirubin is according to different authors. Therefore, in terms of differential diagnosis, the cardiologist should consider Gilbert’s syndrome as a possible cause of hyperbilirubinemia. Description of the clinical case. The article considers a clinical case of differential diagnosis of non-conjugated hyperbilirubinemia detected in a patient after coronary artery stenting. The level of hemoglobin, erythrocytes, reticulocytes did not differ from normal values and did not change over time. This made it possible to exclude the hemolytic genesis of hyperbilirubinemia. Genetic testing was used to establish the homozygous form of Gilbert’s syndrome. However, the presence of fibrotic changes in the liver, an increase in not only unconjugated, but also conjugated bilirubin, hypertriglyceridemia, dyslipidemia, and stenosing atherosclerosis of the coronary arteries did not allow us to state that the patient had only Gilbert’s syndrome. Discussion. According to recent studies, this disease is characterized by a benign course and reduces the risk of developing cardiovascular diseases due to the antioxidant effect of bilirubin. In addition to Gilbert’s syndrome, the patient was diagnosed with an erased form of non-alcoholic fatty liver disease associated with metabolic syndrome. Conclusion. The disease was caused by insulin resistance, a high-calorie diet, excess consumption of saturated fats, refined carbohydrates, and a sedentary lifestyle. The drugs of choice in this case are statins, ezetemibe, and ursodeoxycholic acid. Their appointment allows not only to reduce cardiovascular risk, but also to slow down the further progression of liver fibrosis.