On the issue of pleiotropic effects of febuxostat

Gout is characterised by high comorbidity. Cardiovascular pathology and associated disorders of lipid and carbohydrate metabolism, as well as kidney damage are among the most frequent companions of gout, often significantly worsening the “quality” and limiting the life expectancy of the patient. Experimental and epidemiological data indicate that hyperuricemia, characteristic of gout, can have a pathogenetic influence on the formation of components of the metabolic syndrome. The report presents a clinical case of gout that debuted in a man aged 36 years. The patient had arterial hypertension, widespread atherosclerosis, prediabetes, obesity, dyslipidaemia, and non-alcoholic fatty liver disease. Due to renal damage, the patient with a uric acid level of 713 μmol/l was prescribed febuxostat at a dose of 80 mg/day, which was increased to 120 mg/day after 4 weeks in the absence of achieving the target level of uricemia. One year later, complex therapy including original febuxostat provided improvement of renal functional status and a stable tendency to normalisation of liver function (regression of cytolysis, cholestasis syndromes and improvement of elastogram parameters). Against the background of febuxostat therapy there was a decrease in the severity of insulin resistance (reduction of NOMA index from 4.2 to 2.8) and improvement of carbohydrate metabolism (reduction of fasting glycaemia from 6.7 to 5.9 mmol/l, glycosylated haemoglobin from 6.4 to 5.7%). Probably, febuxostat in the presented clinical case contributed to potentiation of hypolipidemic effects of statins (rosuvastatin), which is consistent with the literature data. The triglyceride level underwent especially expressive dynamics during the follow-up (decrease from 3.07 to 0.93 mmol/l). Recent literature data and the presented clinical observation indicate that febuxostat, along with having a strong urates-lowering potential with a favourable safety profile, is able to exert a pleiotropic positive effect on the metabolic disorders inherent in gout.

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