Abstract
Background: Thyroid dysfunction affects hundreds of millions globally, serum uric acid (UA) elevation has been found to be related to thyroid dysfunction according to some studies. Thyroid dysfunction affects the purine nucleotide metabolism that may increase uric acid concentration, which is the end-product of purine metabolism and is a primary risk factor for development of gout. AIM OF THE WORK: The aim of this study was to estimate the frequency of hyperuricemia in patients with thyroid dysfunction whether hypothyroid or hyperthyroid. Patients and methods: This is a case control clinical study that was conducted in Internal Medicine Outpatient Clinic and Inpatient Department of Internal Medicine at Al-Azhar University Hospital, Damietta. The population of the study were classified into 50 hypothyroid patients (group I), 50 hyperthyroid patients (group II) and 50 normal as control (group III). All were subjected to full history, clinical examination and laboratory tests including, complete blood count, serum urea, serum creatinine, estimated glomerular filtration rate, lipid profile, thyroid stimulating hormone, free triiodothyronine and free thyroxine. Investigations included echocardiography, electrocardiography and thyroid ultrasound. Results: There was significant elevation of body mass index, blood urea, createnine, VLDL, TG, cholesterol, Uric Acid, TSH in group I as compared to group II & III. Additionaly, there was statistically significant elevation of estimated glomerular filteration rate, FT4, FT3 in group II in comparison with groups I & III. Also, there was significant increase in IHD, pericardial effusion, in group I and statistically significant increase in pulmonary HTN in group II. Conclusion: The uric acid level was elevated in both hypothyroidism and hyperthyroidism, the elevation was more in hypothyroidism concomitant with the elevation of other parameters that characterize chronic kidney disease such as creatinine, estimated glomerular filtration rate and blood urea indicating that the decreased excretion of uric acid was the leading pathogenesis to this elevation in hypothyroidism
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