Possible Improvement of Liver Steatosis Associated with Elevated Creatine Phosphokinase Level Due to Subclinical Hypothyroidism by Thyroid Hormone Replacement Therapy
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 4, Issue 1
Abstract
A 71-year-old man suffering from non-alcoholic fatty liver disease, diabetes and dyslipidemia was hospitalized for elevated creatine phosphokinase levels. Discontinuation of antihyperlipidemic agents and rehydration could not normalize creatine phosphokinase levels. Findings of liver biopsy were compatible with non-alcoholic steatohepatitis. Based on the detailed evaluations, he was diagnosed as hypothyroidism. Thyroid hormone replacement therapy gradually improved his thyroid function and creatine phosphokinase levels. Notably, the repeated liver biopsy after the therapy showed histological improvement of steatosis. We should suspect "subclinical” hypothyroidism in case of unexplained elevation of creatine phosphokinase levels during the course or at the onset of non-alcoholic fatty liver/ non-alcoholic steatohepatitis. There are few reports of elevation of creatine phosphokinase (CK) levels and rhabdomyolysis caused by hypothyroidism [13]. On the other hand, hypothyroidism and elevated thyroid stimulating hormone (TSH) levels are reportedly independent risk factors for non-alcoholic steatohepatitis (NASH) [4,5]. Herein, we report a valuable case of NASH in which the elevation of CK levels due to hypothyroidism developed after long-term use of statins for dyslipidemia (DL) and thyroid hormone replacement therapy was most likely to improve CK levels and liver steatosis. Case Report A 71 years-old man who had worked as a landscaper until 5 years ago was admitted to our hospital for the elevation of CK levels (2782 IU/mL, normal range: 0-180) and deterioration of both gastrocnemius muscle pains. His body height was 174 cm and body weight was 80.5 kg (BMI 26.6 kg/m2), thus, he was thought to be obesity. His body temperature was normal (96.4 °F), and no abnormalities were also shown in other vital signs. He had no history of allergy, edema in lower limbs, goiter, hoarseness, and skin roughness. He had been treated hypercholesterolemia by statins for 11 years (pravastatin, atorvastatin, and rosuvastatin in this order) and add-on ezetimibe had been administered since 6 years before. Since 11 years before, his alanine aminotransferase (ALT) had been mildly elevated (approximately 50 IU/L), and ultrasonog-raphy had kept showing fatty liver such as (Figure 1A). He had also been treated diabetes mellitus (DM) by glimepiride, alogliptin, and voglibose since 6 years before. Although self-reported dietary intake was not changed, his body weight was gradually increased (57 kg [body mass index (BMI) 18.8 kg/m2] in 3 years ago, 62 kg [BMI 20.5 kg/m2] in a year ago, and 64 kg [BMI 21.1 kg/m2] in 5 months ago). Therefore, nutrition intervention was performed, but it was not effective. In addition, he had sometimes felt mild both gastroc- nemius muscle pains without specific factors such as exercise since 10 years before, and his CK levels had been slightly elevated (ap- proximately 400 IU/L).
Authors and Affiliations
Satoshi Takakusagi, Ken Sato, Yuhei Suzuki, Takayoshi Kobayashi, Satoru Kakizaki, Hitoshi Takagi
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