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Abstract
Background Morbid obesity is frequently complicated by chronic liver diseases, including nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), and fibrosis. Parathyroid hormone (PTH) is found to be elevated in morbid obesity due to the defective hepatic metabolism of vitamin D. Bariatric surgery is performed to help patients with BMI>40 kg/m2 to effectively lose weight, particularly in patients with obesity who are afflicted with complications such as NAFLD/NASH. Objective This study aimed to evaluate the PTH level as a predictor of hepatic function in individuals with morbid obesity who have undergone bariatric surgery. Methods Ninety subjects with morbid obesity referred for Roux en-Y gastric bypass surgery were recruited. After IRB approval, demographic profiles, anthropometric factors, liver biopsy, and laboratory tests were obtained. The two-dimensional shear wave elastography (2D-SWE) technique was applied to assess hepatic stiffness. Results A significant reduction occurred six months after bariatric surgery in the anthropometric indices (p < 0.001), hepatic elasticity (p=0.002), alanine aminotransferase (p < 0.001), serum alkaline phosphatase (p < 0.001), gamma-glutamyl transpeptidase (GGT) (p < 0.001), and nonalcoholic fatty liver disease fibrosis score (NFS) (p < 0.001). Serum PTH concentration was not predictive of postsurgical liver fibrosis and steatosis at six months but could predict weight loss success rate. No significant alteration in serum PTH levels was observed between presurgical vs. postsurgical time points. Conclusion A significant reduction was observed in the anthropometric parameters, liver enzymes, and hepatic elasticity after bariatric surgery. No significant effect was found on PTH levels.
Highlights
Worldwide, along with a rapid rise in the number of patients with obesity, nonalcoholic fatty liver disease (NAFLD) prevalence is increasing, affecting 20–30% of the population across the world [1]
Metabolic syndrome affected more than half (51.9%) of the participants (considered as the existence of at least three of five to be followed criteria: waist circumference more than 102 cm and 88 cm, high blood pressure (>130/ 85 mmHg), fasting high-density lipoprotein (HDL) cholesterol lower than 40 mg/dL or 50 mg/dL, fasting triglyceride (TG) levels more than 150 mg/dL, and fasting blood glucose higher than 110 mg/dL) by the criteria of the National Cholesterol Education Program expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (NCEP ATP III) [17]
Bariatric surgery is a successful treatment for morbid obesity, it decreases calcium absorption, resulting in a substantial decrease in bone density and, as a result, an increase in Parathyroid hormone (PTH) levels [13]. e elevated levels of PTH before bariatric surgery may be attributed to a vitamin D deficiency caused by NAFLD, which may be exacerbated by postbariatric surgery calcium absorption impairment [18]
Summary
Along with a rapid rise in the number of patients with obesity, nonalcoholic fatty liver disease (NAFLD) prevalence is increasing, affecting 20–30% of the population across the world [1]. Is prevalence is higher with other weightrelated comorbidities such as type 2 diabetes mellitus (T2DM) [2] Another contributor to the formation of NAFLD is assumed to be vitamin D deficiency, which is related to the development of fibrogenesis and insulin resistance (IR) [3, 4]. Parathyroid hormone (PTH) is found to be elevated in morbid obesity due to the defective hepatic metabolism of vitamin D. Is study aimed to evaluate the PTH level as a predictor of hepatic function in individuals with morbid obesity who have undergone bariatric surgery. A significant reduction occurred six months after bariatric surgery in the anthropometric indices (p < 0.001), hepatic elasticity (p 0.002), alanine aminotransferase (p < 0.001), serum alkaline phosphatase (p < 0.001), gamma-glutamyl transpeptidase (GGT) (p < 0.001), and nonalcoholic fatty liver disease fibrosis score (NFS) (p < 0.001).
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