Cushing syndrome (CS), a complex, multisystemic condition resulting from prolonged exposure to cortisol, is frequently associated with nonalcoholic fatty liver disease (NAFLD). In patients with adrenal adenoma(s) and NAFLD, it is essential to rule out coexisting endocrine disorders like CS, so that the underlying condition can be properly addressed. We report a case of a 49-year-old woman with a history of hypertension, prediabetes, dyslipidemia, biopsy-confirmed steatohepatitis, and benign adrenal adenoma, who was referred for endocrine work-up for persistent weight gain. Overt Cushing features were absent. Biochemical evaluation revealed nonsuppressed cortisol on multiple 1-mg dexamethasone suppression tests, suppressed adrenocorticotropic hormone, and low dehydroepiandrosterone sulfate. The patient initially declined surgery and was treated with mifepristone, a competitive glucocorticoid receptor antagonist. In addition to improvements in weight and hypertension, substantial reductions in her liver enzymes were noted, with complete normalization by 20 weeks of therapy. This case suggests that autonomous cortisol secretion from adrenal adenoma(s) could contribute to the metabolic and liver abnormalities in patients with NAFLD. In conclusion, successful management of CS with mifepristone led to marked improvement in the liver enzymes of a patient with long-standing NAFLD.
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http://dx.doi.org/10.1155/2017/6161348 | DOI Listing |
Eur J Prev Cardiol
January 2025
Department of Clinical Sciences and Community Health, University of Milan, Via Commenda 19, Milan 20122, Italy.
Liver Int
February 2025
Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing, China.
Background: Metabolic associated fatty liver disease (MAFLD), previously defined as non-alcoholic fatty liver disease (NAFLD), has been shown to be closely related to many environmental pollutants. Lately, we found methyl tert-butyl ether (MTBE), a new environmental pollutant, could increase NAFLD risk in American adults, which still needs more population epidemiological studies to verify, and its pathogenic mechanism is not yet clear.
Methods: We conducted a cross-sectional study among petrol station workers, diagnosed their MAFLD according to internationally recognised diagnostic criteria, assessed the potential association of MTBE exposure with MAFLD risk, and explored the miR-18a-5p/PXR/SREBP2 pathway as possible pathogenic mechanisms in male Wistar rats and HepaRG cells treated with MTBE.
Nutr Rev
January 2025
Faculty of Medicine, Pelita Harapan University, Tangerang, Banten 15811, Indonesia.
The demonization of seed oils "campaign" has become stronger over the decades. Despite the dietary guidelines provided by nutritional experts recommending the limiting of saturated fat intake and its replacement with unsaturated fat-rich food sources, some health experts ignore the dietary guidelines and the available human research evidence, suggesting the opposite. As contrarians, these individuals could easily shift public opinion so that dietary behavior moves away from intake of unsaturated fat-rich food sources (including seed oils) toward saturated fats, which is very concerning.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, 11651, Cairo, Egypt.
The clinical use of dexamethasone (DXM) is associated with the development of non-alcoholic fatty liver disease (NAFLD). However, the mechanisms by which DXM-induced NAFLD is still incompletely known. Therefore, the current study aims to test the hypothesis that DXM-induced NAFLD is mediated by dysregulation of key genes involved in lipid metabolism and liraglutide (LG) can ameliorate these effects.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang 550000, China.
Objectives: To investigate the regulatory role of nucleotide-bound oligomerized domain-like receptor containing pyrin-domain protein 6 (NLRP6) in liver lipid metabolism and non-alcoholic fatty liver disease (NAFLD).
Methods: Mouse models with high-fat diet (HFD) feeding for 16 weeks (=6) or with methionine choline-deficient diet (MCD) feeding for 8 weeks (=6) were examined for the development of NAFLD using HE and oil red O staining, and hepatic expressions of NLRP6 were detected with RT-qPCR, Western blotting, and immunohistochemical staining. Cultured human hepatocytes (LO2 cells) with adenovirus-mediated NLRP6 overexpression or knock-down were treated with palmitic acid (PA) in the presence or absence of compound C (an AMPK inhibitor), and the changes in cellular lipid metabolism were examined by measuring triglyceride, ATP and β-hydroxybutyrate levels and using oil red staining, RT-qPCR, and Western blotting.
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