Nonalcoholic fatty liver disease: The most common cause of abnormal liver enzymes in the U.S. population

2001 ◽  
Vol 120 (5) ◽  
pp. A65-A65 ◽  
Author(s):  
J CLARK ◽  
F BRANCATI ◽  
A DIEHL
Author(s):  
Anastasia-Stefania Alexopoulos ◽  
Ryan Duffy ◽  
Elizabeth A Kobe ◽  
Jashalynn German ◽  
Cynthia A Moylan ◽  
...  

Abstract Individuals with type 2 diabetes (T2DM) are at high risk for nonalcoholic fatty liver disease (NAFLD), and evidence suggests that poor glycemic control is linked to heightened risk of progressive NAFLD. We conducted an observational study based on data from a telehealth trial conducted in 2018-2020. Our objectives were to: 1) characterize patterns of NAFLD testing/care in a cohort of individuals with poorly-controlled T2DM; and 2) explore how lab-based measures of NAFLD (e.g., liver enzymes, fibrosis-4 [FIB-4]) vary by glycemic control. We included individuals with poorly-controlled T2DM (n=228), defined as hemoglobin A1c (HbA1c) ≥ 8.5% despite clinic-based care. Two groups of interest were: 1) T2DM without known NAFLD; and 2) T2DM with known NAFLD. Demographics, medical history, medication use, glycemic control (HbA1c) and NAFLD testing/care patterns were obtained by chart review. Among those without known NAFLD (n=213), most were male (78.4%) and self-identified as Black race (68.5%). Mean HbA1c was 9.8%. Most had liver enzymes (85.4%) and platelets (84.5%) ordered outpatient over a 2-year period that would allow for FIB-4 calculation, yet only 2 individuals had FIB-4 documented in clinical notes. Approximately one third had abnormal liver enzymes at least once over a 2-year period, yet only 7% had undergone liver ultrasound and 4.7% had referral placed to Hepatology. Among those with known NAFLD (n=15), mean HbA1c was 9.5%. Only 4 individuals had undergone transient elastography, half of whom had advanced fibrosis. NAFLD is underrecognized in poorly-controlled T2DM, even though this is a high-risk group for NAFLD and its complications.


2019 ◽  
Vol 68 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Kyungeh An ◽  
Angela Starkweather ◽  
Jamie Sturgill ◽  
Jeanne Salyer ◽  
Richard K. Sterling

Obesity ◽  
2013 ◽  
Vol 22 (1) ◽  
pp. 292-299 ◽  
Author(s):  
Andrea L. C. Schneider ◽  
Mariana Lazo ◽  
Elizabeth Selvin ◽  
Jeanne M. Clark

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Enzo Ragucci ◽  
Dat Nguyen ◽  
Michele Lamerson ◽  
Andreas G. Moraitis

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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