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The association of serum total bile acid with non-alcoholic fatty liver disease in Chinese adults: a cross sectional study
Background
Non-alcoholic fatty liver disease (NAFLD) is currently the major cause of chronic liver disease globally. Bile acids (BAs) have emerged as relevant signaling molecules that are associated with NAFLD development. This study was aimed to examine the association of serum total bile acids (TBAs) with NAFLD in a large population of Chinese subjects.
Methods
This cross sectional study recruited 152,336 participants from the Second Xiangya Hospital, China. NAFLD was diagnosed based on the presence of hepatic steatosis on ultrasonography, without significant alcohol consumption and other known causes for chronic liver disease. A multivariate logistic regression model was used to test for the association of serum TBAs with NAFLD, adjusting for conventional risk factors of NAFLD.
Results
A total of 27.4% of the participants had NAFLD. Patients with NAFLD had slightly higher TBA levels than those without, 3.4 vs. 3.0 μmol/L (p < 0.001). However, TBA levels were not associated with NAFLD in the multivariate logistic regression model, which adjusted for age, gender and other acknowledged risk factors for NAFLD (OR = 1.00. 95% CI: 1.00–1.00, p = 0.797).
Conclusions
We found that the serum TBA levels were not associated with NAFLD. Future studies in a large population, focusing on serum BA composition may improve the understating of the role of BAs in NAFLD
The Many Faces of Purpura: Vancomycin-Induced Leukocytoclastic Vasculitis
Leukocytoclastic vasculitis is a rare form of immune-mediated vasculitis that might be caused by infections or autoimmune diseases or might be precipitated by specific medications. We describe a 65-year-old patient, who was receiving vancomycin for a methicillin-sensitive Staphylococcus aureus permacath infection. Vancomycin was chosen due to medication non-adherence and the patient’s desire to receive antimicrobial therapy in conjunction with his scheduled dialysis sessions. The patient’s medical history was notable for untreated hepatitis C infection and end-stage renal disease, requiring hemodialysis three times a week. Vancomycin was administered during dialysis sessions. After one week of therapy, the patient developed bilateral lower extremity purpura. Skin biopsy was suggestive of leukocytoclastic vasculitis with an absence of intravascular thrombi. Serum cryoglobulins were negative, making cryoglobulinemia due to HCV infection unlikely. Following cessation of vancomycin therapy, the rash gradually disappeared with scarring in the form of post-purpuric hyperpigmentation. Despite its widespread use, vancomycin is a rare cause of leukocytoclastic vasculitis. Clinicians should keep in mind a wide range of differential diagnosis of bilateral lower extremity purpura as treatment differs depending on its underlying etiology