Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the work was to establish the frequency and conditions in which structural and functional changes of the liver might occur in case of long-term amiodarone use, depending on thyroid dysfunction. The study included 80 patients with cardiosclerosis with atrial fibrillation (AF). The patients were assigned to: group I (n=60) - received amiodarone at a maintenance dose for one year (on background of basic therapy); control group (CG) - patients (n=20) who received on the background of basic therapy digoxin and bisoprolol. Biochemical tests were conducted: fT3, thyroid-stimulating hormone (TSH), fT4, anti-TPO Ab, transaminases (ALT, AST), alkaline phosphatase (AF), total bilirubin, thymol test (TT), arginase, gama glutamil transpeptidase (GGT). Thyroid dysfunction during administration of amiodarone was detected in 20 (33.3%) patients of group I - amiodarone-induced hypothyroidism (AmIH) in 12 (20.0%) patients, amiodarone-induced thyrotoxicosis (AmIT) in 8 (13.3%) patients. Cholestasis was detected in 83,3% of patients with AmIH and 75,0% with AmIT, which was accompanied by an increase of the AF activity and GGT, which were more pronounced in case of AmIH. More than half of patients with AmIT presented with increased total bilirubin, ALT and AST activity opposed to sixth of AmIG patients. Increased arginase activity, tendency to increase of TT was determined in almost half of patients with AmIG and AmIT. Amiodarone-induced thyroid dysfunction is characterized by the development of drug-induced hepatocellular toxicity, which is manifested by a cholestatic, cytolytic syndrome and accompanied by an energetic changes in hepatocytes.
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PMID:[HEPATOCELLULAR TOXICITY IN THE BACKGROUND OF AMIODARON-INDUCED THYROID DYSFUNCTION IN PATIENTS WITH ATRIAL FIBRILLATION]. 3201 1

Thyroid function and type 2 diabetes mellitus (T2DM) are both associated with increased risks of adverse clinical outcomes in nonalcoholic fatty liver disease (NAFLD). Our study is aimed at evaluating the association between thyroid function and NAFLD in T2DM patients with normal thyroid function (euthyroid) and analyzing the potential effects of metformin on the pathological process. Overall, 369 T2DM patients were enrolled between July 2017 and September 2018 and stratified into NAFLD and non-NAFLD groups. Data on age, gender, body mass index (BMI, kg/m2), metformin use, and basal metabolic rate (BMR) were obtained from participants' records. All patients were tested for biochemical markers, indexes of glucose metabolism, lipid metabolism, bone metabolism, and thyroid function at baseline. Multivariate analyses detected increased odds of NAFLD among individuals with T2DM per unit increase in their BMI and free triiodothyronine (FT3) and thyroid stimulating hormone (TSH); the odds ratios (OR) were 1.25, 3.02, and 1.58, respectively (all p < 0.05). Positive correlations were detected between alanine aminotransferase (ALT) and FT3 (r = 0.221, p = 0.010), and negative correlations were noted between TSH and BMR (r = -0.618, p < 0.001) and between BMR and FT3 (r = -0.452, p < 0.001) in T2DM subjects with NAFLD. A significant difference in serum FT3 (t = 2.468, p = 0.0167) and TSH (t = 2.658, p = 0.010) levels was found between obese individuals with NAFLD who used and did not use metformin. The pathological mechanism of T2DM complicated by NAFLD in euthyroid patients may be associated with insulin resistance and a thyroid hormone resistance-like manifestation, i.e., relevant hypothyroidism. Metformin can potentially decrease the double-resistance situation, especially in obese individuals.
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PMID:Association between Thyroid Function and Nonalcoholic Fatty Liver Disease in Euthyroid Type 2 Diabetes Patients. 3296 54


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