Pathogenesis and genetic factors influencing predisposition to antituberculosis drug-induced hepatotoxicity (ATDH) are not clear. Polymorphism at the genetic locus of a drug and xenobiotic compound metabolizing enzyme, N-acetyltransferase type 2 (NAT2), is reported to be associated with the excess generation of toxic reactive metabolites. To date, many case-control studies have been carried out to investigate the relationship between the NAT2 polymorphisms and ATDH, but the results have been inconsistent. To investigate this inconsistency, a meta-analysis was performed. Databases including PubMed, Web of Science, EMBASE and CNKI were searched to find relevant studies. A total of 26 case-control studies, involving 1,198 cases and 2,921 controls were included. Overall, we found significant association between slow acetylator genotype of NAT2 and ATDH (OR = 3.10, 95% CI: 2.47-3.88, P < 10(-5)). Significant results were also found in East Asians, South Asians, Brazilians and Middle Eastern when stratified by ethnicity. However, no significant associations were found for Caucasians. This meta-analysis demonstrated that the slow acetylator genotype of NAT2 is a risk factor associated with increased ATDH susceptibility, but these associations vary in different ethnic populations.
Background: Glycated hemoglobin (HbA1c) is commonly used in the diagnosis and evaluation of glycemic control in diabetes, and it may be influenced by several non-glycemic and glycemic factors, including albumin. This retrospective study investigated the influence of albumin on HbA1c and HbA1c-defined glycemic status.Methods: The demographic, hematological, and biochemical data were collected for 11,922 patients undergoing routine physical examination. Univariate and multivariate linear regression analyses, stratified analyses and interaction analyses, and multiple logistic regression were conducted to identify the association between albumin and HbA1c in people with different glycemic status.Results: HbA1c levels were inversely associated with serum albumin level (P < 0.0001) in all participants. Risk factors leading to the association included age > 45 years, high fasting plasma glucose (≥7.0 mmol/L), and anemia. The negative association between HbA1c and albumin was curved (P < 0.0001) and had a threshold effect in the HbA1c-defined diabetic population; the association was significantly stronger when the albumin level fell below 41.4 g/L (β: −0.31, 95% CI: −0.45 to −0.17, P < 0.0001). A 2 g/L increase in albumin reduced the odds of HbA1c-defined dysglycemia, diabetes, and poor glycemia control by 12% to 36%, after adjustment for all possible confounders.Conclusions: HbA1c was inversely associated with albumin level in all participants, and the association was significantly stronger in people with diabetes (defined by HbA1c criteria). For diabetic patients with lower albumin level, there was an increased risk of an erroneous HbA1c-based identification and management of glycemic status.
Backgound: Glycated hemoglobin (HbA1c) is commonly used in the diagnosis and evaluation of glycemic control in diabetes, and may be influenced by several non-glycemic and glycemic factors, including albumin. This retrospective study investigated the influence of albumin on HbA1c and HbA1c-defined glycemic status. Methods: The demographic, hematological, and biochemical data were collected for 11,922 patients undergoing routine physical examination. Univariate and multivariate linear regression analyses, stratified analyses and interaction analyses, and multiple logistic regression were conducted to identify the association between albumin and HbA1c in people with different glycemic status. Results: HbA1c levels were inversely associated with serum albumin level ( P < 0.0001) in all participants. Risk factors leading to the association included age >45 years, high fasting plasma glucose (≥7.0 mmol/L), and anemia. The negative association between HbA1c and albumin was curved ( P < 0.0001) and had a threshold effect in the HbA1c-defined diabetic population; the association was significantly stronger when the albumin level fell below 41.4 g/L (β: –0.31, 95% CI: –0.45 to –0.17, P < 0.0001). A 2 g/L increase in albumin reduced the odds of HbA1c-defined dysglycemia, diabetes, and poor glycemia control by 12% to 36%, after adjustment for all possible confounders. Conclusions: HbA1c was inversely associated with albumin level in all participants, and the association was significantly stronger in people with diabetes (defined by HbA1c criteria). For diabetic patients with lower albumin level, there was an increased risk of an erroneous HbA1c-based identification and management of glycemic status.
The established two-compartment model with first-order absorption and elimination successfully described the pharmacokinetic characteristics of rE-4 in Chinese patients with T2DM. .
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