Objective:To investigate the influence of cytochrome P450 2A6 (CYP2A6) gene polymorphisms on liver function injury in patients with hyperthyroidism treated with methimazole.Methods:The study selected 90 patients with hyperthyroidism who were treated with methimazole in the Department of Thyroid Surgery at the First Affiliated Hospital of Zhengzhou University from Sept. 2023 to Aug. 2024 as the research subjects. Based on the occurrence of liver injury, they were divided into a liver injury group ( n=36) and a non-liver injury group (n=54). Peripheral blood DNA was extracted from the patients, and the CYP2A6 gene genotypes (rs8192725, rs8192720, and rs28399433) were detected using the polymerase chain reaction (PCR) amplification method. The association between CYP2A6 gene polymorphisms and liver injury induced by methimazole treatment in hyperthyroidism was analyzed. Results:The comparison of genotype distribution frequencies at the rs8192725 locus between the liver injury group and the non-liver injury group showed a statistically significant difference ( P<0.05). The AG and GG genotypes at the rs8192725 locus were protective factors against liver injury in patients with hyperthyroidism (AG vs. AA, OR: 0.21; 95% CI: 0.08-0.57; P<0.05; GG vs. AA, OR: 0.24; 95% CI: 0.06-0.89; P<0.05; AG+GG vs. AA, OR: 0.22; 95% CI: 0.09-0.54; P<0.05). The frequency of the G allele of rs8192725 in the liver injury group was significantly lower than that in the non-liver injury group (G vs. A, OR: 0.36; 95% CI: 0.19-0.70; P<0.05), indicating that it is a protective factor for liver injury in hyperthyroid patients receiving methimazole treatment. Conclusions:The CYP2A6 gene polymorphism at the rs8192725 locus is associated with the occurrence of liver injury in patients with hyperthyroidism treated with methimazole. The G allele may be a protective factor against liver injury in patients with hyperthyroidism, suggesting that individualized treatment plans can be developed based on the patient's genotype.

Objective:To investigate the influence of cytochrome P450 2A6 (CYP2A6) gene polymorphisms on liver function injury in patients with hyperthyroidism treated with methimazole.Methods:The study selected 90 patients with hyperthyroidism who were treated with methimazole in the Department of Thyroid Surgery at the First Affiliated Hospital of Zhengzhou University from Sept. 2023 to Aug. 2024 as the research subjects. Based on the occurrence of liver injury, they were divided into a liver injury group ( n=36) and a non-liver injury group (n=54). Peripheral blood DNA was extracted from the patients, and the CYP2A6 gene genotypes (rs8192725, rs8192720, and rs28399433) were detected using the polymerase chain reaction (PCR) amplification method. The association between CYP2A6 gene polymorphisms and liver injury induced by methimazole treatment in hyperthyroidism was analyzed. Results:The comparison of genotype distribution frequencies at the rs8192725 locus between the liver injury group and the non-liver injury group showed a statistically significant difference ( P<0.05). The AG and GG genotypes at the rs8192725 locus were protective factors against liver injury in patients with hyperthyroidism (AG vs. AA, OR: 0.21; 95% CI: 0.08-0.57; P<0.05; GG vs. AA, OR: 0.24; 95% CI: 0.06-0.89; P<0.05; AG+GG vs. AA, OR: 0.22; 95% CI: 0.09-0.54; P<0.05). The frequency of the G allele of rs8192725 in the liver injury group was significantly lower than that in the non-liver injury group (G vs. A, OR: 0.36; 95% CI: 0.19-0.70; P<0.05), indicating that it is a protective factor for liver injury in hyperthyroid patients receiving methimazole treatment. Conclusions:The CYP2A6 gene polymorphism at the rs8192725 locus is associated with the occurrence of liver injury in patients with hyperthyroidism treated with methimazole. The G allele may be a protective factor against liver injury in patients with hyperthyroidism, suggesting that individualized treatment plans can be developed based on the patient's genotype.

BACKGROUND: Recent study showed that osteocalcin may elevate Insulin secretion and sensitivity, prevent the fat accumulation, play a role in the metablism of glucose and lipid. Undercarboxylated osteocalcin works as the main role. OBJECTIVE: To investigate the effect of different concentrations of glucose on osteoblast undercarboxylated osteocalcin. METHODS: The rib trabeculae were resected and broken, trypsinizated and washed completely by PBS. Bone surface and non-adhesive floating cells in cleaning fluid were observed with inverted microscope. Rib trabeculae was washed by DMEM culture medium once, and cultured in culture bottle. The culture liquid was replaced by new one once a week. The osteoblast was moved from the scledte a week later. The cells were fused monolayer and could be subcultured 4 to 6 weeks later. The active second or third generation cells were inoculated to 6-pore plate forming 5 groups. Osteoblast were stimulated by 5.6 mmol/L., 7.6 mmol/L, 9.6 mmol/L, 12.6 mmol/L, 20.6 mmol/L glucose medium respectively after the 80% cells were fused, the vitamin K_2 was added into the culture liquid until the concentration of it to be 10~(-5) mol/L. Supernatant was collected after half hour culturing, the undercarboxylated osteocalcin level were detected with RIA test kit, and corrected it as the total the undercarboxylated osteccalcin, calculated the carboxylated incomplete osteocalcin rate. RESULTS AND CONCLUSION: The rate of ostecblast carboxylated incomplete osteocalcin was different under different concentration glucose. The rate of 7.6 mmol/L, 9.6 mmol/L, 20.6 mmol/L concentration glucose groups were higher than that of 5.6 mmol/L glucose group [(0.27±0.02)%, (0.29±0.04)%, (0.12±0.02)%, P < 0.05]. It is indicated that osteoblast could sense the change of glucose concentration by regulating the secretion of the undercarboxylated osteocalcin between the concentration of 5.6mmol/L to 9.6mmol/L, while the carboxylated incomplete osteocalcin decreased as the concentration of glucose increased.