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1.
Open Med (Wars) ; 18(1): 20230876, 2023.
Article in English | MEDLINE | ID: mdl-38152330

ABSTRACT

The association of thyroid hormone antibodies and glycolipid metabolism indicators with Type 2 diabetes mellitus (T2DM) was explored. As the disease worsens, the levels of thyroglobulin antibody (TGAb), thyroid peroxidase antibody (TPOAb), and thyroid-stimulating hormone (TSH) was increased, and the levels of total tri-iodothyronine (TT3) and total thyroxine (TT4) was decreased (P < 0.001). The severe, medium, and light group had higher level of high-density lipoprotein (HDL), lower level of total cholesterol (TC), low-density lipoprotein (LDL), glycosylated hemoglobin (HbA1c), triacylglycerol (TAG), and fasting blood sugar (FBG) than the control group (P < 0.05). The level of HDL was lower in the severe group than the light group and the medium group, but the levels of TC, LDL, HbA1c, TAG, and FBG were increased with the progress of T2DM (P < 0.001). The levels of TGAb, TPOAb, and TSH in patients with T2DM were positively correlated with the levels of TC, LDL, HbA1c, TAG, and FBG (P < 0.05), and were negatively correlated with HDL levels (P < 0.05). The life quality score was lower in the severe group than the light and the medium group (P < 0.001). Among the above indicators, the predictive value of TT3, TT4, and HbA1c in T2DM was better. Clinically, detecting the levels of thyroid hormone antibodies and glycolipid metabolism indicators had a certain predictive value for the severity of T2DM. Main findings: The results of this study found that the thyroid hormone antibody and glycolipid metabolism levels in T2DM patients were abnormal, and had different degrees of impact on the quality of life of patients. Thus, monitoring these indicators had certain predictive value for the severity of the disease, and also had a certain degree of suggestive effect on the evaluation of diabetic vascular complications. Clinically, attention should be paid to the screening of thyroid disease in diabetic patients, and the assessment and prognosis of thyroid function on diabetes, the control of diabetes, and the prevention and treatment of complications have important clinical significance.

2.
Diabetes Metab Syndr Obes ; 16: 2225-2232, 2023.
Article in English | MEDLINE | ID: mdl-37525823

ABSTRACT

Background: Thyroxine binding globulin (TBG) deficiency is a rare thyroid disease, mostly caused by genetic mutations and acquired by X-linked recessive inheritance. The clinical features of children with TBG deficiency and their family members were summarised and the Serpina7 gene mutation was analysed, providing a reference for the differentiation of TBG deficiency. Methods: Thyroid function was detected in TBG deficient patients, and genetic analysis was performed using polymerase chain reaction (PCR) and direct DNA sequencing to detect the characteristics of TBG mutants. Using "thyroxine binding globulin, gene and mutation" as keywords, PubMed (biomedical literature database), Web of Science and other databases were searched for relevant studies to collect and summarise relevant information. Results: The TBG (14.7 µg/mL), 70% triiodothyronine (T3) (<0.3 nmol/L), total T3 (Tr3) (<0.05 ng/mL) and thyroxine (T4) (14.72 nmol/L) values were lower than normal, while the thyrotropin (TSH) (2.33 uIU/mL), free T3 (FT3) (1.62 pmol/L), and free T4 (FT4) (11.39 pmol/L) values were normal. These values indicate a TBG partially deficient phenotype. Using PCR amplification and direct sequencing of the target gene, a missense mutation in exon 4 of the Serpina7 gene was found in the patient and the father, and the nucleic acid variant was C.909 (exon 4) g > T; the patient was heterozygous and the father was hemizygous. The literature search retrieved a total of 45 studies, most of which were related to mutations in the Serpina7 gene. The mutation locations included exons, introns, enhancers and promoters, with exons the predominant location. A total of 49 variants of the Serpina7 gene were identified. Conclusion: Serpina7 C.909G (P.L303F) is a mutation acquired from the father by X-linked recessive inheritance. The main clinical features of TBG deficiency patients are low serum T4, T3 and TBG levels, normal TSH, FT3 and FT4 levels, and no clinical manifestations.

3.
Endocr Connect ; 10(12): 1550-1559, 2021 Nov 29.
Article in English | MEDLINE | ID: mdl-34739389

ABSTRACT

OBJECTIVES: A variety of factors differed between rural and urban areas may further influence iodine status and thyroid structure. Hence, this study compared iodine nutrition, the prevalence of thyroid goiter, and nodules between rural and urban residents in Guangzhou, a southern coastal city of China. METHODS: A total of 1211 rural residents and 1305 urban residents were enrolled in this cross-sectional study. A questionnaire regarding personal characteristics was administered. Urinary iodine concentration (UIC) was examined. Ultrasonography of the thyroid was performed to evaluate thyroid goiter and nodules. Multiple logistic analysis was used to identify the potential associated factors. RESULTS: The median UIC was significantly lower in rural residents than in urban residents (120.80 µg/L vs 136.00 µg/L, P < 0.001). Although the coverage rate of iodized salt was much higher in rural residents than in urban residents (99.59% vs 97.29%, P < 0.001), the percentages of seafood intake (8.60% vs 29.29%, P < 0.001), iodine-containing drug consumption (0.33% vs 1.24%, P = 0.011), and iodine contrast medium injection (0.58% vs 1.87%, P = 0.004) were lower in rural residents than in urban residents. Both the prevalence of thyroid goiters and nodules was significantly higher in rural residents than in urban residents (goiter: 8.06% vs 1.20%, P < 0.001; nodules: 61.89% vs 55.04%, P = 0.023). Living in rural areas was associated with thyroid goiter (OR 5.114, 95% CI 2.893-9.040, P < 0.001). CONCLUSIONS: There were differences in iodine nutrition and the prevalence of thyroid goiter and nodules in rural and urban residents in Guangzhou. Differentiated and specialized monitoring is recommended in our area.

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