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Objective: To investigate the correlation of blood glucose and islet function with serum retinol-binding protein 4, serum cystatin C, and nesfatin-1 levels in women with gestational diabetes mellitus. Methods: Between June 2018 and June 2020, 70 patients with gestational diabetes mellitus were included in a study group and 70 healthy pregnant women were recruited into a healthy group. Alterations in fasting blood glucose (FPG), glycated hemoglobin (HbA1c), fasting serum insulin (FINS), homeostatic model assessment for insulin resistance (HOMA-IR), serum retinol-binding protein 4 (RBP4), serum cystatin C (CysC), and nesfatin-1 of all eligible participants were analyzed, and the occurrence of complications was recorded. Correlation analysis of serum RBP4, serum CysC, and nesfatin-1 levels with blood glucose and islet function in women with gestational diabetes mellitus was performed. Results: Gestational diabetes mellitus was associated with significantly higher levels of FPG, HbA1c, and HOMA-IR and lower levels of FINS (6.58 ± 1.41, 9.24 ± 1.09, 3.21 ± 2.03, 8.23 ± 2.21) versus a healthy condition (5.23 ± 0.85, 7.61 ± 0.67, 2.42 ± 1.14, 10.54 ± 2.15) (P < 0.05). Women with gestational diabetes mellitus showed significantly higher levels of serum RBP4, serum CysC, and nesfatin-1 (62.45 ± 7.86, 1.95 ± 0.59, 2.65 ± 0.49) versus healthy pregnant women (45.48 ± 6.15, 1.03 ± 0.67, 1.42 ± 0.62) (P < 0.05). With serum RBP4, serum CysC, and nesfatin-1 as dependent variables, univariate correlation analysis showed that serum RBP4, serum CysC, and nesfatin-1 levels were positively correlated with FPG and HbA1c levels and HOMA-IR, and negatively correlated with FINS in women with gestational diabetes mellitus (P < 0.05). Gestational diabetes mellitus resulted in a significantly higher incidence of preterm delivery, cesarean section, excess amniotic fluid, and premature rupture of membranes versus a healthy status (P < 0.05). Conclusion: Glucose metabolism and islet function in women with gestational diabetes are significantly correlated with serum RBP4, serum CysC, and nesfatin-1 levels, which shows great potential for the prevention and treatment of gestational diabetes mellitus and perinatal complications.
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Background: Atrial fibrillation (AF) has been a worldwide health issue with increasing prevalence and mortality. Recently, increasing attention has been gained to the relationship between heart rate variability (HRV) and the clinical prognosis of AF catheter ablation. We aimed to evaluate the prognostic value of HRV in AF recurrence. Methods: We systematically searched Web of Science, PubMed, and Embase from inception until 17 August 2022 to conduct the systematic review and meta-analysis. We included the studies reporting the predictive value of HRV parameters for AF recurrence or in which HRV parameters in AF recurrence and non-recurrence groups were individually reported. Results: Finally, we enrolled 16 studies, including 2,352 patients. Higher rMSSD could independently predict AF recurrence following catheter ablation (OR: 1.02, 95% CI: 1.00-1.04; p = 0.03). Higher HF (OR: 1.55, 95% CI: 1.05-2.28; p = 0.03) and lower LF/HF (OR: 1.12, 95% CI: 1.03-1.20; p = 0.004) could independently predict AF recurrence within 1 year. Higher SDNN (OR: 1.02, 95% CI: 101-1.02; p = 0.0006) could independently predict AF recurrence among patients with paroxysmal AF. Almost all HRV parameters within 3 days after catheter ablation and lnHF, lnLF, and rMSSD at 3 months after catheter ablation performed significant differences in AF recurrence and non-recurrence groups. Conclusion: Heart rate variability, especially higher rMSSD (within short-term and long-term periods), was closely related to recurrent AF following catheter ablation, highlighting the clinical importance of HRV in the prognosis of AF following catheter ablation.
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Congenital nephrogenic diabetes insipidus (CNDI) is a rare hereditary tubular dysfunction caused mainly by X-linked recessive inheritance of AVPR2 gene mutations. Pathogenic genes are a result of mutations in AVPR2 on chromosome Xq28 and in AQP2 on chromosome 12q13. The clinical manifestations of CNDI include polyuria, compensatory polydipsia, thirst, irritability, constipation, developmental delay, mental retardation, persistent decrease in the specific gravity of urine, dehydration, and electrolyte disorders (hypernatremia and hyperchloremia). Herein, we report a rare case of CNDI caused by an AVPR2 mutation in a 2-year-old Chinese boy who had sustained polyuria, polydipsia, and irritability for more than 20 months. Laboratory examinations showed no obvious abnormality in blood sodium and chloride levels but decreased urine osmolality and specific gravity. Imaging findings were also normal. However, genetic analysis revealed a C > T transition leading to T273M missense mutations in AVPR2. We provided the boy a low-sodium diet and administered oral hydrochlorothiazide and indomethacin for 1 month, after which his clinical symptoms significantly improved. This case report suggests that CNDI is characterized by pathogenic T273M missense mutations alone and expands our understanding of the pathogenesis of CNDI.