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Background The association between serum 25-hydroxy vitamin D (25(OH)D) status and gestational diabetes mellitus (GDM) gained attention in recent years, however the conclusion is still controversial due to many interfering factors, such as region of living, environment, lifestyle, and food supplements. Other metabolites (laboratory parameters) are also important in reflecting gestational states. This study aimed to investigate the association of serum 25(OH)D status in early pregnancy with GDM and other laboratory parameters in pregnant women. Methods A total of 1516 pregnant women whose blood glucose were normal before pregnancy in the city of Foshan in Guangdong, China were enrolled in this study. GDM was diagnosed between 24 to 28 weeks of pregnancy following the guidelines from the American Diabetes Association. Maternal serum 25(OH)D and other laboratory parameters—including hematology, coagulation, chemistry, and bone density—were measured utilizing various analytical methods in clinical laboratory at gestational weeks 11 to 14. Results The average 25(OH)D concentration was 59.1 ± 12.6 nmol/L. None of the study subjects had 25(OH)D < 25 nmol/L; 434 (28.6%) women had 25(OH)D deficiency (< 50 nmol/L), 882 women (58.2%) had 25(OH)D insufficiency (50–74 mmol/L) and 200 women (13.2%) had 25(OH)D sufficiency (≥ 75 nmol/L). There were 264 (17.4%) women diagnosed with GDM. There was not, however, an association between serum 25(OH)D in early pregnancy and GDM. Interestingly, women with more parity and high serum alkaline phosphatase levels had higher serum 25(OH)D levels. There was a possible positive association between serum 25(OH)D and pre-albumin, and a possible negative association between serum 25(OH)D, creatinine, and thrombin time. This study did not find an association between serum 25(OH)D and bone density. Conclusions There were no associations between maternal serum 25(OH)D concentration in early pregnancy and the risk of GDM or bone density. There were, however, correlations between serum 25(OH)D and parity, seasoning at sampling, serum alkaline phosphatase, creatinine, pre-albumin, and coagulation factor thrombin time, which need further study to explain their pathophysiology and clinical significance.

Jiangmen is one of the Guangdong‐Hong Kong‐Macao Greater Bay Areas with frequent commercial intercourse, which is responsible for human immunodeficiency virus type 1 (HIV‐1) rapid circulation and genetic evolution for recent years. As a novel HIV‐1 second‐generation recombinant was previously reported in Jiangmen but the systematic molecular epidemiological investigation was still unknown. A retrospective study on HIV‐1 genotypic characteristics and the emergence of transmitted drug resistance in this region was necessary. A total of 224 newly diagnosed HIV‐positive cases were randomly selected in Jiangmen City of Guangdong Province between 2018 and 2019. The partial gag (1080 bp), pol (840 bp), and env (460 bp) genes were amplified using nested polymerase chain reaction followed by sequencing. The phylogenetic and recombination analysis as well as HIV‐1 drug resistance were performed to surveillance. Sexual transmission was determined to be the major risk factor in Jiangmen. Phylogenetic analysis detected the genotypic distribution as follows: CRF01_AE (36.65%,70 of 191), CRF07_BC (32.46%, 62 of 191), CRF08_BC (4.71%, 9 of 191), CRF55_01B (5.24%, 10 of 191), CRF59_01B (3.14%, 6 of 191), subtype B (4.71%, 9 of 191), subtype C (1.05%, 2 of 191) as well as unique recombinant forms (12.04%, 23 of 191) consisted of seven recombinant patterns, which originated from multiple regions of China. Low‐level prevalence of Surveillance Drug Resistance Mutations (2.1%) were predicted but drug‐resistant mutations showed at a high level (15.4%) especially mutations in RT gene at position 179 were found to be the most frequent in the therapy‐naïve population. Our study highlighted the critical importance of monitoring the emerge of recombinant strains among newly diagnosed HIV‐1 individuals along with drug resistance regularly to prevent multi‐channel introduction and breakout of new HIV strains.