Untreated Prior Pulmonary Tuberculosis Adversely Affects Pregnancy Outcomes in Infertile Women Undergoing in vitro Fertilization and Embryo Transfer: A Large Retrospective Cohort Study.

OBJECTIVE: Prior pulmonary tuberculosis (PTB) on chest X-ray (CXR) was commonly found in infertile patients receiving examinations before in vitro fertilization and embryo transfer (IVF-ET). It was unclear whether untreated PTB would affect pregnancy outcomes after IVF-ET. METHOD: We conducted a retrospective cohort study of 14,254 infertile patients who had received IVF-ET at Peking University Third Hospital in 2017. Prior PTB was defined as the presence of signs suggestive of old or inactive PTB on CXR, with or without a clinical TB history. Patients who had prior PTB on CXR but had not received a clinical diagnosis and anti-TB therapy were included for analysis. Live birth, clinical pregnancy, and miscarriage rates were compared between the untreated PTB and non-PTB groups. RESULTS: The untreated PTB group had significantly lower clinical pregnancy (31.7% vs. 38.1%) and live birth (23.8% vs. 30.6%) rates than the non-PTB group (both P < 0.001). Multivariate analysis revealed that untreated PTB was a risk factor for decreased live birth rate [odds ratio ( OR), 0.80; 95% confidence interval ( CI), 0.66-0.98; P = 0.028] in all patients and for increased miscarriage ( OR, 4.19; 95% CI, 1.69-10.39; P = 0.002) and decreased live birth ( OR, 0.45; 95% CI, 0.24-0.83; P = 0.011) rates in patients with unexplained infertility. CONCLUSIONS: Untreated PTB was associated with adverse pregnancy outcomes after IVF-ET, especially in patients with unexplained infertility, highlighting the clinical significance of PTB in this specific patient population.

Association of gene polymorphisms of tumour necrosis factor-alpha and interleukin-13 with chronic obstructive pulmonary disease in Han nationality in Beijing.

BACKGROUND: Genetic factors are believed to play a role in the individual susceptibility to chronic obstructive pulmonary disease (COPD). A single nucleotide polymorphism (SNP) of tumour necrosis factor-alpha (TNF-alpha) has been reported but inconsistent results may arise from different populations and phenotypes of COPD. There are only a few published studies of interleukin-13 (IL-13) SNPs on COPD. The SNPs of TNF-alpha and IL-13 have not been studied in the Chinese population. This research was conducted to study the frequencies of IL-13 gene promoter 1055 (IL-13-1055) and TNF-alpha gene-308 polymorphisms in the patients with COPD and to investigate the effect of those genetic polymorphisms on COPD in the Chinese population. METHODS: A cohort of COPD patients and age matched controls were recruited from an inpatient hospital service in Beijing. Venous blood was obtained and genomic DNA was extracted from peripheral blood monocytes using standard method. Genomic DNA was used as a template for amplification by polymerase chain reaction (PCR) to determine the polymorphism at -1055 in the IL-13 gene promoter region. PCR restriction fragment length polymorphism (RFLP) was used to determine polymorphisms in the TNF-alpha gene-308 position. The products were investigated by sequence analysis also. RESULTS: One hundred and eleven COPD patients and 97 controls were studied. Seventy-five cases were current smokers in COPD patients and 36 were current smokers in controls. The frequencies of TT genotype in the IL-13 gene promoter region were 11.7% (13/111) in the COPD group and 13.4% (13/97) in the controls (P = 0.713). However, the OR value of TT genotype was significantly increased to 6.4 (95% CI 1.62 - 25.39) in the smokers with COPD. TT genotype was also positively related to family history of COPD, OR = 7.7 (95% CI 1.37 - 43.80). The frequencies of A allele in the TNF-alpha gene were 5.9% in COPD and 3.1% in controls (P = 0.131). The OR value of A allele was 5.0 (95% CI 1.011 to 25.059) in smokers with COPD. CONCLUSIONS: There is no significant difference in the frequencies of the TT genotype of IL-13-1055 or the A allele of the TNF-alpha between Han Chinese patients with COPD versus control. Thus, it does not appear that these SNPs are independent factors in COPD for Han nationality in Beijing. However, these SNPs may increase the risk of COPD among smokers.

[The study of interleukin-13 gene promoter polymorphism in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To study the frequencies of interleukin-13 (IL-13) gene promoter 1055 (IL-13-1055) polymorphism in patients with chronic obstructive pulmonary disease (COPD) and to investigate the effect of this genetic polymorphism on COPD in Chinese. METHODS: The polymorphism in 111 COPD patients and 97 controls who had non-obstructive pulmonary disease were studied. Genomic DNA was extracted from peripheral blood mononuclear cells by using standard high-concentration salt method. Genomic DNA was used as a template for amplification by polymerase chain reaction (PCR)-amplification of specific allele (PASA) to determine the polymorphism at -1055 in the IL-13 gene promoter region. The production was investigated by sequence analysis. SPSS was used for statistical analysis. chi(2) test was used to examine the genotype in COPD patients and controls. Logistic regression analysis was used to exclude confounding factors and evaluate the effect of smoking or family history on COPD combining with gene polymorphism. RESULTS: The frequency of TT genotype in COPD was 11.7% (13/111), and 13.4% (13/97) in control group, P = 0.713. P value was increased to 0.244 using logistic regression analysis excluded confounding factors, including age, gender, smoking and combined diseases. TT genotype can increase the risk of smoking to COPD, OR = 6.40 (95% CI: 1.62 - 25.39) when the data was stratified by smoking status. TT genotype was positively related with family history of COPD, OR = 7.67 (95% CI: 1.37 - 43.80) using multiple factors regression analysis to clinic phenotype and TT genotype. CONCLUSION: TT genotype of IL-13-1055 is not an independent factor for COPD in Chinese Han people in Beijing, but increases the risk for smokers to develop COPD and the one who has COPD family history as well.