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Background: Smoking or weight loss is a risk of tuberculosis (TB) development. However, the impact of weight change after smoking cessation on the occurrence of TB remains elusive. We aimed to determine the relationship between weight change after smoking cessation and the risk of TB development. Methods: We conducted a population-based cohort study using the national database in Republic of Korea. Of the 10,490,491 subjects who underwent health check-up in 2009, we enrolled 9,953,124 subjects without a previous TB history and followed them until 2017. We divided all study participants into the following three groups: never, former, and current smokers. The primary endpoint was newly developed TB. Results: Among 9,953,124 subjects analyzed, 5,922,845 (59.5%) were never smokers, 1,428,209 (14.4%) were former smokers, and 2,602,080 (26.1%) were current smokers. The risk of TB development was significantly higher in current smokers than in never smokers (adjusted hazard ratio (aHR) 1.158; 95% confidence interval [CI] 1.131–1.186). Among current smokers, individuals who stopped smoking and maintained weight after baseline evaluation had a significantly lower risk of TB development compared with those who continued to smoke (aHR 0.771; 95% CI 0.741–0.892). However, even after smoking cessation, individuals who lost weight were at a significantly higher risk of TB development compared with those who continued to smoke (aHR 1.327; 95% CI 1.119–1.715). Conclusions: Our findings suggest that smoking is a risk factor for TB and weight maintenance (neither gaining or losing) after quitting smoking might reduce the risk of TB development. [ABSTRACT FROM AUTHOR]

Aims Individuals without traditional cardiovascular risk factors (CVRFs) still experience adverse events in clinical practice. This study evaluated the predictors of subclinical coronary atherosclerosis in individuals without traditional CVRFs. Methods and results A total of 1250 (52.8 ± 6.5 years, 46.9% male) asymptomatic individuals without CVRFs who underwent coronary computed tomographic angiography for a general health examination were analysed. The following were considered as traditional CVRFs: systolic/diastolic blood pressure ≥140/90 mmHg; fasting glucose ≥126 mg/dL; total cholesterol ≥240 mg/dL; low-density lipoprotein cholesterol (LDL-C) ≥160 mg/dL; high-density lipoprotein cholesterol <40 mg/dL; body mass index ≥25.0 kg/m2; current smoking status; and previous medical history of hypertension, diabetes, and dyslipidaemia. Subclinical atherosclerosis, defined as the presence of any coronary plaque, was present in 20.6% cases; the incidences of non-calcified, calcified, and mixed plaque were 9.6%, 12.6%, and 2.6%, respectively. Multivariate regression analysis showed that LDL-C level [odds ratio (OR): 1.008; 95% confidence interval (CI): 1.001–1.015], together with age (OR: 1.101; 95% CI: 1.075–1.128) and male sex (OR: 5.574; 95% CI: 3.310–9.388), was associated with the presence of subclinical atherosclerosis (All P  < 0.05). LDL-C level was significantly associated with an increased risk of calcified plaques rather than non-calcified or mixed plaques. Conclusion LDL-C, even at levels currently considered within normal range, is independently associated with the presence of subclinical coronary atherosclerosis in individuals without traditional CVRFs. Our results suggest that a stricter control of LDL-C levels may be necessary for primary prevention in individuals who are conventionally considered healthy. [ABSTRACT FROM AUTHOR]

Osteonecrosis of the femoral head (ONFH) is a complex and multifactorial disease that is influenced by a number of genetic factors in addition to environmental factors. Some autoimmune disorders, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), are associated with the development of ONFH. Complement receptor type 2 (CR2) is membrane glycoprotein which binds C3 degradation products generated during complement activation. CR2 has many important functions in normal immunity and is assumed to play a role in the development of autoimmune disease. We investigated whether CR2 gene polymorphisms are associated with risk of ONFH in SLE patients. Eight polymorphisms in the CR2 gene were genotyped using TaqMan™ assays in 150 SLE patients and 50 ONFH in SLE patients (SLE_ONFH). The association analysis of genotyped SNPs and haplotypes was performed with ONFH. It was found that three SNPs, rs3813946 in 5′-UTR (untranslated region), rs311306 in intron 1, and rs17615 in exon 10 (nonsynonymous SNP; G/A, Ser639Asn) of the CR2 gene, were associated with an increased risk of ONFH under recessive model (P values; 0.004~0.016). Haplotypes were also associated with an increased risk (OR; 3.73~) of ONFH in SLE patients. These findings may provide evidences that CR2 contributes to human ONFH susceptibility in Korean SLE patients. [ABSTRACT FROM AUTHOR]