Relationship between NAT2 polymorphisms and onset risk of acute leukemia: a systematic review and meta-analysis.

OBJECTIVE: This meta-analysis aims to clarify the correlation between N-acetyltransferases 2 (NAT2) polymorphisms and susceptibility of acute leukemia. MATERIALS AND METHODS: Articles reporting the correlation between NAT2 polymorphisms and susceptibility of acute leukemia were searched from PubMed, Embase, and Cochrane. Citations in eligible articles were manually reviewed. Only cohort studies and case-control studies which provided odds ratio (OR) and 95% confidence interval (CI) of the correlation between NAT2 polymorphisms and susceptibility of acute leukemia up to December 1st, 2018 were enrolled. The included data were weighted by an inverse variance and analyzed using the fixed-effects or random-effects model. The data acquisition and the heterogeneity test were conducted. STATA 12.0 was used for statistical analysis. RESULTS: This meta-analysis enrolled 10 independent case-control studies with 1,874 leukemia patients and 2,789 healthy volunteers. No significant difference was found between the fast-acetylator incidence of NAT2 haplotype and the onset risk of acute lymphoblastic leukemia (ALL, OR=0.70, 95% CI=0.45-1.08) or acute myeloid leukemia (AML, OR=0.79, 95% CI=0.46-1.47). The subgroup analysis was conducted based on the sources of controls (SOCs). We did not find statistical difference in population-based (PB) group (OR=0.82, 95% CI=0.47-1.42) and hospital-based (HB) group (OR=0.54, 95% CI=0.27-1.08). In addition, the fast-acetylator incidence of NAT2 haplotype was only observed to be higher in ALL patients compared with HB group (OR=0.52, 95% CI=0.33-0.83), rather than the PB group (OR=0.82, 95% CI=0.47-1.44). CONCLUSIONS: Except for ALL patients and those hospital-based controls, no evidence has shown the relationship between NAT2 polymorphisms and the susceptibility of acute leukemia. This conclusion still needs to be further verified in multi-center hospital with a large sample size.

[The clinical analysis of corneal interface fluid syndrome after Laser lamellar corneal refractive surgery].

Objective: To analysis, the clinical characteristics, refractive changes, and clinical treatment of interface fluid syndrome after laser lamellar corneal refractive surgery. Methods: During Dec. 2010 to Apr. 2016. In total 6 cases(9 eyes), 3 cases were bilateral, 3 cases were unilateral. Five patients were male and 1 was female. The age of the patients ranged from 20 to 29 years was (24.83±4.02) years. Six cases(9 eyes)of IFS were diagnosed at our hospital. The history and complete ophthalmic examination that include Slit-lamp examination, Slit-lamp photography, refraction, corneal thickness measurement, corneal endothelial cell counting, IOP, anterior segment OCT(AS-OCT), exams were recorded. Results: Post-lasik Primary open angle glaucoma was 2 eyes in 1 patient. 1 patient(1 eye)was Posner-Schlossmann Syndrome and 1 patient(1 eye)was iritis after femtosecond laser. Post-small incision lenticule extraction by steroid drops induced elevated IOP were 5 eyes in 3 patients. Slit-lamp exam indicated edematous corneal flap or cap, lamellar haze, interface fluids accumulation. AS-OCT showed obvious interface dark area. The corneal flap or cap thickening and wrinkles, IOP change, diopter myopic shift, Corneal thickening. Conclusions: IFS is a rare but serious complication after Laser lamellar corneal refractive surgery. The main causes are high intraocular pressure and/or dysfunction of corneal endothelium. For patients with high IOP after laser lamellar corneal refractive surgery, follow up should be observed closely. accurate diagnosis by OCT and corneal endothelial cell counting. Early diagnosis, accurate treatment, its prognosis is good. (Chin J Ophthalmol, 2017, 53: 847-854).

Association of tumor necrosis factor-α gene polymorphism with osteoarticular tuberculosis prognosis in a Hebei population.

This study investigated the association of tumor necrosis factor-α (TNF-α)-308, -238, and -863 polymorphisms with osteoarticular tuberculosis (OA-TB) prognosis in a Hebei population. Genomic DNA was extracted from venous blood samples of 120 OA-TB patients and 100 healthy volunteers. TNF-α-308, -238, and -863 were analyzed by PCR-restriction fragment length polymorphism; genotype and allele frequencies were calculated. Serum TNF-α level was significantly higher in OA-TB patients (283.16 ± 51.68 ng/L) than in control (122.54 ± 54.65 ng/L; P < 0.05). Higher frequency of TNF-α-308 GG genotype in healthy volunteers (91.0%) than in OA-TB patients (79.2%) indicated that it was a protective factor against OA-TB (OR = 0.405, 95%CI = 0.147-0.657, P = 0.007). Higher frequencies of TNF-α-308 GA genotype and TNF-α-308 allele (A) in OA-TB patients (20.8 and 10.4%, respectively) than in healthy volunteers (8.0 and 5.0%, respectively) indicated an association with increased risk of OA-TB (OR = 3.112, 95%CI = 1.520-6.343, P = 0.003; OR = 3.109, 95%CI = 1.676-6.538, P = 0.006; respectively). Haplotype association analysis of TNF-α polymorphisms (-308/-238/-863) showed a higher frequency of TNF-α AGA in OA-TB patients (12.1%) than in healthy volunteers (3.5%), indicating that it was a risk factor for OA-TB (OR = 4.201, 95%CI = 1.80-9.91, P = 0.010). TNF-α-308 G/A and TNF-α AGA (-308/-238/-863) were associated with a predisposition to OA-TB, which could aid clinical detection, prevention, and prognosis of OA-TB.