Background Combined androgen blockade (cab) is a promising treatment modality for prostate cancer (pca). In the present meta-analysis, we compared the efficacy and safety of first-line cab using an antiandrogen (aa) with castration monotherapy in patients with advanced pca.Methods PubMed, embase, Cochrane, and Google Scholar were searched for randomized controlled trials (rcts) published through 12 December 2016. Hazard ratios (hrs) with 95% confidence intervals (cis) were determined for primary outcomes: overall survival (os) and progression-free survival (pfs). Subgroup analyses were performed for Western compared with Eastern patients and use of a nonsteroidal aa (nsaa) compared with a steroidal aa (saa).Results Compared with castration monotherapy, cab using an aa was associated with significantly improved os (n = 14; hr: 0.90; 95% ci: 0.84 to 0.97; p = 0.003) and pfs (n = 13; hr: 0.89; 95% ci: 0.80 to 1.00; p = 0.04). No significant difference in os (p = 0.71) and pfs (p = 0.49) was observed between the Western and Eastern patients. Compared with castration monotherapy, cab using a nsaa was associated with significantly improved os (hr: 0.88; 95% ci: 0.82 to 0.95; p = 0.0009) and pfs (hr: 0.85; 95% ci: 0.73 to 0.98; p = 0.007)—a result that was not achieved with cab using a saa. The safety profiles of cab and monotherapy were similar in terms of adverse events, including hot flushes, impotence, and grade 3 or 4 events, with the exception of risk of diarrhea and liver dysfunction or elevation in liver enzymes, which were statistically greater with cab using an aa.Conclusions Compared with castration monotherapy, first-line cab therapy with an aa, especially a nsaa, resulted in significantly improved os and pfs, and had an acceptable safety profile in patients with advanced pca.

The cause of ankylosing spondylitis (AS) remains unelucidated. Both genetic and environmental factors are suspected playing an important role in AS development. Peptidyl arginine deiminase type IV (PADI4) is a member of gene family that encodes enzymes responsible for the conversion of arginine to citrulline residues. A strong linkage between PADI4 polymorphism and rheumatoid arthritis has been found in Japanese and Korean patients, but there is no association study about PADI4 in AS. We speculated that PADI4 may be a pivotal gene for AS development. So we investigated the PADI4 polymorphisms in AS in Chinese Han population. A total of 316 Chinese AS patients of Han nationality and 439 healthy controls were recruited. Five single‐nucleotide polymorphisms (SNP), PADI4‐89 (rs11203366), PADI4‐90 (rs11203367), PADI4‐92 (rs874881) PADI4‐94 (rs2240340) and PADI4‐104 (rs1748033), of PADI4 gene were selected, and the major allele frequencies between cases and controls were assessed as 0.571 versus 0.597, 0.565 versus 0.585, 0.565 versus 0.574, 0.446 versus 0.421 and 0.614 versus 620, respectively. No significant differences in the frequency of PADI4 alleles and genotypes between the cases and controls were observed. Two haplotypes ACGGC and GTCGC were significant with AS even after Bonferroni’s correction but were with a tiny frequency in AS cases as 1.0% and 1.2%, respectively. These results indicate that PADI4 polymorphisms may not play an important role in the development of AS in Chinese Han population.

Ankylosing spondylitis (AS) is a chronic inflammatory disorder with a multifactorial genetic basis. HLA‐B27 was reported with the greatest susceptibility to AS but did not act alone. The aim of this study was to search for other gene(s) associated with AS independently of HLA‐B27 using 13 microsatellite markers spanning 1.5 Mb from locus TAP1 to HLA‐Cw and a single‐nucleotide polymorphism marker within NFκBIL1 gene promoter. Genotyping for microsatellites was performed in 175 AS patients of eastern Chinese and 219 ethnically matched healthy controls using polymerase chain reaction with fluorescence‐labelled primers, whereas the SNP marker was genotyped by direct DNA sequencing. Allele as well as haplotype frequencies were compared between cases and controls, and a linkage disequilibrium analysis was performed to estimate the LD relationship between the candidate regions. The frequencies of alleles D6S2811*128, STR_MICA*A5.1 and D6S2672*109, as well as haplotypes D6S2811*128–D6S2927*213–D6S2810*340, D6S2927* 221–D6S2810*350–MICA*A5.1, and D6S2810*350–MICA*A5.1–D6S2800* 136 were significantly increased in B27‐positive AS patients when compared with B27‐positive controls. The results indicated that there may be other gene(s) within the HLA region, especially around locus HLA‐B or HLA‐Cw, with susceptibility to AS independently of HLA‐B27.

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