Cheng-Yao Zhu

Alcohol consumption and psoriatic risk: A meta-analysis of case–control studies

Psoriasis is one of the most common dermatological disorders. The association between alcohol consumption and psoriasis has been inconsistent among studies. To examine the magnitude of the risk of developing psoriasis for drinking populations compared to those with non‐drinking, and to determine causes of the variation in odds ratios (OR) between various case–control studies, we performed a comprehensive published work search and a meta‐analysis of case–control studies considering prevalence. We did electronic searches on Medline, and searched reports to identify case–control studies of prevalent of psoriasis. We did meta‐analyses of study‐specific incremental estimates to determine the risk of psoriasis associated with drinking. The magnitude of the OR was analyzed by combining 15 case–control studies that matched defined criteria. The variance in OR between studies was explored. The overall OR of psoriasis for drinking persons compared to those with non‐drinking was 1.531 (95% confidence interval [CI] = 1.164–2.014, P = 0.002) and the association remains statistically significant across a number of stratified analyses in European descent subgroup (OR = 1.432, 95% CI = 1.085–1.889, P = 0.011) and also persists in sensitivity analyses performed to assess the potential effect of varying psoriasis outcome definitions. Alcohol consumption is associated with increased risk of psoriasis. These epidemiological observations should inform the exploration of biological mechanisms that link alcohol consumption with psoriasis.

Leptin levels in patients with psoriasis: a meta-analysis.

There have been inconsistent results reported for leptin levels in patients with psoriasis.

Adiponectin levels in patients with psoriasis: a meta-analysis.

Conflicting results regarding adiponectin levels in patients with psoriasis have been reported. We carried out a meta‐analysis on studies which compared adiponectin levels of psoriatic patients with controls. A published work search was performed through PubMed (MEDLINE), EMBASE and the Cochrane Library for articles published in English. Pooled standardized mean difference (SMD) and 95% confidence intervals (95% CI) were calculated by using random effects and fixed effect models. Heterogeneity between studies was assessed using the Cochrans Q and I2 statistics. A total of nine studies were enrolled (389 cases and 360 controls) for adiponectin, and three studies were included (132 cases and 132 controls) for high‐molecular weight (HMW) adiponectin. Adiponectin and HMW adiponectin levels were not significantly different in patients with psoriasis compared with controls (SMD, −0.151 [95% CI, −0.616 to 0.315]; P = 0.526 for adiponectin; SMD, 0.999 [95% CI, −2.626 to 4.624]; P = 0.589 for HMW adiponectin). The associations were borderline significantly different in the stratum of those with a mean age of less than 40 years (SMD, −0.516 [95% CI: −1.032 to 0]; P = 0.050). Sensitivity analyses were not substantially altered in the direction of effect when any one study was excluded. No publication bias was detected. The level of adiponectin and HMW adiponectin may not be associated with psoriasis. The relationship between psoriasis and adipokines needs more in‐depth studies with larger sample sizes.

Variants of CARD14 gene and psoriasis vulgaris in southern Chinese cohort

BACKGROUND: Recent mutation analysis identified several missense mutations in CARD14 in psoriasis. OBJECTIVES: We performed the genomic sequence analysis on CARD14 in southern Chinese Han Cantonese with Psoriasis Vulgaris (PsV) to reveal more causative missense mutations. METHODS: A total of 131 patients with PsV and 207 matched controls were included. We conducted sequence analysis of all the exon and exon-intron boundaries of CARD14 in the group of PsV patients and subsequent case control analysis of potential sequence variants of significance. RESULTS: We found five rare mutations and four of them are annotated or reported. Only the variant (c.1291C>G) has not been reported and annotated, but the variant was also found in controls. No significant difference was detected among all rare variant allele frequencies of patients and controls. CONCLUSION: None of the new definite variants were pathogenic. The other pathogenic mutations for PsV are still elusive in our cohort.

The TNFAIP3 polymorphism rs610604 both associates with the risk of psoriasis vulgaris and affects the clinical severity

Genome‐wide association studies in white and Chinese Han populations have found that the single‐nucleotide polymorphism (SNP) rs610604, at the tumour necrosis factor (TNF)‐α‐induced protein 3 (TNFAIP3) locus, is associated with psoriasis, and is also associated with response to TNF blockade in psoriasis.

Combined effect between CHRNB3–CHRNA6 region gene variant (rs6474412) and smoking in psoriasis vulgaris severity

BACKGROUND Many factors associated with causing psoriasis have been reported, such as the genetic and environmental factors. Smoking is one of the well-established environmental risk factors for psoriasis and also associated with the disease severity. In addition, several studies of psoriasis and psoriatic arthritis have documented gene-environment interactions involving smoking behavior. Although gene polymorphisms on nicotinic acetylcholine receptor subunits CHRNB3-CHRNA6 region gene have been found to correlate with smoking behavior and lung cancer susceptibility in Chinese Han population, the combined effect between the smoking-related genetic variants and smoking behavior on psoriasis vulgaris (PV) has been unreported. OBJECTIVE To evaluate the combined effect of the smoking-related (rs6474412-C/T) polymorphism on CHRNB3-CHRNA6 region gene and smoking behavior on PV risk and clinic traits in Chinese Han population. METHODS A hospital-based case-control study including 672 subjects (355 PV cases and 317 controls) was conducted. The variant of rs6474412 was typed by SNaPshot Multiplex Kit (Applied Biosystems Co., USA). RESULTS The higher body mass index (BMI≥25), smoking behavior and alcohol consumption were risk factors for PV, and the estimated ORs were 1.55 (95% CI, 1.09-2.29), 1.74 (95% CI, 1.22-2.49) and 1.81 (95% CI, 1.25-2.62) respectively. The smoking patients had more severe conditions than non-smokers (OR=1.71, 95% CI, 1.08-2.70, P=0.020). The alleles and genotypes of rs6474412 were not associated with risk of PV, but the combined effect of rs6474412 genotype (TT) and smoking behavior increased severity of PV (OR=5.95; 95% CI, 1.39-25.31; P<0.05; adjusted OR=2.20; 95% CI, 1.55-3.14; P<0.001). CONCLUSIONS Our results demonstrate that the combined effect of rs6474412-C/T polymorphism in smoking-related CHRNB3-CHRNA6 region gene and smoking behavior may not confer risk to PV, but may have impact on PV severity in Chinese Han population.

First case of congenital idiopathic hypohidrosis in China

A 43-year-old Chinese man presented with generalized hypohidrosis, which he had had since birth, without obvious abnormalities of other skin appendages except a sparse beard and axillary hairs. The sweat test revealed localized sweating on the face, axillae and palms. Histopathologic examination showed that the sweat glands were absent in the forearm and thigh, but some eccrine and apocrine sweat glands were present in the right axilla. S-100 was expressed in the nerve terminals surrounding the acini and ducts of the eccrine sweat glands, while PGP9.5 was positive in the acini of apocrine glands and the nerve terminals surrounding the eccrine glands in the axilla. To our knowledge, this is the first case of congenital idiopathic hypohidrosis in China.

An association study on the CHRNA5/A3/B4 gene cluster, smoking and psoriasis vulgaris

Genome-wide association and large cohort studies have consistently linked several single nucleotide polymorphisms (SNPs) located in the CHRNA5/A3/B4 gene cluster to smoking behaviors and nicotine dependence. Smoking is one of the well-established environmental risk factors for psoriasis and also associated with severity of the disease. Then we conduct the study to examine whether the genetic variations related to smoking behavior located in the CHRNA5/A3/B4 gene cluster also predict the risk of psoriasis vulgaris (PV). The investigations may help explain the mechanisms of the smoking-PV relationship. This is a hospital base case–control study including 634 subjects (329 PV patients and 305 controls), all Chinese Han population. 8 SNPs were selected based on findings from recent studies on smoking and nicotine dependence, all located in the nicotinic acetylcholine receptor subunits CHRNA5/A3/B4 gene cluster. The variants were typed by SNaPshot Multiplex Kit (Applied Biosystems Co., USA). We confirmed that smoking, alcohol consumption and higher body mass index (BMI ≥25) were risk factors for PV. However, none of the selected SNPs was associated with PV risk in the overall analysis and stratification analysis. And we found no association between the selected SNPs in CHRNA5/A3/B4 gene cluster and the clinical features of PV in case-only analysis. This exploratory study does not provide a relationship between these smoking-related SNPs in the CHRNA5/A3/B4 gene cluster and PV in Chinese Han population.

Alcohol consumption: Is it really a risk factor for psoriasis?: Reply to Emilie Brenaut's letter

Dear Editor, With great interest, we have read the comments of Brenaut et al. The authors are absolutely right to conclude that alcohol consumption as a risk factor requires more data on alcohol consumption before the onset of psoriasis. In our article, we only obtained data about present alcohol consumption from case–control studies, even the study of Jankovic et al. mentioned by Brenaut et al. However, we also agree that many of the case–control studies included in our study describe the alcohol consumption as a risk factor in their papers. In our discussion, we have explained the limitation that we focused on case–control studies of prevalence only, but not incidence. However, despite the limitations, the results of this metaanalysis suggest that alcohol consumption may have involvement in the pathogenesis of psoriasis, regardless of subtype of alcohol consumption and subtype of psoriasis. We have excluded the two studies by Tey et al. and Naldi et al. There was also a strong evidence of significant association between psoriasis and alcohol consumption in drinking versus non-drinking subjects (odds ratio [OR] = 1.620, 95% confidence interval [CI] = 1.206–2.176, P = 0.001) (Tables S1 and S2). In the subgroup analysis, the pooled OR is 1.459 (95% CI; 1.092–1.950; P = 0.011) for European descent and 2.532 (95% CI; 0.854–7.511, P = 0.094) for Asian descent, showing that racial characteristics seem to influence the results. Heterogeneity is one of the limitations of our study. We used the random effects model (the DerSimonian and Laird method). We should highlight this in our discussion and carefully interpret the result.