Causal relationship and potential common pathogenic mechanisms between hidradenitis suppurativa and related cancer.

Background: Hidradenitis suppurativa (HS) is a chronic, inflammatory and common skin disease. Observation studies have reported the association between HS and cancers, however no studies reported whether a causal relationship exists between HS and cancers. This study aimed to explore the causal relationship between HS and differential subtypes of cancers by conducting a bidirectional Mendelian randomization (MR) analysis.

Methods: Genome-wide association study (GWAS) data related to HS and 16 subtypes of cancers were collected. The inverse variance weighted (IVW) method was primarily applied for our MR analysis, MR-Egger, weighted median, simple mode, and weighted mode methods were used additionally. Heterogeneity, horizontal pleiotropy, and potential outliers were assessed for the MR analysis results. Subsequently, disease-related genes were retrieved from the GeneCards database. To investigate the potential functions of these associated genes, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted.

Results: The results of our MR analysis indicated a causal association between HS and pancreatic cancer (PAC). Specifically, HS was found to elevate the risk of developing PAC (odds ratio (OR), 1.074; 95% confidence interval (CI) 1.015-1.135; p = 0.013). Conversely, reverse MR analysis demonstrated that PAC does not exert a causal effect on HS. Furthermore, our findings did not reveal any significant causal relationships between HS and other types of cancer. No evidence of heterogeneity or pleiotropy was identified in the analysis. Additionally, we identified disease-related genes, and subsequent GO and KEGG enrichment analyses indicated that the genes common to both HS and PAC are implicated in pathways associated with immune and inflammatory processes.

Conclusions: The results of this study offer novel evidence regarding the causal relationship between HA and PAC. Our Mendelian randomization analysis indicates that HS may have a causal influence on PAC, which could inform the development of improved treatment strategies for patients suffering from HS. However, the underlying mechanisms warrant further exploration.