Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition characterized by painful nodules, abscesses, and sinus tract formation, primarily affecting intertriginous areas. Although its exact etiology remains unknown, it is likely multifactorial and thought to involve follicular occlusion and inflammation likely influenced by genetic and environmental factors.1 This occlusion causes follicles to swell, eventually leading to rupture and thus triggering an intense inflammatory response. Additionally, certain bacteria, such as Staphylococcus and Streptococcus species, are more abundant in HS lesions while protective species may be less prevalent compared to healthy individuals.1 Finally, HS lesions exhibit upregulation of innate immune pathways, with elevated levels of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-17.1
Previous studies have shown a correlation between HS and the HLA-B27 gene mutation, suggesting a susceptibility to HS among individuals with this genetic predisposition.2 Environmental factors, such as obesity, smoking, and sex, have also been implicated in the development of HS.3 Obesity increases skin friction, thereby fostering the conditions conducive to HS development.3 Moreover, hormonal changes and metabolic syndrome associated with obesity have been linked to an elevated risk of HS.3 Nicotine, a component of cigarettes, is also known to exacerbate HS likely through increased follicular occlusion and slow healing.3 Lastly, sex differences reveal that women are disproportionately affected by HS than men, with a ratio of 3:1.
In contrast, irritable bowel diseases (IBDs), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), are inflammatory gastrointestinal conditions characterized by diarrhea, abdominal pain, and bloody stools.4 Like HS, the exact etiology of IBDs remain unknown, though both genetic and environmental factors are implicated. Studies have demonstrated a correlation between the HLA-B27 gene mutation and the presence of IBDs.5 Smoking has been identified as a risk factor for IBDs, particularly CD attributed to the proinflammatory effects of nicotine.6 Obesity also exhibits strong associations with IBDs, affecting between 15 to 40 percent of IBD patients.7 Additionally, dysbiosis, an imbalance in the gut microbiome, has emerged as a critical factor in IBD pathogenesis, contributing to immune dysregulation and chronic intestinal inflammation. Certain bacterial species, such as Escherichia coli and Fusobacterium, are often overrepresented in IBD patients, while protective species may be diminished, further exacerbating disease progression.8 Sex differences also play a role in the manifestation of IBDs, with women being more predisposed to developing CD and men to UC.9
Despite the similarities between HS and IBDs in terms of inflammatory nature and the involvement of genetic and environmental factors, limited research has been conducted on the association between these two conditions. Nevertheless, existing studies suggest a potential link between HS and IBDs.10 In this systematic review, we aim to synthesize current literature on the association between HS and IBDs and to evaluate the interplay between these conditions and whether individuals affected by one condition face an increased risk of developing the other.
METHODS
A systematic review was conducted on June 29, 2023, using three databases: Ovid Medline, PubMed, and the Cochrane Database. While all three databases were searched, Ovid Medline yielded the most results, with PubMed and Cochrane contributing minimal studies. The search terms included a combination of Medical Subject Headings (MeSH) and free-text terms, systematically combined using Boolean operators (AND, OR). Terms such as “Hidradenitis Suppurativa,” “HS,” “Inflammatory Bowel Disease,” “IBD,” “Crohn’s Disease,” “Ulcerative Colitis,” and variations of these combinations (eg, “HS AND IBD” or “Hidradenitis Suppurativa AND Crohn’s Disease”) were used. Filters were applied to limit results to English-language articles and studies conducted in the United States.
The search initially resulted in 48 articles, with one duplicate removed, resulting in 47 eligible articles for screening. Titles and abstracts were then independently screened by two reviewers to assess relevance, and 22 articles were excluded for focusing on either HS or IBD independently without investigating their association. The remaining 25 full-text articles were sought for retrieval, though one article could not be accessed. Of the 24 articles retrieved, one was excluded for not being conducted in the United States, two were excluded for not being written in English, two discussed both HS and IBD but not in relation to each other, and seven were excluded for being systematic reviews or meta-analyses rather than original research studies. This resulted in a final selection of 12 articles that met both the inclusion and exclusion criteria and were included in the analysis.
Screening and selection were performed independently by two reviewers, with discrepancies resolved through discussion. The study adhered to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and followed principles from the Cochrane Handbook for Systematic Reviews of Interventions where appropriate. A formal risk of bias assessment was not conducted as this systematic review aimed to synthesize and summarize findings from the selected studies rather than perform a meta-analysis. Future meta-analyses examining the association between HS and IBD may benefit from applying standardized tools such as the Newcastle-Ottawa Scale (NOS) or ROBINS-I tool to systematically evaluate study quality.
Key data, including study design, population characteristics, prevalence rates, risk factors, findings, and limitations, were extracted from each included study and synthesized into Table 1 to provide a structured overview of the key findings. Figure 1 shows a visual representation of the paper and data collection discussed here, using the PRISMA model.