# Acne Inversa and Inflammatory Bowel Disease: The Crohn's Connection

Canonical URL: https://acneinversa.life/en/blog/acne-inversa-inflammatory-bowel-disease-crohns/
Markdown URL: https://acneinversa.life/en/blog/acne-inversa-inflammatory-bowel-disease-crohns.md
Plain text URL: https://acneinversa.life/en/blog/acne-inversa-inflammatory-bowel-disease-crohns.txt
Language: en
Category: Treatments
Published: 2026-05-21
Last updated: 2026-05-21
Author: Dr. rer. nat. Dennis Alexander Kwiatkowski (Biochemist, Scientific Writer and Pharma Expert)
Tags: Acne Inversa, Hidradenitis Suppurativa, HS, Treatments, IBD, Crohn's disease, ulcerative colitis, comorbidities, ASCA, TNF inhibitors, perianal disease

> HS and inflammatory bowel disease - particularly Crohn's disease - co-occur at strikingly elevated rates. This article explains the shared biology, the diagnostic overlap in perianal disease, and the treatment implications.

Medical disclaimer: This website is for general educational information only and does not replace medical advice, diagnosis, or treatment. Please speak with qualified medical professionals about symptoms or treatment decisions.

## Article

The association between hidradenitis suppurativa (HS) and inflammatory bowel disease (IBD) — particularly Crohn’s disease — is one of the most well-established comorbidity relationships in HS, and one of the most clinically important to recognize. The two conditions share inflammatory biology, immunological markers, and treatment options. They can also be confused, particularly when both affect the perianal region. Patients with one of these conditions are at meaningfully elevated risk of the other, and integrated management produces better outcomes than disconnected specialist care.

This article addresses the HS-IBD relationship: what the evidence shows about prevalence, the shared biology, the diagnostic challenges (especially in perianal disease), and the treatment implications, including which biologics address both conditions and which may unmask or worsen IBD.

> **Educational content only.** Diagnosis and management of IBD requires gastroenterological evaluation. This article describes general principles relevant to patients who already have one condition and want to understand the connection.

## Key takeaways

- Crohn’s disease occurs in HS patients at 2- to 10-fold the rate of matched controls in published studies, with the wide range reflecting different study populations and methodologies. The lower estimates come from population-based data; higher estimates from tertiary referral cohorts.
- Ulcerative colitis is also elevated in HS but less strongly than Crohn’s disease. The reverse direction is also documented: IBD patients are at approximately 9-fold elevated risk of subsequently developing HS.
- The shared biology involves abnormal immune responses to commensal organisms (reflected in elevated anti-Saccharomyces cerevisiae antibodies in both conditions), shared genetic susceptibility loci, and overlapping cytokine pathways including TNF-α and IL-17.
- Perianal disease is the most clinically important overlap zone — perianal Crohn’s disease and perianal HS can look similar, and distinguishing them affects treatment decisions.
- TNF inhibitors (adalimumab, infliximab) are approved for both conditions and are first-line systemic therapy when both are present. IL-17 inhibitors (secukinumab, bimekizumab) — approved for HS — should not be used in patients with active IBD and may unmask or worsen the bowel disease.

## What the evidence actually shows

The prevalence and odds estimates for IBD in HS populations:

**Crohn’s disease.** Multiple meta-analyses and large population-based studies report elevated rates. A representative example is the population-based Dutch cohort (LifeLines), which reported an odds ratio of 2.69 (95% CI 1.25–5.79) for Crohn’s disease in HS patients versus controls. Some case-control studies report higher figures, including up to 10-fold increased risk in selected populations. Published prevalence of Crohn’s disease in HS cohorts ranges from 1.2% to 23%, depending on population characteristics and ascertainment methods. The general population prevalence of Crohn’s disease is approximately 0.1–0.3%, so even the lower estimates represent substantial relative elevation.

**Ulcerative colitis.** Elevated but less strongly than Crohn’s. The Dutch cohort reported a non-significant trend (OR 0.80, 95% CI 0.36–1.78), though larger studies and meta-analyses generally support some elevation. The overlap with HS is less robust and the mechanisms may differ from those linking HS to Crohn’s specifically.

**Inverse direction.** Studies examining HS prevalence in IBD populations also show elevated rates. A prospective cohort study cited in patient-facing HS literature reported that IBD patients were approximately 9-fold more likely to develop HS compared to the general population. The relationship runs in both directions, supporting a shared underlying susceptibility rather than one condition causing the other.

**Multi-centre cross-sectional data.** Various clinical cohort studies report IBD prevalence in HS populations 4 to 8 times higher than the general population, again with substantial variation depending on study design.

**The 2021 evidence-based screening recommendations** from the US and Canadian Hidradenitis Suppurativa Foundations explicitly include IBD screening among recommended assessments for HS patients, reflecting the strength of the association.

The honest summary: the relationship between HS and Crohn’s disease specifically is robust across study designs. The mechanistic explanation is well grounded. The clinical implication — that HS patients should be assessed for IBD symptoms and that IBD patients should be evaluated if they develop skin lesions resembling HS — is supported by current guidelines.

## The shared biology

The mechanistic overlap between HS and IBD operates at several levels.

**Anti-Saccharomyces cerevisiae antibodies (ASCA).** ASCA, antibodies against mannan in the cell wall of the yeast Saccharomyces cerevisiae, are the characteristic serological marker of Crohn’s disease, where they appear in 50% to 80% of patients. They are also elevated in HS patients compared to controls (Assan et al. 2020, Journal of Allergy and Clinical Immunology), correlating with systemic inflammation and disease severity. The shared antibody pattern provides direct immunological evidence of overlapping immune dysregulation.

**Genetic susceptibility.** Several genome-wide association studies have identified shared susceptibility loci between HS and IBD, including variants in genes related to innate immunity (NOD2, IL-1 signaling), barrier function, and inflammatory regulation. The genetic picture supports shared upstream biology rather than coincidental co-occurrence.

**Microbiome and barrier dysfunction.** Both HS and IBD involve abnormal interactions between the host immune system and commensal organisms at epithelial surfaces — the gut for IBD, the hair follicle for HS. Barrier dysfunction (whether intestinal mucosal or follicular) appears to be an early step in both, allowing exposure of immune cells to microbial components that drive inflammation.

**Cytokine pathways.** Both conditions involve elevated TNF-α and IL-17/Th17 axis activity. This is the immunological basis for the overlap in approved biological therapies (TNF inhibitors for both, with caveats about IL-17 inhibitors discussed below).

**Innate immune dysregulation.** Both involve dysregulated innate immune responses — particularly involving neutrophils and inflammasome-mediated inflammation. The clinical observation of pus-forming inflammatory lesions in HS and acute neutrophilic infiltrates in active IBD reflects shared innate immune pathology.

The picture is of two diseases that share inflammatory and immunological substrate but express it in different tissues. A patient with HS and Crohn’s disease is not coincidentally affected by two diseases; the same underlying biological vulnerability is producing both.

## The clinical overlap: perianal disease

This is the area where clinical confusion is most likely and most consequential.

**Perianal HS** typically presents as recurrent painful nodules, abscesses, and draining sinus tracts in the perianal, gluteal, and perineal regions. Lesions can be deep, can interconnect into extensive tunnel networks, and can persist for months or years. The disease respects the cutaneous boundary of the perianal area in most cases but can extend close to the anal sphincter.

**Perianal Crohn’s disease** presents as anal fissures, fistulas, abscesses, skin tags, and ulceration in and around the anal canal. Perianal fistulas in Crohn’s connect the rectal or anal lumen to the perianal skin, communicating between the gut and the external surface. Anal canal involvement (ulceration, stenosis) is distinctive.

**The distinction matters because:**

- Perianal Crohn’s typically requires gastroenterological management, possibly including biologic therapy, surgery (often by colorectal specialists familiar with Crohn’s-specific approaches), and management of the underlying intestinal disease.
- Perianal HS is dermatological and dermatologic-surgical in primary management.
- The same patient can have both, with complex anatomy that requires combined assessment.
- Treatment decisions — particularly the choice of biologic — depend on whether IBD is present.

**Features that suggest perianal involvement may be Crohn’s rather than (or in addition to) HS:**

- Anal canal involvement, fissures, or stenosis on examination
- Fistulas that clearly communicate with the rectal lumen
- Gastrointestinal symptoms (chronic diarrhoea, abdominal pain, weight loss, rectal bleeding)
- Family history of IBD
- Elevated inflammatory markers (CRP, ESR) beyond what HS alone explains
- Anaemia not explained by other causes
- Positive ASCA antibodies

**Features that suggest perianal involvement is HS:**

- Disease in characteristic HS locations elsewhere (axillae, groin, breasts) consistent with HS pattern
- Sinus tracts respecting cutaneous boundaries rather than communicating with the rectal lumen
- Absence of gastrointestinal symptoms
- Disease morphology and pattern consistent with HS rather than Crohn’s

Patients with extensive perianal disease, particularly those with any gastrointestinal symptoms, warrant gastroenterological evaluation to clarify whether IBD is present in addition to HS. Imaging (MRI of the pelvis) and endoscopic evaluation by gastroenterology can establish or exclude underlying IBD.

## When to screen HS patients for IBD

The clinical question is not whether to screen all HS patients exhaustively for IBD but how to recognize when evaluation is warranted.

**Symptoms that warrant gastroenterological referral:**

- Chronic diarrhoea (loose stools more than three weeks)
- Recurrent abdominal pain, particularly with eating or with bowel movements
- Blood in stool
- Unexplained weight loss
- Chronic fatigue beyond what HS alone explains
- Iron deficiency anaemia not explained by menstrual or other causes
- Mouth ulcers occurring repeatedly
- Joint pain or back pain consistent with spondyloarthritis (covered in a separate companion article)
- Family history of IBD in close relatives

**Other indications:**

- Patients with severe perianal HS, particularly with atypical features
- Patients being considered for IL-17 inhibitor therapy (where IBD exclusion is important before starting)
- Patients with positive ASCA antibodies on testing

**Basic screening that can be initiated in primary care or dermatology:**

- Full blood count and inflammatory markers (CRP, ESR)
- Iron studies and ferritin
- Stool calprotectin (a sensitive marker of intestinal inflammation; widely available)
- Symptom assessment

Elevated stool calprotectin or unexplained anaemia or persistent symptoms warrants gastroenterological referral for further workup, which may include colonoscopy with biopsies, MRI imaging, and serological testing.

## Treatment implications

The HS-IBD overlap has direct treatment implications that affect biologic selection.

### Adalimumab and other TNF inhibitors

Adalimumab is approved for both HS and Crohn’s disease (and for ulcerative colitis) — making it the first-line biologic for patients with both conditions. Infliximab (intravenous, also a TNF inhibitor) is approved for IBD and used off-label for HS, with reasonable evidence in severe HS.

For a patient with both HS and Crohn’s disease, TNF inhibitor therapy can address both conditions simultaneously. This is one of the strongest practical advantages of recognizing the comorbidity: a single treatment may address what could otherwise require separate medications.

### IL-17 inhibitors

Secukinumab and bimekizumab — both approved for HS — should generally not be used in patients with active IBD. The mechanism of action (IL-17A inhibition for secukinumab; IL-17A and IL-17F for bimekizumab) can worsen IBD or unmask previously subclinical disease.

The relationship between IL-17 inhibition and IBD is established. In rheumatology, where IL-17 inhibitors are used for psoriatic arthritis and ankylosing spondylitis, new-onset or worsening IBD has been observed during treatment. For HS patients, this means:

- IL-17 inhibitors should be avoided in patients with known IBD
- Patients being considered for IL-17 inhibitor therapy should be screened for IBD symptoms beforehand, with low threshold for gastroenterological assessment in patients with suggestive symptoms or markers
- IL-17 inhibitor users who develop GI symptoms during treatment should be evaluated for IBD

### Ustekinumab

Ustekinumab, an IL-12/23 inhibitor approved for psoriasis, psoriatic arthritis, Crohn’s disease, and ulcerative colitis, is sometimes used off-label for HS in patients with both HS and IBD. The evidence in HS specifically is limited but supportive for use as second- or third-line therapy in selected patients, particularly those with concurrent IBD where it addresses both conditions.

### Other treatments

Standard IBD-directed therapy (5-ASA compounds, corticosteroids, immunomodulators like azathioprine or methotrexate, newer biologics like vedolizumab) is determined by gastroenterology. HS-specific treatment continues in parallel as needed. Coordination between dermatology and gastroenterology is important to avoid conflicting prescriptions or missed treatment opportunities.

### Surgery

Surgical management of perianal disease in patients with both HS and Crohn’s requires specialist input. The standard HS approach (deroofing, wide excision) may not be appropriate without first controlling underlying IBD. Conversely, surgical management of perianal Crohn’s typically requires gastroenterological-surgical collaboration, often involving colorectal surgeons familiar with both pathologies.

## Practical points for patients

If you have HS and are reading this with concerns about possible IBD:

- **Discuss any GI symptoms with your general practitioner.** Persistent diarrhoea, abdominal pain, rectal bleeding, or unexplained weight loss warrants evaluation regardless of HS.
- **Ask for stool calprotectin if symptoms are suggestive.** This is a sensitive, non-invasive screening test for intestinal inflammation.
- **If you are starting an IL-17 inhibitor, ensure your dermatologist has screened for IBD symptoms.** This is part of appropriate pre-treatment assessment but is sometimes overlooked.
- **If you have known IBD and are considering an HS biologic, the choice differs.** TNF inhibitors (adalimumab) are usually preferred over IL-17 inhibitors for patients with concurrent IBD.

If you have IBD and are reading this with concerns about possible HS:

- **HS lesions are typically nodules and abscesses in skin folds**, not gastrointestinal symptoms. The two diseases have distinct presentations even when both occur in the same patient.
- **Any new recurrent painful lumps in axillae, groin, or buttocks** warrant dermatological evaluation.
- **Perianal HS can coexist with perianal Crohn’s** and may not be distinguished without specialist evaluation.

## Frequently asked questions

**Should I be tested for ASCA antibodies?**

Not routinely. ASCA testing can be informative in specific clinical situations — suspected Crohn’s disease with equivocal findings, patients with both HS and gastrointestinal symptoms, patients considering yeast-elimination dietary intervention. It is not part of routine HS workup. Discuss with your dermatologist or gastroenterologist whether it is appropriate for your situation.

**Will treating my HS help my Crohn’s, or vice versa?**

If you are on a TNF inhibitor that addresses both, yes. The same drug working on both diseases produces parallel benefit. Other treatments are more disease-specific.

**Can I have HS biologics on top of my IBD biologics?**

In most cases, no — combination of multiple biologics is generally avoided due to additive infection risk. The exception is when a single biologic (TNF inhibitor) addresses both conditions, which is the usual approach. Conflicting biologic prescriptions for different diseases by different specialists should be flagged and reconciled.

**My family has Crohn’s disease — am I at higher risk of HS?**

Family history of Crohn’s disease modestly elevates HS risk, and conversely. The genetic susceptibility shared between the two conditions runs in families to some degree. This is not a clinical screening test, but family history of either condition is relevant medical information.

**What if I want to try yeast elimination — is that relevant to my Crohn’s too?**

The brewer’s yeast hypothesis covered in the companion article on diet and HS has overlap with Crohn’s disease, given the shared ASCA biology. Some patients with both conditions report benefit from yeast elimination affecting both. This is observational, and yeast elimination is not a substitute for standard IBD treatment. Discuss with your gastroenterologist before undertaking elimination diets if you have IBD.

**Should I see a gastroenterologist as part of routine HS care?**

Not necessarily, in the absence of symptoms or signs suggesting IBD. Most HS patients do not have or develop IBD. Routine gastroenterological referral is not part of standard HS management. Targeted referral based on symptoms, signs, or specific biologic-related considerations is the appropriate pathway.

**What about other gastrointestinal conditions — IBS, celiac, microscopic colitis?**

Irritable bowel syndrome (functional, not inflammatory) is more common in HS populations but does not have the same biological implications as IBD. Celiac disease has been examined and may be modestly elevated; if you have suggestive symptoms (persistent GI complaints, iron deficiency, family history), testing is appropriate. Microscopic colitis and other inflammatory GI conditions are less specifically studied.

**Can pregnancy affect my HS and IBD together?**

Pregnancy commonly affects both conditions, often in opposite directions. Some women experience improvement in HS during pregnancy and Crohn’s flare postpartum; others experience the opposite. Pre-pregnancy planning and pregnancy management require coordination between dermatology, gastroenterology, and obstetrics. A separate article in the planned series addresses pregnancy and HS in detail.

> **Disclaimer.** This article is for general education and does not constitute personal medical advice. Diagnosis and management of inflammatory bowel disease requires evaluation by qualified gastroenterological clinicians. Biologic therapy selection in patients with both HS and IBD requires coordination between dermatology and gastroenterology.

## References

1. Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: Evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. - Journal of the American Academy of Dermatology, 2022
2. Vossen ARJV et al. New insights in hidradenitis suppurativa from a population-based Dutch cohort: prevalence, smoking behaviour, socioeconomic status and comorbidities. - British Journal of Dermatology, 2022
3. Assan F et al. Anti-Saccharomyces cerevisiae IgG and IgA antibodies are associated with systemic inflammation and advanced disease in hidradenitis suppurativa. - Journal of Allergy and Clinical Immunology, 2020
4. Garg A, Hundal J, Strunk A. Overall and subgroup prevalence of Crohn disease among patients with hidradenitis suppurativa: A population-based analysis in the United States. - JAMA Dermatology
5. Zouboulis CC et al. European S2k guideline on the treatment of hidradenitis suppurativa / acne inversa. - European S2k guideline