Metabolic Syndrome and Acne Inversa: What Your Internist Should Know

Written by Dr. rer. nat. Dennis Alexander Kwiatkowski

Hidradenitis suppurativa (HS) is most often discussed as a skin disease. The cardiovascular and metabolic dimensions of the disease are less prominent in patient education and routine clinical care, despite some of the strongest comorbidity data in the HS literature. Patients with HS have approximately 4-fold higher odds of metabolic syndrome than matched controls, elevated rates of each of its components (obesity, diabetes, hypertension, dyslipidemia), and nearly 2-fold higher cardiovascular-related mortality.

This article addresses the metabolic dimension of HS directly: what the evidence shows about the elevated cardiovascular risk, why this matters for life expectancy and not just current quality of life, what screening is appropriate, and how the dermatology-cardiology-internal medicine pathway should function for patients with significant HS. It is written for patients who want to understand why their HS clinician (or their internist) should be paying attention to factors beyond the skin.

Educational content only. Cardiovascular and metabolic management requires individualized assessment by a general practitioner or internist. This article describes general principles and what screening is reasonable to ask about.

Key takeaways

• Metabolic syndrome — a cluster of obesity, hypertension, dyslipidemia, and impaired glucose metabolism — occurs in HS at approximately 4 times the rate of matched controls.
• HS patients have approximately 2-fold higher risk of cardiovascular-related death and elevated rates of major cardiovascular events (myocardial infarction, stroke) compared to general populations.
• The increased risk is not fully explained by obesity alone; chronic systemic inflammation from HS itself contributes to cardiovascular risk independently.
• Screening for metabolic syndrome components in HS patients is recommended by current guidelines and is often underutilized.
• Treatment of metabolic syndrome components proceeds through standard pathways (lifestyle, medication when indicated); some HS treatments may have indirect metabolic benefit by reducing systemic inflammation.

What metabolic syndrome actually is

Metabolic syndrome is a clinically defined cluster of cardiovascular risk factors that, when occurring together, identify patients at substantially elevated risk of cardiovascular disease and type 2 diabetes. The diagnostic criteria most commonly used in Europe (International Diabetes Federation, with similar definitions from NCEP-ATP III) require central obesity plus at least two of the following:

• Central obesity: waist circumference exceeding ethnic-specific thresholds (for European populations: >94 cm in men, >80 cm in women)
• Elevated triglycerides: ≥150 mg/dL (1.7 mmol/L), or specific treatment for this abnormality
• Reduced HDL cholesterol: <40 mg/dL (1.03 mmol/L) in men, <50 mg/dL (1.29 mmol/L) in women, or specific treatment
• Elevated blood pressure: systolic ≥130 mmHg or diastolic ≥85 mmHg, or treatment of previously diagnosed hypertension
• Elevated fasting glucose: ≥100 mg/dL (5.6 mmol/L), or previously diagnosed type 2 diabetes

The diagnosis identifies a state of metabolic dysregulation. Each component independently contributes to cardiovascular and metabolic disease risk; their co-occurrence amplifies risk beyond what each would predict alone. Approximately 25% to 30% of adults in Western populations meet criteria for metabolic syndrome; the prevalence rises with age.

What the HS-specific evidence shows

The metabolic syndrome literature in HS is consistent and substantial.

Overall metabolic syndrome prevalence. A frequently cited Danish study of 358 HS patients reported approximately 4-fold higher odds of metabolic syndrome compared to matched controls. Multiple subsequent studies in different populations have confirmed substantial elevation, with point estimates ranging from approximately 2- to 4-fold depending on study population.

Individual component prevalence.

• Obesity: approximately 2.5-fold higher odds in HS populations (2024 meta-analysis OR 2.48).
• Type 2 diabetes: approximately 2.8-fold higher odds (OR 2.78 in the same meta-analysis).
• Hypertension: elevated in HS populations, with reported odds ratios typically around 2.
• Dyslipidemia: elevated, with both elevated triglycerides and reduced HDL contributing.

Cardiovascular events and mortality. A population-based cohort study (n=5,964 HS patients) showed approximately 2-fold higher risk of major adverse cardiovascular events and 1.7- to 2-fold higher cardiovascular-related mortality compared to controls.

Independent effect beyond BMI. Several studies have shown that the metabolic and cardiovascular risk in HS is not fully explained by obesity alone. Even after adjusting for BMI, HS independently contributes to cardiovascular risk — a pattern consistent with chronic inflammation as an independent risk factor, similar to the well-established cardiovascular risk associated with chronic inflammatory diseases like rheumatoid arthritis and psoriasis.

The 2021 evidence-based screening recommendations from the US and Canadian Hidradenitis Suppurativa Foundations explicitly list metabolic syndrome, obesity, dyslipidemia, type 2 diabetes, hypertension, and cardiovascular disease among comorbidities for which screening is recommended in HS patients.

Why this matters more than it sounds

Three reasons the metabolic dimension deserves attention rather than being dismissed as an incidental finding.

Mortality is increased. Approximately 2-fold higher cardiovascular-related mortality is not a minor finding. For a 30-year-old patient with moderate-to-severe HS, the cardiovascular trajectory over the next 40 years matters as much as the trajectory of skin disease. Lifetime cardiovascular events are a meaningful contributor to overall HS burden that is poorly captured by skin-focused outcome measures.

Risk is modifiable. Unlike many comorbidity associations, the metabolic syndrome components are amenable to specific interventions — lifestyle changes, medications for hypertension and dyslipidemia, glucose management, smoking cessation. The increased risk is not fixed. Active management produces measurable reduction in cardiovascular events.

The inflammation argument has therapeutic implications. If chronic inflammation contributes to cardiovascular risk in HS, effective treatment of the inflammation may reduce cardiovascular events. This is established for rheumatoid arthritis and psoriasis, where biologic therapy has been shown to reduce cardiovascular event rates beyond what is explained by traditional risk factor management. For HS, the cardiovascular outcomes data from biologic therapy is still emerging but the parallel is plausible.

Screening gaps are real. Multiple audit studies have shown that HS patients are screened for cardiovascular and metabolic comorbidities less consistently than would be appropriate given the elevated risk. The screening burden falls between specialties — dermatology focuses on skin, internal medicine sees the patient less often or not at all — and patients often fall through the gap.

The biological connection

The mechanistic story linking HS to metabolic and cardiovascular disease is increasingly well characterized.

Chronic systemic inflammation. HS produces sustained elevation of inflammatory markers (CRP, IL-6, TNF-α, IL-1β, IL-17). Chronic systemic inflammation is a well-established contributor to atherosclerosis through effects on endothelial function, lipoprotein metabolism, plaque stability, and thrombogenic factors. The same inflammatory profile that drives HS at the skin level produces measurable cardiovascular effects.

Adipose tissue inflammation. Obesity in HS is associated with particularly inflammatory adipose tissue, producing additional cytokine load that drives both HS activity and metabolic dysfunction. The relationship is bidirectional: obesity contributes to inflammation, and inflammation contributes to metabolic dysfunction.

Insulin resistance. Chronic inflammation produces insulin resistance through TNF-α and other cytokine effects on insulin signaling. Insulin resistance in turn contributes to obesity, dyslipidemia, hypertension, and atherosclerosis — connecting the metabolic syndrome components mechanistically.

Shared risk factors. Several modifiable risk factors are common to HS and metabolic syndrome: obesity, smoking, sedentary lifestyle, certain dietary patterns. These shared factors contribute to both conditions and explain part (but not all) of the comorbidity association.

Vascular effects. Some research suggests direct effects of HS-related inflammation on vascular health, including measurable endothelial dysfunction in HS patients independent of traditional cardiovascular risk factors. This is consistent with the pattern observed in other inflammatory diseases.

The combined picture: HS contributes to cardiovascular risk through both shared risk factors (obesity, smoking) and through systemic inflammation independent of those factors. Both pathways are addressable.

Appropriate screening

Recommended screening for metabolic and cardiovascular comorbidities in HS patients, based on current guidelines and clinical practice:

Annually (or at appropriate intervals):

• Blood pressure measurement
• Weight, height, BMI calculation
• Waist circumference
• Fasting lipid panel (total cholesterol, LDL, HDL, triglycerides)
• Fasting glucose or HbA1c
• Symptom review for cardiovascular symptoms (chest pain, dyspnea on exertion, palpitations)

Initial baseline assessment (especially in patients with moderate-to-severe HS):

• Full cardiovascular risk assessment using validated tools (SCORE, Framingham, or local equivalents)
• Assessment of family history of cardiovascular disease
• Smoking status and cessation status
• Sleep history (sleep apnea is more common in HS and contributes to cardiovascular risk)

Additional assessment when indicated:

• ECG for patients with symptoms or specific risk factors
• Echocardiography for specific indications
• Cardiology referral for high-risk patients or specific findings

This screening is appropriately performed by the general practitioner (Hausarzt in Germany) rather than the dermatologist — the dermatologist’s role is to flag the need for screening and to communicate the elevated risk picture to the primary care clinician. In Germany under GKV, routine preventive examinations (Gesundheits-Check-up) provide a framework for this screening, and HS patients should ensure they are using these proactively rather than relying on episodic disease-focused visits.

What treatment looks like

Management of metabolic syndrome components in HS patients follows standard pathways.

Lifestyle interventions

The foundation for all metabolic syndrome management. Specific approaches:

• Weight management in patients with elevated BMI, addressed in the companion article on weight and HS.
• Smoking cessation, addressed in the companion article on smoking. The combined cardiovascular benefit of cessation plus HS-specific benefit makes this one of the highest-yield interventions.
• Physical activity as tolerated by disease state, with the dual benefit of cardiovascular protection and metabolic improvement.
• Dietary patterns consistent with anti-inflammatory and cardioprotective principles. Mediterranean dietary pattern has the strongest evidence for combined metabolic and cardiovascular benefit.
• Sleep optimization, particularly identifying and treating sleep apnea where present.

Medication for individual components

Specific medications for components of metabolic syndrome are managed by general practitioners and internists following standard guidelines. Brief summary of what HS patients should know:

Hypertension. Treated with standard antihypertensive agents (ACE inhibitors, ARBs, calcium channel blockers, thiazides) per general guidelines. ACE inhibitors and ARBs have specific advantages in patients with diabetes or proteinuria. No specific HS-related considerations for choice of antihypertensive.

Dyslipidemia. Statins remain first-line for elevated LDL cholesterol or for primary cardiovascular prevention in patients with elevated risk. No specific HS-related contraindication to statins. The reduction of cardiovascular events from statin therapy is well established and applies to HS patients with elevated risk.

Type 2 diabetes. Metformin is first-line, with additional advantages in PCOS overlap and possible direct anti-inflammatory effects relevant to HS. GLP-1 receptor agonists (semaglutide, liraglutide) and SGLT2 inhibitors (empagliflozin, dapagliflozin) provide both glycemic control and additional cardiovascular benefits. The companion articles on weight reduction and PCOS cover these in more detail.

Aspirin for primary prevention is no longer routinely recommended; the decision depends on individual cardiovascular risk and bleeding risk. This is a primary care decision.

Treatment of HS itself

Effective HS treatment may indirectly benefit metabolic and cardiovascular outcomes through reduction of systemic inflammation. The direct evidence in HS is limited, but parallels with psoriasis and rheumatoid arthritis suggest that effective biologic therapy may reduce cardiovascular event rates beyond what would be predicted from skin improvement alone. This is an additional rationale for aggressive treatment of significant HS rather than chronic suboptimal management.

The integrated care problem

A patient with significant HS and metabolic syndrome often sees:

• A dermatologist focused on skin disease
• A general practitioner managing primary care
• Possibly an endocrinologist for diabetes
• Possibly a cardiologist for cardiovascular risk
• Possibly a gynaecologist or other specialists

Each specialist tends to focus on their own domain. The combined picture — chronic inflammation driving both skin and cardiovascular disease, multiple modifiable factors that affect both, shared therapeutic targets — often falls between the cracks.

What helps with this:

• Active coordination by one clinician (usually the general practitioner) who has the overall picture
• Bringing the HS dimension to general practice visits explicitly, including any biologic therapy and current disease activity
• Bringing the cardiovascular dimension to dermatology visits explicitly, including current cardiovascular medications and any cardiac symptoms
• Asking specialists to communicate through shared electronic records or summary letters where possible
• Annual integrated review at general practice, looking at all conditions together rather than each in isolation

Patients who advocate for this integration tend to receive better-coordinated care than those who passively accept fragmented specialist contacts.

In Germany specifically

The German healthcare context for metabolic screening in HS:

• Gesundheits-Check-up (general preventive examination) is available under GKV every 3 years for adults aged 35+, and once between ages 18-34. This is the appropriate framework for routine metabolic and cardiovascular screening. HS patients should ensure they are using this.
• Hausarzt (general practitioner) coordinates standard cardiovascular and metabolic care.
• Specialist referrals to endocrinology, cardiology, or other relevant specialties are made by the Hausarzt as needed.
• DMP (Disease Management Programmes) exist for type 2 diabetes, coronary heart disease, and other chronic conditions; HS patients with these conditions can enroll for structured follow-up.

The system supports the integrated screening this article describes — what is often missing is the active patient awareness that this screening is warranted given the comorbidity profile.

Frequently asked questions

Should I see a cardiologist as part of my HS care?

Not as a routine, but if you have specific symptoms (chest pain, dyspnea), known cardiovascular disease, or substantially elevated cardiovascular risk on standard assessment, cardiology referral through your general practitioner is appropriate. Most patients can be adequately managed in primary care.

Will treating my HS reduce my cardiovascular risk?

Possibly. The evidence is suggestive but not definitive specific to HS. The parallel with psoriasis and rheumatoid arthritis — where effective biologic therapy reduces cardiovascular events — supports the expectation that effective HS treatment has cardiovascular benefits beyond skin improvement. This adds to the rationale for active HS treatment rather than chronic suboptimal management.

Are biologics safe from a cardiovascular perspective?

Generally yes. The biologics approved for HS (adalimumab, secukinumab, bimekizumab) have favourable cardiovascular safety profiles in the indication populations studied. TNF inhibitors have been studied extensively in cardiovascular contexts in rheumatology and dermatology. Patients with specific advanced cardiovascular conditions (e.g., NYHA class III/IV heart failure) have specific considerations with TNF inhibitors and should be evaluated individually.

Does my CRP being elevated matter?

C-reactive protein (CRP) is a marker of systemic inflammation that is often elevated in HS, particularly during flares. Persistently elevated CRP is associated with cardiovascular risk independent of traditional factors. Active HS treatment that reduces CRP may indirectly reduce cardiovascular risk. CRP is a useful biomarker but not a treatment target in itself in HS management.

Should I be on a statin because of my HS?

Statin therapy is determined by cardiovascular risk assessment, not by HS diagnosis alone. If your overall cardiovascular risk calculation supports statin therapy (typically based on age, lipid levels, blood pressure, diabetes status, smoking, family history), HS does not contraindicate it. The relevant decision is made with your general practitioner using standard cardiovascular risk frameworks.

What about NSAIDs and my cardiovascular risk?

NSAIDs (ibuprofen, naproxen, diclofenac, etc.) used for HS pain have established cardiovascular risk in regular long-term use, particularly at higher doses. For patients with significant cardiovascular risk, this warrants discussion with the prescribing clinician. Short-term use during flares is generally low-risk; chronic use at maximum doses for years carries meaningful cardiovascular implications.

Are GLP-1 agonists relevant for me?

For HS patients with type 2 diabetes, significant obesity, or both, GLP-1 receptor agonists offer benefits for glycemic control, weight management, and cardiovascular events. They may also have indirect benefits for HS through weight reduction. Reimbursement in Germany varies and is evolving; specific indications and access should be discussed with your general practitioner or endocrinologist.

My family has heart disease — should I worry more?

Family history of premature cardiovascular disease (men <55, women <65) is an additional cardiovascular risk factor that compounds with the HS-related elevation. This warrants more proactive cardiovascular risk management — earlier and more frequent screening, lower thresholds for intervention, and active modification of all risk factors. Discuss family history specifically with your general practitioner.

Disclaimer. This article is for general education and does not constitute personal medical advice. Cardiovascular and metabolic management requires individualized assessment by qualified clinicians, typically including your general practitioner and, where relevant, internal medicine or cardiology specialists.