Hidradenitis Suppurativa (Boils)
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Hidradenitis Suppurativa (Boils)
Hidradenitis suppurativa (HS), also called acne inversa, is a chronic inflammatory skin disease characterized by painful, recurring abscesses, nodules, and tunnels (sinus tracts) in areas where skin rubs together. It results from blocked hair follicles that become inflamed and rupture, triggering an immune response that destroys surrounding tissue and creates chronic wounds. This condition affects 1-4% of the population, typically beginning after puberty, and significantly impacts quality of life due to pain, drainage, and scarring.
Recognizing Hidradenitis Suppurativa (Boils)
Common symptoms and warning signs to look for
Painful, deep lumps under the skin - often in armpits, groin, buttocks, or under breasts
Recurring boils that rupture and drain foul-smelling pus or blood
Tunnels under the skin (sinus tracts) connecting multiple abscesses
Thick, rope-like scarring (hypertrophic or keloid) in affected areas
Double comedones (blackheads with multiple openings) - a hallmark sign
What a Healthy System Looks Like
In a healthy individual, the pilosebaceous unit (hair follicle and associated sebaceous gland) functions as a normal skin appendage: The hair follicle undergoes regular cycling (anagen, catagen, telogen) with normal keratinization preventing follicular occlusion. Apocrine and eccrine sweat glands produce sweat that reaches the skin surface through unobstructed ducts, regulating temperature and providing antimicrobial peptides. The skin microbiome maintains balanced bacterial populations (Staphylococcus epidermidis, Cutibacterium acnes) without pathogenic overgrowth. Terminal hair follicles in intertriginous areas (axilla, groin, perianal) remain patent with normal keratinocyte turnover. The immune system maintains surveillance without triggering excessive inflammation. Wound healing proceeds through normal phases (hemostasis, inflammation, proliferation, remodeling) without chronic tissue destruction or tunnel formation.
How the Condition Develops
Understanding the biological mechanisms
Hidradenitis suppurativa involves multi-stage pathogenesis: (1) Follicular occlusion - Hyperkeratosis of the follicular infundibulum blocks the hair follicle, creating a dilated, keratin-filled follicle (follicular retention); (2) Follicular rupture - Accumulated sebum, keratin, and bacteria cause follicular distension and rupture, releasing contents into the dermis; (3) Intense inflammatory response - Ruptured follicular material triggers massive neutrophilic infiltration, IL-1β, IL-17, IL-23, and TNF-α release, creating sterile abscesses initially; (4) Bacterial colonization - Anaerobic bacteria (Prevotella, Porphyromonas) and Staphylococcus aureus colonize the damaged tissue, forming biofilms that resist treatment; (5) Chronic inflammation and tissue destruction - Persistent inflammation destroys surrounding tissue, creating sinus tracts (tunnels) lined with granulation tissue and epithelium; (6) Fibrosis and scarring - Chronic wound healing leads to hypertrophic scarring, keloid formation, and contractures; (7) Sinus tract formation - Epithelialized tunnels connect multiple lesions, allowing continuous drainage and bacterial persistence; (8) Hormonal influence - Androgens stimulate apocrine gland activity and keratinocyte proliferation, explaining post-pubertal onset and female predominance; (9) Genetic factors - Gamma-secretase mutations (NCSTN, PSENEN, PSEN1) in familial HS impair Notch signaling and follicular integrity.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| TNF-Alpha | <8 pg/mL | <4 pg/mL | Key inflammatory cytokine elevated in HS; correlates with disease severity (Hurley stage); target of adalimumab therapy |
| IL-17 (Interleukin-17) | <5 pg/mL | <2 pg/mL | Th17 cytokine elevated in HS lesions; drives neutrophilic inflammation and tissue destruction |
| IL-1β (Interleukin-1 Beta) | <5 pg/mL | <2 pg/mL | Inflammasome-derived cytokine central to HS pathogenesis; triggers initial inflammatory cascade after follicular rupture |
| IL-23 (Interleukin-23) | <10 pg/mL | <5 pg/mL | Th17 cell maintenance cytokine; elevated in HS; target of emerging biologic therapies |
| CRP (C-Reactive Protein) | <3 mg/L | <1 mg/L | Non-specific inflammation marker; elevated in active HS; correlates with disease activity and cardiovascular risk |
| Testosterone (Total) | 300-1000 ng/dL (men), 15-70 ng/dL (women) | 400-700 ng/dL (men), 20-50 ng/dL (women) | Androgens stimulate apocrine activity and follicular occlusion; hormonal assessment guides anti-androgen therapy |
| DHEA-S | 120-520 mcg/dL (men), 35-430 mcg/dL (women) | 150-350 mcg/dL | Adrenal androgen precursor; elevated levels may contribute to HS pathogenesis |
| Fasting Insulin | <25 mIU/L | <8 mIU/L | Hyperinsulinemia and insulin resistance common in HS; associated with metabolic syndrome and disease severity |
| Hemoglobin A1c | <5.7% | <5.4% | HS patients have increased diabetes risk; glycemic control affects inflammation and wound healing |
| 25-Hydroxy Vitamin D | 30-100 ng/mL | 50-80 ng/mL | Vitamin D deficiency common in HS; immunomodulatory effects may reduce inflammation |
| Zinc | 60-120 mcg/dL | 80-120 mcg/dL | Zinc essential for wound healing and immune function; deficiency impairs tissue repair |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Predisposition","contribution":"30-40% of HS patients have family history; gamma-secretase gene mutations (NCSTN, PSENEN, PSEN1) in familial cases impair Notch signaling; first-degree relatives have 20% lifetime risk","assessment":"Family history assessment; genetic testing for gamma-secretase mutations in early-onset or familial cases"}
{"cause":"Follicular Occlusion and Hyperkeratosis","contribution":"Universal in HS - Abnormal keratinization blocks hair follicles; follicular retention syndrome creates dilated, keratin-filled follicles that rupture","assessment":"Clinical examination for double comedones; histopathology if biopsy performed; assessment of lesion morphology"}
{"cause":"Hormonal Factors","contribution":"Androgens stimulate apocrine gland activity and keratinocyte proliferation; post-pubertal onset; female predominance; flares with menstrual cycle; improves with anti-androgen therapy","assessment":"Hormonal panel (testosterone, DHEA-S, androstenedione); menstrual history; assessment of disease pattern relative to hormonal changes"}
{"cause":"Obesity and Mechanical Friction","contribution":"Major risk factor - Body mass index strongly correlates with disease severity; skin friction in intertriginous areas triggers follicular damage; adipose tissue produces pro-inflammatory cytokines","assessment":"BMI calculation; waist circumference; body composition analysis; assessment of skin friction areas"}
{"cause":"Smoking","contribution":"70-90% of HS patients are current or former smokers; nicotine affects immune function and wound healing; smoking cessation improves outcomes","assessment":"Smoking history (pack-years); cotinine levels if needed; readiness to quit assessment"}
{"cause":"Bacterial Colonization and Biofilms","contribution":"Anaerobic bacteria (Prevotella, Porphyromonas) and Staphylococcus aureus form biofilms in sinus tracts; biofilms resist antibiotic treatment and perpetuate inflammation","assessment":"Wound cultures; bacterial sequencing; assessment of treatment resistance patterns"}
{"cause":"Immune Dysregulation","contribution":"Core mechanism - Dysregulated Th1/Th17 response, elevated TNF-α, IL-1β, IL-17, IL-23; impaired regulatory T-cell function; autoinflammatory component","assessment":"Cytokine panels; inflammatory markers; response to immunomodulatory therapy"}
{"cause":"Nutritional Factors","contribution":"Dairy consumption may trigger some patients; high-glycemic diet promotes inflammation; vitamin D deficiency common; zinc deficiency impairs wound healing","assessment":"Dietary history; food sensitivity testing; nutritional panel (vitamin D, zinc, iron, B12)"}
{"cause":"Psychological Stress","contribution":"Stress triggers flares through HPA axis activation; depression and anxiety worsen disease; stress-induced behaviors (picking, scratching) damage skin","assessment":"Stress history; PHQ-9 for depression; GAD-7 for anxiety; identification of stress triggers"}
Risks of Inaction
What happens if left untreated
{"complication":"Progressive Scarring and Contractures","timeline":"Months to years","impact":"Chronic inflammation leads to extensive hypertrophic and keloid scarring; contractures limit range of motion in axilla, groin, and limbs; may require surgical release; permanent disfigurement"}
{"complication":"Chronic Pain and Disability","timeline":"Ongoing","impact":"Persistent pain affects daily activities, work productivity, and sleep; average HS patient loses 2-3 work days monthly; disability claims common in severe disease"}
{"complication":"Psychological Morbidity","timeline":"Chronic, progressive","impact":"50% of HS patients experience depression; 2-3x increased suicide risk; social isolation, relationship difficulties, and reduced quality of life; body image disturbances affect intimacy"}
{"complication":"Squamous Cell Carcinoma","timeline":"10-20+ years of disease","impact":"Long-standing HS lesions (especially perianal) can develop Marjolin's ulcer; aggressive SCC with poor prognosis; requires regular surveillance in chronic cases"}
{"complication":"Lymphedema","timeline":"Years of chronic inflammation","impact":"Scarring and inflammation damage lymphatic vessels; chronic limb swelling increases infection risk and impairs mobility; difficult to treat once established"}
{"complication":"Anemia and Systemic Inflammation","timeline":"Chronic","impact":"Chronic blood loss and inflammation cause anemia; elevated cardiovascular risk from persistent inflammation; increased risk of metabolic syndrome and diabetes"}
{"complication":"Treatment Complications","timeline":"With chronic therapy","impact":"Long-term antibiotic use causes resistance and microbiome disruption; chronic opioid use for pain leads to dependence; repeated surgeries create additional scarring"}
{"complication":"Social and Economic Burden","timeline":"Lifetime","impact":"Average HS patient spends $3000+ annually on treatments; lost wages from disability; relationship strain and social withdrawal; reduced educational and career attainment"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Hurley Staging Assessment","purpose":"Classify disease severity and guide treatment","whatItShows":"Stage I: Single or multiple isolated abscesses without sinus tracts or scarring; Stage II: Recurrent abscesses with sinus tract formation and scarring, separated by normal skin; Stage III: Diffuse or near-diffuse involvement with interconnected sinus tracts and abscesses across entire area"}
{"test":"International Hidradenitis Suppurativa Severity Score System (IHS4)","purpose":"Objective disease activity measurement","whatItShows":"Scores nodules, abscesses, and draining tunnels; IHS4 <3 mild, 3-8 moderate, >8 severe; tracks treatment response over time"}
{"test":"Cytokine Panel (TNF-α, IL-17, IL-1β, IL-23)","purpose":"Assess inflammatory burden and guide biologic selection","whatItShows":"Elevated inflammatory cytokines confirm immune-driven pathogenesis; helps predict response to specific biologic therapies"}
{"test":"Hormonal Assessment","purpose":"Identify hormonal contributors","whatItShows":"Testosterone, DHEA-S, androstenedione levels; PCOS workup in women; guides anti-androgen therapy decisions"}
{"test":"Metabolic Panel","purpose":"Screen for comorbidities","whatItShows":"Fasting glucose, HbA1c, insulin levels, lipid panel; identifies metabolic syndrome and diabetes risk; informs holistic treatment"}
{"test":"Bacterial Culture and Sensitivity","purpose":"Guide antibiotic therapy","whatItShows":"Identifies dominant organisms (S. aureus, anaerobes) and resistance patterns; biofilm assessment; informs targeted antimicrobial therapy"}
{"test":"Nutritional Assessment","purpose":"Identify modifiable nutritional contributors","whatItShows":"Vitamin D, zinc, iron, B12 levels; deficiencies impair immune function and wound healing; guides supplementation"}
{"test":"Wound Assessment and Mapping","purpose":"Document extent and track healing","whatItShows":"Photographic documentation, lesion count, surface area measurement, sinus tract mapping; essential for monitoring treatment response"}
{"test":"Psychological Screening","purpose":"Identify mental health comorbidities","whatItShows":"PHQ-9 for depression, GAD-7 for anxiety; quality of life assessment (Dermatology Life Quality Index); informs supportive care needs"}
Our Treatment Approach
How we help you overcome Hidradenitis Suppurativa (Boils)
Healers HS Remission Protocol
Healers HS Remission Protocol
Diet & Lifestyle
Recommendations for optimal recovery
Recovery Timeline
What to expect on your healing journey
{"initialImprovement":"4-8 weeks - Reduced pain and inflammation, decreased drainage from lesions, fewer new nodules forming, improved wound healing","significantChanges":"3-6 months - Marked reduction in active lesions (IHS4 score improvement), healing of sinus tracts, reduced scarring progression, improved quality of life scores","maintenancePhase":"6-12 months - Sustained remission with minimal active lesions, stable disease without progression, reduced treatment requirements, maintained quality of life improvements"}
How We Measure Success
Outcomes that matter
IHS4 score reduction >50% from baseline
Hurley stage improvement or stabilization
Pain score reduction >50% (validated pain scales)
Reduction in draining lesions by >75%
No new nodule formation for 3+ months
Sinus tract healing or significant improvement
Improved quality of life (DLQI score improvement)
Reduced antibiotic requirements
Weight loss goal achievement if indicated
Smoking cessation if applicable
Improved metabolic markers (glucose, insulin, lipids)
Patient-reported satisfaction and well-being
Frequently Asked Questions
Common questions from patients
What is the best treatment for hidradenitis suppurativa?
The most effective HS treatment combines biologic therapy (adalimumab is FDA-approved for moderate-severe HS), hormonal modulation for appropriate patients, targeted antibiotics, and lifestyle modifications. For early disease, topical clindamycin and lifestyle changes may suffice. Severe cases may require combination biologics or surgical intervention. At Healers Clinic, we develop personalized protocols based on your Hurley stage, inflammatory markers, and hormonal profile.
Can hidradenitis suppurativa be cured?
While there is no definitive cure for HS, it can be effectively controlled and many patients achieve long periods of remission with modern treatments. Biologic therapies have revolutionized HS management, with many patients experiencing significant improvement. Early intervention is key - treating HS in Stage I can prevent progression to more severe disease with scarring. The goal is sustained remission with minimal active lesions and preserved quality of life.
What triggers hidradenitis suppurativa flare-ups?
HS flare-ups are triggered by multiple factors: hormonal changes (menstruation, stress hormones), friction and sweating from tight clothing or exercise, heat and humidity, smoking, stress, certain foods (dairy, high-glycemic foods in some patients), weight gain, and poor sleep. Identifying your personal triggers through a symptom diary is essential. At Healers Clinic, we help you identify and manage your specific triggers through comprehensive assessment.
Is hidradenitis suppurativa an autoimmune disease?
HS is classified as an autoinflammatory disease rather than a classic autoimmune condition. It involves dysregulated innate immune responses with elevated cytokines (TNF-α, IL-1β, IL-17, IL-23) driving inflammation. While not autoimmune in the traditional sense (no specific autoantibodies), the immune system is clearly dysregulated. This distinction is important because it explains why HS responds to immunomodulatory therapies like biologics.
Does weight loss help hidradenitis suppurativa?
Yes, weight loss significantly improves HS. Studies show that even 5-10% weight reduction reduces disease severity, flare frequency, and pain levels. Weight loss reduces skin friction in intertriginous areas, improves insulin sensitivity, and decreases systemic inflammation. Bariatric surgery has shown dramatic improvements in some patients. At Healers Clinic, we incorporate weight management as a core component of HS treatment when appropriate.
Why does hidradenitis suppurativa smell?
The odor in HS comes from anaerobic bacteria (Prevotella, Porphyromonas) colonizing sinus tracts and draining lesions. These bacteria produce sulfur compounds and other metabolic byproducts with strong odors. The chronic drainage and trapped bacteria in tunnels create an environment where odor-producing organisms thrive. Proper wound care, targeted antibiotics, and healing of sinus tracts significantly reduce odor. We understand this is distressing and address it compassionately as part of treatment.
Medical References
- 1.1. Zouboulis CC, Desai N, Emtestam L, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatol Venereol. 2015;29(4):619-644. doi:10.1111/jdv.12966
- 2.2. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2019;81(1):76-90. doi:10.1016/j.jaad.2019.02.077
- 3.3. Kimball AB, Okun MM, Williams DA, et al. Two Phase 3 Trials of Adalimumab for Hidradenitis Suppurativa. N Engl J Med. 2016;375(5):422-434. doi:10.1056/NEJMoa1504370
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Hidradenitis Suppurativa (Boils).