Pyoderma gangrenosum !

A rare inflammatory skin disease causing fast-growing, very painful leg ulcers; it is not an infection and is linked to bowel and blood diseases.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

A non-infectious neutrophilic dermatosis in which a tender pustule or nodule breaks down into a rapidly enlarging, painful ulcer with a violaceous, undermined edge. Despite its name it is neither pyogenic nor gangrenous. It is a diagnosis of exclusion and often signals an underlying systemic disease.

Who gets it

Rare; it can appear at any age but is more frequent after 50 and slightly more frequent in women. About half of patients have an associated disease, most often inflammatory bowel disease (seen in roughly 1–3% of people with IBD, more with ulcerative colitis). No specific Colombian data exist; cases are seen in dermatology and IBD clinics, and it is often first mistaken for an infected wound or a venous ulcer.

Causes

Inflammatory bowel disease: ulcerative colitis and Crohn disease
Inflammatory arthritis, especially rheumatoid arthritis
Myeloid blood disorders: myelodysplastic syndrome, acute myeloid leukaemia, monoclonal gammopathy (often IgA)
Others: autoimmune hepatitis, Behçet disease, granulomatosis with polyangiitis, autoinflammatory syndromes (PAPA), levamisole-adulterated cocaine
About half of cases are idiopathic

Risk factors

Active inflammatory bowel disease
Rheumatoid arthritis or other inflammatory arthritis
Haematological malignancy or monoclonal gammopathy
Skin trauma or surgery (pathergy), including surgical wounds and stomas
Age over 50

Pathophysiology

Dysregulated innate immunity drives uncontrolled recruitment and activation of neutrophils in the dermis. Cytokines such as IL-1, IL-8, IL-17 and TNF-α amplify the response and destroy tissue, producing the ulcer. Minor trauma can trigger new lesions or enlarge existing ones (pathergy), which explains why debridement or surgery may worsen the disease.

Classification

Ulcerative (classic): painful ulcer with violaceous undermined border, mostly on the legs
Bullous: superficial haemorrhagic blisters, strongly linked to myeloid neoplasms
Pustular: sterile pustules, typically during IBD flares
Vegetative: localized, less aggressive, superficial ulcers
Peristomal: around ileostomies or colostomies

Symptoms and signs

A small pustule, papule or nodule that breaks down within days into an ulcer
Severe pain, out of proportion to the size of the lesion
Ulcer with a violaceous, undermined edge and a purulent or necrotic base
Most often on the lower legs (pretibial area); may be multiple
Healing with thin, cribriform (sieve-like) scars
Fever, malaise and joint pain in some patients

Diagnosis

Clinical: A clinical diagnosis of exclusion: rapidly progressive painful ulcer with a violaceous undermined border, a history of pathergy, cribriform scarring and an associated disease. Validated criteria (major criterion: neutrophilic infiltrate at the ulcer edge, plus several minor criteria) support the diagnosis.
Tests: Biopsy from the ulcer edge to show a neutrophilic infiltrate and exclude infection, vasculitis and cancer. Tissue cultures (bacteria, fungi, mycobacteria). Blood count, inflammatory markers, serum protein electrophoresis, liver tests, autoimmune and ANCA screen; endoscopy or colonoscopy if bowel symptoms are present.
Imaging: Not diagnostic. Vascular studies (Doppler, ankle-brachial index) help exclude venous or arterial ulcers on the legs.

Differential diagnosis

Venous, arterial or diabetic ulcer
Infections: ecthyma, necrotizing soft-tissue infection, deep fungal infection, cutaneous leishmaniasis (important in Colombia), mycobacterial infection
Vasculitis and antiphospholipid syndrome
Ulcerated skin cancer (squamous cell carcinoma, lymphoma)
Calciphylaxis and spider bites (loxoscelism)

Goal of treatment

Stop the inflammation quickly to relieve pain and allow the ulcer to heal, avoid further trauma, control the associated disease and prevent infection and scarring.

Treatment

Medical: Mild or localized disease: potent topical or intralesional corticosteroids and topical calcineurin inhibitors (tacrolimus), sometimes with anti-inflammatory tetracyclines.
Medical: Extensive or rapidly progressing disease: systemic corticosteroids or ciclosporin as first-line options; anti-TNF biologics (especially when IBD coexists) and other immunosuppressants as steroid-sparing therapy.
Conservative: Moist, non-adherent dressings, gentle cleaning, compression only if tolerated, oedema control and adequate pain relief; avoid aggressive surgical debridement during the active phase.
Follow-up: Nursing: measure and photograph the ulcer, assess pain, watch for infection, steroid side effects (glucose, blood pressure) and tell surgical teams about the pathergy risk.

Complications

Secondary infection and sepsis
Severe chronic pain and disability
Cribriform scarring and recurrence
Complications of long-term immunosuppression
Spread to new sites after surgery or minor trauma

Prognosis

Most lesions heal over months with treatment, but recurrences are common and depend on control of the associated disease. Outcome is worse when it is linked to a haematological malignancy or treated late.

Prevention

Avoid unnecessary procedures and trauma in known patients; plan surgery with peri-operative immunosuppression
Keep the associated disease (IBD, arthritis) well controlled

Test yourself

Think of the answer, then tap the question to see it.

Which systemic disease is most commonly associated with pyoderma gangrenosum?

Inflammatory bowel disease, especially ulcerative colitis; rheumatoid arthritis and myeloid blood disorders follow.

What is pathergy and why does it matter in pyoderma gangrenosum?

New or worse lesions after minor skin trauma; it means surgical debridement can enlarge the ulcer.

What does the classic ulcer look like?

A very painful ulcer with a violaceous, undermined border, usually on the lower legs, healing with cribriform scars.

What are first-line systemic treatments for extensive disease?

Systemic corticosteroids or ciclosporin; anti-TNF biologics when IBD coexists or as steroid-sparing therapy.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Pyoderma Gangrenosum: Symptoms, Causes, and Treatment (DermNet, 2026).

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Representative model, for educational purposes only.

Skin highlighted on the Durgical 3D model