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Chapter 22: Pyoderma Gangrenosum

Alexandra Coromilas; Misha Rosenbach

PYODERMA GANGRENOSUM

Therapeutic Approach

Pyoderma gangrenosum (PG) is a rare neutrophilic inflammatory skin condition that often occurs in association with underlying systemic inflammatory conditions. PG can be classified into ulcerative (classic), bullous, pustular, vegetative, and peristomal subtypes. Therapy is largely based on small uncontrolled and observational studies; there are no FDA-approved therapies and thus a strict guideline for treatment does not exist. A multi-facted approach is needed with a two-fold goal: (1) stop the inflammation, (2) heal the wound. It is essential to identify any associated systemic conditions that may be driving inflammation, and ensure they are adequately treated. The type of underlying disease may influence the therapeutic approach to PG. Multimodality therapy is often used, including topical/local anti-inflammatory therapies (to target PG), topical antimicrobial therapies (to eliminate colonization/superinfection), and systemic anti-inflammatory therapies. Topical therapy can be sufficient for mild, superficial PG, and specifically the vegetative and peristomal subtypes. However, in patients with multiple, more extensive lesions, and/or rapid progression, systemic therapy is indicated. Prednisone, cyclosporine, and infliximab are first-line systemic therapy, with initial choice based on severity, physician comfort, and patient comorbidities. Infliximab should be considered in patients with underlying inflammatory bowel disease or rheumatoid arthritis. Evidence for use of additional immunosuppressive or biologic therapy is based on case reports and case series, and these are typically used as adjunctive and glucocorticoid-sparing therapy in severe, refractory cases. Once inflammation is treated, focus should turn to wound healing with dressings and local wound care. Surgical therapy such as with skin grafts, bioengineered keratinocyte autografts, and allogeneic dermal substitutes is controversial given the potential for pathergy, but can be considered in select patients with chronic wounds with delayed healing despite sufficient control of the underlying PG. See Table 22-1.

Table 22-1Pyoderma Gangrenosum Treatment Table
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Table 22-1 Pyoderma Gangrenosum Treatment Table
MEDICATION NAME INDICATION MECHANISM OF ACTION DOSING ADVERSE EFFECTS SUGGESTED MONITORING LEVEL OF EVIDENCE (REFERENCE)
Topical Therapy
Topical steroids Limited, small, superficial slowly progressive lesions including vegetative, peristomal; adjunct to systemic therapy. Anti-inflammatory Clobetasol propionate 0.05% Cutaneous atrophy, striae None III1,2
Topical calcineurin inhibitors Limited, small, superficial slowly progressive lesions including vegetative, peristomal; adjunct to systemic therapy Anti-inflammatory Tacrolimus 0.03%-0.3%, cyclosporine ophthalmic emulsion 0.05% Burning, irritation, excessive granulation tissue, rarely systemic absorption None III1-3
Intralesional steroids Adjunct to systemic therapy; consider as monotherapy for limited, small, superficial slowly progressive lesions including vegetative, peristomal. Anti-inflammatory Intralesional triamcinolone 5-40 mg/mL Cutaneous atrophy, pathergy None III4,5
Topical dapsone Adjunct to systemic therapy Anti-inflammatory Dapsone 5% Dryness, erythema, peeling, burning None III6
First-Line Systemic Therapy
Glucocorticoids First-line treatment for extensive, rapidly progressive lesions Anti-inflammatory Prednisone 0.5-2 mg/kg po daily or its equivalent; rarely pulse methylprednisolone for severe disease Hyperglycemia, hypertension, weight gain, edema, opportunistic infection, bowel perforation, peptic ulcer disease, cataracts, glaucoma, osteoporisis, osteonecrosis None, consider baseline DEXA scan if ...

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