Pyoderma Gangrenosum

Table of Contents

  1. What is Pyoderma Gangrenosum?
  2. Pathogenesis: Neutrophilic Dysregulation and Autoinflammation
  3. Clinical Variants: Ulcerative, Pustular, Bullous, and Vegetative
  4. The Pathergy Phenomenon: Trauma and Surgery
  5. Associated Systemic Diseases
  6. Diagnosis: Exclusion, Biopsy, and Validated Criteria
  7. Differential Diagnosis
  8. Wound Care: Protecting the Fragile Edge
  9. Systemic Treatment: Corticosteroids and Cyclosporine
  10. Biologic Therapy: Anti-TNF Agents and Other Targeted Drugs
  11. Prognosis and Quality of Life
  12. Key Research Papers
  13. Connections
  14. Featured Videos

What is Pyoderma Gangrenosum?

Pyoderma gangrenosum (PG) is a rare, non-infectious neutrophilic dermatosis that presents with rapidly developing, painful skin ulcers with undermined borders and surrounding redness. Despite its name, PG is not an infection: the ulcers are sterile, and it is generally considered an autoinflammatory disorder (Maverakis 2020, PubMed PMID: 33033263). The legs are the most commonly affected site, but other parts of the skin and mucous membranes can be involved, and the course can be mild or severe, chronic or relapsing (Wollina 2007, PubMed PMID: 17433111).

In a UK population-based cohort of 313 people, the incidence standardized to the European population was 0.63 per 100,000 person-years, the median age was 59 years and 59% were women (Langan 2012, PubMed PMID: 22534879); a 2020 review puts average age at onset in the mid-40s and incidence at a few cases per million person-years. In the same UK cohort, a recognized disease association was present in 33% of patients: inflammatory bowel disease (IBD) in 20.2%, rheumatoid arthritis in 11.8% and hematological disorders in 3.9%. Hospital series report higher figures — in a Boston review of 103 patients, 34% had IBD, 20% hematological disorders and 19% seronegative arthritis, and 76% were women (Binus 2011, PubMed PMID: 21824126).

Pathogenesis: Neutrophilic Dysregulation and Autoinflammation

The cause of PG is not well understood. It is classed among the autoinflammatory diseases — conditions of recurrent sterile inflammation without circulating autoantibodies or autoreactive T cells — and research has also focused on T cells at the wound margin, which may support the destructive innate immune response (Maverakis 2020, PubMed PMID: 33033263; Marzano 2016, PubMed PMID: 27106250).

Molecules found in PG lesions include:

Genetic evidence for the autoinflammatory model comes from PAPA syndrome (pyogenic sterile arthritis, PG, and acne), an inherited early-onset disorder caused by mutations in the CD2BP1 gene (the human counterpart of murine PSTPIP1); the original authors proposed classing it as an autoinflammatory disease (Wise 2002, PubMed PMID: 11971877). PSTPIP1 mutations, via increased binding to pyrin, induce inflammasome assembly and IL-1β activation (Marzano 2016, PubMed PMID: 27106250).

Clinical Variants: Ulcerative, Pustular, Bullous, and Vegetative

PG has several recognized subtypes (Zaino 2024, PubMed PMID: 38423678). The features below come from the cited studies.

Ulcerative PG (Classic)

The classic presentation is an ulcer with an erythematous-to-violaceous undermined border (Zaino 2024, PubMed PMID: 38423678). Lesions typically start as sterile pustules that rapidly progress to painful ulcers of variable depth and size (Wollina 2007, PubMed PMID: 17433111). In German wound centres the lower legs were affected in 71.9% of 121 patients, wound size ranged from 1 to 600 cm² and pain was predominantly very high (mean 7 on a 10-point scale) (Jockenhöfer 2016, PubMed PMID: 27767288); in the Boston series 78% of ulcers were on the lower leg and 65% of patients had two or more ulcers (Binus 2011, PubMed PMID: 21824126).

Pustular PG

Besides the classic ulcer, atypical presentations include pustular, bullous and vegetative lesions (García-Abellás 2022, PubMed PMID: 36578743). How often the pustular form occurs and how it relates to IBD activity are not reported in the abstracts cited on this page.

Bullous PG

Bullous PG is considered an extremely rare form. In the reported case, a 76-year-old man with a recent diagnosis of hairy cell leukemia, the atypical presentation mimicked necrotising fasciitis; he received several antibiotics and surgical procedures before histopathology raised the suspicion of a neutrophilic dermatosis (García-Abellás 2022, PubMed PMID: 36578743). Hematological disorders are among the recognized associations of PG overall (Langan 2012, PubMed PMID: 22534879).

Vegetative PG

Vegetative PG is the subject of a 2005 case report and literature review (Langan 2005, PubMed PMID: 16101860); PubMed carries no abstract for it, so its findings are not summarized here.

Peristomal PG

A systematic review of 335 patients from 79 studies describes peristomal PG as a painful, rapidly progressing ulcer with undermined, violaceous borders, often with a history of ostomy leakage and local skin irritation or trauma. Systemic steroids were first-line therapy; infliximab and adalimumab also controlled active IBD; and, unlike classic PG, surgical approaches such as stoma closure and resection of active IBD had an effective role (Afifi 2018, PubMed PMID: 29288099).

The Pathergy Phenomenon: Trauma and Surgery

Pathergy — new lesions or worsening at sites of skin injury — is one of the 8 minor criteria in the Delphi diagnostic criteria (Maverakis 2018, PubMed PMID: 29450466), and "localization of lesion at the site of trauma" is a minor criterion in the PARACELSUS score (Jockenhöfer 2019, PubMed PMID: 29388188). Pathergy complicates management of PG (Haag 2020, PubMed PMID: 31927079).

Misdiagnosis is the other side of the problem. In a Mayo Clinic review of 240 patients diagnosed with PG plus the literature, 95 patients had ulcers that resembled PG but had another cause — vascular occlusive or venous disease, vasculitis, cancer, primary infection, drug-induced or external tissue injury, or other inflammatory disorders. Of the 64 who had been treated for PG (median 10 months), 36% did not respond to PG treatment and 12% were made worse by it (Weenig 2002, PubMed PMID: 12409543).

What the surgical literature reports:

Associated Systemic Diseases

PG is often associated with other immune-mediated diseases, most commonly IBD and rheumatoid arthritis (Maverakis 2020, PubMed PMID: 33033263). How often depends on the setting: 33% of patients in a UK population cohort had a recognized association (Langan 2012, PubMed PMID: 22534879), while a 2024 study states that up to 75% of cases develop in association with an underlying systemic disease (Saeidi 2024, PubMed PMID: 38795175).

Inflammatory bowel disease: 20.2% of the UK cohort (Langan 2012, PubMed PMID: 22534879), 34% of the Boston series (Binus 2011, PubMed PMID: 21824126) and 9.9% of a German wound-centre cohort (ulcerative colitis 5.8%, Crohn's disease 4.1%) (Jockenhöfer 2016, PubMed PMID: 27767288). Seen from the IBD side, a meta-analysis of 61,695 IBD patients found PG in 0.4% to 2.6% across individual studies, and PG was associated with female sex, Crohn's disease, erythema nodosum and eye involvement (States 2020, PubMed PMID: 31925675).

Inflammatory arthritis: rheumatoid arthritis in 11.8% of the UK cohort (Langan 2012, PubMed PMID: 22534879); seronegative arthritis in 19% and psoriasis in 11% of the Boston series (Binus 2011, PubMed PMID: 21824126); rheumatic comorbidities in 14.1% of the German cohort (Jockenhöfer 2016, PubMed PMID: 27767288).

Hematological disorders and cancer: 3.9% (UK) and 20% (Boston) had hematological disorders; in the German cohort neoplasms were found in 20.6% (6.6% hematological, 14.0% solid) (Langan 2012, PubMed PMID: 22534879; Binus 2011, PubMed PMID: 21824126; Jockenhöfer 2016, PubMed PMID: 27767288).

Monoclonal gammopathy: of 106 PG patients screened at one institution, 27% had a gammopathy (IgA 41%, IgG 28%, biclonal 14%), and cancer, especially hematologic cancer, developed in 28% of those with gammopathy versus 6% without (Saeidi 2024, PubMed PMID: 38795175).

Metabolic factors: in the German cohort, obesity was found in 69.4%, high blood pressure in 57.9% and diabetes in 33.9% (Jockenhöfer 2016, PubMed PMID: 27767288).

PAPA, PASH and related syndromes: PG also occurs within syndromes — PAPA (pyogenic arthritis, PG, acne), SAPHO and PASH (PG, acne, suppurative hidradenitis), which researchers regard as one clinicopathological spectrum of autoinflammation (Marzano 2016, PubMed PMID: 27106250). PASH was first described in two patients who had PG, acne and hidradenitis but no arthritis; one responded, though not completely, to the IL-1 receptor antagonist anakinra (Braun-Falco 2012, PubMed PMID: 21745697).

Diagnosis: Exclusion, Biopsy, and Validated Criteria

PG has long been called a "diagnosis of exclusion" (Maverakis 2018, PubMed PMID: 29450466). Laboratory tests of biopsied wound tissue together with clinical examination are needed, and validated criteria now help (Maverakis 2020, PubMed PMID: 33033263). In the Boston series only 7% of patients had a biopsy suggestive of PG, and the authors concluded that pathology should not be used to exclude the diagnosis (Binus 2011, PubMed PMID: 21824126). The Mayo review found that ulcers misdiagnosed as PG were later shown to be vascular disease, vasculitis, cancer, infection, drug-induced or external injury, or other inflammatory disorders (Weenig 2002, PubMed PMID: 12409543).

Validated Diagnostic Criteria

Delphi consensus criteria (Maverakis 2018): an international expert Delphi exercise produced 1 major criterion — biopsy of the ulcer edge showing a neutrophilic infiltrate — and 8 minor criteria: (1) exclusion of infection; (2) pathergy; (3) history of IBD or inflammatory arthritis; (4) a papule, pustule or vesicle ulcerating within 4 days of appearing; (5) peripheral redness, undermining border and tenderness at the ulcer; (6) multiple ulcers, at least one on the front of the lower leg; (7) cribriform or "wrinkled paper" scars at healed ulcer sites; and (8) decreased ulcer size within 1 month of starting immunosuppressive medication. Meeting 4 of the 8 minor criteria gave a sensitivity of 86% and a specificity of 90% (PubMed PMID: 29450466).

PARACELSUS score (Jockenhöfer 2019): a 10-criterion score developed on 60 patients with leg PG and 50 with venous leg ulcers. Major criteria are rapidly progressing disease, assessment of relevant differential diagnoses, and a reddish-violaceous wound border (present in 98% of PG patients); minor criteria are improvement with immunosuppressants, irregular ulcer shape, pain above 4/10, and location at a site of trauma; additional criteria are suppurative inflammation on histopathology, undermined borders, and an associated systemic disease. A total of 10 points or more indicates a high likelihood of PG and separated PG from venous leg ulcers (PubMed PMID: 29388188).

Differential Diagnosis

Because no histopathologic, immunologic or imaging finding is specific for PG, misdiagnosis is frequent and leads to added illness and death (Becker 2025, PubMed PMID: 40155526). In the Mayo series, the conditions eventually found in ulcers misdiagnosed as PG were:

Of the misdiagnosed patients treated for PG, 12% got worse on that treatment (Weenig 2002, PubMed PMID: 12409543). "Exclusion of infection" is one of the Delphi minor criteria, and "assessment of relevant differential diagnoses" is a PARACELSUS major criterion (Maverakis 2018, PubMed PMID: 29450466; Jockenhöfer 2019, PubMed PMID: 29388188). PG and Sweet syndrome share an autoinflammatory profile in lesional skin, with chemokine signals lower in Sweet syndrome (Marzano 2014, PubMed PMID: 24903614).

Wound Care: Protecting the Fragile Edge

Reviews describe appropriate wound care as essential alongside drug treatment (Maverakis 2020, PubMed PMID: 33033263), and describe modern wound dressings as useful for limiting pain and the risk of secondary infection (Wollina 2007, PubMed PMID: 17433111).

A wound-care specialist review summarizes the principles as pathergy avoidance, moisture balance and reduction of inflammatory stimuli: gentle cleansing without sharp debridement, limited topical antibacterial use, and a moist environment to support epithelial migration. Dressings are matched to the wound type (superficial, eschar, exudative, granulating, colonized), and the review describes compression therapy as important for reducing swelling and overgranulation (Croitoru 2020, PubMed PMID: 32320358).

Topical therapy: in a prospective UK cohort of 66 patients whose PG was considered suitable for topical treatment (mainly topical corticosteroids, most often clobetasol propionate 0.05%, and tacrolimus), 43.8% of ulcers healed by 6 months, the median time to healing was 145 days, larger ulcers healed more slowly, and 15% recurred. The study had no randomized comparator (Thomas 2016, PubMed PMID: 27502313).

Skin grafting: grafts have generally been avoided for fear of pathergy; a systematic review of case reports and series found complete healing in 75.5% of grafted wounds and pathergy in 5.2% of patients, with the evidence limited to case-level data (Morgenstjerne-Schwenck 2021, PubMed PMID: 33377584).

Systemic Treatment: Corticosteroids and Cyclosporine

Treatment typically starts with fast-acting immunosuppressive drugs (corticosteroids and/or cyclosporine) followed by slower-acting drugs with better adverse-event profiles, including biologics (Maverakis 2020, PubMed PMID: 33033263). A 2005 evidence review of more than 350 patients concluded that efficacy is best documented for systemic corticosteroids and cyclosporine, and listed alternatives for non-responders: corticosteroids with mycophenolate mofetil, mycophenolate mofetil with cyclosporine, tacrolimus, infliximab, or plasmapheresis (Reichrath 2005, PubMed PMID: 16021123).

STOP GAP trial (prednisolone vs cyclosporine): 121 patients at 39 UK hospitals (112 analysed) were randomized to oral prednisolone 0.75 mg/kg/day (maximum 75 mg/day) or cyclosporine 4 mg/kg/day (maximum 400 mg/day). Speed of healing at 6 weeks did not differ (P=0.97). By 6 months ulcers had healed in 47% of each group, and 30% (cyclosporine) and 28% (prednisolone) of healed patients had a recurrence. Adverse reactions were similar overall (68% vs 66%), but serious adverse reactions, especially infections, were more common with prednisolone. The authors concluded that the two drugs did not differ across objective and patient-reported outcomes, and that side-effect profiles and patient preference can guide the choice (Ormerod 2015, PubMed PMID: 26071094).

Real-world comparison: in a German retrospective study of 52 patients, complete remission or improvement was recorded in 48.8% of treatment attempts with corticosteroids and 20.0% with cyclosporine; adverse events occurred in 40% of cyclosporine-treated and 10.4% of corticosteroid-treated cases (Herberger 2019, PubMed PMID: 30592563).

Intravenous immunoglobulin (IVIG): in the same German study, 66.7% (10/15) of patients given IVIG had complete remission or improvement, and adverse events occurred in 20% (Herberger 2019, PubMed PMID: 30592563).

Biologic Therapy: Anti-TNF Agents and Other Targeted Drugs

A 2023 treatment review reports a growing number of studies on biologics that block tumour necrosis factor-α, interleukin-1, interleukin-17, interleukin-23 or complement factor C5a, and states that biologics have become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities (Dissemond 2023, PubMed PMID: 37610614).

Infliximab (anti-TNF-α): the first randomized placebo-controlled trial of any drug for PG. Thirty patients received a single infusion of infliximab 5 mg/kg or placebo; at week 2, 46% (6/13) on infliximab had improved versus 6% (1/17) on placebo (p=0.025). Non-responders were offered open-label infliximab; of all 29 who received it, 69% responded, 21% were in remission at week 6, and 31% did not respond (Brooklyn 2006, PubMed PMID: 16188920).

Adalimumab (anti-TNF-α): in a 26-week open-label phase 3 study in 22 Japanese patients (160 mg at week 0, 80 mg at week 2, then 40 mg every week from week 4), 54.5% achieved complete re-epithelialization of the target ulcer at week 26; adverse events were reported by 18 patients, most often infections, and serious adverse events by four. The study had no placebo arm and was sponsored by the drug's manufacturer (Yamasaki 2020, PubMed PMID: 32804433).

Other biologics in a retrospective cohort: complete remission or improvement was recorded in 63.6% of patients on infliximab, 57.1% on adalimumab, 71.4% (5/7) on etanercept and 66.6% (6/9) on ustekinumab (Herberger 2019, PubMed PMID: 30592563).

IL-1 blockade: case-level evidence only. A patient with a PAPA-like syndrome and a homozygous PSTPIP1 variant went into rapid remission on canakinumab (Geusau 2013, PubMed PMID: 23426477), and one of the two original PASH patients responded partially to anakinra (Braun-Falco 2012, PubMed PMID: 21745697).

JAK inhibitors: a 2026 systematic review of published case reports found 59 PG patients treated with tofacitinib, upadacitinib, baricitinib, abrocitinib or ruxolitinib, with 33 complete and 26 partial responses and adverse events in 6; the authors note the evidence is limited to small case reports with variable outcome definitions and call for controlled studies (Vahabi 2026, PubMed PMID: 42472066).

Prognosis and Quality of Life

Despite advances in therapy, the prognosis of PG remains unpredictable (Wollina 2007, PubMed PMID: 17433111).

Healing and recurrence: in the STOP GAP trial, 47% of ulcers in each arm had healed by 6 months, and about 3 in 10 healed patients had a recurrence (Ormerod 2015, PubMed PMID: 26071094). In the topical-therapy cohort, the median time to healing was 145 days (Thomas 2016, PubMed PMID: 27502313).

Scarring: cribriform or "wrinkled paper" scars at healed ulcer sites are one of the Delphi minor criteria (Maverakis 2018, PubMed PMID: 29450466).

Quality of life: a narrative review of nine studies found the physical, emotional and psychological domains most affected; patients tend to feel depressed or anxious, isolated and embarrassed, pain is a major contributor, and comorbidities such as Crohn's disease, ulcerative colitis and monoclonal gammopathy can worsen the impact (Sanchez-Melendez 2024, PubMed PMID: 37424357). In the Boston series, 14% had major depression (Binus 2011, PubMed PMID: 21824126).

Mortality: in the UK population cohort, the risk of death was three times that of general-population controls (adjusted hazard ratio 3.03), 72% higher than that of IBD controls, and borderline higher than that of rheumatoid arthritis controls (Langan 2012, PubMed PMID: 22534879). The Boston series recorded a 16% mortality rate over its 8-year study period (Binus 2011, PubMed PMID: 21824126).

Decisions about diagnosis and treatment belong with a dermatologist or other clinician.

Key Research Papers

Key peer-reviewed studies on pyoderma gangrenosum pathogenesis, diagnosis, and treatment. Each PMID link opens the study on PubMed; every entry was checked against its PubMed record.

  1. Maverakis E, et al. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020;6(1):81. — PubMed PMID: 33033263
  2. Brooklyn TN, et al. Infliximab for the treatment of pyoderma gangrenosum: a randomised, double blind, placebo controlled trial. Gut. 2006;55(4):505–509. — PubMed PMID: 16188920
  3. Ormerod AD, et al. Comparison of the two most commonly used treatments for pyoderma gangrenosum: results of the STOP GAP randomised controlled trial. BMJ. 2015;350:h2958. — PubMed PMID: 26071094
  4. Jockenhöfer F, et al. Tricenter analysis of cofactors and comorbidity in patients with pyoderma gangrenosum. J Dtsch Dermatol Ges. 2016;14(10):1023–1030. — PubMed PMID: 27767288
  5. Maverakis E, et al. Diagnostic Criteria of Ulcerative Pyoderma Gangrenosum: A Delphi Consensus of International Experts. JAMA Dermatol. 2018;154(4):461–466. — PubMed PMID: 29450466
  6. Langan SM, et al. Incidence, mortality, and disease associations of pyoderma gangrenosum in the United Kingdom: a retrospective cohort study. J Invest Dermatol. 2012;132(9):2166–2170. — PubMed PMID: 22534879
  7. Reichrath J, et al. Treatment recommendations for pyoderma gangrenosum: an evidence-based review of the literature based on more than 350 patients. J Am Acad Dermatol. 2005;53(2):273–283. — PubMed PMID: 16021123
  8. Jockenhöfer F, et al. The PARACELSUS score: a novel diagnostic tool for pyoderma gangrenosum. Br J Dermatol. 2019;180(3):615–620. — PubMed PMID: 29388188
  9. Yamasaki K, et al. Adalimumab in Japanese patients with active ulcers of pyoderma gangrenosum: Twenty-six-week phase 3 open-label study. J Dermatol. 2020;47(12):1383–1390. — PubMed PMID: 32804433
  10. Binus AM, et al. Pyoderma gangrenosum: a retrospective review of patient characteristics, comorbidities and therapy in 103 patients. Br J Dermatol. 2011;165(6):1244–1250. — PubMed PMID: 21824126
  11. Herberger K, et al. Biologics and immunoglobulins in the treatment of pyoderma gangrenosum - analysis of 52 patients. J Dtsch Dermatol Ges. 2019;17(1):32–41. — PubMed PMID: 30592563
  12. Wollina U. Pyoderma gangrenosum--a review. Orphanet J Rare Dis. 2007;2:19. — PubMed PMID: 17433111
  13. Wise CA, et al. Mutations in CD2BP1 disrupt binding to PTP PEST and are responsible for PAPA syndrome, an autoinflammatory disorder. Hum Mol Genet. 2002;11(8):961–969. — PubMed PMID: 11971877
  14. Marzano AV, et al. Expression of cytokines, chemokines and other effector molecules in two prototypic autoinflammatory skin diseases, pyoderma gangrenosum and Sweet's syndrome. Clin Exp Immunol. 2014;178(1):48–56. — PubMed PMID: 24903614
  15. Marzano AV, et al. Pyoderma gangrenosum and its syndromic forms: evidence for a link with autoinflammation. Br J Dermatol. 2016;175(5):882–891. — PubMed PMID: 27106250
  16. Braun-Falco M, et al. Pyoderma gangrenosum, acne, and suppurative hidradenitis (PASH)--a new autoinflammatory syndrome distinct from PAPA syndrome. J Am Acad Dermatol. 2012;66(3):409–415. — PubMed PMID: 21745697
  17. Geusau A, et al. Identification of a homozygous PSTPIP1 mutation in a patient with a PAPA-like syndrome responding to canakinumab treatment. JAMA Dermatol. 2013;149(2):209–215. — PubMed PMID: 23426477
  18. Weenig RH, et al. Skin ulcers misdiagnosed as pyoderma gangrenosum. N Engl J Med. 2002;347(18):1412–1418. — PubMed PMID: 12409543
  19. Becker SL, et al. Clinical Mimickers Misdiagnosed as Pyoderma Gangrenosum. Am J Clin Dermatol. 2025;26(4):511–523. — PubMed PMID: 40155526
  20. States V, et al. Pyoderma Gangrenosum in Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis. Dig Dis Sci. 2020;65(9):2675–2685. — PubMed PMID: 31925675
  21. Saeidi V, et al. Monoclonal gammopathy in the setting of Pyoderma gangrenosum. Arch Dermatol Res. 2024;316(6):268. — PubMed PMID: 38795175
  22. Afifi L, et al. Diagnosis and management of peristomal pyoderma gangrenosum: A systematic review. J Am Acad Dermatol. 2018;78(6):1195–1204.e1. — PubMed PMID: 29288099
  23. Haag CK, et al. Perioperative management of pyoderma gangrenosum. J Am Acad Dermatol. 2020;83(2):369–374. — PubMed PMID: 31927079
  24. Morgenstjerne-Schwenck LET, et al. Efficacy and safety of skin grafting in treatment of vasculitic ulcer and pyoderma gangrenosum-A systematic review. Wound Repair Regen. 2021;29(2):240–253. — PubMed PMID: 33377584
  25. Croitoru D, et al. A Wound Care Specialist's Approach to Pyoderma Gangrenosum. Adv Wound Care (New Rochelle). 2020;9(12):686–694. — PubMed PMID: 32320358
  26. Thomas KS, et al. Clinical outcomes and response of patients applying topical therapy for pyoderma gangrenosum: A prospective cohort study. J Am Acad Dermatol. 2016;75(5):940–949. — PubMed PMID: 27502313
  27. Dissemond J, et al. Pyoderma Gangrenosum: Treatment Options. Drugs. 2023;83(14):1255–1267. — PubMed PMID: 37610614
  28. Vahabi SM, et al. JAK Inhibitors for Treatment of Pyoderma Gangrenosum and Sweet Syndrome: A Systematic Review of Published Case Reports. Dermatol Res Pract. 2026;2026:7086209. — PubMed PMID: 42472066
  29. Sanchez-Melendez SN, et al. Pyoderma gangrenosum and impact on quality of life: A narrative review. Exp Dermatol. 2024;33(1):e14876. — PubMed PMID: 37424357
  30. Zaino ML, et al. Pyoderma Gangrenosum: Diagnostic Criteria, Subtypes, Systemic Associations, and Workup. Dermatol Clin. 2024;42(2):157–170. — PubMed PMID: 38423678
  31. García-Abellás P, et al. Pure Bullous Pyoderma Gangrenosum, a Challenging Clinico-Pathological Diagnosis: Critical Literature Review with Emphasis on Diagnostic Criteria. Indian J Dermatol. 2022;67(4):409–414. — PubMed PMID: 36578743
  32. Langan SM, Powell FC. Vegetative pyoderma gangrenosum: a report of two new cases and a review of the literature. Int J Dermatol. 2005;44(8):623–629. — PubMed PMID: 16101860

PubMed Topic Searches

  1. PubMed: PG pathogenesis
  2. PubMed: Adalimumab PG
  3. PubMed: PG and IBD
  4. PubMed: PG diagnosis criteria
  5. PubMed: PG pathergy
  6. PubMed: PG cyclosporine
  7. PubMed: PAPA syndrome
  8. PubMed: PG wound care

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