Pyoderma gangrenosum developing during therapy with TNF-alpha antagonists in a patient with rheumatoid arthritis

Vandevyvere, K.; Luyten, Frank P.; Verschueren, Patrick; Lories, Rik; Segaert, Siegfried; Westhovens, René

doi:10.1007/s10067-007-0733-8

Cited by 35 publications

(14 citation statements)

References 12 publications

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“…Cases of drug‐induced PG were mainly gathered from PubMed searches using a variety of combined search terms including ‘pyoderma gangrenosum’, ‘drug‐induced pyoderma gangrenosum’, ‘neutrophilic dermatosis’, ‘treatment’ and ‘therapy’. A list of cases of drug‐induced PG is provided in Table and the proposed pathogenic mechanisms for each drug are illustrated in Figure .…”

Section: Summary Of Each Of the 43 Published Reports Of Drug‐induced mentioning

confidence: 99%

Drug-induced pyoderma gangrenosum: a model to understand the pathogenesis of pyoderma gangrenosum

Patel

Ortega‐Loayza

2017

Br J Dermatol

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This study aimed to explore how drug-induced pyoderma gangrenosum develops in the body. Pyoderma gangreno-sum (PG) is a rare autoinflammatory disease (a genetic disease caused by a malfunctioning immune system) that causes tissue cells to die, resulting in severe and painful ulcers. Drug-induced disease is where a disease occurs, or is triggered, as a result of taking medication/drugs. In this study 43 cases of patients diagnosed with drug-induced PG were reviewed. The authors found that most of the medications associated with drug-induced PG affected more the one element in the pathway that leads to a person developing drug-induced PG. Abnormal neutrophil migration and function, dysregulated inflammation, keratinocyte apoptosis, and alteration of epigenetic mechanisms were all found to be associated with the development of drug-induced PG. Abnormal neutrophil migration and function refers to the irregular movement and function of a specific type of white blood cell (which forms part of the body's immune system). Dysregulated inflammation refers to an abnormal inflammation response in the body's cells and tissue. Ker-atinocyte apoptosis means the death of keratinocyte cells (the cells that form the majority of the outer layer of skin). Alteration of epigenetic mechanisms means a change to the way in which a cell reads and understands its own genes, which in turn affects how the cell behaves. The authors conclude that, in order to better understand how PG develops, further research is needed into the immune system, epigenetics (the way in which a cell reads and acts upon its genes) and NETosis (a form of cell death).

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Section: Summary Of Each Of the 43 Published Reports Of Drug‐induced mentioning

confidence: 99%

Drug-induced pyoderma gangrenosum: a model to understand the pathogenesis of pyoderma gangrenosum

Patel

Ortega‐Loayza

2017

Br J Dermatol

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“…Since the introduction of anti-TNF treatment, an increasing number of cutaneous adverse reactions have been recognized including psoriasiform and pustular eruptions, lupus-like disorders, dermatomyositis, vasculitis, granulomatous reactions, infections, infusion and injection site reactions and malignancies [21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38]. These entities have been summarized in table 2.…”

Section: Discussionmentioning

confidence: 99%

Amicrobial Pustulosis-Like Rash in a Patient with Crohn’s Disease under Anti-TNF-Alpha Blocker

Lee¹,

Pelivani²,

Beltraminelli³

et al. 2011

Dermatology

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Amicrobial pustulosis of the folds (APF) is a recently described entity characterized by relapsing pustular lesions predominantly involving the cutaneous flexures and scalp. This disease typically occurs in association with systemic lupus erythematosus and a variety of other autoimmune diseases. We here describe an APF-like pustular eruption predominantly affecting the scalp, face and trunk, occurring during long-term infliximab treatment for Crohn’s disease. Immunohistochemical staining of skin biopsy specimens for myxovirus resistance protein A, a marker for type 1 interferon-inducible proteins, showed increased staining in the epidermis and dermal mononuclear inflammatory infiltrate. Our observation further extends the spectrum of cutaneous adverse reactions potentially related to anti-tumor necrosis factor-α, the clinical context in which APF can occur as well as its clinical presentations.

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“…The underlying mechanisms are unknown, but cutaneous vasculitis and ulcer may be worsened with the use of TNF inhibitors. Vandevyvere et al [26] presented a case of a patient with RA who developed PG under IFX and persistent cutaneous inflammation when switching to etanercept. Additional case studies and large prospective studies are needed to establish the appropriate use of IFX for PG patients with RA.…”

Section: Discussionmentioning

confidence: 98%

Use of infliximab in a patient with pyoderma gangrenosum and rheumatoid arthritis

et al. 2010

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Pyoderma gangrenosum (PG) is characterized by ulcerative skin lesions. Infliximab (IFX) may promote PG healing in patients with inflammatory bowel disease, but whether IFX is effective for treating PG in patients with rheumatoid arthritis (RA) has not reported. We report the case of a 53-year-old woman with PG complicated by RA who was treated using IFX therapy. This case suggests that IFX therapy might offer effective treatment for such patients.

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Pyoderma gangrenosum developing during therapy with TNF-alpha antagonists in a patient with rheumatoid arthritis

Cited by 35 publications

References 12 publications

Drug-induced pyoderma gangrenosum: a model to understand the pathogenesis of pyoderma gangrenosum

Drug-induced pyoderma gangrenosum: a model to understand the pathogenesis of pyoderma gangrenosum

Amicrobial Pustulosis-Like Rash in a Patient with Crohn’s Disease under Anti-TNF-Alpha Blocker

Use of infliximab in a patient with pyoderma gangrenosum and rheumatoid arthritis

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