Pirfenidone photosensitization in patients with idiopathic pulmonary fibrosis: a case series

Droitcourt, Catherine; Adamski, H.; Polat, Alaadin; Polard, Élisabeth; Kerjouan, M.; Arnouat, Baptiste; Garrec, M. Le; Oger, E.; Dupuy, Alain; Jouneau, S.

doi:10.1111/bjd.16016

Cited by 15 publications

(10 citation statements)

References 8 publications

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“…The anti-fibrotic drug pirfenidone reduces the profibrotic and contractile phenotype of differentiated human dermal myofibroblasts [146]. Pirfenidone is a pyridine (5-methyl-1-phenyl-2-(1H)-pyridone) that is FDA-approved for the treatment of idiopathic pulmonary fibrosis [147,148]. Pirfenidone reduces hypertrophic scarring following a burn, animal bites, and in diabetic ulcer wounds [149][150][151][152] and a study by Wells and Leung [146] have shown that pirfenidone may reduce fibrosis through inhibition of fibroblast differentiation into myofibroblasts.…”

Section: Myofibroblasts and Apoptosismentioning

confidence: 99%

Current Approaches Targeting the Wound Healing Phases to Attenuate Fibrosis and Scarring

Ayadi

Jay

Prasai

2020

IJMS

168

130

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Cutaneous fibrosis results from suboptimal wound healing following significant tissue injury such as severe burns, trauma, and major surgeries. Pathologic skin fibrosis results in scars that are disfiguring, limit normal movement, and prevent patient recovery and reintegration into society. While various therapeutic strategies have been used to accelerate wound healing and decrease the incidence of scarring, recent studies have targeted the molecular regulators of each phase of wound healing, including the inflammatory, proliferative, and remodeling phases. Here, we reviewed the most recent literature elucidating molecular pathways that can be targeted to reduce fibrosis with a particular focus on post-burn scarring. Current research targeting inflammatory mediators, the epithelial to mesenchymal transition, and regulators of myofibroblast differentiation shows promising results. However, a multimodal approach addressing all three phases of wound healing may provide the best therapeutic outcome.

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Section: Myofibroblasts and Apoptosismentioning

confidence: 99%

Current Approaches Targeting the Wound Healing Phases to Attenuate Fibrosis and Scarring

Ayadi

Jay

Prasai

2020

IJMS

168

130

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“…Cutaneous AE include photosensitivity and unspecified rash. Recently, it has been described that pirfenidone can induce both phototoxic 2,3 and photoallergic reactions 2,4 . Here we present a patient with a phototoxic reaction induced by pirfenidone and a review of the literature.…”

Section: Figurementioning

confidence: 91%

“…In pivotal clinical trials, between 12% and 50% of patients developed skin reactions or photosensitivity, 1 and a significant percentage discontinued the drug. Droitcourt et al 2 . recently published the largest patient series describing pirfenidone cutaneous AE in detail, where 24% of cases (13/54) presented with cutaneous AE: 2% (1/54), urticaria, and the remainder, photosensitivity.…”

Section: Figurementioning

confidence: 99%

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Pirfenidone‐induced phototoxic reaction

2020

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“…It is assumed that pathomechanism of pirfenidone photosensitivity involves photoallergy and phototoxicity. It induces erythematous, burning, pruritic lesions followed by hyperpigmentation [ 246 , 247 ].…”

Section: Characteristics Of Drugs With Photosensitive Potentialmentioning

confidence: 99%

Drug-Induced Photosensitivity—From Light and Chemistry to Biological Reactions and Clinical Symptoms

et al. 2021

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Photosensitivity is one of the most common cutaneous adverse drug reactions. There are two types of drug-induced photosensitivity: photoallergy and phototoxicity. Currently, the number of photosensitization cases is constantly increasing due to excessive exposure to sunlight, the aesthetic value of a tan, and the increasing number of photosensitizing substances in food, dietary supplements, and pharmaceutical and cosmetic products. The risk of photosensitivity reactions relates to several hundred externally and systemically administered drugs, including nonsteroidal anti-inflammatory, cardiovascular, psychotropic, antimicrobial, antihyperlipidemic, and antineoplastic drugs. Photosensitivity reactions often lead to hospitalization, additional treatment, medical management, decrease in patient’s comfort, and the limitations of drug usage. Mechanisms of drug-induced photosensitivity are complex and are observed at a cellular, molecular, and biochemical level. Photoexcitation and photoconversion of drugs trigger multidirectional biological reactions, including oxidative stress, inflammation, and changes in melanin synthesis. These effects contribute to the appearance of the following symptoms: erythema, swelling, blisters, exudation, peeling, burning, itching, and hyperpigmentation of the skin. This article reviews in detail the chemical and biological basis of drug-induced photosensitivity. The following factors are considered: the chemical properties, the influence of individual ranges of sunlight, the presence of melanin biopolymers, and the defense mechanisms of particular types of tested cells.

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Pirfenidone photosensitization in patients with idiopathic pulmonary fibrosis: a case series

Cited by 15 publications

References 8 publications

Current Approaches Targeting the Wound Healing Phases to Attenuate Fibrosis and Scarring

Current Approaches Targeting the Wound Healing Phases to Attenuate Fibrosis and Scarring

Pirfenidone‐induced phototoxic reaction

Drug-Induced Photosensitivity—From Light and Chemistry to Biological Reactions and Clinical Symptoms

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