Syndrome de Raynaud compliqué de gangrène digitale au cours d'un traitement par l'interféron alpha

Liozon, É.; Delaire, L; Lacroix, Pascal G.; Labrousse, François; Ly, Kim-Heang; Fauchais, Anne-Laure; Loustaud‐Ratti, Véronique; J, Vidal; Liozon, F; Vidal, É.

doi:10.1016/s0248-8663(97)84017-9

Cited by 17 publications

(7 citation statements)

References 13 publications

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“…We could not identify the precise nature of the arterial lesion in our patient because a biopsy of the arteries was refused. Such arterial lesions have previously been described as corresponding to arteritis containing eosinophils in the inflammatory infiltrate of the vessel wall with secondary thrombosis 10 or to thrombi without underlying vasculitis 11 . Our case did not have any other skin lesions concomitant with the digital necrosis, demonstrating that digital necrosis in HES can occur independent of cutaneous (eosinophilic) vasculitis.…”

supporting

confidence: 60%

Digital necrosis in a patient with hypereosinophilic syndrome in the absence of cutaneous eosinophilic vasculitis

et al. 2001

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supporting

confidence: 60%

Digital necrosis in a patient with hypereosinophilic syndrome in the absence of cutaneous eosinophilic vasculitis

et al. 2001

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“…RP is a known side effect of treatment with interferon supported by numerous cases reports [41,[108][109][110][111][112][113][114][115][116]. On direct questioning of patients taking IFN [117], symptoms of RP were reported by more than half.…”

Section: Drugs Increasing Blood Viscosity and Enhancing Vasoconstrictionmentioning

confidence: 99%

“…Although some case reports of RP induced by interferons are described without any immune deficiency [122] it is known that interferon therapy can be related to an autoimmune disease [123,124]. Increasing blood viscosity by induction of serum cryoprecipitation [125], deposition of immune complexes [126] and arterial occlusion by thrombi due to the procoagulant activity of interferon [112,113] have been proposed. A study of 108 patients with SSc found a higher level of IFN-γ in patients with associated RP and suggested a pathogenic role of INF-γ in SSc patients with RP, but this role still remains unclear [127].…”

Section: Drugs Increasing Blood Viscosity and Enhancing Vasoconstrictionmentioning

confidence: 99%

Drug‐induced Raynaud's phenomenon: beyond β‐adrenoceptor blockers

Khouri

Blaise

Carpentier

et al. 2016

Brit J Clinical Pharma

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AIMDrug-induced Raynaud's phenomenon (RP) has long been associated with the use of different drugs, including cancer chemotherapy or β-adrenoceptor blockers. However, sources report extremely variable prevalence and the level of evidence for each class is heterogeneous. Moreover, new signals are emerging from case reports and small series. Our objective was therefore to review available evidence about this adverse drug effect and to propose a mechanistic approach of drug-induced RP. METHODSA systematic review of English and French language articles was performed through Medline (1946Medline ( -2015 and Embase (1974Embase ( -2015. Further relevant papers were identified from the reference lists of retrieved articles. RESULTSWe identified 12 classes of drugs responsible for RP, with a variety of underlying mechanisms such as increased sympathetic activation, endothelial dysfunction, neurotoxicity or decreased red blood cell deformability. Cisplatin and bleomycin were associated with the highest risk, followed by β-adrenoceptor blockers. Recent data suggest a possible involvement of tyrosine kinase inhibitors (TKI), through an unknown mechanism. CONCLUSIONDrug-induced RP is a probably underestimated adverse drug event, with limited available evidence regarding its prevalence. Although rare, serious complications like critical digital ischaemia have been reported. When these treatments are started in patients with a history of RP, careful monitoring must be made and, if possible, alternative therapies that do not alter peripheral blood flow should be considered. IntroductionRaynaud's phenomenon (RP) is characterized by transient ischaemia of the extremities in response to environmental stress or emotions [1]. It typically manifests as changes to the fingers, with pallor (vasospasm and decreased blood flow), cyanosis (deoxygenation of the static venous blood) and rubor (reperfusion), often accompanied by pain. RP can be primary (i.e. idiopathic) or secondary to an underlying cause. In both cases, abnormalities of the cutaneous microcirculation are primarily involved in the pathophysiology of RP [2]. The prevalence of RP in the general population varies between 0.5 and 19%, with major geographic variability [3][4][5][6]. While primary RP is the most frequent form (80-90%) [7], RP may also be secondary to various auto-immune diseases (such as systemic sclerosis (SSc), systemic lupus erythematosus, vasculitis, etc.), or other systemic diseases [1]. Several drugs with peripheral vascular effects leading to decreased microvascular perfusion may induce or aggravate RP. Drug-induced RP probably goes unrecognized because of the limited knowledge of this side effect. British Journal of Clinical PharmacologyLiterature reviews and textbooks usually have comprehensively reviewed drugs that have long been known to be responsible for RP [8]. However, new signals are emerging from numerous case reports. Yet, to our knowledge, no systematic review has been performed and little is known about the prevalence and the level of evidence ...

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“…Additionally, IFN‐α promotes intravascular thrombosis by diminishing endothelial urokinase‐type plasminogen inhibitor 19 . In one case of IFN‐α‐associated Raynaud's syndrome, histopathological examination of the arteries in an amputated finger showed multifocal arterial occlusion by thrombi 15 . Vascular thrombosis has also been described associated with IFN‐β‐induced cutaneous ulcers 20,21 .…”

Section: Discussionmentioning

confidence: 99%

“…19 In one case of IFN-αassociated Raynaud's syndrome, histopathological examination of the arteries in an amputated finger showed multifocal arterial occlusion by thrombi. 15 Vascular thrombosis has also been described associated with IFN-β -induced cutaneous ulcers. 20,21 However, the exact mechanism of IFN-α -induced vascular abnormalities is unknown.…”

Section: Discussionmentioning

confidence: 99%

Livedo reticularis associated with interferon α therapy in two melanoma patients

Ruíz‐Genao

García‐F‐Villalta

Hernández‐Núñez

et al. 2005

Acad Dermatol Venereol

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We report two patients who developed intense livedo reticularis clearly related to the administration of interferon alpha 2b as an adjuvant therapy for melanoma. Histological studies showed scattered perivascular infiltrates without vasculitis. Laboratory tests excluded any underlying condition. Resolution of the symptoms was observed in both patients when interferon alpha was withdrawn. These cases highlight the occurrence of livedo reticularis as an uncommon side-effect of interferon alpha treatment.

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Syndrome de Raynaud compliqué de gangrène digitale au cours d'un traitement par l'interféron alpha

Cited by 17 publications

References 13 publications

Digital necrosis in a patient with hypereosinophilic syndrome in the absence of cutaneous eosinophilic vasculitis

Digital necrosis in a patient with hypereosinophilic syndrome in the absence of cutaneous eosinophilic vasculitis

Drug‐induced Raynaud's phenomenon: beyond β‐adrenoceptor blockers

Livedo reticularis associated with interferon α therapy in two melanoma patients

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