Fênomeno de Raynaud grave associado a terapia com interferon-beta para esclerose múltipla: relato de caso

Cruz, Bóris Afonso; Queiroz, Eustáquio De; NUNESi, Simone Vilela; Filho, Achiles Cruz; Campos, Gilberto Belisário; Monteiro, Ernesto Lentz De Carvalho; Crivellari, H

doi:10.1590/s0004-282x2000000300025

Cited by 11 publications

(3 citation statements)

References 15 publications

(9 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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%

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

Khouri

Blaise

Carpentier

et al. 2016

Brit J Clinical Pharma

View full text Add to dashboard Cite

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 ...

show abstract

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

View full text Add to dashboard Cite

show abstract

“…La esclerosis múltiple es una patología neurológica crónica caracterizada por in amación de la sustancia blanca y desmielinización y un curso clínico alternante entre recaídas y remisiones 4 . El tratamiento con interferón (IFN) beta natural intratecal y la administración subcutánea de IFN beta-1b recombinante ha demostrado disminuir la frecuencia de las exacerbaciones 4,5,6 .…”

Section: Discussionunclassified

“…Otro caso reportado en el año 2000, una mujer de 58 años con E.M que, dos semanas después de iniciar tratamiento con IFN beta-1b, desarrolla cianosis y dolor en dedos de una mano seguido de necrosis isquémica en el pulpejo del 4to dedo, tratada con heparina, bolos de ciclofosfamida (1 gramo) mensuales y metilprednisolona (1 gramo), seguidos de 60 mg/día de prednisona vía oral, con lo que se logra limitar los síntomas 4 .…”

Section: Discussionunclassified

Vasculitis con necrosis digital asociada con interferón beta

Miretti¹,

Encinas²,

Colazo³

et al. 2013

Rev. Argent. Reumatol.

View full text Add to dashboard Cite

El Interferón (IFN) es una citoquina producida por distintas poblaciones de células y, a partir de su estructura, se han desarrollado varias drogas biológicas utilizadas en un amplio espectro de enfermedades. Se han descripto lesiones cutáneas y casos de síndrome de Raynaud severo con gangrena digital con IFN alfa y beta. En este reporte presentamos una paciente con necrosis digital asociada a la administración de IFN beta.

show abstract

Onset and enhancement of systemic sclerosis after treatments for multiple sclerosis

2007

View full text Add to dashboard Cite

The coexistence of systemic sclerosis (SSc) and multiple sclerosis (MS) in the same patient has been described in few cases. We refer here a further case of association between these diseases, which highlight the difficulty of treating such patients. A 57-year-old male with relapsing-remitting MS since 20 years, shortly after having received high-dose corticosteroids for a relapse of MS, suddenly developed SSc, with onset of Raynaud phenomenon simultaneous to that of scleroderma skin involvement, new appearance of accelerated arterial hypertension, and rapidly progressive oliguric renal failure, indicative of scleroderma renal crisis, that was controlled with ramipril, irbesartan and amlodipin. A further disabling relapse of MS was treated with interferon-beta, but 19 months later he developed multiple severe digital necrotic ulcers, that resolved with interferon discontinuation and therapy with iloprost. This case report shows that some form of treatment useful for MS might enhance the manifestations of SSc.

show abstract

Fênomeno de Raynaud grave associado a terapia com interferon-beta para esclerose múltipla: relato de caso

Cited by 11 publications

References 15 publications

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

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

Vasculitis con necrosis digital asociada con interferón beta

Onset and enhancement of systemic sclerosis after treatments for multiple sclerosis

Contact Info

Product

Resources

About