Acrocyanosis Induced by Interferon α&lt;sub&gt;2a&lt;/sub&gt;

Campo‐Voegeli, A.; Estrach, Teresa; Marti, R.; Corominas, Núria; Tuset, Montserrat; Mascaró, J M

doi:10.1159/000017917

Cited by 30 publications

(11 citation statements)

References 12 publications

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“…47,151,152 Up to 6% of renal transplant patients treated with sirolimus may develop acrocyanosis. 48 In rare cases, acrocyanosis has been associated with treatment with clonidine, 49 interferon, 43,44 alphaprodine, 118 amphotericin B, 50 and intra-arterial injection of propoxyphene. 52 The exact mechanisms are not well-studied.…”

Section: Secondary Acrocyanosismentioning

confidence: 99%

Acrocyanosis: The Flying Dutchman

2011

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Acrocyanosis is symmetric, painless, discoloration of different shades of blue in the distal parts of the body that is marked by symmetry, relative persistence of the skin color changes with aggravation by cold exposure, and frequent association with local hyperhidrosis of hands and feet. Described over a century ago and despite seeming familiarity, it remains a poorly understood condition that shares much in clinical presentation with other conditions characterized by skin color changes in the distal parts of the body. The diagnosis remains mostly clinical, and pathological mechanisms vary suggesting that acrocyanosis may not be a single entity. We performed an extensive literature review to summarize existing knowledge about the demographics, pathology, diagnosis, and treatment of this condition.

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Section: Secondary Acrocyanosismentioning

confidence: 99%

Acrocyanosis: The Flying Dutchman

2011

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“…23 There is evidence to suggest that AGS results from a primary genetic defect of IFN-α metabolism. 8 Briefly, CSF IFN-α levels are consistently raised in the early stages of the disease, 2 3 treatment with IFN-α in a number of clinical settings can induce skin lesions similar to those seen in AGS, [24][25][26][27] and, of particular importance, astrocyte specific chronic overproduction of IFN-α in transgenic mice 28 29 recapitulates the neuropathological findings observed in AGS 30 31 and Cree encephalitis. 5 Notably, as in AGS, serum levels of IFN-α are raised in SLE [32][33][34][35] and therapy with IFN-α can actually induce the clinical and immunological features of the latter condition.…”

Section: Discussionmentioning

confidence: 86%

Cree encephalitis is allelic with Aicardi-Goutieres syndrome: implications for the pathogenesis of disorders of interferon alpha metabolism

Crow

2003

Journal of Medical Genetics

105

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Aicardi-Goutières syndrome (AGS) is an early onset, progressive encephalopathy characterised by calcification of the basal ganglia, white matter abnormalities, and a chronic cerebrospinal fluid (CSF) lymphocytosis. Cree encephalitis shows phenotypic overlap with AGS although the conditions have been considered distinct because of immunological abnormalities observed in Cree encephalitis. We report that levels of interferon alpha (IFN-α), a marker of AGS, are raised in Cree encephalitis. Moreover, linkage analysis indicates that the disorders are allelic and refines the AGS1 locus to a 3.47 cM critical interval. Our data show that a CSF lymphocytosis is not necessary for the diagnosis of AGS and strongly suggest that AGS and pseudo-TORCH syndrome are the same disorder. Recognition of immunological dysfunction as part of the AGS phenotype provides further evidence of a primary pathogenic role for abnormal IFN-α production in AGS.

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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%

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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Acrocyanosis Induced by Interferon α<sub>2a</sub>

Cited by 30 publications

References 12 publications

Acrocyanosis: The Flying Dutchman

Acrocyanosis: The Flying Dutchman

Cree encephalitis is allelic with Aicardi-Goutieres syndrome: implications for the pathogenesis of disorders of interferon alpha metabolism

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

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