Fingerkuppennekrosen nach Dihydroergotaminmedikation bei limitierter systemischer Sklerodermie

Hahne, Torsten; Balda, Bernd‐Rüdiger

doi:10.1007/s001050050816

Cited by 6 publications

(1 citation statement)

References 3 publications

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“…Moreover, they are α 1 ‐ , α 2 ‐adrenergic and dopaminergic D 2 ‐receptor agonists. Numerous case reports illustrating this effect are found in the literature . However, the accountability of ergot alkaloids in RP is difficult to assess because of a significantly higher prevalence of RP in the migraine population .…”

Section: Resultsmentioning

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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Section: Resultsmentioning

confidence: 99%