Scientific article
Sildenafil as a Therapeutic Option for Digital Ischemic Ulceration: Case Report

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We report the case of a 37-year-old woman who developed critical upper limb ischemia caused by a cervical rib. Because the malformation was initially undiagnosed, a vascular bypass was performed, and failure occurred. Following a 6-month therapy with sildenafil, revascularization of the arm was successful and amputation was avoided. A 6-year follow-up shows a rich collateral network at the compression site and normal values of digital plethysmography. Because hand surgeons often see patients with digital ulcerations and other manifestations of peripheral vascular pathology, therapy of ischemia with sildenafil could be an effective treatment option in patients not responding to classic drugs.

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Case Description

A 37-year-old woman presented to the emergency unit of our hospital with critical upper limb ischemia. She complained of increasing pain in the right forearm and a freezing cold feeling in the hand. Her past medical history included a nontreated Raynaud phenomenon of the right hand diagnosed 5 months before. She also had multiple associated risk factors including heavy smoking with oral contraception use. She was screened for coagulopathy or hypercoagulative state, but nothing could be found.

Discussion

In this case report, the patient avoided amputation after sildenafil administration. This patient experienced ischemic pain for months without any relief, and the naturally developed collateral circulation was not enough to relieve the patient's pain and measured O2 levels. Therefore, we think that improvement was likely related to sildenafil administration.

Sildenafil is known to activate the nitric oxide/protein kinase G pathway, which has an important role in vascular tone regulation and in

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    Salloum et al108 showed that tadalafil attenuates ischemic cardiomyopathy and preserves LV function. Krähenbühl et al109 reported that sildenafil could be an effective option in patients with ischemia that does not respond to classic drugs. Gong et al110 showed that long-term inhibition of cGMP-specific PDE5 prevents cardiac fibrosis through inhibition of tumor growth factor-β–induced Smad signaling.

No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.

S.M.K. and M.D. contributed equally to this work (co-first authors), and L.A.A. and W.R. contributed equally to this work (co-last authors).

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