Durvalumab-associated vasculitis presenting as 'the blue toe syndrome'.

Durvalumab is a selective, high-affinity human immunoglobulin monoclonal antibody in a class called check point inhibitors, that blocks PD-L1 on tumour cells. Despite clinical success in increasing progression-free survival rates in patients with stage III non-small-cell lung cancer, durvalumab has been associated with immune-related side effects such as pneumonitis and colitis. We present a case of an 84-year-old woman with acral vasculitis presenting as blue toe syndrome, associated with prolonged use of durvalumab. After 1 year of fortnightly durvalumab therapy postchemoradiation therapy, the patient came in with a left blue big toe, and later developed bilateral livedo racemosa. The diagnosis of durvalumab-associated vasculitis was made and treatment with prednisolone was started with clinical improvement.

[Blue toe syndrome--a rare but possible complication of anticoagulant therapy]. / Sinisten varpaiden oireyhtymä-- antikoagulanttihoidon harvinainen komplikaatio.

Cholesterol microembolization syndrome (CMS) is a multiorgan ischemic disorder resulting from occlusion of small vessels by cholesterol crystals that are derived from atherosclerotic plaques of major arteries. Flow distribution of cholesterol crystals determines the clinical picture of CMS. Cholesterol crystals distributed to the lower extremities cause a typical "blue toe" appearance. The predisposing factors of CMS include various vascular procedures that scratch the luminal surface of the vascular wall and make the release of cholesterol crystals from the atherosclerotic plaques possible. However, CMS can also occur as a consequence of continuous anticoagulant use. Therefore, patients on anticoagulant therapy complaining even minor toe symptoms should be examined for possible CMS.

Blue toe syndrome and sunitinib.

We present a patient with metastatic renal cell carcinoma treated with sunitinib, a multitargeted tyrosine kinase inhibitor. The patient experienced bilateral blue toe syndrome which we related to sunitinib use. Discontinuation of sunitinib to lower the patient's prothrombotic state and increase the ability to form collaterals, together with the addition of low-molecular-weight heparin to treat the occluding thrombi, resulted in waning of the blue toe syndrome. This case adds to the accumulating evidence of possible untoward cardiovascular side effects that should be taken into consideration in patients on tyrosine kinase inhibitors such as sunitinib.

Late onset purple toe syndrome with warfarin successfully treated with fondaparinux.

Purple toe syndrome is a rarely reported adverse effect of warfarin. In all described cases, the syndrome occurred relatively quickly after initiation of warfarin with little recommendation for treatment in patients needing continued anticoagulation. We encountered a patient who developed purple toes after 1 year of warfarin therapy. The warfarin was stopped, and fondaparinux was substituted with prompt resolution of all his symptoms. This is the first case describing late onset purple toe syndrome with warfarin with successful substitution with fondaparinux.

[Purple extremities in black-skinned patients: blue toe syndrome as presenting sign of antiphospholipid antibody syndrome]. / Extrémités violettes sur peau noire: orteils pourpres révélateurs d'un syndrome des antiphospholipides.

Although acral ischemia can involve several underlying mechanisms, suspicion of lupus warrants testing for antiphospholipid antibodies in patients with blue toe syndrome.

Blue toe syndrome after initiation of low-dose oral anticoagulation.

Cholesterol emboli are a known complication after arterial catheterization, arterial surgery, and after lysis with plasminogen activators. The clinical presentation of cholesterol emboli is variable ranging from a localized blue toe syndrome to a multisystem disease. The purpose of this case report is to report on a patient with blue toe syndrome and livedo reticularis occuring two months after initiation of low-dose oral anticoagulation with phenproucomon. The non-invasive studies revealed an infrarenal abdominal aneurysma lined by a thin wall thrombus as a potential source of cholesterol emboli. The patient had a benign course with resolution of toe pain after a period of four weeks, without development of an ulceration. The case report demonstrates that cholesterol emboli may also occur in patients treated with low-dose oral anticoagulation and no previous arterial catheterization.

Atheromatous embolization precipitated by oral anticoagulants.

Five patients with a "blue or purple" toe syndrome due to atheromatous embolization probably precipitated by oral anticoagulant therapy are reported. In four, the symptoms started a few weeks after initiation of oral anticoagulants and in the fifth they were clearly aggravated by coumarinic drugs. Prior to anticoagulation, one patient had received a course of thrombolytic therapy and two had undergone an arterial catherization without embolic events. A diagnostic arteriography performed in four patients caused no new symptoms. All patients had advanced atherosclerosis. A shaggy aorta and/or pelvic arteries were found in four and in the fifth a highly stenotic femoral lesion appeared the source of peripheral embolization. Oral anticoagulants were interrupted in all five and four underwent reconstructive vascular surgery to eradicate the nidus of atheromatous emboli. One died postoperatively from multiple organ failure. The poor condition of the fifth patient precluded aorto-iliac surgery. No new episodes of embolization occurred and the symptoms disappeared, although one patient needed a toe amputation for a skin lesion that had proceeded to gangrene. The possible role of anticoagulant drugs in precipitating atheromatous embolization is discussed and the importance of recognizing the syndrome is emphasized.