Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65-year-old patient developed nonpruritic purpuric skin eruptions following 10 days of coumadin treatment. Skin biopsy revealed vasculitis and immunofluorescent studies demonstrated the presence of IgM and C3 deposits in the walls of the affected blood vessels. Rechallenge with coumadin was followed by reappearance of the skin eruptions. Indirect mast cell degranulation test and migration inhibiting factor test were positive in the presence of coumadin. These findings strongly suggest that the skin lesions were induced by an immunologic reaction to warfarin.
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PMID:Dermal vasculitis due to coumadin hypersensitivity. 675 87

An elderly man experienced recurrent transient episodes of right arm weakness and expressive aphasia. He was initially treated with aspirin and then with coumadin. Thirteen days after initial presentation, he became febrile and had signs of meningitis. The illness progressed relentlessly to death 9 weeks after admission to the hospital. Necropsy showed prominent meningitis with vasculitis extending into the left frontal lobe. Polymerase chain reaction identified the organism as Listeria monocytogenes.
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PMID:Neurolisteriosis presenting as recurrent transient ischemic attacks. 1102 51

Eosinophilic variant of CML (eoCML) is a unique disease with a poor prognosis. Like the hypereosinophilic syndrome (HES), eoCML has no clinically identifiable reason for an increased eosinophil count in the peripheral blood. In contrast to HES, eoCML patients carry a distinct chromosomal abnormality. The bcr/abl fusion gene (Philadelphia chromosome) is the genetic basis of this clonal disease. Recently, eoCML has been separated from HES. Patients with eoCML frequently suffer organ damage including the heart and lungs. This damage is related to the release of eosinophilic granules in the blood, which results in fibrosis of the endothelial lining. We report a case of a peripheral vasculitis complicated by gangrene of the fingers in a patient with eoCML. Despite an almost complete response to CML treatment with Gleevac, combined with prednisone, aspirin and coumadin the patient sustained irreversible damage to the vascular lining of the distal arteries of the upper extremities.
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PMID:Eosinophilic variant of chronic myeloid leukemia with vascular complications. 1456 66

Cutaneous pseudovasculitis represents a heterogeneous collection of disorders that are capable of simulating cutaneous vasculitis and can be broadly classified into diseases that produce hemorrhage (petechiae, purpura, and ecchymoses) or vessel occlusion with resultant livedo, cyanosis, ulcers, digital necrosis, and/or gangrene. Overlap is not uncommon, but if present, one mechanism dominates. Hemorrhagic pseudovasculitis is due to vessel wall dysfunction (incompetence), which can be related to diverse factors that include vessel wall deposition of metabolic substances (amyloid, calcium), nutritional deficiencies (scurvy), nonvasculitic inflammatory purpura (pigmented purpuric dermatitis, arthropod, viral and drug reactions), degeneration of the vessel wall and supporting stroma (senile/solar purpura), direct vessel wall invasion of infective organisms, coagulation-fibrinolytic disorders (eg, thrombocytopenia), and vessel wall trauma. Cyanotic-infarctive pseudovasculitis is due vaso-occlusion by emboli, thrombi, or fibrointimal hyperplasia (endarteritis obliterans) and includes varied conditions such as purpura fulminans, Coumadin necrosis, antiphospholipid antibody syndrome, cardiac myxoma, cholesterol embolization, calciphylaxis, and radiation arteritis. Delayed and inappropriate diagnosis of pseudovasculitis leads to incorrect management and exposure to potentially deleterious treatment modalities such as corticosteroids and cytotoxic agents. The diagnosis of a pseudovasculitic disorder requires a high index of suspicion and should always be part of the differential diagnosis of vasculitis. Skin biopsy is a crucial step in differentiating pseudovasculitis from authentic vasculitis; absence of histologic evidence of vasculitis, particularly after multiple biopsies, should direct evaluation and diagnosis towards pseudovasculitis.
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PMID:Cutaneous pseudovasculitis. 1728 61

A 40-year-old white male developed Mycoplasma pneumoniae pneumonia (IgM titer 1:256) as well as autoimmune hemolytic anemia due to cold agglutinins (titer of 1:512). Four days after admission to the hospital, he developed an acute superior mesenteric artery (SMA) thrombosis. Four feet of ischemic small bowel were resected. A follow-up angiogram again showed SMA thrombosis and a left popliteal artery thrombosis. The patient was returned to the operating room and underwent thrombectomy of the affected arteries. The following day, he again developed a left popliteal artery thrombosis requiring thrombectomy. Plasmapheresis, Coumadin and prednisone were implemented. No further thrombotic events occurred. Hypercoagulability workup was negative. Pathology samples revealed vasculitis. Based on a negative hypercoagulability workup, nonrecurrence of thrombotic events after treatment, and in the absence of any structural abnormalities of the affected arteries, an autoimmune phenomenon with damage to the endothelium was thought to have played a role in the mechanism of thrombosis.
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PMID:Mycoplasma pneumoniae associated with hemolytic anemia, cold agglutinins, and recurrent arterial thrombosis. 1733 Jun 97

Acute cutaneous necrosis is defined as a sudden onset of gangrenous skin changes in the skin, associated with significant morbidity and mortality. The following diseases are included in this discussion: coumadin necrosis, heparin necrosis, brown recluse spider bite, necrotizing fasciitis, vasculitis, pyoderma gangrenosum, calciphylaxis, clotting abnormalities and embolic phenomena. The importance of early diagnosis, early distinction and early drug therapy or drug withdrawal must match the diagnosis for maximal preservation of the skin and underlying tissue.
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PMID:Use of drug therapy to manage acute cutaneous necrosis of the skin. 2051 91

The objective of this study was to describe a novel presentation of peripheral vasculitis associated with levamisole-adulterated cocaine. Cocaine abuse is widespread in the United States with 5.3 million people using cocaine in 2008. Over the past decade, drug enforcement officials have noticed the presence of levamisole in confiscated cocaine samples as an adulterant. Known side effects of cocaine-related levamisole ingestion have included agranulocytosis and a cutaneous acral purpura that is histopathologically characterized by a mixture of inflammation (vasculitis) and occlusion (vasculopathy). A 54-year-old man who nasally ingested cocaine laced with levamisole developed widespread necrotic/purpuric skin lesions on approximately 20% of his body with an acral accentuation. These lesions were complicated by multiple areas of sloughing and necrosis. He was initially treated with topical silver sulfadiazine dressing changes but progressed to require debridement and split-thickness skin grafting. Peripheral vasculitis/vasculopathy with severe necrosis resembling Coumadin necrosis is a relatively recently recognized sequelae from levamisole-adulterated cocaine use.
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PMID:Necrotizing peripheral vasculitis/vasculopathy following the use of cocaine laced with levamisole. 2222 33

Warfarin is widely prescribed for patients with atrial fibrillation. In addition to unexpected bleeding, allergic skin reaction is one of its uncommon adverse effects. We herein report an 89-year-old man who, after taking warfarin for 4 years, suffered extensive skin eruptions. The skin biopsy disclosed leukocytoclastic vasculitis. The causal relationship between skin lesions and warfarin was confirmed after re-challenge of warfarin. A literature review revealed only 13 such cases reported from 1980 to 2011. Clinicians should be aware of this potential adverse effect of warfarin.
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PMID:Warfarin-induced leukocytoclastic vasculitis: a case report and review of literature. 2244 68

Kawasaki disease (KD) is an acute vasculitis syndrome of unknown etiology. It occurs in infants and young children, affecting mainly small and medium-sized arteries, particularly the coronary arteries. Generalized microvasculitis occurs in the first 10 days, and the inflammation persists in the walls of medium and small arteries, especially the coronary arteries, and changes to coronary artery aneurysms.We report the case of a 10-month-old girl referred to our center three months after the onset of disease due to the aneurysms of the coronary arteries. During the acute phase of her illness, she received 2 gr/kg intravenous gamma globulin; and after her referral to us, the patient was treated by antiaggregant doses of acetylsalicylic acid (ASA) (5 mg/kg) and Warfarin (1 mg/daily). At three months' follow-up, the aneurysms still persisted in the echocardiogram.
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PMID:Segmented coronary artery aneurysms and kawasaki disease. 2307 12

A patient with a history of deep vein thrombosis presented with painful bruising and blistering on his left leg 7-10 days after warfarin treatment. A complicated 2-month treatment followed, where vasculitis was originally diagnosed from histological findings before the final diagnosis of warfarin-induced skin necrosis (WISN) was made on clinical grounds. Warfarin was stopped, reversed and low molecular weight heparin started but, the lesions had progressed to full thickness necrosis. This was originally treated with conventional surgical debridement before introducing maggot debridement therapy (MDT) in an effort to try to salvage the limb.
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PMID:Warfarin-induced skin necrosis diagnosed on clinical grounds and treated with maggot debridement therapy. 2336 73


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