1/129. Anticoagulant-induced skin necrosis in a patient with hereditary deficiency of protein S.skin necrosis is a rare but debilitating complication of treatment with vitamin k antagonist anticoagulants such as warfarin. A clinically similar syndrome has been reported less frequently with heparin therapy. We recently managed a thirty-year-old female patient who developed skin necrosis on her left lower extremity while on warfarin for postpartum DVT. The lesions started to develop 48 hr after stopping heparin therapy. Discontinuation of warfarin and reinstitution of heparin was complicated by a rapid decrease in platelet count consistent with heparin-induced thrombocytopenia (HIT) and its associated risk of platelet activation and thrombosis. The diagnosis was supported by the identification of antibodies against heparin/platelet factor 4 complexes in the patient's serum. The platelet count recovered and the patient improved after switching to therapy with the heparinoid danaparoid. Evaluation for a hypercoagulable state revealed a partial deficiency of protein S, a condition that previously was identified in two of her family members. It is not clear if this patient suffered from warfarin-induced skin necrosis, a manifestation of heparin-mediated platelet activation, or a complex condition in which both drugs contributed. HIT may affect 1-3% of patients who receive unfractionated heparin, and this case raises the possibility that heparin may contribute to, or cause, some episodes of skin necrosis attributed to warfarin. Because many patients who develop warfarin-induced skin necrosis have been treated initially with heparin, it would seem prudent to consider HIT in these situations.- - - - - - - - - - ranking = 1keywords = thrombosis (Clic here for more details about this article) |
2/129. Severe cerebral venous sinus thrombosis and dural arteriovenous fistula in an infant with protein s deficiency.A 12-month-old infant presented with cerebral seizures and neurological deficits. MRI scan of the brain and angiography showed massive cerebral venous sinus thrombosis complicated by a dural arteriovenous fistula. Subsequent clotting analysis revealed a protein s deficiency. Screening for inherited coagulation inhibitor deficiency is recommended in children with unexplained or atypical thrombotic events.- - - - - - - - - - ranking = 5keywords = thrombosis (Clic here for more details about this article) |
3/129. Acquired protein s deficiency with multiple thrombotic complications after orthotopic liver transplant.BACKGROUND: Orthotopic liver transplantation (OLT) is frequently complicated by thrombotic events that may threaten the viability of the allograft and severely compromise the overall outcome in these patients. Although multiple prothrombotic pathogenic mechanisms may be involved, a role for inadequate natural anticoagulant levels in the early postoperative period has been postulated. methods: We describe a case of a woman who suffered multiple thrombotic complications after a second OLT. Prospective assays of procoagulant and natural anticoagulant factor levels, in addition to screening tests for a variety of inherited and acquired hypercoagulable states, were carried out. RESULTS: Serial studies confirmed an acquired, isolated deficiency of Protein S associated with the second transplanted liver. Protein S levels were normal after the patient's first and third OLTs. There was no laboratory evidence of other underlying prothrombotic conditions. CONCLUSIONS: This unusual case of acquired protein s deficiency demonstrates that the hypercoagulable phenotype may develop in the recipient of a liver from a heterozygous deficient donor. Furthermore, isolated low Protein S may be causally associated with hepatic artery thrombosis after OLT.- - - - - - - - - - ranking = 1keywords = thrombosis (Clic here for more details about this article) |
4/129. Inherited protein c deficiency, protein s deficiency and hyperhomocysteinaemia in a patient with hereditary spherocytosis.We report a family with hereditary spherocytosis in whom there is, in addition, a cluster of genetic predispositions to thrombosis. Although inherited prothrombotic abnormalities are prevalent in the general population, the likelihood of this combination of abnormalities being found in a single family is extremely low. The management of such high risk individuals is discussed.- - - - - - - - - - ranking = 1keywords = thrombosis (Clic here for more details about this article) |
5/129. Mesenteric and portal vein thrombosis in a young patient with protein s deficiency treated with urokinase via the superior mesenteric artery.A 32-year-old man, who was previously healthy, had acute abdominal pain without peritonitis. Diffuse mesenteric and portal vein thrombosis were shown by means of a computed tomography scan. A protein s deficiency was found by means of an extensive workup for hypercoagulable state. Successful treatment was achieved with urokinase infusion via the superior mesenteric artery without an operation. This represents an attractive alternative approach to treating patients with this disease. The previous standard of operative intervention(1) can now be reserved for complications, such as bowel infarction with peritonitis, or for those patients with absolute contraindications to thrombolytic therapy.- - - - - - - - - - ranking = 5keywords = thrombosis (Clic here for more details about this article) |
6/129. Cardiac transplantation in a patient with protein s deficiency.Cardiac transplantation was successfully performed in a patient with end-stage ischemic cardiomyopathy and hereditary protein s deficiency who had undergone two previous coronary artery bypass graft procedures. Routine intraoperative heparinization and reversal with protamine was undertaken, and the antifibrinolytic agent aprotinin was infused throughout the procedure without perioperative hemorrhage or thrombosis. Systemic anticoagulation with intravenous heparin was resumed on postoperative day 2, and the patient was then converted to Lovenex as outpatient anticoagulation to facilitate routine surveillance endomyocardial biopsies.- - - - - - - - - - ranking = 1keywords = thrombosis (Clic here for more details about this article) |
7/129. Intermittent left coronary occlusion caused by native aortic valve thrombosis in a patient with protein s deficiency.A 77-year-old woman presented with chest pain and cardiogenic shock. Transesophageal echocardiography showed a mobile mass occluding intermittently the left coronary ostium. The mass was surgically resected, and histologic examination revealed an organized thrombus. Coagulation study demonstrated a protein s deficiency. This is the first case of aortic thrombosis associated with protein s deficiency, and it is the first time that transesophageal echocardiography provided definite evidence that a mass can cause intermittent left ostium coronary obstruction.- - - - - - - - - - ranking = 5keywords = thrombosis (Clic here for more details about this article) |
8/129. Postinfection purpura fulminans in a patient heterozygous for prothrombin G20210A and acquired protein S resistance.purpura fulminans usually consists of large, often symmetrical, spreading ecchymosis, which may later develop into extensive areas of skin necrosis and peripheral gangrene. Postinfectious purpura fulminans associated with an autoantibody directed against protein S has been described. The interaction and the contribution of recently described mutations such as factor v Leiden and prothrombin G20210A to the development and progression of postinfectious purpura fulminans and venous thrombosis is not known. The authors describe a patient heterozygous for prothrombin G20210A who developed purpura fulminans and extensive venous thrombosis secondary to acquired protein s deficiency.- - - - - - - - - - ranking = 2keywords = thrombosis (Clic here for more details about this article) |
9/129. Mesenteric vein thrombosis secondary to protein s deficiency.Mesenteric vein thrombosis is an uncommon condition. diagnosis is often difficult because of the nonspecific clinical presentation and findings on routine laboratory and radiological evaluation. endoscopy is usually unrevealing. An underlying hypercoagulable state is often present, but protein s deficiency has rarely been implicated. We describe a case in which chronic inferior mesenteric vein thrombosis, with remarkable endoscopic findings, occurred as the initial presentation of type I protein s deficiency.- - - - - - - - - - ranking = 6keywords = thrombosis (Clic here for more details about this article) |
10/129. Dural sinus thrombosis in a patient with protein s deficiency--case report.A 23-year-old female presented with dural sinus thrombosis caused by protein s deficiency. She suffered superior sagittal sinus thrombosis 6 days after delivering her first child. Past history showed deep vein thrombosis at the age of 20. While conservative management was initiated because of the potential risk of increasing intracranial hemorrhage, several hours later she deteriorated rapidly because of severe brain swelling with massive hemorrhage. The patient died despite surgical decompression. autopsy disclosed organized thrombus in the superior sagittal and transverse sinuses. Although the total concentration of protein S was normal, the free protein S concentration and protein S activity were decreased. protein s deficiency is a rare cause of dural sinus thrombosis, but is associated with a high mortality rate, so accurate diagnosis and urgent intervention are required.- - - - - - - - - - ranking = 8keywords = thrombosis (Clic here for more details about this article) |
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