Cases reported "Protein C Deficiency"

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1/146. Recurring myocardial infarction in a 35 year old woman.

    A 35 year old woman presented with acute myocardial infarction without any of the usual risk factors: she had never smoked; she had normal blood pressure; she did not have diabetes; plasma concentrations of total cholesterol and high and low density lipoprotein cholesterol, fibrinogen, homocysteine, and Lp(a) lipoprotein were normal. She was not taking oral contraceptives or any other medication. coronary angiography showed occlusion of the left anterior descending coronary artery but no evidence of arteriosclerosis. Medical history disclosed a previous leg vein thrombosis with pulmonary embolism. Coagulation analysis revealed protein c deficiency. The recognition of protein c deficiency as a risk factor for myocardial infarction is important as anticoagulation prevents further thrombotic events, whereas inhibitors of platelet aggregation are ineffective.
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ranking = 1
keywords = thrombosis, vein thrombosis
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2/146. Atrial and venous thrombosis secondary to septic arthritis of the sacroiliac joint in a child with hereditary protein c deficiency.

    Septic arthritis and osteomyelitis in children is seldom accompanied by calf vein thrombosis and rarely by atrial thrombosis. We report the case of an 11-year, 5-month-old boy with septic arthritis and osteomyelitis of the sacroiliac region who developed deep venous thrombosis, in addition to life-threatening right atrial thrombosis. After an intensive hematologic investigation, a hereditary protein c deficiency was revealed. The association of venous thrombosis with septic arthritis or osteomyelitis should raise the possibility of the presence of protein c deficiency.
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ranking = 10.247027147447
keywords = thrombosis, venous thrombosis, vein thrombosis, deep
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3/146. Ophthalmic manifestation of congenital protein c deficiency.

    Under normal conditions activated protein C is a natural anticoagulant that cleaves 2 activated coagulation factors, factor va and factor viiia, thereby inhibiting the conversion of factor X to factor xa and of prothrombin to thrombin. Additionally, activated protein C enhances tissue-plasminogen activator-mediated fibrinolysis by inhibition of plasminogen activator inhibitor-1. This results in an increase in circulatory plasminogen activator levels. protein c deficiency, a genetic or acquired thrombophilic abnormality, has been demonstrated to predispose to episodes of potentially blinding and lethal thromboembolic events. Heterozygous-deficient subjects usually remain asymptomatic until adolescence or adulthood. In homozygous-deficient patients, protein C activity is usually less than 1% (reference range, 70%-140%), resulting in thromboembolism as early as in the neonatal period. The major clinical symptoms in affected newborn infants have been purpura fulminans, vitreous hemorrhage, and central nervous system thrombosis. The age of onset of the first symptoms has ranged from a few hours to 2 weeks after birth, usually after an uncomplicated full-term pregnancy and delivery. In contrast to the genetic form, acquired neonatal protein c deficiency occurs particularly in ill preterm babies. Typical complications of prematurity such as respiratory distress syndrome, necrotizing enterocolitis, and neonatal sepsis may also be present. In the medical literature, there are only a few reports of homozygous protein c deficiency in neonates. We present 2 cases of homozygous protein c deficiency with ocular and extraocular manifestation.
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ranking = 0.91474126248014
keywords = thrombosis
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4/146. Mesenteric venous thrombosis associated with protein c deficiency.

    An 83-year-old man had gradually worsening abdominal pain and vomiting. laparotomy revealed segmental intestinal infarction resulting from thrombosis in the superior mesenteric vein. Necrosed intestine was resected and anastomosis was performed successfully. The patient was anticoagulated with intravenous heparin and nafamostat mesilate followed by oral aspirin. He recovered rapidly. Blood chemistry revealed protein c deficiency, while protein S and antithrombin iii levels were normal. Laboratory evaluation of these proteins may help define the cause of mesenteric venous thrombosis.
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ranking = 7.0956426731548
keywords = thrombosis, venous thrombosis
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5/146. 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.
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ranking = 0.91474126248014
keywords = thrombosis
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6/146. Acquired protein c deficiency following cisplatinum-navelbine administration for locally advanced breast cancer. Case report.

    Thromboembolic events have recently been reported following diverse regimens of chemotherapy for breast cancer. This is a report of a 39-year-old woman, a diagnosed case of locally advanced breast cancer, who received many regimens of chemotherapy. She presented with deep venous thrombosis 2 months after starting the cisplatinum-navelbine regimen. protein c deficiency was the only abnormal coagulation test that normalized after cessation of chemotherapy.
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ranking = 1.236643211812
keywords = thrombosis, venous thrombosis, deep
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7/146. stroke after zoster ophthalmicus in a 12-year-old girl with protein c deficiency.

    A 12-year-old girl who had zoster ophthalmicus 10 months earlier presented with hemiparesis and corresponding basal ganglionic infarction related to middle cerebral artery branch thrombosis ipsilateral to the zoster. Hematologic evaluation disclosed protein c deficiency. This represents the first zoster-associated stroke reported in childhood associated with protein c deficiency, with extension of the latency period between zoster and infarction, previously reported to be 6 months.
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ranking = 0.91474126248014
keywords = thrombosis
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8/146. Superior sagittal sinus thrombosis occurring at high altitude associated with protein c deficiency.

    A 42-year-old male presented with right-sided weakness, dysphasia and seizures while climbing the French Alps at an approximate altitude of 3,000 m. Imaging studies were consistent with superior sagittal sinus thrombosis with hemorrhage. Laboratory testing for thrombophilic states, 18 days after presentation at our hospital, showed a low protein C level (0.32 U/ml, normal 0.80-1.60 U/ml). A family member was also found to have protein c deficiency without a history of thrombosis. The patient gradually improved and was discharged on warfarin and valproic acid. This is the first reported case of cerebral venous thrombosis in a patient with congenital protein c deficiency who ascended to high altitude. We postulate that the ascent to high altitude represented an additional prothrombotic risk factor to the congenital protein c deficiency leading to cerebral thrombosis.
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ranking = 7.6393691194959
keywords = thrombosis, venous thrombosis
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9/146. Case report: portal vein thrombosis associated with hereditary protein c deficiency: a report of two cases.

    protein c deficiency is one of the causes of curable or preventable portal vein thrombosis. We report two patients of portal vein thrombosis associated with hereditary protein c deficiency. The first patient presented with continuous right upper quadrant pain and high fever. The abdominal sonography revealed normal liver parenchyma but portal vein and superior mesenteric vein thrombosis. Based on a 55% (normal 70-140%) plasma protein C level, he was diagnosed as having protein c deficiency. A trace of his family history showed that his elder brother also had protein c deficiency with a 50% plasma C level. Both patients received anticoagulant therapy. The younger brother showed good response. Unfortunately, the elder one suffered from recurrent episodes of variceal bleeding and received a life-saving splenectomy and devascularization. We herein remind clinicians that early screening and therapy are helpful in preventing late complications of protein c deficiency with portal vein thrombosis.
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ranking = 8
keywords = thrombosis, vein thrombosis
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10/146. Protein-losing enteropathy caused by mesenteric venous thrombosis with protein C deficiency.

    A 64-year-old man presented with leg edema and hypoproteinemia. His alpha-1 antitrypsin clearance rate of 174 mL/day indicated the presence of protein-losing enteropathy (PLE). Computed tomographic scans demonstrated thickened ileal wall and mesenteric edema. Angiography revealed occlusion in a peripheral branch of the superior mesenteric vein. Furthermore, both the patient and his son had low protein C levels. The patient was treated successfully with partial resection of the ileum. Histologic examination of the resected ileum revealed multiple erosions and submucosal fibrosis with organized venous thrombi in the mesenteric veins. This is the first case report of PLE caused by mesenteric venous thrombosis, and our findings suggest that serum protein was lost through erosion of the ileum caused by ischemia due to mesenteric venous thrombosis.
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ranking = 7.4170816928095
keywords = thrombosis, venous thrombosis
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