Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-six patients undergoing elective splenectomy have been investigated preoperatively and postoperatively by serial platelet counts and leg scanning using iodine 125-labeled fibrinogen. The presence of deep leg vein thromboses detected by labeled fibrinogen was confirmed by dye phlebography. In only five patients (6%) did deep venous thrombosis develop. In none of these five patients did an elevation in platelet count to 600,000/cu mm develop before or at the time of development of the thrombosis. None of 21 other patients who did have a rise in platelet count greater than 1,000,000/cu mm had evidenced of venous thrombosis. These data do not substantiate the need for routine prophylactic antithrombotic therapy in patients in whom postsplenectomy thrombocytosis develops.
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PMID:Deep venous thrombosis and postsplenectomy thrombocytosis. 63 13

71 patients with traumatic splenic rupture are reported. Most had severe associated injuries. In 44 patients the mechanism of trauma was blunt, in 10 penetrating, and in 17 iatrogenic, occurring most commonly (11/17) during operations for peptic ulcer. Splenectomy gave use to thrombocytosis which reached its peak about 2 weeks and returned to normal within one month after operation. Postoperative complications occurred in 24 of the 60 surviving patients (40%) of which most, 17 patients (30%) were infectious in origin. One patient developed deep venous thrombosis. Mortality was 16%. Associated injuries were the main cause of death in most patients (9/11), the ruptured spleen being responsible for only 2 deaths. None of the 17 patients with injury to the spleen alone died, whether associated with fractures of the left lower ribs or not. Primary unconsciousness, shock on admission, and multiple injuries, especially renal and hepatic, increased the mortality rate markedly. The necessity of drainage, the possibility of increased susceptibility of splenectomized patients to infection and thromboembolic complications and their prevention are briefly discussed.
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PMID:Traumatic splenic rupture. 87 6

No significant excess of deep vein thrombosis (DVT) as measured by the 125I-labelled fibrinogen method was observed in patients having staging laparotomy and splenectomy for Hodgkin's disease (HD) compared with patients having elective cholecystectomy under highly standardized surgical conditions. Patients who did have DVT all had splenic involvement with HD. There was no correlation between the post-splenectomy thrombocytosis and the occurrence of DVT. Patients with non-Hodgkin's lymphoma (NHL) and splenomegaly had a high incidence of DVT after splenectomy.
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PMID:Thrombotic risks of staging laparotomy with splenectomy in Hodgkin's disease. 731 64

Two patients with angiographically proven longitudinal sinus thrombosis were studied from a coagulation point of view. In the first case, marked primary thrombocytosis was found. This patient was treated with aspirin, dipyridamole and radioactive phosphorus. In the second case, fibrinogen and whole blood plasma viscosity were elevated. This patient developed deep vein thrombosis of the left leg a few weeks after the cerebral episode and was treated with coumarin drugs. The importance of a coagulation study in every patient with cerebral vein thrombosis is emphasized.
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PMID:Clotting changes in two patients with longitudinal sinus thrombosis. 735 20

The association of deep vein thrombosis with systemic necrotizing vasculitis is infrequent. Herein are referred two patients with microscopic polyarteritis and one patient with overlap syndrome who developed deep vein thrombosis which complicated in two cases with pulmonary embolism. The clinical features and the pathogenic mechanisms involved in this infrequent association are analyzed. In two patients the thrombosis was simultaneous with the diagnosis of vasculitis. In one patient deep vein thrombosis was the cause of hospital admission. Advanced age and thrombocytosis are factors associated to vasculitis, which may favor the development of thromboembolic disease. The presence of antiphospholipid syndrome was discarded. Although infrequent, this association should be considered because of the potential severe complications.
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PMID:[Deep venous thrombosis associated with necrotizing vasculitis]. 811 40

The prevalence of specific thrombotic accidents recognized in 260 patients with thrombocytosis are reported. Ninety one were affected by PV, 86 by ET, 20 by MF and 63 by ST. The highest incidence of thrombosis was in the PV group. About half of ET and MF patients experienced a thrombosis. In all the patients thrombosis preferentially affected the cerebrovascular district (17.3% of the cases). Coronary artery disease occurred in PV while peripheral vascular disease was frequent in ET. Portal vein district thrombosis is not rare during the course of all MPD (7.1%). Apparently, deep vein thrombosis occurs in all patients with both primary and secondary thrombocytosis.
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PMID:Prevalence of specific thrombotic accidents in patients with thrombocytosis. 811 27

The authors describe a clinical case with a peculiar sequence of unhealthy events. An operated by osteotomy woman presented a deep venous thrombosis of lever lower extremity with following pulmonary embolism. The patient was treated with heparin. After 5 days, the patient showed a thrombocytopenia, that was not determined by an immune mechanism. The heparin was stopped and the thrombocythemia returned to normal values. But the patient still presented somnolence, asthenia and hypotension. The tests of adrenocortical function showed below normal values. The abdominal CAT showed haemorrhagic necrosis of the suprarenal glands.
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PMID:[Acute adrenal failure due to adrenal hemorrhagic necrosis secondary to heparin-induced thrombocytopenia]. 823 35

The authors report a 69-year-old woman with a hypercoagulable state manifesting as superior sagittal sinus thrombosis, thrombocytosis, right lower extremity deep venous thrombosis, and subsequent pulmonary embolus. The liver enzyme values were elevated in a cholestatic pattern. Carcinoembryonic antigen level was markedly elevated. Evaluation revealed that her longstanding "goiter" had slowly enlarged during the past 6 years. The serum calcitonin level was markedly elevated. Subsequent biopsy revealed medullary thyroid carcinoma. Surgical debulking of the tumor and lymph nodes resulted in substantial reduction of the calcitonin and carcinoembryonic antigen levels in a matter of days. Long-term follow-up revealed normalization of cholestasis and resolution of the hypercoagulable state. Review of the literature revealed no previously reported cholestasis or hypercoagulable state associated with medullary thyroid carcinoma. The literature on paraneoplastic cholestasis, carcinoembryonic antigen production, and hypercoagulable states is reviewed.
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PMID:Paraneoplastic cholestasis and hypercoagulability associated with medullary thyroid carcinoma. Resolution with tumor debulking. 829 93

In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.
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PMID:Acute-phase response and the hypercoagulable state in pulmonary tuberculosis. 870 31

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59


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