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  • 1
    ISSN: 1436-2813
    Keywords: prostaglandin ; aspirin ; renal insuffiency ; endotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of the anticoagulants, heparin and low molecular weight heparin (LMWH), and the antiplatelet agents, prostaglandin E1 (PGE1) and aspirin, on endotoxin-induced renal insufficiency not induced by prerenal factors, were investigated using rabbits to evaluate the clinical usefulness of these drugs and their possible involvement in the activation of hemostasis in renal insufficiency. The intravenous administration of PEG1, at 0.4 μg/kg/min, or aspirin, at 5 mg/kg, significantly restored all the parameters of renal function measured in the present study, namely, effective renal plasma flow, glomerular filtration rate and urine N-acetyl-β-D-glucosaminidase, as well as histological renal ischemic changes. On the other hand, neither heparin nor LMWH, even at a high dose, improved any parameter. As the antiplatelet effect is the common property of PGE1 and aspirin, it is suggested that the activation of platelets may be prerequisite to the occurrence of renal insufficiency induced by endotoxin. The results of this study thus show that PGE1 or aspirin may be applied in clinical use for renal insufficiency complicated by sepsis or endotoxemia.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1436-2813
    Keywords: dysplasminogenemia ; varicose veins ; deep vein thrombosis ; hemostasis activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Sclerotherapy combined with ligation has become a widely accepted treatment for varicose veins; however, it is associated with some risk of the serous complications of deep vein thrombosis (DVT). We investigated the incidence of thrombophilia in 164 consecutive patients undergoing treatment for varicose veins and determined the activities of antithrombin-III, protein C, and plasminogen. Of the 164 patients, 10 were diagnosed as having dysplasminogenemia (DPG), showing an incidence of 6.1%, in accordance with previous reports. DVT was not found to be caused by DPG in any patient, and no difference was found between patients with and those without DPG, suggesting that DPG is not a risk factor for varicose veins. We also investigated the activation of coagulation by measuring the thrombin-antithrombin III complex (TAT). The activation of coagulation after sclerotherapy was inhibited when ligation was performed 1 month prior to sclerotherapy, whereas it was increased when sclerotherapy and ligation were performed simultaneously. Of the 10 patients with DPG, 5 were treated uneventfully, and their TAT level increased to 4.0 μg/l, which was comparable to the level after sclerotherapy and ligation. These findings indicate that sclerotherapy can be performed safely in the majority of patients with DPG, and that the temporal separation of sclerotherapy and surgery is an alternative for these patients to prevent the activation of coagulation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1436-2813
    Keywords: portal vein calcification ; superior mesenteric vein thrombosis ; dysplasminogenemia ; abnormal plasminogen ; idiopathic portal hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report herein a case of a 68-year-old Japanese woman in whom calcification of the portal vein was recognized by plain abdominal X-ray radiograph and computed tomography (CT) scan when she presented with repeated thrombosis of the portal system. Following emergency small bowel resection for intestinal necrosis caused by superior mesenteric vein thrombosis, hematological studies revealed the association of dysplasminogenemia. A review of 21 cases of portal vein calcification reported between 1940 and 1990 revealed the average age to be 53.7±10.2 years and the male/female ratio 17:4. Although the majority of cases suffered from portal hypertension (81%), only 38% had any evidence of liver cirrhosis, while 52% had normal liver function, being comparable to idiopathic portal hypertension. The calcified lesions were located in the portal vein in 100% of cases, the splenic vein in 62%, the superior mesenteric vein in 33%, and the inferior mesenteric vein in 0%. The precise etiology of the calcification was not elucidated in any of the reviewed cases. The patient reported herein is the first reported case of portal vein calcification due to repeated thrombosis of the portal system caused by dysplasminogenemia, which could be accounted as a cause of idiopathic portal hypertension.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1436-2813
    Keywords: sepsis ; systemic inflammatory response syndrome (SIRS) ; hepatocyte growth factor (HGF) ; endotoxin ; beta-glucan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Interleukin-1 (IL-1), a cytokine released from macrophages by endotoxin stimulation, has been shown to upregulate the genetic expression of the hepatocyte growth factor (HGF). The present study was conducted to determine whether plasma HGF is increased in patients with systemic inflammatory response syndrome (SIRS). The plasma levels of HGF, endotoxin, and beta-glucan were measured in 41 surgical patients without hepatic diseases, 18 of whom had been diagnosed with sepsis, and 33, with nonseptic SIRS. The plasma HGF was found to be significantly increased in the 18 patients with sepsis, at 0.69±0.47 ng/ml (mean ± SD), and in the 23 patients with nonseptic SIRS, at 0.49±0.37 ng/ml, compared to values in 40 normal controls, at 0.10±0.03 ng/ml (P〈0.001). No significant correlations were observed between the plasma levels of HGF and endotoxin (r=0.02) or beta-glucan (r=−0.05) in any of the patients; however, plasma HGF was significantly correlated with the WBC count (r=0.34, P〈0.05) and with total bilirubin (r=0.45, P〈0.01). Plasma HGF was also strongly correlated with alanine transaminase (ALT) in 8 patients with ALT levels higher than 50 U/I (r=0.70), but there was no such correlation in 33 patients with ALT levels of 50 U/I or less (r=0.30). Thus, although the clinicopathologic significance of HGF is not well understood, the present findings indicate that plasma HGF increases in response to infection or inflammation.
    Type of Medium: Electronic Resource
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