Biomedical subjects

M G Conlan

Publications and source records attributed to M G Conlan.

23 records · Page 2Linked to original sources

PubMed1989

Prothrombotic abnormalities in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is known to be associated with a thrombotic tendency, which is often attributed to thrombocytosis, elevated fibrinogen, or decreased antithrombin III. We prospectively studied eight patients with IBD, seven of whom had little or no disease activity, to determine if they had any laboratory abnormality known to be associated with an increased risk of thrombosis. Abnormalities in fibrinolysis were noted in five patients: four with high plasminogen activator inhibitor levels and one with poor release of tissue plasminogen activator following venous occlusion. Circulating immune complexes were present in the sera of five patients. Fibrinogen was mildly elevated in one patient, and two patients had mild thrombocytosis. Decreased levels of antithrombin III, protein C, or protein S were not observed. There appears to be a high incidence of abnormalities in fibrinolysis in inactive IBD, which may contribute to the high frequency of thrombosis seen in IBD. The presence of circulating immune complexes may contribute to vascular injury and thrombosis.

Adult↗

PubMed1988

Familial type II protein C deficiency associated with warfarin-induced skin necrosis and bilateral adrenal hemorrhage.

A family is described in which venous thromboembolic disease is associated with reduced plasma protein C activity and normal levels of protein C antigen. Immunoelectrophoretic analysis of protein C antigen gave an abnormal pattern in all affected members, suggesting that the disorder is related to the presence of a structurally and functionally abnormal form of protein C. The propositus developed simultaneous warfarin-induced skin necrosis and bilateral adrenal hemorrhage. This is the first reported instance of warfarin-induced skin necrosis associated with a dysfunctional protein C molecule and the first reported instance of simultaneous warfarin-induced skin necrosis and bilateral adrenal hemorrhage.

Adrenal Gland Diseases↗

PubMed1988

Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation.

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.

Animals↗

PubMed1986

Epsilon-aminocaproic acid in the treatment of patients with acute promyelocytic leukemia and acquired alpha-2-plasmin inhibitor deficiency.

Patients with acute promyelocytic leukemia often develop bleeding diatheses during treatment. In seven patients who had this disease, the plasma level of alpha-2-plasmin inhibitor was the best predictor of severity of coagulopathy and bleeding. Clinical bleeding occurred when alpha-2-plasmin inhibitor levels measured less than 30% of normal levels. Patients with acute promyelocytic leukemia who had acquired deficiencies of alpha-2-plasmin inhibitor were considered to have deficits similar to those in persons congenitally deficient in alpha-2-plasmin inhibitor, and were assumed to be at increased risk for bleeding. Treatment with the fibrinolytic inhibitor, epsilon-aminocaproic acid, along with heparin resulted in prompt cessation of bleeding, reversal of laboratory evidence of fibrinolysis, and a decreased need for blood product support. The only thrombotic complication--thrombosis around a central venous catheter--resolved when treatment with epsilon-aminocaproic acid was discontinued. Epsilon-aminocaproic acid is a safe and effective therapy for those patients with acute promyelocytic leukemia who develop coagulopathy associated with low levels of alpha-2-plasmin inhibitor.

Aminocaproates↗

PubMedDate not supplied

Postoperative adjuvant irradiation of rectal and rectosigmoid cancer.

Local recurrence is a major problem for approximately 40% of stage B and C rectal cancer patients following successful complete resection by either anterior (AR) or abdominoperineal resection (APR). We retrospectively analyzed the sites of local recurrence in 138 patients following curative surgery, and evaluated the effect of 5,000 rad adjuvant postoperative pelvic EXRT in reducing the incidence of local recurrence in 40 patients.

Combined Modality Therapy↗