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Biomedical subjects

E F Mammen

Publications and source records attributed to E F Mammen.

At least 91 records · Page 5Linked to original sources
PubMed1982

Altered coagulation protein content after albumin resuscitation.

Previous studies showed that the random addition of supplemental albumin to a resuscitation regimen of blood, salt, and frozen plasma caused a significant (p = less than 0.05) fall in fibrinogen clotting activity (FC) and a rise in prothrombin times (PT) in seriously injured patients; the partial thromboplastin times (PTT) were insignificantly prolonged. Based upon these findings, frozen plasma samples, prospectively collected in 41 non-albumin patients and 35 albumin patients, were analyzed immunologically, in duplicate, for protein content of coagulation factor VIII (VIIIAg), prothrombin (IIAg), fibrinogen (FAg), antithrombin III (ATAg), and fibrin(ogen) split products (FSP). Supplemental albumin resuscitation was associated with a significant fall in FAg (83 +/- 9 versus 124 +/- 10 SE mg/dl), VIIIAg (97 +/- 13 versus 127 +/- 135 SE %), IIAg (54 +/- 3 versus 80 +/- 4 SE %), and ATAg (14 +/- 0.8 +/- 19 +/- 0.8 SE mg%) with no significant changes in FSP. FSP, however, were more than 20 micrograms/ml in 13 of 41 nonalbumin patients versus four of 35 albumin patients (X2 = 4.5, p less than 0.05). Reduced coagulation activity following albumin supplementation seems partly caused by a decrease of coagulation protein content; increased fibrinolysis in the albumin patients is not the cause. Decreased coagulation protein content parallels the fall in coagulation activity and the need for postresuscitation blood transfusions. The role of reduced coagulation synthesis in these changes needs further study.

Adult↗
PubMed1982

Primary hemostasis after massive transfusion for injury.

Primary hemostasis, the formation of a platelet plug, was studied in 22 injured patients receiving an average of 21 transfusions during the operation for control of bleeding. The storage age of the blood averaged 15 days; no platelet transfusions were given. Platelet counts (PLT) and bleeding time (BT) were studied intraoperatively; postoperatively at 6 hours, 25 hours, day 2, day 4; and during convalescence (8 days to 3 months). Serial PLT and BT levels were correlated with the number of transfusions and age of blood. During operation, the PLT fell to 109,000/mm3 and the BT was greater than 15 minutes. Thrombocytopenia did not correlate with the number of transfusions or age of blood. The PLT averaged 106,000/mm3 at 6 hours and then fell significantly to 73,000/mm3 at 15 hours and to 76,000/mm3 on day 2. The PLT rose significantly to 110,000/mm3 by day four and increased to supernormal levels by convalescence. The BT remained elevated at 6 hours, 15 hours, day 2, and day 4, and declined to normal by convalescence. Thrombocytopenia and prolonged BT after massive transfusion for injury indicate platelet dysfunction which may protect against disseminated intravascular coagulation. Correction of the thrombocytopenia should be reserved for patients with bleeding.

Bleeding Time↗
PubMed1977

Fat embolism prophylaxis: a study of four treatment modalities.

Significant coagulation and blood gas changes may occur with uncomplicated extremity fractures. To more accurately define the effect of therapy on these changes, a prospective study of 58 patients with uncomplicated fractures was undertaken. An initial group of 10 selected patients was studied to determine the changes with "standard therapy." The remaining 48 patients were then randomized into five groups: control, increased fluid intake, increased glucose intake, aspirin, and massive steroids. The patients were studied on 5 consecutive days. Treatment of patients in the latter four groups with aspirin or steroids resulted in significant normalization of blood gases, coagulation proteins, and platelet numbers when compared to controls. These measurements in patients treated with fluid loading or increased glucose intake were not significantly different from controls.

Adolescent↗
PubMed1969

Congenital dysfibrinogenemia: fibrinogen Detroit.

A 17 yr old female with a congenital bleeding disorder was found to suffer from dysfibrinogenemia. Whole blood and plasma coagulation times were delayed and thrombelastograms were grossly abnormal. Clottability of plasma fibrinogen by addition of thrombin was not demonstrated during the 30 min test period. Fibrinogen was revealed by turbidometric and immunologic techniques. Other coagulation factors were present in normal amounts and prothrombin activation was normal. Patient's plasma inhibited thrombin clotting times of normal plasma and purified normal fibrinogen. Fibrinolysis was not detected. The plasma fibrinogen migrated normally on paper and cellulose acetate electrophoresis, but on immunoelectrophoresis it displayed a faster mobility than normal fibrinogen. On immunodiffusion the antigenic determinants were similar to those of normal fibrinogen. The patient's fibrinogen-antifibrinogen precipitins required longer to appear and the resultant precipitin was broader and hazier than those elicited with normal fibrinogen. These findings suggest the presence of two discrete populations of fibrinogen molecules. Investigation of the family of the patient suggested that the defect has an autosomal dominant pattern of heredity. Immunologic comparisons of our patient's plasma and of her relatives with plasma of patients with "Fibrinogen Baltimore" and "Fibrinogen Cleveland" revealed certain differences in immunoelectrophoretic mobility as well as in immunodiffusion. In keeping with the nomenclatures of abnormal fibrinogens in the literature, we propose the term "Fibrinogen Detroit" for this fibrinogen.Physicochemical properties of "Fibrinogen Detroit" were investigated also and compared with those of normal fibrinogen. Purified normal fibrinogen (clottability 96.7%) and "Fibrinogen Detroit" revealed homogeneity when studied by ultracentrifugation and immunoelectrophoresis. Native and cleaved "Fibrinogen Detroit" had the same sedimentation constants and molecular weights as the normal. In fresh samples. 3 moles of free SH groups/mole of fibrinogen were titrated in both. Determination of the amino acid composition revealed a decreased content of lysine, glucosamine, and galactosamine in abnormal fibrinogen. Total carbohydrates, protein-bound hexoses, sialic acid, and hexosamine were decreased in the abnormal fibrinogen. In an investigation with Doctors Blombäck a specific molecular defect was revealed in the N-terminal disulfide knot of the alpha (A) chain in which the arginine at the 19th position was replaced by serine. It is believed that the substitution of a strongly basic amino acid with a neutral hydroxy acid may result in considerable conformational changes in the N-terminal disulfide knot of fibrinogen which might affect the "active site" for polymerization. The lower carbohydrate content observed in "Fibrinogen Detroit" may have been the result of a change in primary and tertiary structure of the protein.

Adolescent↗