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Biomedical subjects

R Egbring

Publications and source records attributed to R Egbring.

At least 91 records · Page 5Linked to original sources
PubMed1977

Fibrinogen Marburg a new genetic variant of fibrinogen.

A new case of congenital dysfibrinogenemia has been discovered in a 20 year old woman, who suffered from a severe postpartal hemorrhage after the delivery of her first child, followed by episodes of thrombosis. Coagulation studies reveal a prolongation of thrombin time, reptilase time was immeasurable. Thromboplastin time and partial thromboplastin time were slightly prolonged. Low fibrinogen levels were obtained by techniques, which depend on the coagulation velocity following addition of thrombin, while immunological procedures gave slightly diminished values of fibrinogen. Patients's fibrinogen had a moderate inhibitory effect on the fibrin formation in normal plasma. However, inhibitors of the fibrinogen-fibrin conversion could not be detected. Coagulation factors were normal, fibriolysis as well. The cause of the coagulation disorder was found to be a defect of the fibrinogen molecule, leading to an abnormal fibrin polmerization of patient's fibrin monomers. The release of the fibrinopeptides in the paperelectrophoresis was normal. The defect of the fibrinogen molecule did not protect from thrombotic complications. The same defect could be found in the lower scale in patient's father, 4 of her 7 brothers and sisters, and her son.

Adult↗
PubMed1977

Demonstration of granulocytic proteases in plasma of patients with acute leukemia and septicemia with coagulation defects.

To show whether direct proteolysis of coagulation factors may play a role in patients with so-called consumption coagulopathy, granulocytic neutral proteases in the plasma of patients with acute myelocytic leukemia and septicemia were assayed by one- and two-dimensional Laurell electrophoresis. Complexes between serum alpha1-antitrypsin and elastase-like granulocytic protease could be demonstrated in those patients with acute myelocytic leukemia and septicemia who also had moderate or severe coagulation defects. Despite the presence of a high antiprotease potential, addition of the elastase-like enzyme to normal plasma resulted in coagulation defects in vitro comparable to those seen in the patients. These results and the ability of the elastase-like protease to destroy isolated clotting factors suggested that in certain types of coagulation factor deficiencies direct proteolysis rather than consumption of clotting factors due to disseminated intravascular coagulation may be operational.

Blood Coagulation Disorders↗
PubMed1976

[Longtime therapy of congenital factor XIII deficiency using factor XIII concentrate].

Factor XIII was determined by enzymatic and immunochemical methods in 3 patients with congenital factor XIII deficiency. Factor XIII activity measured by trans-glutaminase assay was below 1% of normal value in each of these cases. Immunelectrophoresis determination revealed the absence of the functionally active subunit A, whereas subunit S was only slightly diminished (30 to 50% of the normal value). Substitution with factor XIII concentrate caused a parallel increase of factor XIII activity and subunit A concentration. No uptake of factor XIII activity or of subunit. A by platelets could be demonstrated. Despite discontinuous substitution over a period of six years no antibody against factor XIII activity could be demonstrated in one patient with congenital factor XIII deficiency.

Antibodies↗