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Biomedical subjects

J J Veltkamp

Publications and source records attributed to J J Veltkamp.

At least 55 records · Page 3Linked to original sources
PubMed1976

The influence of the thyroid function on the metabolic rate of prothrombin, factor VII, and factor X in the rat.

The influence of the thyroid function on the metabolic rate of prothrombin, factor VII, and X was studied in the rat. Disappearance rates of the three coagulation factors were measured after synthesis had been blocked with appropriate doses of warfarin, and reappearance rates were assessed upon induction of synthesis by high doses of vitamin K1 injected into rats displaying coumarin induced hypocoagulability. No statistically significant difference in the disappearance and production rates of any of the factors could be found between normal euthyroid rats and thyroxin-treated hypothyroid rats proven to be euthyroid. The differences between the two euthyroid groups and the hypothyroid group were highly significant, however: hypothyroidism results in an approximately 50% decrease of the metabolic rates of the three coagulation factors under study. The reappearance of the three factors, under euthyroid as well as hypothyroid conditions, showed a biphasic pattern: in the first two hours after vitamin K1 administration to warfarin treated rats, a rapid reappearance was observed, to the same extent for all three factors, in hypo- as well as euthyroid rats. This finding suggests that in vitamin K1 deficiency an intracellular accumulation of precursor proteins (PIVKAs) occurs, which after rapid conversion into biologically active coagulation factors by vitamin K1 are shed into circulation. The subsequent phase of reappearance is much slower and reflects the synthesis rate of coagulation enzymes. It is characteristic for each factor and clearly slower in hypothyroid rats than in euthyroid rats. From this an influence of thyroid function on the synthesis rate of the protein moiety of coagulation factors can be inferred. An apparent difference between disappearance and reappearance rate of the coagulation factors in the plasma, particularly pronounced for factors VII and X in euthyroid rats, could theoretically be explained as the consequence of the model used for derivation of these rates.

Animals↗
PubMed1976

Molecular variant of factor VII.

Two patients with severe factor VII deficiency appeared to be different with respect to the presence of inactive factor VII-like material in their plasma. The inactive material, demonstrated in one patient's plasma and adsorbable onto BaSO4, inhibits the thrombotest-system and is capable of neutralizing a heterologous antibody against factor VII in a fluid phase system.

Cross Reactions↗
PubMed1976

Hereditary antithrombin III deficiency and thromboembolic disease.

Two teenage brothers with recurrent thromboembolic disease were found to have antithrombin III deficiency. A family study spanning four generations revealed a total of 10 members with antithrombin III deficiency. Five of the 10 affected family members have had thrombotic problems. Antithrombin III deficiency was documented by coagulation assays measuring heparin cofactor, anti-Factor Xa, and progressive antithrombin activity; the level of antithrombin III antigenic material measured by immunoelectrophoresis was low in subjects with abnormal coagulation assays. The clinical features which may lead one to suspect the hereditary hypercoagulable condition of antithrombin III deficiency are reviewed.

Antithrombins↗
PubMed1976

Automation in the hematology laboratory.

In the routine laboratory for hematology conflicting results may be obtained for the red blood cell parameters with the Coulter Counter Model S. These parameters2) are: mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC). When the values of the MCHC are above 36 g/dl something must be wrong with the blood sample of the patient. One of the reasons can be agglutination e.g. by cold agglutinins. The blood sample should be reanalysed before and after heating for 1 hour at 37 degrees C. If the values change: cold agglutinins are present; if no change occurs paraproteins, or other disturbing factors, such as bilirubin or high leucocyte levels, will be found. MCH values may also be high in some cases e.g. if the red blood cells are coated with antibodies (Coombs test positive) or after ingestion of medicines like Azathioprine. These examples show that it is possible in some cases to correlate immunological findings with the red blood cell parameters. In addition to the results with the Coulter Counter Model S, some observations on the Hemalog (Technicon) are also presented.

Blood Cell Count↗
PubMed1975

Potentially thrombogenic materials in factor IX concentrates.

Factor XI concentrates manufactured from human plasma and intended for therapeutic infsuion in man have been suspected for some time of being potentially thrombogenic. In the current studies, assays were carried out in vitro and in vivo for potentially thrombognic materials. It was possible to rank the various materials tested according to the amount of thromboninic material detected. For concentrates not containing heparin, there was substantial agreement between the in vivo and in vitro assays, with a coefficient of correlation of 0.77. There was no correlation between the assays for thrombogenicity and the antithrombin III content. We conclude that many presently availabel concentrates of Factor IX contain substantial amounts of potentially thrombogenic enzymes, and that this fact must be considered in arriving at the decision whether or not to use them therapeutically.

Animals↗
PubMed1975

Orthotopic liver transplantation: an experimental study on mechanisms of hemorrhagic diathesis and thrombosis.

The hemorrhagic diathesis after transplantation of preserved livers generally is attributed to intravascular coagulation, whereas postoperative "hypercoagulability" of the blood is considered the main cause of thrombosis of the hepatic artery anastomosis. Since our preliminary studies, however, suggested other mechanisms, parameters of coagulation, fibrinolysis, and platelet function were prospectively studied before and after 28 orthotopic liver transplantations, with and without preservation, in dogs and pigs. In addition, the arterial anastomoses were evaluated routinely by angiography and, after removal at reintervention or autopsy, inspected for thrombosis and tested for fibrinolytic activity and fibrin deposition. Concerning the hemorrhagic diathesis, prolongation of bleeding time without concomitant thrombocytopenia was the main abnormality found and occurred only in the nine dogs with liver transplants previously preserved for 3 to 6 hours. As only two of the nine dogs had postoperative hemorrhage of clinical significance, we consider surgically imperfect hemostasis facilitated by an acquired platelet dysfunction the principal cause of hemorrhage. Thrombosis of the arterial anastomosis was found in 38 percent of animals in which an end-to-end anastomosis was made but was not encountered with celiac artery-aorta anastomoses. Local factors due to surgical technique therefore appear most important in the pathogenesis of thrombosis of the hepatic artery anastomosis, although the postoperative hyperfibrinogenemia and diminished local and systemic fibrinolytic activity may contribute as well.

Animals↗