Biomedical subjects

D Colhon

Publications and source records attributed to D Colhon.

8 recordsLinked to original sources

PubMed1996

Plasma fibronectin in overweight men and women: correlation with serum triglyceride levels and serum cholinesterase activity.

When compared with 67 age- and sex-matched normal weight control subjects, the 71 overweight patients displayed obviously higher levels of plasma fibronectin. For a similar body mass index (BMI) the 16 overweight men younger than 45 years had a significantly (P < 0.01) higher plasma fibronectin level (455 +/- 99.3 mg/l; mean +/- SD) than the 16 age-matched overweight women (351 +/- 105 mg/l) while there was no significant difference between the 22 overweight men (446 +/- 89.2 mg/l) and the 17 overweight women (475 +/- 111 mg/l) older than 45 years. Particularly high plasma fibronectin levels were noted in the five women with upper body (android) obesity. Plasma fibronectin was positively correlated with BMI, serum triglyceride concentration, plasma fibrinogen and serum cholinesterase activity. It is considered that metabolic disturbances related to upper body obesity may lead to an enhanced hepatic secretion of VLDL and of several plasma proteins including fibronectin.

Adult↗

PubMed1994

Homozygous or compound heterozygous qualitative antithrombin III deficiency.

A male patient of 24 years who had experienced thrombotic episodes since the age of 15 displayed an unusually low antithrombin III (AT III) activity measured as heparin cofactor (13% of the normal), while a similarly decreased value (16% of normal) was found in a 26 year old brother who had suffered from thrombotic events since the age of 12 years. AT III heparin cofactor activities were close to 50% of normal in the father, mother, another brother and a sister, none of whom had experienced thrombotic episodes. Since all available members of the family, including the patient, displayed near normal AT III antigen levels (73-85%) normal total progressive antithrombin activities (92-110%) as assessed by the thrombin agarose diffusion technique and normal total progressive anti-Xa activities, the propositus and his brother could be considered to be homozygotes or compound heterozygotes for a qualitative familial AT III deficiency probably caused by an abnormality of the heparin binding site. Molecular techniques would be required to elucidate the precise mutation giving rise to the deficiency.

Adolescent↗

PubMedDate not supplied

Plasma protein C and antithrombin III in patients with acute leukemia.

When compared to values recorded in the 32 healthy control subjects, plasma protein C activity was found to be significantly decreased in the 29 patients with acute leukemia and especially in those considered to be in a critical condition. On the other hand, plasma antithrombin III activity did not significantly differ from the values noted in control subjects. The concomitantly occurring high plasma fibrinogen levels and low serum cholinesterase activity were highly suggestive for a switch of hepatic protein synthesis towards the production of acute phase proteins. It is therefore considered that in the absence of a consumption coagulopathy, changes affecting plasma protein C and antithrombin III should be related to a modified pattern of hepatic protein synthesis.

Acute Disease↗

PubMedDate not supplied

Antithrombin III deficiency.

Data on clinical features and laboratory diagnosis of familial antithrombin deficiency, a rather heterogeneous group of disorders, are illustrated by observations on two Romanian kindreds afflicted by recurrent thrombotic episodes. In a first family, both plasma antithrombin III antigen and activity were reduced to 50% of normal, a condition characteristic for a heterozygous type I (quantitative) familial antithrombin III deficiency. In a second kindred, the two brothers who had experienced thrombotic events since they were teenagers, displayed exceedingly low AT III heparin cofactor activity (13% and 16% of the normal, respectively) while values around 50% of the normal were recorded in their parents who had not experienced thrombotic episodes. Since plasma antithrombin III antigen and total progressive antithrombin III activity were within normal limits in all the investigated members of this family it was considered that the two brothers were homozygotes or compound heterozygotes and the parents were heterozygotes for a qualitative-antithrombin III deficiency caused by an abnormality of the heparin binding site.

Adolescent↗

PubMedDate not supplied

Hemostatic balance during the acute inflammatory reaction. (II). With special reference to plasma protein C.

While plasma fibrinogen level and clotting factor VIII activity obviously increased during the acute inflammatory reaction caused by intramuscular injections of turpentine in 10 rabbits, the activity of plasma protein C, with anticoagulant and antithrombotic effects, was found to display a slight yet significant (p < 0.02) decrease. When compared to protein C activity in humans, this vitamin K-dependent serine protease was found to be lower in rabbits (52, 7% +/- 3,63 of standard human plasma) and this activity decreased to 45,8% +/- 2,80 (mean +/- SEM), 48 hours after the injection of turpentine. This slight decrease should however be interpreted in the context of other disturbances of the hemostatic balance caused by inflammation and may contribute to the intravascular deposition of fibrin.

Acute-Phase Reaction↗

PubMedDate not supplied

Hemostatic balance during the acute inflammatory reaction; with special reference to antithrombin III.

Inflammatory reaction caused by intramuscular injections of turpentine in 5 rabbits led to an obvious increase of not only plasma fibrinogen and factor VIII: C levels, but also of plasma antithrombin III activity, measured by a chromogenic assay as heparin cofactor. This activity rose from 80% +/- 10,8 (mean +/- SEM) before the injection to 123% +/- 6,56 48 hours later. Changes affecting plasma fibrinogen level and antithrombin II activity were much lesser in a group of 5 rabbits given small doses of intravenous endotoxin. It is considered that acute inflammation is accompanied by the setting of the hemostatic balance at a higher level.

Acute-Phase Reaction↗

PubMedDate not supplied

Acute phase reaction and the hemostatic balance.

Data in the literature as well as authors own observations concerning a possible relationship between the acute phase reaction and changes of the hemostatic variables, which may favour or trigger a thrombotic event, are reviewed. Acute phase reaction is usually accompanied by increased plasma levels of fibrinogen, von Willebrand factor and clotting factor VIII, while endothelial cells in culture added proinflammatory cytokines were found to express tissue factor activity, to release von Willebrand factor and to increase the production of plasminogen activator inhibitor. Evidence is also provided that inflammation would lead to an increase of plasma antithrombin III while the protein C system is down regulated. It is also considered that the above-mentioned changes of hemostatic variables would favour the local deposition of fibrin and platelets while attempting to prevent an intravascular dissemination of fibrin formation.

Acute-Phase Proteins↗

PubMedDate not supplied

Increased plasma factor VIII:c activity in patients with unstable angina pectoris.

Plasma factor VIII:c activity was found to be significantly (p < 0.01) higher in the 17 patients with unstable angina pectoris (201% +/- 121; x +/- SD) than in the 10 healthy control subjects (97% +/- 16). Plasma fibrinogen level was also significantly (p < 0.003) higher in patients (455 mg/dl +/- 188) than in controls (260 mg/dl +/- 35) but there was no significant correlation between these two variables within the group of patients with unstable angina. No difference could be noted between plasma antithrombin III activities in patients and in controls. It is considered that the increased factor VIII:c activity in patients with unstable angina pectoris could be subsequent to the acute phase reaction induced by cytokines and/or by an enhanced adrenergic stimulation, although the possible presence of genetically-conditioned hyperactive factor VIII:c molecules can not be excluded. Since the outcome of a ruptured plaque may also depend on the systemic thrombotic propensity at the time of rupture, the presently reported findings could be pathogenically relevant.

Adult↗