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Biomedical subjects

F Jobin

Publications and source records attributed to F Jobin.

At least 19 recordsLinked to original sources
PubMed1999

Recombinant factor VIIa is effective for bleeding and surgery in patients with Glanzmann thrombasthenia.

Recombinant activated factor VII (rFVIIa) was found to be effective and safe in treating 24 bleeding episodes and to prevent bleeding during one bilateral herniorrhaphy in four children with Glanzmann thrombasthenia. One of the patients had alloantibodies to platelet membrane glycoprotein (GP) IIb/IIIa and was refractory to platelet transfusion. rFVIIa was administered at 89 to 116 microg/kg per injection every 2 hours, in association with antifibrinolytic drugs. Bleeding stopped in all cases, but platelet transfusion was required in one. Two bleeding episodes recurred 36 and 63 hours after discontinuation of rFVIIa, but were successfully treated with additional doses. No adverse effects of rFVIIa were observed. Although the number of patients is small, our study suggests that rFVIIa may be an alternative to platelet transfusions in patients with a severe congenital thrombocytopathy.

Blood Loss, Surgical↗
PubMed1994

The use of vitreous humor levels of glucose, lactic acid and blood levels of acetone to establish antemortem hyperglycemia in diabetics.

Glucose and lactic acid concentrations were measured in 328 autopsy cases. Glucose and lactic acid in vitreous humor and blood levels of acetone were found to be valuable indicators of antemortem hyperglycemia in diabetics. Resuscitation significantly increased glucose concentrations in vitreous humor whereas blood levels of acetone were not significant (< 1 mg/dl: detection limit). Values encountered in postmortem cases are presented and case results are discussed.

Acetone↗
PubMed1992

Prevention of deep vein thrombosis after major knee surgery--a randomized, double-blind trial comparing a low molecular weight heparin fragment (enoxaparin) to placebo.

Consecutive patients undergoing knee arthroplasty or tibial osteotomy at four participating hospitals received either enoxaparin, 30 mg subcutaneously every 12 h (n = 66) or an identical-appearing placebo (n = 65). All study medications started the morning after the operation and were continued up to a maximum of 14 days. Patients underwent surveillance with 125I-fibrinogen leg scanning and impedance plethysmography. Bilateral contrast venography was performed routinely at Day 14 or at time of discharge, if sooner. Deep vein thrombosis was detected by venography in 35 of 54 patients (65%) in the placebo group and in 8 of 41 patients in the enoxaparin group (19%), a risk reduction of 71%, P less than 0.0001. For the entire study group, deep vein thrombosis was detected by either venography of non-invasive tests in 37 of 64 patients (58%) in the placebo group and in 11 of 65 patients (17%) in the enoxaparin group, a risk reduction of 71%, P less than 0.0001. Proximal vein thrombosis was found in 19% of the placebo patients and in none of the enoxaparin patients, a risk reduction of 100%, P less than 0.001. Bleeding complications occurred in 5 of 65 patients (8%) in the placebo group and in 4 of 66 patients (6%) in the enoxaparin group, P = 0.71. There were no differences in the amount of blood loss, minimum hemoglobin levels and number of units of packed red cells given between the two treatment groups. We conclude that a fixed dose regimen of enoxaparin, started post-operatively, is an effective and safe regimen for reducing the frequency of deep vein thrombosis after major knee surgery.

Aged↗
PubMed1991

Two cases of inherited triple deficiency in a large kindred with thrombotic diathesis and deficiencies of antithrombin III, heparin cofactor II, protein C and protein S.

Thirty-three subjects, belonging to a large family with functional antithrombin III (ATIII) deficiency (type IIa) and recurrent thromboembolism, were investigated for ATIII, heparin cofactor II (HCII), protein C (PC) and protein S (PS). We report the exceptional finding of two cases of triple deficiency: ATIII combined with HCII and PC in the first case aged 15 and ATIII combined with HCII and PS in the second case aged 27. Interestingly, both are asymptomatic thus far. Twenty-five other deficient members were found, among which seven are affected with a double deficiency. Totally, the results of our study show 38 deficiencies of four distinct antithrombotic protein: ATIII (n = 9), HCII (n = 9), PC (n = 7) or PS (n = 13). Two types of HCII deficiency were observed and type I PC deficiency was found. Functional PS deficiency was characterized by reduced levels of cofactor activity for activated PC. Our report demonstrates that combined deficiencies should be sought in a family already known to be deficient in one antithrombotic protein.

Adolescent↗
PubMed1986

[Oral anticoagulant therapy: analysis of the efficacy of a dosage guide].

An empirical protocol for dosage adjustment in warfarin therapy was evaluated by means of retrospective analysis of the medical records of 106 outpatients at an anticoagulation clinic followed from January 1981 to August 1984. There were 203 cases in which the prothrombin time was abnormal (below the therapeutic range in 123 cases and above the range in 80). The protocol was successful in about 60% of cases in which the prothrombin time before dosage adjustment was below the therapeutic range and in 80% of cases in which it was above the range. Statistical analysis showed that the success rate could be improved by more precise definition of the percentage of dosage change in certain situations. However, individual variation in response of the prothrombin time to a standard dosage change limits the success that can be expected after the initial adjustment. We propose an improved protocol for adjustment of warfarin dosage.

Adult↗
PubMed1978

[Fibrinogen Quebec I and Quebec II: two new families of dysfibrinogenemia (author's transl)].

Two new families of congenital dysfibrinogenemia originating from French Canada are reported. The dysfibrinogenemia in the first family is characterized by an abnormal aggregation of the fibrin monomers; the defect in the second family is due to a faulty release of fibrinopeptides during the proteolytic phase of the thrombin-fibrinogen reaction.

Blood Coagulation Disorders↗