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Biomedical subjects

J P Frontroth

Publications and source records attributed to J P Frontroth.

9 recordsLinked to original sources
PubMed2003

Acenocoumarol therapy in pediatric patients.

To determine guidelines for administering and monitoring acenocoumarol therapy in children, 93 patients (median 5.1 years, range: 0.2-18 years) were prospectively evaluated over a 33-month period. The loading doses used were: <1 year, 0.20 mg x kg-1; >1-5 years, 0.09 mg x kg-1; 6-10 years, 0.07 mg x kg-1; 11-18 years, 0.06 mg x kg-1. In this study, the loading dose and the dose to achieve and maintain target therapeutic range (TTR) for acenocoumarol are age-dependent, with infants having the highest and teenagers having the lowest requirements. The use of a different loading dose according to age has allowed most of the children (80%) in all the age groups to achieve TTR in less than 1 week. No patients had serious bleeding or thrombotic complications. We conclude that there is an age-dependent response to acenocoumarol in pediatric patients. The implementation of an age-adjusted loading dose regimen reduces the length of hospitalization required to achieve effective anticoagulant therapy.

Acenocoumarol↗
PubMed1999

Prethrombotic disorders in children with arterial ischemic stroke and sinovenous thrombosis.

BACKGROUND: Arterial ischemic stroke (AIS) and sinovenous thrombosis (SVT) are relatively rare events in children. The contribution of prethrombotic disorders to the etiology of these entities has not been completely elucidated. OBJECTIVES: To determine the frequency of inherited and acquired prethrombotic disorders in a pediatric population with AIS and SVT and to report clinical and radiological features. METHODS: From May 1992 to April 1997, 30 consecutive children with AIS and 10 children with SVT were assisted at a single institution. Hemostatic evaluation was performed for all the children. Evaluation included the following assays: protein C, protein S, antithrombin, plasminogen, activated protein C resistance, factor V Leiden mutation, and the detection of antiphospholipid antibodies. Data concerning baseline demographics, risk factors, presenting features, family history of thrombosis, and radiological findings were also recorded. RESULTS: One or more prethrombotic disorders were present in 9 children (30%) with AIS (inherited protein S deficiency, 2 patients; inherited protein C deficiency, 1 patient; acquired antithrombin deficiency, 2 patients; antiphospholipid antibodies, 3 patients; and antiphospholipid antibodies and plaminogen deficiency, 1 patient) and in 5 children (50%) with SVT (inherited protein S deficiency, 1 patient; acquired antithrombin deficiency, 3 patients; and antiphospholipid antibodies, 1 patient). CONCLUSIONS: Most children studied presented both a variety of risk factors for thrombosis and concomitant prethrombotic disorders. Therefore, a complete hemostatic evaluation for all children with AIS and SVT should be performed, despite the presence of obvious clinical risk factors or lack of family history of thrombosis.

Adult↗
PubMed1995

Reduction of platelet surface GPIb expression induced by polymorphonuclear leukocytes.

It has been demonstrated that soluble factors released from PMNs such as proteases, free radicals and arachidonic acid metabolites are able to induce platelet activation (1). More recently, it has been demonstrated that PMNs can also inhibit platelet functional responses. It has been suggested that the inhibitory effect of PMNs could be related to the release of nitric oxide (NO) (2-3). In contrast, we have previously observed that coincubation of platelets with unstimulated PMNs, results in the inhibition of platelet aggregation and ATP release by a yet non-identified mechanism that does not involves NO (4). Considering that an alteration in surface receptors could be one of the phenomena accounting for impaired platelet responses, in the present study we evaluated the ability of PMNs to modulate the expression of the glycoproteins (GP) involved in platelet adhesion and aggregation, GPIb-IX and GPIIb-IIIa.

Blood Platelets↗
PubMed1992

A simple enzyme-immunoassay test for von Willebrand factor binding in human arterial subendothelium.

In order to determine the binding of vWF, subendothelium from everted human umbilical arteries was perfused with dialysed serum containing different concentrations of purified vWF using an annular perfusion chamber at a wall shear rate of 1100 sec-1 for 30 min. After perfusion, control (not perfused) and perfused vessel segments were washed and incubated with a diluted rabbit antibody against human vWF. Then the nonbound anti-vWF from both samples were used to determine indirectly vWF by EIA. Although in our experiments normal vWF serum concentrations were not enough to exert vWF binding, a substantial binding could be attained with vWF levels around 2.5 U/ml. To estimate the pre-existing subendothelial vWF amount, three different experiments were developed: a) diluted IgG from a nonimmunized rabbit, b) a diluted rabbit antibody to human vWF, c) PBS-BSA. After washing, vessel segments were incubated with rabbit antibody to human vWF. After incubation, the nonbound anti-vWF was used to determine indirectly vWF by EIA. The results obtained showed that the amount of pre-existing vWF was approximately 1.1x10(-3) U vWF/cm2 subendothelium.

Endothelium, Vascular↗
PubMed1991

Visualization of platelet glycoproteins Ib and IIIa by immunoenzymatic stain using avidin-biotin peroxidase complex.

A method is described here for the identification and quantitation of antigens by monoclonal antibodies. This method is based upon 1) separation (crossed-immunoelectrophoresis) and immunoprecipitation (rocket immunoelectrophoresis and crossed immunoelectrophoresis) of glycoproteins Ib and IIIa with a polyspecific antiserum; 2) binding of the non precipitating monoclonal antibody to glycoproteins precipitated by the rabbit antibody; 3) visualization of the monoclonal antibody with secondary biotinylated antibody and after addition of avidin biotin peroxidase complex, the peroxidase activity is detected by 4-Cl-1-naphtol. By this technique, the agarose gel plate could be stained directly and this allowed us to eliminate electrophoretic transblotting and radioactive compounds.

Animals↗
PubMed1988

Purification and partial characterization of a bioactive substance from rat's vessel wall independent of prostacyclin production.

The bioactive substance from rat's vessel wall was purified by Sephadex G-75 gel filtration and by a combination of DEAE Cellulose ion exchange and Sephadex G-50 gel filtration chromatographies. Purifications of 12.5 fold and 70 fold over the initial material were achieved. PAGE of the purified material resulted in a single major band with a molecular weight estimated at 55kd-65kd. Trypsin (0.3 mg/ml) and chymotrypsin (30 mg/ml) abolished platelet antiaggregating activity. Neuraminidase (1.2 units) had no effect on platelet antiaggregating activity. This is the report of purification of aortic vessel wall antiaggregating activity independent of prostacyclin production.

Animals↗
PubMedDate not supplied

Prothrombotic abnormalities in children with venous thromboembolism.

PURPOSE: The aim of this study was to determine the frequency of acquired or inherited prothrombotic disorders in a pediatric population with venous thromboembolism (VTE). PATIENTS AND METHODS: From May 1992 to April 1998, 56 consecutive children with VTE were prospectively studied at a single center. RESULTS: The median age was 8.4 years (range, 0.1-18 years). There was a male predominance. Fifty (89%) children had thrombosis in the lower venous system. Risk factors were detected in 54 (96%) children. Twenty-one (38%) thrombotic episodes were related to central venous lines. Family history of thrombosis was positive in 13 (23%) patients. In 26 (46%) patients, a prothrombotic disorder was detected. Nine of them had inherited disorders (protein C deficiency, 5 patients; protein S deficiency, 3 patients; Factor V Leiden mutation, 1 patient), and 13 children had acquired disorders (antiphospholipid antibodies, 5 patients; antithrombin deficiency, 8 patients). The remaining four showed combined abnormalities (Factor V Leiden mutation associated with inherited protein S deficiency, 1 patient; acquired antithrombin deficiency, 2 patients and inherited antithrombin deficiency, 1 patient). CONCLUSIONS: In the series, a high percentage of prothrombotic disorders was detected; thus, a complete hemostatic evaluation should be performed in all of the children with VTE whether the patients have one or more risk factors.

Adolescent↗