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Biomedical subjects

J Monasterio

Publications and source records attributed to J Monasterio.

At least 37 records · Page 2Linked to original sources
PubMed1987

Low-dose acetylsalicylic acid (ASA) plus dipyridamole versus dipyridamole alone in the prevention of stroke in patients with reversible ischemic attacks.

A total of 243 patients who had reversible ischemic attacks (RIA) were submitted to clinical trial to determine whether dipyridamole (400 mg/day) (D) or aspirin (100 mg/48 hours) + dipyridamole (300 mg/day) (ASA + D) would produce significant reduction in the subsequent occurrence of RIA and completed stroke. One hundred and fifteen were selected for Group ASA + D and 71 were treated with dipyridamole only. The treatment groups were similar in relation to age, sex, risk factors, duration and presumed vascular territory of RIA, incidence of alterations of arterial supra-aortic trunks, cerebral infarct (CT scan), and platelet function. Patients were followed for a mean time of 21 months. At the end of the study, 21.7% of the ASA + D group and 19.7% in the D group had suffered new episodes of RIA or completed stroke (p = 0.88). Frequency of stroke (reversible ischemic neurologic deficit or completed stroke) was 7.8% in the ASA + D patients and 9.8% in the D patients (p = 0.83). Subgroup analysis did not show significant differences either. It is concluded that ASA + D has no significantly greater beneficial effect than that observed with D alone in the secondary prevention of atherothrombotic cerebral ischemia. However, a statistical Type II error cannot be excluded by the reduced number of recurrences.

Adult↗
PubMed1983

Microhaemorheological properties of binifibrate. Part II: Preliminary open studies in patients with peripheral arteriopathies.

3-Pyridinecarboxylic acid 2-[2-(4-chlorophenoxy)-2-methyl-1-oxo-propoxy]-1,3-propanediyl ester (binifibrate, Biniwas) an anti-arteriosclerotic and hypolipidaemic agent which showed an effect on microhaemorheological properties during studies in experimental animals (rat and rabbit), was administered to six hyperlipidaemic patients who suffered from circulatory disturbances in the lower limbs. The treatment with binifibrate was applied at a dosage of 3 X 600 mg/day during one month. Both subjective symptoms such as paraesthesia, dysthaesia, coldness at rest and functional weakness of movements were improved, as well as objective symptoms measured by oscillometry. The microhaemorheological analyses demonstrated a positive variation in relative parameters. The correlation between microhaemorheological parameters and clinical symptoms is discussed.

Adult↗
PubMed1980

Antithrombin III contribution to cholestasis differential diagnosis: its correlation with one stage prothrombin time and factor V.

Levels of antithrombin III (AT III) measured by two different methods, Factor V (FV) and One Stage Prothrombin Time, have been studied in two groups of patients: 55 with chronic liver disease and 22 with extra hepatic cholestasis. Results show a statistically significant correlation between the decrease of AT III and FV in the first group, and the normality of these parameters (unrelated to One Stage Prothrombin Time) in the second group. Levels at AT III and FV correlate directly with the functional integrity of hepatic parenchyma, so they may help in the differential diagnosis of different types of cholestasis.

Antithrombin III↗
PubMedDate not supplied

Plasma concentrations and bioavailability of propranolol by oral, rectal, and intravenous administration in man.

Eight normal male volunteers received 80 mg doses of propranolol by the oral and rectal routes and 2.2 mg by intravenous administration in a crossover fashion. Plasma concentrations of propranolol were measured by a gas chromatographic method using an electron capture detector. Individual subject concentration-time data were analysed and results indicated that the data fit a two compartment model with first order absorption. An approximately two-fold higher plasma propranolol concentration was observed after rectal administration as compared with oral dosing. Statistical analysis of the difference in the total AUCs indicates a significantly higher bioavailability of propranolol administered by the rectal route. The reduced bioavailability after oral administration indicates a substantial first pass effect but that it is possible to bypass the liver, at least partially, by giving the drug rectally to man.

Administration, Oral↗
PubMedDate not supplied

Comparative study on the antithrombotic efficacy of hirudin, heparin and a low-molecular weight heparin in preventing experimentally induced venous thrombosis.

In a random, blind study, we compared the antithrombotic potential of unfractioned heparin, a low-molecular weight heparin (LMWH) and a recombinant hirudin (r-hirudin) given subcutaneously in a jugular vein thrombosis model in rabbits. All drugs and placebo were injected subcutaneously 2 h before inducing experimental thrombosis. A good thromboprophylactic effect was obtained with either LMWH and r-hirudin as compared with placebo. By contrast, no significant differences were found between groups in bleeding time. We also found a small (non-significant) prolongation of the activated partial thromboplastin time in the r-hirudin-treated animals. As for thrombin time, r-hirudin-treated rabbits exhibited too much sensitivity, with noncoagulable end-points. In our study, r-hirudin at the dose used seemed to be as effective as LMWH is in the prophylaxis of venous thrombosis.

Animals↗
PubMedDate not supplied

Inflammatory mediators and their influence on haemostasis.

Sepsis is the most important cause of mortality in the Intensive Care Units. At present, sepsis is understood to be the inflammatory response of the host to infection, rather than a direct effect of microbial aggression. From the clinical standpoint, this inflammatory response is known as systemic inflammatory response syndrome (SIRS). Pathophysiologically, SIRS is characterized by the activation of several groups of cell (monocytes/macrophages, PMNs, and endothelial cells) and by the release of inflammatory mediators (cytokines and others). Tumor necrosis factor (TNF) is the first cytokine released by endotoxin action over monocyte/macrophage. TNF secretion, modulated by interferon gamma (IFN gamma) and interleukin 10 (IL-10), is followed by release of other cytokines such as interleukins (IL) (IL-1, IL-6 and IL-8). These mediators are able to act over hemostasis activating the extrinsic pathway through tissue factor expression. The action of the mediators over endothelial cells induces an increase in plasminogen activator inhibitor type 1 (PAI-1) levels with inhibition of fibrinolysis. Both coagulation activation and fibrinolysis blockade result in fibrin deposit in the microvascular system. The complexity of the mechanisms implicated in systemic inflammatory response make a general rule so difficult to establish, because patient response is highly individualized and it is not possible to know which moment of this dynamic process is being analyzed.

Animals↗
PubMedDate not supplied

Clinical and therapeutic aspects associated to phospholipid binding antibodies (lupus anticoagulant and anticardiolipin antibodies).

Antiphospholipid antibodies (APA) comprise a family of immunoglobulins characterized by their pattern of reactivity in a number of laboratory tests. Included in this family are lupus anticoagulant (LA) anticardiolipin antibodies (ACA) and antibodies causing biologic false positive serologic tests for syphilis (BFP-STS). LA and ACA occur in a variety of conditions, including other autoimmunes disorders, infectious diseases, neoplasic disorders, in association with certain drugs and in otherwise healthy individuals. Clinical interest in LA and ACA is increasing. Antiphospholipid antibody syndrome is characterized by a triad of clinical features which include fetal loss, thromboembolic disease and thrombocytopenia. Other clinical manifestations related with APA are livedo reticularis, cutaneous necrosis, hemolytic anemia, heart valve disease, chorea, migraine and obstetric problems as fetal growth retardation, pre-eclampsia, post-partum serositis or neonatal thrombosis or catastrophic antiphospholipid syndrome. Therapy is mainly directed against the widespread and diverse manifestations associated with the obstruction of small and large vessels. Long-term treatment with oral anticoagulation therapy is advised, even if the venous or arterial occlusion occurred many years previously. In patients with primary antiphospholipid syndrome there is no evidence that the prophylactic administration of steroids or immunosuppression will prevent thromboembolic events. Although the administration of more energetic immunosuppression with cyclophosphamide in pulse form is effective in reducing elevated antibody levels, there is usually a rapid rebound to pretreatment levels shortly after discontinuation of the therapy. A history of recurrent fetal loss requires mandatory treatment during pregnancy. Although the actual prospective risk of pregnancy loss in women with antiphospholipid syndrome and prior pregnancy loss is unknown, it may exceed 60%. Because of this many investigators have treated women with antiphospholipid syndrome with either antiplatelet agents, immunosuppressive agents, or anticoagulants in an attempt to improve pregnancy outcome. Unfortunately, there is no unequivocal proof that any of these therapies are fully efficacious. Despite varying treatment protocols, the live birth rate with treatment was 70%, similar to that reported in the recent randomized clinical trial. Thrombocytopenia and autoimmune hemolytic anemia in patients with APA are treated similarly as patients without APA. Treatment of asymptomatic patients isn't indicated, because only approximately 10-15% of patients with APA developed complications.

Abortion, Habitual↗