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Biomedical subjects

M Cortellaro

Publications and source records attributed to M Cortellaro.

At least 55 records · Page 3Linked to original sources
PubMed1984

A pharmacokinetic and platelet function study of the combined administration of metoprolol and sulfinpyrazone to healthy volunteers.

In a double-blind study on healthy subjects who underwent three 3-week periods of treatment with metoprolol (M) + sulfinpyrazone (S), M + placebo, and S + placebo, pharmacokinetics and plasma levels of M were not affected by concurrent administration of S. Analysis of variance change-over demonstrated a significant difference between treatments only for serum uric acid levels. Analysis of post-treatment and baseline data within each treatment showed: decreased platelet count by M, lowered serum 6-keto PGF1 alpha by all three treatments, decreased serum TXB2 generation and arachidonic acid-induced platelet aggregation by S + M. No negative interaction between S + M was found.

Adult↗
PubMed1984

Effects of chronic metoprolol and sulphinpyrazone on human lymphocyte beta-adrenoceptors.

Multiple (100 mg twice daily for 21 days) but not single (100 mg) oral doses of metoprolol significantly reduced the number (Bmax) and the KD of beta-adrenoceptors on intact lymphocytes from nine healthy volunteers. Sulphinpyrazone (400 mg twice daily for 21 days) did not change lymphocyte beta-adrenoceptors and did not modify their reaction to chronic metoprolol. In vitro sulphinpyrazone (10-4M) increased [3H]-DHA specific binding on intact lymphocytes. This effect was not modified by metoprolol, sulphinpyrazone or the two combined. Metoprolol and sulphinpyrazone did not interact in the experimental model of beta-adrenoceptors on intact lymphocytes in conditions mimicking long-term treatment.

Adult↗
PubMed1984

Response to vincristine treatment in a case of idiopathic hypereosinophilic syndrome with multiple clinical manifestations.

A case is reported of idiopathic hypereosinophilic syndrome involving many organs and systems and with a wide range of clinical findings: hematologic, cardiovascular, skin, pulmonary, spleen, liver, and gastrointestinal. Mortality in such patients is very high, but aggressive medical treatment (vincristine 2 mg/week for 5 weeks) produced a significant clinical benefit and considerably improved our patient's prognosis.

Aspirin↗
PubMed1984

Pharmacokinetics of S-adenosyl-L-methionine in healthy volunteers.

S-Adenosyl-L-methionine (AdoMet) kinetics was studied in 6 male subjects given 100 and 500 mg i.v. Drug concentrations in plasma and urine were assayed using a radioenzymatic method. Pharmacokinetic parameters were estimated according to an open two-compartment model. The apparent volumes of distribution after the 100 and 500 mg doses were 407 +/- 27 and 443 +/- 36 ml/kg (mean +/- SEM), terminal half-lives 81 +/- 8 and 101 +/- 7 min and body clearances 3.7 +/- 0.5 and 3.1 +/- 0.2 ml/min per kg. Urinary excretion was 34 +/- 3 and 40 +/- 2% of the administered dose. The results demonstrate that drug disposition occurs more via metabolism than via renal excretion, and it is not dependent on the administered dose. Binding of AdoMet to serum proteins is negligible.

Humans↗
PubMed1984

Liver dysfunction rather than intravascular coagulation as the main cause of low protein C and antithrombin III in acute leukemia.

Protein C, a newly identified inhibitor of blood coagulation, was measured immunologically in 58 patients with untreated acute leukemias and compared with that of normal subjects. On the average, slightly lower values were found. However, the 17 patients with overt laboratory pictures of decompensated disseminated intravascular coagulation (DIC), including 11 cases with acute promyelocytic leukemia, had protein C concentrations no lower than those of the remaining 41 patients without DIC. Antithrombin III activity and antigen were normal and, like protein C, not lowered in DIC. The concentrations of both proteins were closely correlated with changes in the indexes for liver synthetic function. A subgroup of 13 patients with hyperleukocytic leukemias had lower protein C and antithrombin III, in line with the more compromised synthetic function of their livers. Our findings indicate that liver impairment rather than DIC is the main cause of the changes in the two naturally occurring inhibitors of blood coagulation.

Adult↗
PubMed1983

Transcoronary platelet thromboxane A2 formation without platelet trapping in patients with coronary stenosis-effect of sulphinpyrazone treatment.

Platelet count, and plasma thromboxane B2 (TXB2) and circulating platelet aggregates (CPA) were determined in the coronary sinus (CS), aortic bulb (AO) and cubital vein (V) in 21 patients with stable angina and in 6 control subjects before and after atrial pacing (AP). TXB2 measurements were repeated before and after AP in 6 of the 21 angina patients after 15 days' sulphinpyrazone treatment. Platelet count and CPA ratio were similar in angina patients and controls at all three sampling sites and were unchanged at AP peak. In the controls, basal TXB2 values in CS, AO and V were not significantly different and were unchanged at AP peak. In the angina patients compared with the controls, basal TXB2 values in the AO, CS and V were not significantly different whereas the CS/AO TBX2 ratio was significantly higher; at AP-induced ischaemia, CS TXB2 was significantly increased and the CS/AO TXB2 ratio was increased. A weak but significant direct correlation was found between CS/AO TXB2 ratio and coronary score. Sulphinpyrazone treatment reduced CS TXB2 levels at rest and after AP, but not the ischaemic threshold at AP.

Adult↗
PubMed1981

In vivo platelet hyperactivity and factor VIII related antigen increase long after myocardial infarction. A controlled effect of sulfinpyrazone.

In the Anturane Reinfarction Italian Study the trend of some specific and quantitative haemostatic parameters is being investigated in different series of patients balanced for sulfinpyrazone and placebo. In a series of young male patients who had had myocardial infarction 6 months previously, it has been shown that the placebo treatment subsample presented shortened platelet production time (PPT), increased levels of plasma beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), and increased factor VIII related antigen (VIII:RAg) compared with a matched control group. A close correlation between plasma concentration of VIII:RAg and PPT was evidenced in the same treatment subsample. The sulfinpyrazone treatment subsample presented normalized PPT accompanied by reduction of VIII:RAg but not of beta-TG or PF4 levels.

Adult↗
PubMed1981

Haemostatic function changes in a trial on the secondary prevention of myocardial infarction with sulphinpyrazone.

The trend of some haemostatic parameters was investigated in a series of 186 myocardial infarction patients randomly allocated to sulphinpyrazone and placebo 15-25 days after the myocardial infarction episode in order to ascertain if one or more of these parameters may be considered as forecasting elements. The tests were performed a treatment allocation (basal values) and after 1, 6, and 12 months. In comparison with 44 healthy volunteers, the results have provided striking confirmation of 'hyperactive' platelets in the early phase of myocardial infarction expressed by the shorter bleeding time, increasing plasmatic beta-thromboglobulin, increased platelet factor 4 release and shorter heparin thrombin clotting time, and by the increased platelet sensitivity to threshold concentrations of adenosine diphosphate and collagen. Significant changes in bleeding time, platelet factor 4 release and heparin thrombin clotting time persist at successive testing times. Platelet aggregation by low collagen concentrations was inhibited in the sulphinpyrazone subsample patients.

Adult↗
PubMed1979

A controlled study of the effect of sulfinpyrazone on platelet survival and on platelet-bound 14C-serotonin release in patients with previous myocardial infarction.

Preliminary data obtained in the ambit of Anturan Reinfarction Italian Study (ARIS) show that, in postmyocardial infarction, reduced platelet survival time occurred in hyperbetalipoproteinemic patients treated with placebo, but not in the group of patients treated with sulfinpyrazone (interaction between treatment and lipemic level is at p approximately equal to 0.1). The sulfinpyrazone effect on platelet survival is probably related to the release reaction inhibition as suggested by our ex vivo results on platelet-bound 14C-serotonin release.

Adult↗
PubMed1975

[Pharmacological and clinical aspects of S-adenosylmethionine (SAMe) in primary degenerative arthropathy (osteoarthrosis)].

After some preliminary remarks of a biochemical and pharmacological nature, the authors have started a clinical study to test the antiinflammatory activity of the S-adenosyl-methionine (SAMe). An open trial, carried out on 90 patients with severe degenerative arthropathies has shown that 30 mg SAMe intravenously twice a day for 14 days have a marked anti-inflammatory effect a rather term and no side-effects. In a "double-crossover" investigation, SAMe was next compared to indomethacin by i.m. administrations to 15 arthropathic patients. The therapeutic responses of the two drugs proved exactly alike, whereas the side-effects following indomethacin administration were not present after SAMe. In 9 patients affected with rheumatoid arthritis administrations of SAMe have proved less effective, although some clinical parameters showed improvements.

Adult↗
PubMed1975

Human platelet aggregation by mixed cryoglobulins.

Glomerulonephritis in idiopatic mixed cryoglobulinemia represents perhaps a glomerular damage by immune complexes. In this study, a sigmoidal-like curve was obtained after addition of 13 different mixed cryoglobulins to both autologous and isologous platelet-rich plasma, tested in platelet aggregometer. The lag phase of the curve corresponds to platelet phagocytosis of cryoglobulin-binding ferritin, as shown in electron microscopy and the optical density decrease phase corresponds to the aggregation of platelets that shows the same ultrastructural characteristics of ADP-induced platelet aggregation. This platelet aggregation is inhibited by different drugs. Intraglomerular platelet aggregation by cryoglobulins might play a key role in determining the glomerular damage in cryoglobulinemia by the release of nucleotides and vasoactive amines.

Blood Platelets↗