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Biomedical subjects

J Kutti

Publications and source records attributed to J Kutti.

At least 91 records · Page 5Linked to original sources
PubMed1986

Evaluation of platelet reactivity in diabetes mellitus.

Seventeen patients with insulin-dependent diabetes mellitus, all below the age of 45 years, were studied. Five of them had retinopathy but no other micro- or macrovascular diabetic complications. None of them had any other concurrent disorder or were on any medication but insulin. The results were compared to those of 17 healthy volunteers of comparable age. There was no difference between the two groups in venous platelet counts, serum production of thromboxane B2 (TXB2), ADP-induced platelet aggregation or bleeding times. As compared to the controls, the diabetics had significantly elevated blood glucose and glycosylated hemoglobin values. The mean plasma values of beta-thromboglobulin, platelet factor 4 and TXB2 were significantly lower in the patients than in the controls. Thus, our results do not lend support to the current concept that platelet reactivity is enhanced in diabetes mellitus.

Adenosine Diphosphate↗
PubMed1985

Plasma concentrations of platelet-specific proteins and serum thromboxane B2 production in response to treatment with dipyridamole. A pilot study of 27 post-myocardial infarction patients.

In the present study 27 post-myocardial infarction patients were treated with Persantin capsules (Depot-Kapseln, sustained release form), containing 200 mg dipyridamole, b.i.d. over a period of 3 weeks. Baseline levels for plasma beta-thromboglobulin (BTG), platelet factor 4 (PF4), and serum thromboxane B2 (TXB2) were obtained on day 0 and subsequently on days 1, 3, 5, 7, 14 and 21. The baseline levels for plasma BTG and PF4 as well as for serum TXB2 significantly exceeded those for a control group consisting of healthy subjects. The plasma values for BTG and PF4 remained unchanged during the whole study period. During the first week of study the levels for serum X TXB2 were unchanged; however, on days 14 and 21 the means for TXB2 dropped significantly. There is experimental work to suggest that dipyridamole may exert an inhibitory effect on platelet thromboxane biosynthesis. The present results support this concept.

Adult↗
PubMed1985

ADP-induced platelet aggregation in young female survivors of acute myocardial infarction and their female controls.

Adenosine diphosphate (ADP)-induced platelet aggregation was studied in 35 young female survivors of acute myocardial infarction (AMI) 14-46 (median 30) months after the infarction. The results were compared to those obtained for 35 control females of comparable age. Five different final ADP concentrations (0.2-1.0 microM) were employed, and the object was to assess the slope for the primary wave of aggregation as well as the threshold ADP concentration for secondary aggregation. The results showed that AMI patients and control subjects did not differ with respect to the primary wave of aggregation. However, secondary platelet aggregation was recorded to a significantly higher extent (p less than 0.02) in AMI patients than in their controls. The results therefore support the concept that enhanced platelet reactivity is present in patients with documented ischemic heart disease.

Adenosine Diphosphate↗
PubMed1985

ADP-induced platelet aggregation and metoprolol treatment of myocardial infarction patients. A controlled study.

The effect of metoprolol on platelet aggregation was investigated in a group of postmyocardial infarction (MI) patients. The study was double-blind and included 63 subjects; 30 patients were maintained on metoprolol and 33 received placebo treatment. Adenosine diphosphate (ADP)-induced platelet aggregation was carried out in each subject close to 4 weeks after the acute MI. It was demonstrated that metoprolol as compared to placebo did not influence ADP-induced platelet aggregation in the present clinical setting.

Adenosine Diphosphate↗
PubMed1985

The blood volume in pheochromocytoma patients before and during treatment with phenoxybenzamine.

Total blood volume (TBV), red cell volume (RCV) and plasma volume (PV) were determined in 15 pheochromocytoma patients (9 males and 6 females) prior to and during preoperative treatment with phenoxybenzamine. Seventeen healthy male volunteers served as controls. Untreated male patients did not differ from the controls with respect to TBV, RCV or PV. In the total group of pheochromocytoma patients, phenoxybenzamine, in a dose of 145.6 +/- 45.2 (SD) mg/day over 14.3 +/- 5.7 (SD) days, induced significant increases in TBV (+9.4%) and PV (+14.5%), whereas RCV remained unchanged. During phenoxybenzamine, the mean PV in male patients significantly exceeded the control mean. We conclude that pheochromocytoma patients adapt their TBV to excessive catecholamine production and that they rarely present with profound hypovolemia. Moderate but higher doses of phenoxybenzamine than previously recommended induced marked increases in TBV secondary to PV expansion. Phenoxybenzamine counteracts the development of hypovolemia most effectively, thereby constituting one of several important measures for successful surgical management of pheochromocytoma patients.

Adrenal Gland Neoplasms↗
PubMed1985

Effect of Iloprost (ZK 36 374), a novel prostacyclin analogue, on ADP-induced platelet aggregation.

The effect of Iloprost (ZK 36 374), a chemically stable carboprostacyclin derivative, on ADP-induced platelet aggregation was investigated using platelet-rich plasma obtained from healthy male volunteers. It was shown that Iloprost in a dose-dependent fashion powerfully inhibits both the primary and secondary wave of ADP-induced platelet aggregation. Similarly, Iloprost immediately and most effectively disaggregates preformed platelet aggregates.

Adenosine Diphosphate↗
PubMed1984

The effect of acetylsalicylic acid in 3 different formulations on in vitro and in vivo platelet function tests. An experimental study on healthy male volunteers.

The template bleeding time (TBT), ADP-induced platelet aggregation, and serum production of TXB2 were measured in healthy young male subjects immediately before, and on days 1, 4 and 6 after the ingestion of 1 single dose of 500 mg acetylsalicylic acid (ASA) in 3 different formulations: Aspirin (Bayer), and the 2 enteric-coated formulations Reumyl (Hässle) and Premaspin (Lääke). The ingestion of Aspirin resulted in a significant prolongation of the TBT over a period of 6 d. However, after the ingestion of the same amount of ASA in the 2 enteric coated formulations, the TBT as measured on day 6 had become normalized. After the ingestion of Aspirin, there was no reappearance of the second wave of ADP-induced platelet aggregation during the study period; however, after the ingestion of the 2 enteric-coated formulations, secondary platelet aggregation occasionally returned on day 6. In response to the intake of each of the 3 ASA formulations, the serum TXB2 production as measured 24 h later was almost completely inhibited. In each of the 3 study groups, the TXB2 formation as measured on day 6 was still significantly impaired.

Adult↗
PubMed1984

Successful treatment of refractory autoimmune haemolytic anaemia by plasmapheresis.

A 16-year-old female was admitted because of rapidly progressive fatigue, severe anaemia and icterus. The S-bilirubin was 190 mumol/l, COHb 7.3% and high amounts of free Hb in plasma were present. The Coombs' direct test was strongly positive with anti-IgG but negative with anti-IgM and anti-C3. Conventional therapy with very high doses of hydrocortisone i.v., cyclophosphamide, azathioprine, and transfusions of washed packed red cells proved ineffective. During 5 consecutive days she also received i.v. infusions of gamma-globulin (25 g each day). Nevertheless, her condition deteriorated and 3 plasma exchanges were carried out with impressive clinical and laboratory effects. After the 3rd plasma exchange, the patient did not require further transfusions of packed red cells. Therapy with corticosteroids could be rapidly reduced and she was discharged after 5 weeks with a normal blood picture. Since then she has remained in excellent health.

Adolescent↗
PubMed1983

Plasma concentrations of platelet-specific proteins in young female acute myocardial infarction survivors and their age-matched female controls.

The steady state plasma concentrations of the two platelet-specific proteins beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were determined in two groups of females: 36 acute myocardial infarction (AMI) survivors, and 38 age-matched control subjects. For the AMI patients the mean BTG and PF4 values were 57 +/- 4 and 14.1 +/- 1.7 ng/ml, respectively. These two means significantly exceeded the corresponding means for the controls, 40 +/- 2 and 10.3 +/- 0.6 ng/ml, respectively. Similar results have recently been reported by other workers who investigated patients with coronary artery disease; however, in no previous study were the values for BTG and PF4 related to those obtained for control subjects matched with respect to sex and age. The present results therefore further support the concept that increased platelet activation and secretion is taking place in steady state patients who previously have sustained an AMI.

Adult↗
PubMed1983

The peripheral platelet count and ADP-induced platelet aggregation in response to metoprolol and propranolol as studied in young healthy male volunteers.

In previous studies, we have demonstrated that the oral administration of one single dose of metoprolol as well as of propranolol causes a significant increase in the venous platelet concentration. In the present study, we investigated the effect of metoprolol, administered twice daily over a period of 1 week, on the venous platelet count in a group of healthy volunteers. The results showed that the drug significantly raised the venous platelet concentration over the whole study period. Further, the effect of 1 week's metoprolol and propranolol medication on ADP-induced platelet aggregation was investigated in another group of healthy subjects; the results were compared to those obtained during 1 week of placebo medication. It was demonstrated that neither of the two beta-blocking drugs affected ADP-induced platelet aggregability; this was true on the first as well as on the last day of study.

Adenosine Diphosphate↗
PubMed1983

Stress and platelet activation.

Severe stress, with increased secretion of adrenaline, is likely to cause platelet activation. The aim of the present study was to investigate if moderate stress, which usually is not accompanied by adrenaline secretion, could induce activation of platelets, as measured by changes in the plasma concentrations of platelet factor 4 (PF-4). Noise stimulation (100 dBA for 10 min) caused a significant increase in the diastolic (10%, p less than 0.01) and mean arterial pressures (4%, p less than 0.01) of 10 healthy male volunteers. The plasma levels of PF-4 and the venous platelet concentrations were, however, unaffected during noise exposure. The results therefore suggest that stress not accompanied by adrenal medullary activation, does not induce platelet activation.

Adrenal Medulla↗
PubMed1983

Plasma platelet factor 4: a potentially useful predictor of ischaemic heart disease?

The aim was to investigate whether plasma platelet factor 4 (PF-4) in suspected acute myocardial infarction (AMI) patients could serve as a prognostic tool and identify patients at risk for future death from AMI or ischaemic heart disease (IHD). Therefore, upon admission to our coronary care unit plasma PF-4 was measured on 109 consecutive patients. 53 of them proved to have AMI, and 50 IHD but no AMI; the remaining 6 had no evidence of IHD. 24 patients died in hospital or during the follow-up period which was an average of 16.7 +/- 2.4 months. The decreased were subgrouped into those dying of AMI (n = 16), and those dying of IHD but with no AMI (n = 8). No deaths from other causes were recorded. As compared with survivors there was a tendency towards higher PF-4 values among those who died of AMI. However, patients who during follow-up suffered death from IHD proved to have significantly (p less than 0.05) higher PF-4 levels than survivors.

Adult↗
PubMed1982

Bone marrow megakaryocytes and platelet kinetics in systemic lupus erythematosus. With special reference to corticosteroid and azathioprine therapy.

The megakaryocyte number and mean megakaryocyte area were determined in histological sections of sternal bone marrow from 26 patients with systemic lupus erythematosus (SLE). Also 20 platelet survival studies were carried out in these patients. The results were analyzed with respect to corticosteroid (CS) and CS + azathioprine (AT) therapy. The mean bone marrow megakaryocyte number as highest in untreated SLE patients, slightly lower in patients receiving CSs and lowest in those receiving CSs + AT. The difference was, however, not significant. The mean megakaryocyte areas were smallest in untreated SLE patients, slightly larger in those treated with CSs and significantly (p less than 0.05) larger in patients who received CSs + AT than in untreated patients. Platelet production rate was normal in all 3 groups of SLE patients. The results suggest that CS and AT therapy in SLE intervenes with the bone marrow megakaryopoiesis without affecting the production rate of platelets.

Adrenal Cortex Hormones↗
PubMed1982

The platelet factor 3 assay and circulating immune complexes as studied on non-thrombocytopenic patients with systemic lupus erythematosus.

Sera from 21 patients with systemic lupus erythematosus (SLE) were tested with a platelet factor 3 (PF3) assay. A control serum (pooled blood group AB serum) was always run in parallel with the test sera. The test and control sera were run in duplicate and for each patient the mean recalcification time was used for the calculation of the test serum: AB serum ratio. Concomitantly, the patients' serum concentrations of circulating immune complexes (CIC) were measured by using the Raji cell radioimmunoassay. 20 healthy hospital employees served as controls. In the latter subjects the mean test serum: AB serum ratio was 0.99 (range 0.92-1.09), their CIC concentrations being less than or equal to 16 micrograms/ml. 7 of the SLE patients had CIC values less than or equal to 16 micrograms/ml, and their test serum: AB serum ratios ranged 0.95-1.09. All the remaining SLE patients had elevated values for CIC. In the total material of SLE there was a highly significant (r = -0.87; P less than 0.001) negative correlation between the test serum: AB serum ratios and the values for CIC. It is widely held that the so-called PF3 immunoinjury test detects circulating antiplatelet antibodies. The present results, however, strongly suggest that the assay rather or also detects CIC which like antiplatelet antibodies may damage platelets as we and others have shown in prior publications.

ABO Blood-Group System↗