PubMed Health⌕ Search

Biomedical subjects

F E Preston

Publications and source records attributed to F E Preston.

At least 199 records · Page 11Linked to original sources
PubMed1984

Protein C, an anticoagulant protein, is increased in healthy volunteers and surgical patients after treatment with stanozolol.

On both oral and intramuscular administration, the anabolic steroid stanozolol was found to increase protein C antigen concentrations in circulating blood. In fourteen healthy young volunteers (who received stanozolol orally, dose 10 mg/day) the average increase was 1.5-1.6 times the normal concentrations after 3-6 weeks' treatment and was accompanied by more moderate increases in the other vitamin K-dependent factors II, IX and X to 1.4, 1.4 and 1.2 times their normal concentration respectively. However, there was no change in factor VII. In sixteen elderly surgical patients, intramuscular injection (50 mg) one day prior to surgery induced a moderate increase within 24 hours (to 1.11 times the pretreatment concentration) and seven days after operation (to 1.19 times), and reduced the postoperative fall in protein C. Stanozolol administration seems to be a promising pharmacological method for increasing anticoagulant protein C levels in congenital and acquired deficiencies.

Adult↗
PubMed1984

Near-normal glycaemic control does not correct abnormal platelet reactivity in diabetes mellitus.

The effect of improved glycaemic control, effected by 16 weeks continuous subcutaneous insulin infusion (CSII), on platelet aggregation and platelet prostaglandin biosynthesis has been assessed in a group of 11 diabetic patients with painful peripheral neuropathy. Before CSII and compared with results obtained on samples from age- and sex-matched control subjects, there was enhanced reactivity of the platelets from diabetic patients to ADP, collagen and sodium arachidonate (NaAA). There was also increased thromboxane B2 (TXB2) production after platelet stimulation by NaAA. In contrast, collagen-induced thromboxane production by platelets from diabetic patients was significantly less than that of platelets from controls. Treatment by CSII resulted in a statistically significant improvement in glycaemic control and this was maintained for the 16 week period of the study. At 16 weeks and in the presence of near-normal glycaemic control, the enhanced platelet reactivity in response to collagen and NaAA persisted and that to ADP was further increased. Collagen-induced thromboxane production was, however, corrected by CSII.

Adenosine Diphosphate↗
PubMed1984

The effect of beta-adrenoceptor antagonists on the pharmacokinetics and pharmacodynamics of warfarin after a single dose.

The effects of three beta-adrenoceptor antagonists (propranolol, metoprolol and atenolol) on the serum kinetics and pharmacodynamics of warfarin given in a single oral dose (15 mg) were studied in six normal subjects. At the same degree of beta-adrenoceptor blockade, as assessed by the decrease of exercise tachycardia, propranolol increased the area under the serum warfarin concentration time curve (AUC) by 16.3 +/- 14.2 s.d.% (P less than 0.01) and the maximum serum warfarin concentration by 23.0 +/- 14.3 s.d.% (P less than 0.001). Atenolol increased the maximum serum warfarin concentration by 12.5 +/- 12.3% s.d. (P less than 0.05) but was without effect on warfarin AUC. Metoprolol had no effect on warfarin kinetics. The extent of changes in the prothrombin time and the plasma clotting Factor VII activity caused by warfarin were not altered by any of the beta-adrenoceptor antagonists.

Adult↗
PubMed1984

The platelet defect in acute myeloid leukaemia.

In a study of platelets from 13 patients with acute myeloid leukaemia abnormal aggregation and release reactions were found. A previously unrecognised quantitative defect of thromboxane B2 production may, at least in part, explain these findings. In contrast to a previous report, we were unable to show a convincing storage pool defect in these platelets. The platelet membrane glycoproteins were largely normal.

Adenosine Diphosphate↗
PubMed1983

The use of dichloromethylene diphosphonate for the management of hypercalcaemia in multiple myeloma.

We have assessed the effects of the diphosphonate, dichloromethylene diphosphonate (Cl2MDP), in 19 patients with hypercalcaemia and increased bone resorption due to myeloma. Cl2MDP (800-3200 mg daily by mouth or 300 mg daily by intravenous infusion) decreased plasma calcium and biochemical indices of increased bone resorption in 16 of 19 patients. This effect persisted for the duration of treatment (up to 14 weeks). Prolonged treatment was associated with a progressive rise in serum alkaline phosphatase and only a transient fall in hydroxyproline suggesting the stimulation of bone repair. Since myeloma is associated with significant morbidity and mortality due to progressive bone loss, these results suggest that long-term treatment of myeloma with Cl2MDP is worthy of further study.

Aged↗
PubMed1983

Acquired von Willebrand's disease: demonstration of a circulating inhibitor to the factor VIII complex in four cases.

We have studied four patients suffering from acquired von Willebrand's disease. All patients had a severe bleeding diathesis with recurrent life-threatening haemorrhages. Three of the patients had a monoclonal gammopathy and one of these developed multiple myeloma. In three patients tested, a plasma inhibitor to ristocetin cofactor activity was detected. In each case this was localized to the IgG fraction of plasma. In addition, VIII:C activity was found to be associated with the IgG fraction of patients' plasma and altered mobility of VIII:C was detected on Laurell immunoelectrophoresis. Furthermore, plasma from all four patients and the IgG fraction therefrom resulted in a dissociation of normal VIII:C into two components separable by gel-filtration on Sepharose 6B. Finally the circulating half-life of the three factor VIII activities was found to be markedly reduced in the patients with acquired von Willebrand's disease. We conclude that in the patients studied the coagulation defect was related to the presence of a circulating inhibitor to the factor VIII complex and that this inhibitor was associated with the IgG fraction of plasma.

Aged↗
PubMed1983

Haemorrhage and factor IX deficiency in pituitary insufficiency.

Acquired isolated factor IX deficiency is rare. A case presenting with haemorrhage after dental extraction is described. The factor IX deficiency was associated with pituitary insufficiency and was completely corrected following the administration of thyroxine. This contrasts with a previously reported case in which both thyroxine and cortisone were required for complete correction of the factor IX deficiency. The underlying mechanism and the consequences are briefly discussed.

Hemophilia B↗
PubMed1983

Computed tomography: qualitative and quantitative recognition of liver disease in haemophilia.

Thirty haemophiliac patients have been investigated by computed tomography (CT). Quantitative studies using dual energy scans with and without contrast enhancement, together with autocorrelation function analysis of the characteristics of the liver and spleen, revealed significant changes in the liver. The CT findings corresponded to the presence of liver disease, including chronic active hepatitis and cirrhosis, in 13 patients confirmed by percutaneous liver biopsy.

Hemophilia A↗
PubMed1982

A study of the stimulation of human venous prostacyclin synthesis by dipyridamole.

The synthesis of prostacyclin by human venous tissue in vitro and the effects of aspirin and dipyridamole thereon were investigated. Dipyridamole significantly stimulated prostacyclin production in a concentration range of 25 to 100 microM. Dipyridamole significantly attenuated the inhibitory effect of 0.1 mM aspirin in a concentration range of 12.5 to 100 microM. Isobutylmethylxanthine 0.1 mM, an unrelated inhibitor of phosphodiesterase, had similar effects to dipyridamole. Cyclic AMP 3.0 mM had an inhibitory effect on prostacyclin synthesis in the presence of dipyridamole. Adenosine 0.1 mM and nitrobenzylthioguanosine 0.1 mM, an inhibitor of adenosine uptake, did not significantly influence prostacyclin synthesis in this system. We conclude that the stimulation of prostacyclin synthesis by dipyridamole is unrelated to the ability of this drug to block the high-affinity uptake of adenosine by endothelial cells and that the effect may also be independent of changes in the concentration of cAMP induced by the drug.

Aspirin↗
PubMed1982

Low-dose aspirin inhibits platelet and venous cyclo-oxygenase in man.

In a group of normal subjects we have compared rates of recovery of venous prostacyclin (PGI2) and platelet thromboxane B2 (TXB2) production after a single 300 mg dose of aspirin. Marked inhibition of both venous PGI2 synthesis and platelet TXB2 synthesis persisted for the 72 hours duration of the study. We also examined the effect of four daily doses of 40 mg aspirin on platelet and vessel wall prostaglandin biosynthesis. This produced a cumulative inhibitory effect on TXB2 production with 98.6 per cent mean inhibition at 72 hours. At this time 81-100 per cent inhibition of PGI2 was demonstrated in the four subjects studied. We conclude that the cyclo-oxygenase enzyme in human vein is sensitive to inhibition by very low doses of aspirin. No evidence was found to substantiate the view that rapid recovery of vessel wall cyclo-oxygenase activity occurs after inhibition by a single dose of aspirin.

Aspirin↗
PubMed1982

Plasma 6-keto-prostaglandin F1alpha: fact or fiction.

A radioimmunoassay for 6-keto-prostaglandin F1alpha was developed and validated. The apparent concentration of 6-keto-prostaglandin F1alpha in human venous plasma was found to be less than 50 pg/m1. A rise in plasma 6-keto-prostaglandin F1alpha was detected on infusion of prostacyclin or of DDAVP in human subjects. Various methods of organic extraction were applied to plasma samples prior to radioimmunoassay. Organic extraction and silicic acid chromatography introduced marked and unacceptable nonspecific interference on subsequent radioimmunoassay. This interference was abolished by high pressure liquid chromatography of eluates and extracts prior to assay. Using these methods, a very low concentration of 6-ketoprostaglandin F1alpha in human venous plasma was confirmed.

6-Ketoprostaglandin F1 alpha↗