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Biomedical subjects

R G Malia

Publications and source records attributed to R G Malia.

At least 37 records · Page 2Linked to original sources
PubMed1988

Anticardiolipin antibodies in systemic sclerosis: immunological and clinical associations.

Anticardiolipin antibodies of IgG/IgM class were detected in seven of 28 patients with systemic sclerosis including five of 16 patients severely affected by extensive visceral disease. This severely affected sub-group also showed significant elevations of plasma levels of von Willebrand factor antigen in 10 cases and serum C1q binding activity in seven cases respectively. This triple association raises the possibility that multiple immunological mechanisms are involved in the pathogenesis of systemic sclerosis and its vascular lesions.

Adult↗
PubMed1987

Demonstration of abnormal factor VIII multimers in acquired von Willebrand's disease associated with a circulating inhibitor.

We have studied the factor VIII multimeric structure in four patients with acquired von Willebrand's disease associated with a circulating inhibitor to the factor VIII complex. In three of the four patients tested, the high and medium molecular weights bands were absent when assessed by sodium dodecyl sulphate-agarose electrophoresis. Plasma from the fourth patient contained all the factor VIII multimeric forms, although the high molecular weight bands were markedly decreased in concentration. Intravenous infusion of 1-deamino-(8-D-arginine)-vasopressin (DDAVP) resulted in the appearance of a full complement of multimers in the plasma of the two patients tested. This response was, however, transient and a return to pre-infusion multimeric composition occurred within 2-4 h. In the patients studied, an inhibitor to the factor VIII complex has induced an acquired variant von Willebrand's disease which transiently corrects after the infusion of DDAVP.

Deamino Arginine Vasopressin↗
PubMed1986

Changes in plasma osteocalcin concentration following treatment with stanozolol.

Treatment of healthy, adult, human volunteers with stanozolol, 5 mg twice daily, for six weeks caused a marked elevation in circulating levels of osteocalcin. Plasma osteocalcin concentrations did not fall to pretreatment values for a period in excess of four weeks after the cessation of treatment but remained similar to levels whilst on treatment. At the same time, as the rise in plasma osteocalcin was seen, plasma alkaline phosphatase activity fell; however, in this case, a return to pretreatment levels occurred within four weeks of treatment ending. These data demonstrate that stanozolol has a detectable effect on the plasma concentration of a protein thought to be a marker of osteoblast activity, and that this effect continues for a period after treatment has been discontinued.

Adult↗
PubMed1986

Abnormal vitamin K metabolism in the presence of normal clotting factor activity in factory workers exposed to 4-hydroxycoumarins.

The case histories of two patients exposed to the novel anticoagulants brodifacoum and difenacoum are reported. Abnormal vitamin K1 metabolism, as indicated by elevated vitamin K1 2,3-epoxide plasma concentrations after i.v. administration of vitamin K1, could be detected for more than 18 months after exposure to the anticoagulants. There was a marked prolongation of prothrombin time (greater than 50 s) in both cases, at the time of exposure. However, subsequent haematological investigations (prothrombin time and vitamin K-dependent clotting factor activity) have been shown to be normal in both cases for at least 18 months. These cases confirm the long-acting nature of brodifacoum and difenacoum and present an apparent dissociation between the effect of coumarin anticoagulants on vitamin K1 metabolism and clotting factor activity.

4-Hydroxycoumarins↗
PubMed1984

Stanozolol-induced changes in fibrinolysis and coagulation in healthy adults.

The effect of orally-administered stanozolol, 5 mg b.d. on fibrinolysis, coagulation and on various haematological and biochemical parameters have been studied in 16 healthy adults, 8 males and 8 females. Statistically significant enhancement of extrinsic (tissue-type) plasminogen activator activity was detected in all subjects studied. This was associated with significant increases in plasma plasminogen and a concomitant reduction in histidine-rich glycoprotein. There were no changes in plasma urokinase activity. Changes in the coagulation system included significant reduction in plasma fibrinogen and elevation of protein C and antithrombin III. Changes in plasma lipids included significant reduction of HDL cholesterol associated with an increase in LDL triglycerides. No change occurred in total cholesterol. There were no major differences between the sexes, nor were there serious side effects. The effects of stanozolol on extrinsic (tissue-type) plasminogen activator activity, "free" plasminogen, protein C and antithrombin III, argue strongly in favour of its therapeutic potential.

Adult↗
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

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↗
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↗
PubMed1980

Evidence against vitamin K deficiency in normal neonates.

Umbilical cord plasmas from 24 normal full-term neonates were studied. We confirmed the prolonged prothrombin time and low levels of Vitamin K dependent clotting factors previously described (1), but using a number of recently developed immunological and coagulation techniques we could find no evidence of vitamin K deficiency. We conclude that the decreased levels of vitamin K dependent clotting factors of normal neonates are the result of decreased synthesis by the immature liver and that it is questionable whether vitamin K prophylaxis is necessary for these infants.

Blood Coagulation Factors↗
PubMed1977

Heparinised clotting factor concentrates in patients with Christmas disease and liver disease.

Evidence has been sought of activation of the coagulation system in two groups of patients following the infusion of two heparinised clotting factor concentrates. No changes were detected in 13 patients with mild hepatic dysfunction. In six studies on patients with Christmas disease induced abnormalities occurred in only one. Activation of the coagulation mechanism did not occur in another individual who had received the same batch of material.

Blood Cell Count↗
PubMed1975

Serial changes in the coagulation system following clotting factor concentrate infusion.

Various parameters of the coagulation system have been monitored in patients with Christmas disease following the infusion of clotting factor concentrates. Significant reduction of clotting factor VIII and serum antithrombin III were observed in each of the five studies, whilst the plasma fibrinogen level fell in four subjects. The induced abnormalities were shortlived and there were no clinical sequelae. Further studies are required to assess the effects of similar concentrates in patients with liver disease.

Antithrombins↗
PubMed1974

Essential thrombocythaemia and peripheral gangrene.

Six patients are described in whom gangrene of one or more toes occurred as the presenting feature of essential thrombocythaemia. Spontaneous platelet aggregation was observed in platelet-rich plasma from four patients and platelet aggregation after the addition of adenosine diphosphate and collagen was highly abnormal in samples from all six. All of the patients described dramatic relief of pain within six hours of ingestion of aspirin and this coincided with disappearance of the spontaneous platelet aggregation and collagen-induced platelet aggregation. Treatment with phosphorus-32 corrected the platelet count and there were no further recurrences of peripheral vascular disease. Platelet function tests performed at the time all gave normal results. It is concluded that essential thrombocythaemia is an important and treatable cause of peripheral vascular disease.

Adenosine Diphosphate↗
PubMed1974

Disseminated intravascular coagulation as a consequence of cerebral damage.

Three cases with intracranial lesions developed evidence of disseminated intravascular coagulation which was confirmed at necropsy. The factors engendering this state, including release of potent thromboplastin from neural tissue are discussed and the danger of this intermediary mechanism of disease increasing the mortality of intracranial disease is demonstrated. Careful haematological investigation of all patients with intracranial disease is therefore advised, especially if they manifest evidence of a bleeding tendency.

Adult↗
PubMed1973

Intravascular coagulation and E. coli septicaemia.

Eight patients with E. coli septicaemia had oliguric renal failure which was associated with haematological evidence of intravascular coagulation. Five of these patients also had the characteristic blood picture of microangiopathic haemolytic anaemia. In an attempt to prevent further deposition of fibrin, intravenous heparin was administered to six patients, three of whom recovered fully and three died. The diagnosis of intravascular coagulation was subsequently confirmed by histological examination of necropsy material and it is suggested that some of the complications of E. coli septicaemia may be attributable to disseminated intravascular coagulation.

Anemia, Hemolytic↗