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Biomedical subjects

C Sparling

Publications and source records attributed to C Sparling.

6 recordsLinked to original sources

Preparation of hydrogen from water by reduction with lithium aluminium hydride for the analysis of delta(2)H by isotope ratio mass spectrometry.

An off-line technique is described for the preparation of H(2) from water prior to analysis of delta(2)H by dual-inlet isotope ratio mass spectrometry. H(2) is produced from sample water by reaction with LiAlH(4). This provides a rapid and inexpensive method for the analysis of delta(2)H in small (10 microL) samples of water. Precision was +/- 4.2 to 8.0 (1sigma(n), n = 8) delta(2)H(VSMOW) for samples between 428 and 1500 delta(2)H(VSMOW), +/- 14.5 delta(2)H(VSMOW) for water enriched to 3750 delta(2)H(VSMOW) and +/- 26.0 delta(2)H(VSMOW) for water enriched to 6100 delta(2)H(VSMOW). Accuracy was +/- 1.1 to 4.2 delta(2)H(VSMOW) for water standards from natural abundance to 1000 delta(2)H(VSMOW) (the highest enrichment at which water of accepted delta(2)H is currently available). This method for delta(2)H determination is most appropriate for use with small (<50 microL) samples of high delta(2)H enrichment such as those produced from doubly labelled water studies of small animals. The levels of measurement precision of delta(2)H would contribute 2.6-3.8% to the precision error in estimates of small animal energy expenditure made using the doubly labelled water technique when duplicate analyses are performed.

Aluminum Compounds↗

The influence of developmental haemostasis on the laboratory diagnosis and management of haemostatic disorders during infancy and childhood.

The physiology of the hemostatic system in children is different from that in adults. Reference ranges for components of the hemostatic system are age dependent. During early childhood, physiologic values may overlap with values observed in congenital deficiencies of acquired pathological conditions. Physiologically decreased plasma concentrations of hemostatic components also influence the response to antithrombotic therapy. The relevance of developmental hemostasis for the laboratory diagnosis and management of hemorrhagic and thrombotic disorders during childhood is discussed.

Adolescent↗

Acquired von Willebrand factor deficiency during high-dose infusion of recombinant factor VIII.

Constant infusion of factor VIII (FVIII) into patients with haemophilia A after major surgery has been recommended as optimal treatment to avoid peaks and valleys in the circulating levels of FVIII and to allow the use of much lower doses of FVIII than are historically required. One of our young patients with severe (< 0.01 U/ml FVIII) haemophilia suffered a subdural haematoma for which he received treatment with 815190 recombinant FVIII (rFVIII) units over a period of 52d. 2 weeks after admission, because of low FVIII levels and the presence of FVIII inhibitors, the infusion rate was increased to > 100 U/kg/h for 14d. During this time the FVIII level fluctuated between 0.6 and 4.2 U/ml. For some period it was not possible to detect ristocetin co-factor activity in this patient's plasma and the von Willebrand factor (VWF) level and VWF multimer pattern resembled those of a patient with von Willebrand's disease. Subsequently, when the rFVIII dose was increased 2-fold, this was not reflected by the plasma level of FVIII although antibodies were not detected. The data suggest that the prolonged infusion of very high levels of rFVIII which is deficient in von Willebrand factor can result in depletion of VWF from existing stores, producing a laboratory picture which is consistent with the diagnosis of von Willebrand's disease. Further, in the absence of complexing with VWF, FVIII appears to be cleared from the circulation at an increased rate. This is expensive and potentially compromising. Therefore, when administering very high doses of FVIII concentrates devoid of VWF for prolonged periods of time, ristocetin cofactor and VWF levels should be monitored.

Factor VIII↗

Hypoprothrombinemia in childhood systemic lupus erythematosus.

Three children with systemic lupus erythematosus who developed hemorrhagic tendencies as a consequence of a clotting factor II (prothrombin) deficiency are described. All three responded rapidly to treatment with corticosteroids. A literature review added 25 case reports, with the following findings. First, factor II deficiency occurs in the presence of the lupus anticoagulant, although the interrelationship between the two is not understood. Second, the deficiency is presumed to be secondary to rapid clearing of the antigen/antibody factor II complex in the liver. Finally, most cases respond to corticosteroid therapy with or without the coadministration of vitamin K or fresh frozen plasma. In corticosteroid-dependent patients, the addition of antimetabolites such as azathioprine has enabled reduction in steroid doses.

Adolescent↗

Inherited bleeding disorders.

Congenital bleeding disorders comprise a heterogeneous group of diseases that reflect abnormalities of blood vessels, coagulation proteins and platelets. Studies of these diseases, many of which are rare and several of which result in a mild bleeding diathesis only, have significantly increased our understanding of normal haemostasis. Two lessons have been learned. First, quantitative abnormalities of coagulation proteins and platelets are an important, but not the only, cause of significant haemorrhage; some cases of inherited bleeding disorders reflect synthesis of a dysfunctional coagulation protein or production of abnormal platelets. Diagnostic tests that reflect qualitative abnormalities are therefore important in the evaluation of selected patients with inherited bleeding disorders. Second, in occasional patients the inherited disorder is complex and reflects combined abnormalities of coagulation proteins alone or in association with platelet disorders. In clinical practice it is useful to distinguish disorders that cause significant clinical bleeding from those that cause few or no symptoms. Examples of the former include severe deficiencies of factors VIII and IX, and the homozygous forms of factor II, V, VII, X, XI, XIII, fibrinogen and von Willebrand factor. Comparable platelet disorders include the inherited thrombocytopenias with platelet counts less than 20 x 10(9) litre-1 and the homozygous forms of Bernard-Soulier syndrome and Glanzmann's thrombasthenia. The most frequently encountered mild haemostatic abnormalities include type I von Willebrand's disease, the platelet storage pool deficiency syndromes and the mild and moderate forms of haemophilia A and B; occasionally heterozygous or homozygous forms of the rarer coagulation disorders, e.g. factor XI deficiency, may present with a mild bleeding diathesis. Finally, some disorders are entirely asymptomatic, e.g. factor XII deficiency and deficiencies of other contact coagulation factors. Management of patients with inherited bleeding disorders should reflect knowledge of the specific disorder to be treated plus careful consideration of the clinical circumstance for which therapy is proposed. In all cases, once a decision to treat has been made, the safest efficacious therapy should be given (for example DDAVP in the treatment of patients with mild haemophilia A or type I von Willebrand's disease). Although blood products are now much safer and the risk of blood transmitted viral infections is low, there still remains a risk that transfusion of any blood product may be associated with serious side-effects. As a result, therapy should be given only after careful consideration of the risk: benefit ratio and not merely to treat an abnormal laboratory result.(ABSTRACT TRUNCATED AT 400 WORDS)

Afibrinogenemia↗

A variant form of Bernard-Soulier syndrome: mild haemostatic defect associated with partial platelet GPIb deficiency.

Platelets from patients with Bernard-Soulier syndrome (BSS) are larger than normal and demonstrate characteristic aggregation abnormalities. A molecular defect involving platelet membrane glycoproteins has been established as the primary abnormality, and the major defect is described as an absence of GPIb, the receptor for von Willebrand factor, which prevents the adhesion of BSS platelets to damaged endothelium. Associated deficiencies of GPV and GPIX are also recognized. The overall clinical effect is a haemorrhagic tendency which, although variable, is severe at times in all patients. We report a child who presented with the typical morphological and aggregation abnormalities associated with BSS, but who had negligible bleeding problems. Further investigation revealed a significant but incomplete deficiency of GPIb and of GPV and GPIX. This case suggests that BSS may be a heterogeneous disorder with clinical consequences dependent on the extent and complexity of the platelet membrane glycoprotein deficiency.

Bernard-Soulier Syndrome↗