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D M Adcock

Publications and source records attributed to D M Adcock.

11 recordsLinked to original sources
PubMed2000

Enhanced standardization of the International Normalized Ratio through the use of plasma calibrants: a concise review.

The INR was introduced in 1983 as a means of standardizing the prothrombin time test and improving management of patients receiving warfarin-based oral anticoagulant therapy. Despite the eventual widespread use of the INR system, unacceptable levels of inter-laboratory variation persist. The use of certified plasma calibrants has been studied as a means to reducing INR variation. This review examines the pre-analytical and analytical variables contributing to INR problems. Also, the findings of several multicenter studies in which plasma calibrants were deployed are presented. Issues such as the number of calibrants used and their composition, calibrant format, plasma citrate concentration, reference thromboplastins used, methods of calibrant certification and alternative techniques for local system calibration are examined. The development of consensus guidelines on the use of plasma calibrants for INR standardization is recommended.

Calibration↗
PubMed1998

Minimum specimen volume requirements for routine coagulation testing: dependence on citrate concentration.

We evaluated the effect of sample volume and citrate concentration on results of routine coagulation assays (prothrombin time [PT] and activated partial thromboplastin time [APTT]). The study was performed on samples obtained from healthy persons and patients receiving oral anticoagulant therapy. Standard evacuated tubes (3.2% and 3.8% sodium citrate) were filled to varying total sample volumes ranging from 3.0 to 5.0 mL, and results of routine coagulation tests were compared. Underfilling may significantly affect the APTT and PT, resulting in artifactual prolongation of results. This effect is most pronounced in samples drawn into 3.8% citrate. By using 3.8% citrate, there is a statistically significant difference in the results of PT assays in the samples less than 80% filled compared with those that are 100% filled. For APTT assays performed on samples drawn into 3.8% citrate, a statistical difference occurred at less than 90% filled. This effect was less pronounced when samples were drawn into 3.2% sodium citrate. We found no statistically significant difference in PT results from a 3.2% citrate tube between fill volumes of 60% and 100% and none for APTT results between fill volumes of 70% and 100%. This study further supports the recommendation to use 3.2% sodium citrate concentration, because 60% of the optimum filled volume for PT and 70% of the optimum filled volume for APTT are acceptable.

Anticoagulants↗
PubMed1997

Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing.

The effects of 3.2% and 3.8% sodium citrate concentration on the results of routine coagulation assays (prothrombin time [PT] and activated partial thromboplastin time [aPTT]) were evaluated by means of two sets of reagents, one responsive and the other nonresponsive. Five groups were entered in the study: healthy volunteers; outpatients receiving stable oral anticoagulant therapy; and hospitalized patients receiving intravenous (i.v.) heparin therapy, both i.v. heparin and oral anticoagulant therapy, or no anticoagulant therapy. With use of nonresponsive PT and aPTT reagents, varying the citrate concentration has little clinical significance except in patients receiving i.v. heparin therapy. In contrast, when responsive PT and aPTT reagents are used, the concentration of sodium citrate anticoagulant has a significant effect on assay results. Eighteen percent of samples from patients receiving stable oral anticoagulant therapy demonstrated a change of less than 0.7 INR (International Normalized Ratio) units between citrate concentrations. Nineteen percent of patients receiving i.v. heparin therapy had a greater than 7-second difference when aPTT results were compared. These data demonstrate that citrate concentration affects the results of coagulation tests. On the basis of these data, it is recommended that 3.2% citrate be used for all coagulation tests.

Anticoagulants↗
PubMed1997

A laboratory approach to the evaluation of hereditary hypercoagulability.

The concept of hypercoagulability and especially its evaluation in the clinical laboratory has changed dramatically during the last few years. The genetic basis and the mechanisms of the various factors responsible for hypercoagulability are briefly reviewed with emphasis on the most common genetic deficiencies. The major thrust of this review centers on the cost-effective approach to examining patients with a personal or family history of venous thrombosis. Several new concepts dealing with thrombotic risk are presented with a focus on the theory that multiple factors cause thrombosis in affected patients. A proposal for a cost-effective sequential testing scheme for the accurate diagnosis of hereditary hypercoagulability is discussed. The knowledge of thrombotic risk factors is evolving rapidly, requiring the clinical laboratory to remain flexible. Ultimately, the clinical laboratory must take a leading role in the diagnosis of hereditary thrombotic disease by serving as the consultant to the primary caregiver by providing an up-to-date and cost-effective evaluation.

Antithrombin III↗
PubMed1992

Activated partial thromboplastin time reagent sensitivity to the presence of the lupus anticoagulant.

The lupus anticoagulant (LA) is an acquired abnormality that is associated with a prolonged activated partial thromboplastin time (aPTT). It is one of the most frequent coagulation abnormalities seen in the routine clinical laboratory. The sensitivity of various commercial aPTT reagents varies in their ability to detect the LA. We undertook this evaluation by using a single coagulation instrument to determine the sensitivity of five different commercial aPTT reagents to the presence of the LA. We evaluated 23 patients with known LA using five different reagents, two of which were marketed as having enhanced LA sensitivity. All samples and testing were performed under the same conditions in a timely manner. Based on these data, essentially all of the commercial reagents that were tested could detect patients with known LA by at least minimally prolonging the aPTT. Some reagents were slightly better than others in their ability to detect the LA. For most hospitals, the detection of the LA is not the highest priority for the use of the aPTT assay. In most cases, heparin anticoagulation monitoring is the most common use of the aPTT assay. Since all five reagents are sensitive to the LA, then the best overall reagent will be the one with the best sensitivity to the most important need for the laboratory (usually heparin monitoring). Therefore, a reagent should be chosen based on the primary monitoring requirements of the aPTT assay, and greater than 90% of the patients with the LA will be detected.

Female↗
PubMed1990

Hereditary dysfunctional protein C molecules (type II): assay characterization and proposed classification.

Protein C (PC) deficiency is among the increasing number of recognized causes of hereditary thrombotic disease. Two types of PC deficiency have been described: 1) Type I, which is characterized by a concomitant decrease in PC activity and antigen, and 2) Type II, characterized by disproportionately low activity compared to antigen (i.e. a dysfunctional molecule). To date, only a small number of Type II patients have been described. This study was undertaken to evaluate a number of dysfunctional PC molecules by comparing PC clotting and amidolytic activities with antigen levels. For these studies, an automated PTT-based clotting PC assay was developed. This assay was sensitive to 1% of a normal plasma pool, specific, accurate, and reproducible (+/- 12%). A good correlation (r = 0.918) of the clotting activity to antigen was found in normal individuals and Type I heterozygous and homozygous patients. To classify Type II PC deficient patients, the antigen, amidolytic and clotting PC levels were compared in ten affected families. The clotting activities were decreased in all affected members, whereas the antigen levels were within the normal limits. In four of the 10 families, the amidolytic activity was normal and similar to the antigen levels. This suggests that in certain families, defects in the PC molecule occur in regions not associated with amidolytic functions. From these studies, the molecular basis of Type II PC deficiency is varied and complex, involving different functional domains of the PC molecule. Therefore, we have suggested a nomenclature algorithm for Type II PC deficiency based on the location of the defect within the specific domains of the PC molecule.

Amides↗
PubMed1990

Dermatopathology of skin necrosis associated with purpura fulminans.

Dermal vascular skin necrosis is associated with a complex group of clinical disorders. Many of these disorders are associated with an underlying abnormality of the PC anticoagulant system or DIC, or both. The clinical appearance and histopathologic features of dermal vascular skin necrosis are similar regardless of the etiology. Acute infectious purpura fulminans is distinct in that an acute vasculitis may be present in addition to microvascular thrombosis. Skin biopsy is a valuable diagnostic tool in the early recognition of these clinical disorders, since skin involvement is frequently an early manifestation of the disease process. Prompt recognition and institution of appropriate therapy at the reversible stages of dermal vascular thrombosis will, it is hoped, reduce the morbidity and mortality currently associated with skin necrosis and purpura fulminans.

Heparin↗
PubMed1990

Proposed classification and pathologic mechanisms of purpura fulminans and skin necrosis.

The syndromes of purpuric lesions associated with a thrombotic mechanism are very rare in the general population. Dermal vascular thrombosis, however, can be devastating and associated with significant morbidity and mortality. These syndromes share common features in their clinical course, pathogenesis, and histology. Although these syndromes can be initiated by either the hemostatic or inflammatory pathways, both pathways center around perturbations of the endothelial cell, which promote thrombosis. If animal models or better testing can be developed, enhanced appreciation of mechanisms underlying purpura fulminans may be deduced. Characterization of the pathophysiology may then allow directed treatment modalities that could limit the course of these syndromes and reduce morbidity and mortality.

Endothelium, Vascular↗
PubMed1990

Mycotic pseudoaneurysm of the thoracic aorta with purulent pericarditis.

Mycotic pseudoaneurysms are vascular lesions composed of laminated clot and fibrous tissue and containing bacterial microorganisms. The case reported here it the third in the English literature to describe the association of purulent pericarditis with rupture of a mycotic aortic aneurysm. A 65-year-old male developed cardiac tamponade secondary to Staph. aureus pericarditis. Following a surgical procedure to drain the pericardial sac, the postoperative course was complicated by fatal hemorrhage from a ruptured thoracic pseudoaneurysm. Postmortem examination indicated that the aortic pseudoaneurysm originated at the site of an ulcerated atherosclerotic plaque. A Staph. aureus infection of the aortic lesion, with erosion into the pericardial space, was the apparent cause of purulent pericarditis.

Aneurysm, Infected↗
PubMed1989

Clinical evaluation of protein C: a comparative review of antigenic and functional assays.

Thromboembolic disease is a major complication of protein C (PC) deficiency, which is among the increasing number of recognized causes of hereditary thrombotic disease. The laboratory evaluation of PC is of the utmost importance in the accurate diagnosis of this deficiency. In this review, we describe the various types of clinical antigenic and activity assays of PC. The attributes of each type of assay are discussed, as well as the value of each assay in diagnosing the various acquired and hereditary deficiencies of PC. This basic review is intended for laboratories planning to institute PC assays.

Antigens↗