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Biomedical subjects

W R Swaim

Publications and source records attributed to W R Swaim.

At least 19 recordsLinked to original sources

Laboratory and clinical evaluation of white blood cell differential counts. Comparison of the Coulter VCS, Technicon H-1, and 800-cell manual method.

Eight hundred-cell manual white blood cell differential count evaluations of Coulter VCS and Technicon H-1 included estimates of accuracy, imprecision, random and systematic errors, clinical relevance, and detection of immature neutrophils. Accuracy was acceptable, except for H-1 testing of monocytes. Instrument imprecision was similar, except for tighter monocyte values as measured by the VCS. Deming regression determined random errors were greater for H-1 monocytes and proportional errors were similar. Constant errors for the VCS were less than the H-1 for neutrophils and monocytes and greater than the H-1 for eosinophils and lymphocytes. H-1 morphologic false-negative rates were twice those for VCS. True-positive and false-negative rates in cases with immature neutrophils were 70.6% and 20.3% for the VCS and 35% and 55.9% for the H-1. The reference false-positive rate was 4.4%. Clinically appropriate VCS flags were generated in distributionally abnormal cases. Predictive values were higher for the VCS.

Cell Survival

Factor XI deficiency: genetic and clinical studies of a single kindred.

A four-generation 25-member kindred with Factor XI:C deficiency is reported. Factor XI:C levels in heterozygotes varied from 15 to 58%, suggesting that Factor XI:C values for homozygote determination should be less than 15%. The frequency of bleeding was not correlated with Factor XI:C levels in this range. Individuals with joint pain had significantly lower Factor XI:C levels than members without joint pain and pain occurred more frequently in frequent bleeders. Lod scores showed no close genetic linkage of Factor XI:C deficiency with blood group MNSs (chromosome 4), complement components Bf and C4B (chromosome 6), or blood group P.

Adult

Structural features of endotoxin required for stimulation of endothelial cell tissue factor production; exposure of preformed tissue factor after oxidant-mediated endothelial cell injury.

Cultured human umbilical vein endothelial cells synthesize the procoagulant, tissue factor, after exposure to bacterial endotoxin. Wild-type lipopolysaccharide from Escherichia coli 0127:B8 stimulates a five- to 20-fold increase in cellular tissue factor. Similarly, rough or incomplete lipopolysaccharide subunits from mutant bacterial strains, or lipid A prepared by mild acid hydrolysis of whole endotoxin, are also stimulatory. In addition, a lipid A biosynthetic precursor, consisting of a phosphorylated glucosamine disaccharide substituted with four beta-hydroxymyristoyl residues, is stimulatory at nanomolar concentrations. Endothelial cell tissue factor is not detectable on the surface of undisrupted cells, but can activate clotting on the cell surface after oxidant-mediated cell injury. The procoagulant, tissue factor, is synthesized by endothelial cells after stimulation mediated by a moiety contained within the lipid A region of lipopolysaccharide. Exposure of clotting factors at the endothelial cell surface after cell injury suggests a mechanism for the microvascular thrombosis associated with disseminated intravascular coagulation with sepsis.

Cells, Cultured

Budd-Chiari syndrome in a patient with the lupus anticoagulant.

Lupus anticoagulant is an immunoglobulin that interferes with prothrombin conversion to thrombin and is manifested biochemically by prolongation of the partial thromboplastin time. Paradoxically, bleeding is rare in association with this anticoagulant, and deep leg vein thromboses, pulmonary emboli, and cerebrovascular accidents have been described in patients with this clotting inhibitor. This report describes the first case of Budd-Chiari syndrome associated with the lupus anticoagulant. The patient presented with abdominal pain and massive ascites. The Budd-Chiari syndrome was confirmed by liver biopsy and venography. No medical condition known to predispose to an increased thrombotic tendency could be identified, and the presence of the lupus anticoagulant in the patient's plasma may provide an explanation for his hypercoagulability and development of the Budd-Chiari syndrome.

Adult

Measurement of canine von Willebrand factor using ristocetin and Polybrene. Diagnosis of canine von Willebrand's disease.

Dogs with VWD provide useful models for the study of the factor VIII complex. However, the study of canine VIIIR:WF has been hampered by the lack of a routine plasma assay for canine RCF, an activity that is usually used as a measure of VIIIR:WF. This study shows that canine plasma can be assayed for RCF with a macroscopic tilt-tube method using formalin-fixed human platelets, ristocetin, and extra canine albumin (5.0 mg/ml) to prevent plasma precipitation. An assay was also developed for canine plasma PBCF, an activity that is closely related to RCF. In 45 normal canine plasmas, VIII:C was not correlated with RCF, PBCF, or VIIIR:AG. However, RCF, PBCF, and VIIIR:AG were well correlated with each other. In 26 canine VWD plasmas, VIII:C was frequently normal, whereas VIIIR:AG, RCF, and PBCF were almost always deficient. The patterns of VIIIR:AG, RCF, and PBCF deficiencies in the canine VWD plasmas suggested that some canine breeds have a "classic" form of VWD whereas other breeds have "variant" forms of disease.

Animals

Acquired von Willebrand's disease, platelet-release defect and angiodysplasia.

A previously healthy elderly man with gastrointestinal bleeding was found to have criteria for von Willebrand's disease. The late clinical onset of the disorder and negative family studies suggest that the von Willebrand's disease may be acquired. The findings in the patient were similar to the abnormalities reported in the small number of other patients thought to have acquired von Willebrands disease. An inhibitor of factor VIII could not be demonstrated in this patient. This patient also had platelet aggregation abnormalities that are atypical for patients with congenital or acquired von Willebrand's disease. Vascular abnormalities were also found in this patient and in several other previously described patients with von Willebrand's disease.

Adenosine Diphosphate

IgM pyroglobulinemia with erythrocytosis presenting as hyperviscosity syndrome. I. Clinical features and viscometric studies.

The hyperviscosity syndrome is described in a patient with erythrocytosis and an immunoglobulin M with kappa light chain (IgMK) macroglobulinemia. Viscometric studies were carried out on whole blood and demonstrated the contribution of both the increased hematocrit value and the macroglobulinemia to the whole blood viscosity. Clinical improvement followed phlebotomy and was accompanied by a decrease in whole blood viscosity. Continued treatment with chlorambucil has been associated with a long symptom-free period. The macroglobulin was characterized as a monoclonal IgMK pyroglobulin which retained its thermoprecipitability was reduced to 7S monomers. The presence of IgMK aggregates in the serum may have contributed to the increase in blood viscosity.

Aged

Disseminated intravascular coagulation in the urologic patient.

Gram-negative septicemia and metastatic prostatic cancer are frequent causes of disseminated intravascular coagulation. The clinical manifestations of this condition as well as the laboratory data vary considerably, depending on the patient's compensatory mechanisms in relation to the magnitude and duration of the thromboplastin or endotoxin release. Treatment centers primarily on correcting the underlying disorder. Secondly, deficient clotting factors and platelets should be replaced in the appropriate patient. Heparinization is often unnecessary. The use of drugs that inhibit the protective fibrinolytic mechanism is contraindicated in disseminated intravascular coagulation.

Adenocarcinoma

Urine concentration and dilution: effect on red cell survival.

Survival time of 51Cr-labeled red cells was determined in dogs subjected to water restriction excreting concentrated urine and again following a 6-week period of ad lib. water intake. During water restriction, RBC survival was reduced to one-seventh of normal. In rats with untreated diabetes insipidus, 51Cr RBC survival was reduced 30% as compared to the pitressin-treated state. It appears that RBC survival may be influenced by osmotic stress associated with the state of urine concentration and dilution.

Animals