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Biomedical subjects

J Kizer

Publications and source records attributed to J Kizer.

10 recordsLinked to original sources
PubMed1996

Vertebrobasilar thrombosis associated with nonpenetrating cervical spine trauma.

Vertebral artery injuries associated with blunt trauma to the cervical spine are rare. Five cases of vertebrobasilar complications after blunt trauma to the cervical spine are reported. Four were involved in motor vehicle accidents, and one suffered a diving injury. All of these patients had documented cervical spine fractures. For two patients, the diagnosis of vertebral artery thrombosis was made on the basis of magnetic resonance angiography (MRA), and for the remaining three, cervical four-vessel arteriograms (CFVAs), were used. All the patients had occlusion of flow in either the vertebral artery or in the vertebrobasilar circulation. The patients presented with acute, non-specific changes in neurological status. Two patients had infarctions in the vertebrobasilar tertiary, one had an infarction in the middle cerebral artery territory, and two did not show evidence of cerebral infarction. Three of the patients were treated with anticoagulants. Of these, two showed a stabilization of their neurological status, and one died. The four surviving patients improved with early physical and occupational therapy. Although CFVA remains the "gold standard" for diagnosing these injuries, newer modalities, such as MRA, may be useful adjuncts. Early stabilization of the cervical spine injury and anticoagulation are beneficial.

Accidents, Traffic↗
PubMed1992

Postfiltration factor VIII and fibrinogen levels in cryoprecipitate stored at room temperature and at 1 to 6 degrees C.

The 13th edition of the standards of the American Association of Blood Banks specified storage at 1 to 6 degrees C for cryoprecipitated anti-hemophilic factor (Cryo) administered up to 6 hours after thawing if the Cryo is used for factor VIII (FVIII) content (Standard J4.210). Previous editions specified room-temperature (RT) storage for up to 6 hours. Currently, the temperature specification has been deleted. There are few data addressing the optimal storage temperature and maximum storage time for FVIII and fibrinogen in thawed Cryo. Thirty bags of Cryo were assayed for FVIII and fibrinogen. Each bag was divided into two aliquots; one was stored at RT and the other at 1 to 6 degrees C. Assays were performed immediately after thawing (Base) and 6 and 24 hours after thawing, respectively. All samples were filtered through 200-mu blood component infusion sets before assay. Three hundred analyses were performed, 150 each for FVIII and fibrinogen by conventional clotting technique. Data were analyzed by using a paired t test. Cryo stored at 1 to 6 degrees C for 6 and 24 hours showed an FVIII loss of 35 percent (p less than 0.0001) and 63 percent (p less than 0.0001), respectively. Cryo stored at RT for 6 and 24 hours had an FVIII loss of 8 percent (p greater than 0.05) and 20 percent (p less than 0.0001). Cryo stored at 1 to 6 degrees C for 6 and 24 hours had a fibrinogen loss of 20 percent (p less than 0.0001) and 43 percent (p less than 0.0001). Cryo stored at RT for 6 hours had no fibrinogen loss and a 2 percent loss at 24 hours (p greater than 0.05). These preliminary data show a significant loss of FVIII and fibrinogen activity in Cryo stored at 1 to 6 degrees C and filtered before assay. The FVIII and fibrinogen activity at RT is clearly maintained up to 6 hours after thawing.

Blood Coagulation Tests↗
PubMed1991

Platelet dysfunction in Noonan's syndrome. A case with a platelet cyclooxygenase-like deficiency and chronic idiopathic thrombocytopenic purpura.

Individuals with Noonan's syndrome are likely to have one or more coagulation abnormalities: complex platelet function defects, partial Factor XI deficiency, or von Willebrand's disease. A distinctive platelet function defect has not been identified. The authors describe a 24-year-old women with Noonan's syndrome, chronic idiopathic thrombocytopenic purpura (ITP), and a platelet function defect characterized by a greater than 15-minute bleeding time, failure of aggregation and release with 10 microM ADP, 10 microM epinephrine, 750 microM arachidonic acid or 0.019 g/L collagen. A mixture of aspirin-treated platelets with the patient's platelets failed to correct the defect. Addition of 2.5 microM U46619 (a PGG2 analogue) corrected the aggregation and release defect. An electron microscopic analysis failed to reveal structural abnormalities. Thus, the platelet function defect in this patient appears to be a functional deficiency of cyclooxygenase. The presence of autoantiplatelet antibodies in a clinical setting consistent with chronic ITP raises the possibility that the defect may be acquired.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

The laboratory diagnosis of lupus anticoagulants.

With the well-documented association of lupus anticoagulants with thrombotic disease and recurrent spontaneous abortion, the laboratory approach to diagnosing these inhibitors is more critical now. To this end, we examined plasma samples from 21 patients who initially presented with a prolonged prothrombin time or activated partial thromboplastin time or both for the presence of lupus anticoagulants. We used a battery of coagulation tests, including both immediate and two-hour mixing studies, a platelet neutralization procedure, a tissue thromboplastin inhibition test, and dilute Russell viper venom times. Two patients (10%) had only a prolonged prothrombin time, seven (33%) had only a prolonged activated partial thromboplastin time, and in 12 (57%) both were abnormal. In 15 patients, inhibition was evident on immediate assay of equal-volume mixture studies of patient plasma and normal pooled plasma, but in three additional patients it was evident only after a two-hour incubation. Fifteen of 18 samples showed correction of the abnormal screening study when platelets were used as a source of phospholipid. Both the tissue thromboplastin inhibition test and dilute Russell viper venom times were sensitive assays, being abnormal in 20 of 21 and 13 of 14 samples, respectively. In four patients, discordance of studies necessitated specific coagulation factor levels being measured to confirm the presence of the inhibitor. Because of the variable effect of the inhibitors on all currently available assay procedures, we would suggest that any evaluation will require a laboratory to have a battery of tests available before such an inhibitor can be excluded.

Adolescent↗
PubMed1988

Acquired von Willebrand's syndrome associated with an extranodal pulmonary lymphoma.

A case of acquired von Willebrand's syndrome associated with an extranodal pulmonary lymphoma is reported in a 58-year-old man. His initial factor VIII-von Willebrand factor (vWF) complex parameters included a factor VIII activity of 29 U/dL, a vWF protein of 17 U/dL, and a ristocetin cofactor of less than 10 U/dL. A specific factor VIII inhibitor could not be demonstrated in mixtures of his plasma and normal pooled plasma nor could immune complexes of IgG-factor VIII be detected in similar mixtures using protein A in a solid phase. Following surgical removal of the patient's tumor, all factor VIII-vWF complex parameters returned to normal. Immunoperoxidase stains of the lymphoid tumor cells were negative for von Willebrand protein. The patient's acquired von Willebrand's syndrome recurred approximately one year later, presumably indicative of recurrent lymphoma.

Factor VII↗
PubMed1986

Acquired von Willebrand syndrome due to an inhibitor specific for von Willebrand factor antigens.

A patient with acquired von Willebrand syndrome associated with polycythemia rubra vera is described. Her plasma factor VIII procoagulant activity (67 U/dl) and factor VIII-related antigen (117 U/dl) were normal but no von Willebrand factor activity could be detected. Factor VIII crossed immunoelectrophoresis revealed decreased levels of less anodic polymeric forms of factor VIII. Mixture of her plasma or immunoglobulin G (IgG) fraction with normal plasma resulted in complete recovery of factor VIII activity and related antigen but no measurable von Willebrand factor activity, confirming the presence of an unique inhibitor. The limited specificity of this inhibitor to antigenic sites solely on the von Willebrand portion of the factor VIII bimolecular complex is distinct from all previous reports of this syndrome. This unique inhibitor offers a molecular probe to examine the von Willebrand factor: platelet interaction.

Antigens↗
PubMed1986

Factor V inhibitor associated with immune complex formation.

A 72-year-old man was noted, shortly after surgery, to have a bleeding diathesis secondary to the development of a high-titer anti-factor V inhibitor. We documented the presence of factor V:anti-factor V IgG immune complexes and their disappearance following a short course of steroid therapy.

Abdomen↗
PubMedDate not supplied

Impaired platelet function associated with parenteral nafcillin.

A 44-year-old Caucasian female was admitted with a subarachnoid hemorrhage owing to a multilobular tubular anterior communicating artery aneurysm. Eleven days after the original craniotomy, an epidural hematoma was evacuated. The patient was placed on empiric nafcillin antimicrobial coverage (two g every six hours). Within 24 hours, the onset of epistaxis and oozing of blood from the endotracheal tube and craniotomy site was noted. Recurrent subdural and epidural hematomas necessitated a third emergent craniotomy. The development of an acquired qualitative platelet defect was suggested by the findings of a prolonged template bleeding time and markedly abnormal platelet aggregation/ATP release studies despite a normal platelet count. Nafcillin therapy was immediately discontinued. Clinical bleeding resolved. Subsequent bleeding times and platelet aggregation studies confirmed the nafcillin-induced platelet dysfunction.

Adult↗
PubMedDate not supplied

Lupus anticoagulants in children.

Although a great deal of information is available in the literature on the frequency, clinical/laboratory findings and significance of lupus anticoagulants in adults, little is known about such acquired inhibitors in children. Clinical and laboratory findings are presented on seven non-hemophiliac children, four females and three males, ranging in ages from three to 14 years, who developed such inhibitors. In most, the inhibitor is a transient phenomena and is not associated with a bleeding or thrombotic diathesis.

Adolescent↗