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Biomedical subjects

W McGehee

Publications and source records attributed to W McGehee.

11 recordsLinked to original sources
PubMed1998

The factor V Leiden mutation increases the risk of venous thrombosis in patients with inflammatory bowel disease.

BACKGROUND & AIMS: Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). The aim of this study was to determine the incidence and possible association of the factor V Leiden mutation with the development of thrombosis in patients with IBD. METHODS: This retrospective study included 11 patients with IBD and arterial or venous thrombosis and 51 patients with IBD and no history of thrombosis who were matched for age, sex, ethnic/racial origin, and type of IBD (controls). The presence of the factor V Leiden mutation was determined by coagulation assay and confirmed by a polymerase chain reaction method. RESULTS: Four of 11 IBD patients (36%) with thrombosis and 2 of 51 IBD controls (4%) were heterozygotes for the factor V Leiden mutation (relative risk, 14.00; 95% confidence interval, 1.55-169.25; P = 0.009, Fisher exact test). All thrombotic events in the patients with activated protein C resistance were venous with a calculated prevalence of 50% (4 of 8 patients) and a relative risk of venous thrombosis in IBD patients with factor V Leiden of 23 (95% confidence interval, 2-294; P = 0.005). CONCLUSIONS: In patients with IBD, inheritance of the factor V Leiden mutation results in a significant increased risk of venous thrombosis.

Adolescent↗
PubMed1997

A Protac-based screening test for activated protein C-resistant factor Va and other defects of the protein C anticoagulant pathway.

We have standardized a simple screening test for abnormalities of the protein C anticoagulant system. The test is basically a modified prothrombin time in which one aliquot of a test plasma is incubated for 3 min at 37 degrees C with Protac and another is incubated with buffer. During the incubation the Protac activates both protein C and factor V. The plasmas are then clotted with thromboplastin plus Ca2+, and the clotting time difference reflects the ability of the activated protein C (APC) to inactivate factor Va. With the use of Thromboplastin C Plus as the activator, clotting time differences found in 31 normal subjects (10.4 +/- 3.5 s, mean +/- 2SD) were distinct from clotting time differences found in 57 of 58 subjects with established APC-resistant factor Va (3.6 +/- 3.0 s). In addition, the Protac-based test detected six of seven patients with isolated protein C deficiency and 20 of 28 patients with isolated protein S deficiency. Because of the reported high prevalence of heterozygous APC-resistant factor Va in Caucasian populations, it should be particularly useful in determining whether this genetic risk is present in individuals who have experienced or are at increased environmental risk of venous thrombosis.

Anticoagulants↗
PubMed1996

Preeclampsia and liver infarction in early pregnancy associated with the antiphospholipid syndrome.

BACKGROUND: Usually, preeclampsia is a disease of the second half of pregnancy (i.e., beyond 20 weeks' gestation). Early-onset preeclampsia has been reported in association with the antiphospholipid syndrome, however, the cases reported have been at 25-30 weeks' gestation. CASES: Three pregnant women presented with clinical and laboratory features of severe preeclampsia and the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) before 20 weeks' gestation. On evaluation, they were found to have antiphospholipid antibodies (anticardiolipin and/or lupus anticoagulant). Two of the patients had abdominal computed tomography scans that showed a low-density area along the hepatic periphery, compatible with hepatic infarction. Spontaneous resolution of all clinical and laboratory manifestations of preeclampsia and HELLP syndrome was observed after fetal death and pregnancy termination. CONCLUSION: Preeclampsia and HELLP syndrome can present before 20 weeks' gestation in association with the antiphospholipid syndrome and may be associated with hepatic infarction.

Adult↗
PubMed1996

Evaluation of a tissue factor dependent factor V assay to detect factor V Leiden: demonstration of high sensitivity and specificity for a generally applicable assay for activated protein C resistance.

Resistance to the anticoagulant effects of activated protein C (APC) is now considered the most prevalent cause of inherited thrombophilia. The great majority of patients with activated protein C resistance (APCR) have a missense mutation in the factor V molecule (factor V Leiden, FVR506Q) resulting in defective inactivation of factor Va due to a loss of an APC cleavage site. The diagnosis of APCR has been based upon the inability of APC to prolong the activated partial thromboplastin (aPTT) clotting time in subjects with APCR. However, this assay has a number of deficiencies which limit its general use. We have evaluated a newly described one-stage tissue factor dependent factor V coagulation assay for APCR in 117 patients and controls and compared the results of this assay in a blinded manner to a polymerase chain reaction (PCR) based assay for the molecular defect of factor V Leiden. 43% (50/117) of the patients studied were receiving coumadin or heparin, or had a lupus anticoagulant. The tissue factor dependent factor V assay had 100% specificity and sensitivity for factor V Leiden and successfully predicted a homozygous state in the three documented homozygotes. The PCR-based assay for factor V Leiden resulted in a single false positive assay due to a silent A to C transition at nucleotide 1692 resulting in the loss of the Mnl restriction endonuclease cleavage site. The single-stage tissue factor dependent factor V assay is a highly sensitive and generally applicable assay for APCR.

Blood Coagulation Tests↗
PubMed1991

Measurement of the activated partial thromboplastin time from a capillary (fingerstick) sample of whole blood. A new method for monitoring heparin therapy.

The monitoring of heparin anticoagulation is fraught with difficulties because of the need for repetitive venipunctures and the vagaries of sample handling and processing. The authors evaluated a new aPTT monitoring system with the potential to eliminate many of these difficulties. The Ciba Corning Diagnostics 512 Coagulation Monitor (CCD monitor) is a hand-held portable instrument that can measure an aPTT from a fingerstick sample of capillary whole blood. Fingerstick aPTTs from 319 subjects (including controls and individuals on heparin and/or warfarin) were compared to venipuncture-derived standard laboratory plasma aPTTs using different aPTT reagents on conventional instruments. The correlation coefficients between fingerstick and standard aPTTs (0.79-0.83) were the same as the correlation coefficient between standard laboratory aPTTs using different reagents (0.79). When venipuncture-derived whole blood was compared to fingerstick samples on the new instrument, the correlation coefficient was excellent (0.93). A high degree of precision, as demonstrated by low coefficients of variations, was shown for within-day and between-day testing using the CCD monitor and normal controls. This capillary whole blood, aPTT system is the first to provide the clinician with a means of rapidly and reliably assessing the anticoagulant response to heparin therapy at the bedside, and its use may ultimately lead to more efficient and effective therapy overall.

Blood Coagulation Tests↗
PubMed1986

Arthropathy associated with factor XIII deficiency.

A 47-year-old man with congenital factor XIII deficiency developed recurrent hemarthrosis of the right ankle. He had radiologic evidence of permanent joint damage. A review of the literature revealed that hemarthrosis is not a rare manifestation of factor XIII deficiency; however, destructive changes in the joints are relatively uncommon in this disorder, in contrast with those changes seen in patients with classic hemophilia and arthropathy. The bleeding manifestations of factor XIII deficiency are readily correctable by plasma or cryoprecipitate infusions; this may account for the preservation of joint function and structure.

Ankle Joint↗
PubMed1986

Cerebral infarct, TIA, and lupus inhibitor.

A lupus inhibitor paradoxically prolongs phospholipid-dependent coagulation assays, but may increase risk of thromboembolism. We studied seven patients with cerebral infarcts and one with TIA who had lupus inhibitor. The average age at onset of cerebral ischemia was 41 years. Three patients had multiple cerebral ischemic events. The activated partial thromboplastin time was longer than that of controls, but usually within normal limits. Other abnormalities included biologic false-positive VDRL, antinuclear antibodies, thrombocytopenia (three patients each), and deep vein thrombosis (two patients).

Adult↗
PubMed1984

Prolonged defibrination after a bite from a 'nonvenomous' snake.

The distinction between venomous, potentially dangerous snakes and snakes considered to be harmless to humans is not always clear. A man was bitten by an assumed harmless pet snake, Rhabdophis subminatus (the red neck keelback), that had been obtained from a pet store. The patient experienced a severe coagulopathy with life-threatening hemorrhage unresponsive to transfusion. Since this snake frequently is sold legally in the United States, we wish to alert the medical community to its potential danger and to discuss the pathophysiological mechanism by which the coagulopathy was produced.

Adult↗
PubMed1982

Depression of functional and antigenic plasma antithrombin III (AT-III) due to therapy with L-asparaginase.

Eleven patients with leukemia and lymphoma were treated with 14 courses of E. coli L-asparaginase. Abnormalities of the coagulation screening tests and decreased fibrinogen levels were observed in all patients during treatment. Significant depressions of functional (mean 32%) and antigenic (mean 48%) antithrombin III were observed by day 14 of therapy. There was no laboratory evidence of intravascular coagulation during 11/14 courses of L-asparaginase. Crossed immunoelectrophoresis of plasma obtained at the antithrombin nadir did not demonstrate an abnormal pattern which can be associated with an abnormal antithrombin III or an increase in antithrombin III-coagulation factor complexes. The major underlying mechanism of this depression is believed to be decreased hepatic synthesis, and the low levels of antithrombin III may be associated with an increased risk of thrombosis.

Adult↗
PubMedDate not supplied

Cefotaxime-induced immune hemolytic anemia due to antibodies reacting in vitro by more than one mechanism.

Until recently, all cephalosporin-induced immune hemolytic anemias appeared to react by a "penicillin-type" drug adsorption mechanism, and hemolysis was extravascular. In 1987 and 1988, the first two cases of cephalosporin-induced immune hemolytic anemia with intravascular hemolysis associated with a so-called immune complex mechanism were reported. This report describes a case of extravascular hemolysis due to a third-generation cephalosporin, cefotaxime, which, to the authors' knowledge, is the first to show in vitro characteristics of both the drug adsorption and the so-called immune complex mechanisms.

Adult↗