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Results for “Factor VII Deficiency”

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PubMed1991

Factor VII clotting assay: influence of different thromboplastins and factor VII-deficient plasmas. CISMEL Study Group.

Being a putative predictor of ischemic heart disease, the measurement of factor VII (FVII) coagulant activity will be presumably requested to clinical laboratories with increasing frequency. To assess the influence on FVII assays of different thromboplastins and FVII-deficient plasmas we compared performances of all possible combinations of 5 thromboplastins and 6 deficient plasmas. The reproducibility of the clotting times of the dose-response curves for human and rabbit thromboplastins were acceptable (CV lower than 7%), whereas bovine thromboplastin had a higher CV. Reproducibility was very similar for all deficient plasmas when they were used in combination with a given thromboplastin. Responsiveness of the dose-response curve did not depend on the deficient plasma but rather on the thromboplastin: one rabbit thromboplastin was the least responsive, the bovine thromboplastin the most responsive, the human and the remaining two rabbit thromboplastins had intermediate responsiveness. Assay sensitivity to cold-activated FVII varied according to the thromboplastin: the bovine thromboplastin was the most sensitive, the human thromboplastin the least sensitive, of the three rabbit thromboplastins two were relatively sensitive, one was almost insensitive. In conclusion, our results indicate that thromboplastin rather than deficient plasma is the crucial factor in the standardization of FVII assay.

Adult↗
PubMed1986

Electroimmunoassay of factor VII antigen.

A clear precipitating arc of factor VII antigen appeared by immunoelectrophoresis using 125I-labelled anti-factor VII antibody incorporated in the Laurell plate to enhance the sensitivity. A plasma sample could be electrophoresed directly on 1% agarose containing 1% rabbit anti-human factor VII antiserum, 0.1% 125I-labelled anti-human factor VII specific IgG and 0.5% polyethyleneglycol 6000, and after washing, autoradiographed at -70 degrees C for 24 hr. A distinct rocket was seen from 45 ul standard reference plasma to 16-fold after auto-radiography. Of 4 patients with congenital factor VII deficiency, 3 patients had no detectable factor VII antigen, one patient had reduced factor VII antigen.

Antigens↗
PubMed2003

Pitfalls in molecular diagnosis in a family with severe factor VII (FVII) deficiency--misdiagnosis by direct sequence analysis using a PCR product.

Molecular diagnostic tests are becoming a routine analysis in many laboratories. These modern analyses are widely used in clinical medicine, forensic, genetic and prenatal diagnosis and also in preimplantation genetic diagnosis. The accuracy of analysis is highly dependent on the success achieved in minimising genotyping errors. The pitfalls in molecular diagnostic tests can be due to a simple technique such as the polymerase chain reaction (PCR) used universally. This technique is routinely used for its apparent accuracy, but it is also a well-known source of errors. We report an error introduced during PCR reaction that leads to a wrong sequence result and consequently to a 'false' molecular result in a next prenatal diagnosis in a family with severe factor VII (FVII) deficiency. This error was verified using an unsuitable primer design in a rich repetitive sequence of the FVII gene that leads to a false annealing and then to a wrong molecular diagnosis. It is essential to link closely molecular data with clinical and phenotype analysis in order to avoid false-negative or false-positive results, which is of great importance to diagnosis and molecular prevention.

Adult↗
PubMed2003

Inherited bleeding disorders in Indian women with menorrhagia.

In order to define the prevalence of haemostatic defects in women presenting with menorrhagia in our region, the coagulation data on women bleeders investigated in the Department of Haematology, AIIMS, were analysed. A total of 337 of the 2200 menorrhagic women investigated were characterized to have an inherited bleeding disorder; 221 of these 337 women presented with menorrhagia alone while 116 also had other associated bleeding manifestations as prolonged bleeding from injury site, ecchymotic patches in the skin, epistaxis, haematomas, haemarthroses and major bleeds like intracerebral bleeding. The tests performed included bleeding time (BT), platelet count, prothrombin time (PT), prothrombin consumption index (PCI), activated partial thromboplastin time (APTT), PF3 release with adenosine diphosphate (ADP) at 0 and 20 min, total PF3 assay and platelet Aggregation studies with collagen, ADP, adrenaline, arachidonic acid and ristocetin. Coagulation factor assays, von Willebrand antigen estimation, ristocetin cofactor assay and electron microscopy were performed wherever necessary. Inherited platelet dysfunction was seen in 283 (83.9%) of the patients. Amongst these, isolated PF3 availability defect was seen in 163 (48.4%) cases. Glanzman's thrombasthenia was seen in 30 (8.9%) patients, Storage pool disease in eight (2.4%) patients, arachidonic acid pathway defect in five (1.5%) patients and Bernard-Soulier Syndrome in six (1.8%) patients. In 71 (21.1%) patients, the platelet function defect could not be classified into any specific subtypes. Inherited defects of coagulation were observed in 54 (16%) of the cases. Amongst these, von Willebrand disease (vWD) was the most frequent being seen in 40 (11.9%) of the cases. Factor XIII deficiency was seen in one (0.3%), factor X deficiency in four (1.2%), factor VII deficiency in one (0.3%) and factor XII deficiency in one (0.3%) of the patients. It is concluded that although hereditary platelet function defects constitute a large majority of women bleeders in India but among the coagulation defects, vWD is the commonest as reported from the caucasian population. It is thus suggested that in women presenting with menorrhagia, screening tests for haemostasis especially for vWD and inherited platelet function defects must be performed.

Adolescent↗
PubMed1975

The K-test (trypsin clotting time) in coumarin treated patients and in congenital deficiencies and abnormalities of the prothrombin complex.

The behavior of K-test (Trypsin clotting time) has been studied in 38 patients on long-term coumarin therapy and in 19 patients with congenital coagulation disorders of the prothrombin complex. All coumarin treated patients showed a clear prolongation of the test. The results obtained were compared with the standard prothrombin time, the Hepato-Quick-test (P-P test) and the Factor II + X test values, observed in the same patients. A good correlation was observed in each instance. The highest correlation was observed between K-test and the Factor II + X test (r=+0,78;t=7,80;p less than 0.001). All congenital coagulation disorders of the prothrombin complex yielded a prolonged K-test value but for Factor VII deficiency. In three patients with this latter condition a perfectly normal value was obtained. The K-test together with the prothrombin time may be useful in the differential diagnosis of factor VII deficiency from factor X deficiency and from the factor X Friuli abnormality.

Blood Coagulation Disorders↗