Method for locating defects in the clotting system

Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving blood clotting factor

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C435S004000, C530S380000, C530S381000, C436S066000

Reexamination Certificate

active

06183980

ABSTRACT:

The present invention relates to a method for identification of defects in the clotting, fibrinolysis and complement system.
Thromboses and hemorrhage are now among the most frequent causes of illness and death, especially in the industrial countries. The most well-known are cardiac infarction, apoplexy and pulmonary embolism. If thromboembolism or hemorrhage is survived, the vitality of the patient is limited in most cases, and on the one hand there are secondary symptoms, such as paralysis, post-thrombotic syndrome or organ damage, and on the other hand there are labor- and cost-intensive follow- up treatments, such as convalescence, physiotherapy and medication to improve the health situation and prevent further complications.
Great advances have been made in recent years, especially in research into the causes of thrombosis, and these include the discovery of APC resistance, lupus, anticoagulants, hyperhomocysteinemia and the prothrombin variant G20210A. Nevertheless, no cause is detectable in about 50% of all cases. The most important hemostaseological causes of hemorrhage are known, and these include the various forms of hemophilia, the von-Willebrand-Jurgens syndrome and rarer mutations of the individual clotting factors.
If such defects exist, the hemostatic equilibrium is disturbed and the ratio between pro- and anticoagulatory factors is shifted in favor of one side. Defects which result in an increased secretion of procoagulatory factors, for example the prothrombin variant G20210A, deficient release of inhibitors, such as with protein C, protein S or AT III deficiency, or the prevention of inhibition by modified receptors, in its best-known form resistance to the active form of protein C (APC resistance: Bertina R M, Clin Chem; 43(9): 1678-83), usually lead to thromboses. To these are added defects in the fibrinolysis system which reduce the breakdown of clots formed.
It is the task of the laboratory to identify such defects so that the doctor performing the treatment can estimate the individual risk of the patient and react to this. Various methods of diagnosis are employed here: global tests determine the interaction of several components of the clotting system. The prothrombin time (PT) determines the state of the exogenous clotting system and the partial thromboplastin time (aPTT) determines the state of the endogenous clotting system. Modified global tests are furthermore employed in the analysis of the protein C system and in the diagnosis of lupus anticoagulants. In contrast to these there are individual tests, each of which determine only an individual component and allow both qualitative and quantitative analysis. Modified individual tests are employed in the question of acquired inhibiting bodies. In spite of the diverse methods which can be chosen, an accurate diagnosis is often not possible: the boundaries between a “positive” and “negative” finding are not clear, or medicaments, such as, for example, anticoagulants, have a persistent influence on the test result.
DNA analysis provides unambiguous diagnoses of congenital defects. This is suitable above all for defects which are based on an individual mutation, such as factor V condition (a form of APC resistance) or the prothrombin variant G20210A. If heterogeneous defects exist, genetic analysis is also made extremely difficult. Needless to say, other problems arise in connection with DNA analysis. Only few laboratories are capable of conducting such an investigation, and there are also the high costs associated with it.
It is therefore an aim to select the patient group before the DNA analysis in order to save work and costs. The best known example here is resistance to protein C. There are various tests for investigating for APC resistance. If a positive finding is obtained, a genetic analysis can be carried out to discover whether the very frequent form of factor V condition exists. Such a separation between “positive” and “negative” also has a second decisive advantage. If an unknown defect is to be searched for, patient groups could be separated and selected out as “potentially positive” and analyzed by gene sequencing. To date, these groups have been selected according to the case history.
The prothrombin variant G20210A is a very good example of these problems. This point mutation is associated with increased prothrombin levels which lead to an increased risk of thrombosis (Poortn, Blood 1996; 88 (10): 3698-703). Publications indicate an increased risk of cardiac infarctions (Rosendahl, Blood 1997; 90(5) 1747-50) and venous thromboses (Brown, Br. J. Haematol; 98(4): 907-9). However, it has also been possible to demonstrate that discrimination between mutation carrier and the wild type is not possible with the aid of the prothrombin level, since the two groups cannot be separated (Poortn, Blood 1996; 88(10): 3698-703; see also our own results). Patients under oral anticoagulation had to be excluded.
Surprisingly, we found a possibility of achieving a very good separation between carriers of the mutation and carriers of the wild type gene. This was to be achieved by relating the result of an individual test to an associated search test. The tests which belong together are known to the expert. The relationship in which the individual test and search test can be placed is preferably the ratio. The sensitivity, specificity and cut-off are parameters which are important for the discrimination. As can be seen from the examples, the specificity can be increased at the expense of the sensitivity by varying the cut-off. A lower sensitivity is preferably taken, in order to increase the specificity. Preferably, a sensitivity of a maximum of 100%, particularly preferably a sensitivity of 95-100%, especially preferably a sensitivity of 80-95% is taken to increase the specificity. On the basis of the technical doctrine of the present invention, the expert can set the desired ratio of sensitivity and specificity by determination of a suitable cut-off value by simple experiments.
Acquired diseases can thus also be diagnosed, since these likewise cause hypo- or hypercoagulatory states which are distinguished by only a slight, in itself often insignificant change in the activity of the parameter affected.


REFERENCES:
patent: 5197017 (1993-03-01), Carroll et al.
patent: 5834223 (1998-11-01), Griffin et al.
patent: WO 91 01383 (1991-02-01), None
patent: WO 95 12127 (1995-05-01), None
Bertina, R.M. et al., “Spectrophotometric Assays Of Prothrombin In Plasma Of Patients Using Oral Anticoagulants”, Thrombois and Haemostasis, vol. 42:1296-1305 (1979).
Corrigan, Jr., J.J. et al., “Factor II Antigen In Liver Disease And Warfarin-Induced Vitamin K Deficiency: Correlation With Coagulant Activity Using Echis Venom”, American Journal of Hematology, vol. 8:249-255 (1980).
Rosendaal, F.R. et al., “A Common Prothrombin Variant (20210 G To A) Increases The Risk Of Myocardial Infarction In Young Women”, Blood, vol. 90:1747-1750 (Sep. 1, 1997).
Brown, K. et al., “Risk Of Venous Thromboembolism Associated With A G To A Transition At Position 20210 In The 3′-Untranslated Region Of The Prothrombin Gene”, British Journal Of Haematology, vol. 98:907-909 (1997).
Rosendaal, F.R. et al., “A Common Prothrombin Variant (20210 G to A) Increases The Risk Of Myocardial Infarction In Young Women”, Blood, vol. 90(5): 1747-1750, (1997).
Bertina, Rogier, “Factor V Leiden And Other Coagulation Factor Mutations Affecting Thrombotic Risk”, Clinical Chemistry, vol. 43(9): 1678-1683, (1997).
Brown, Karen et al., “Risk Of Venous Thromboembolism Associated With a G To A Transition At Position 20210 In The 3′-Untranslated Region Of The Prothrombin Gene”, British Journal of Haematology, vol. 98: 907-909, (1997).
Poort, Swibertus R. et al., “A Common Genetic Variation In The 3′-Untranslated Region Of The Prothrombin Gene Is Associated With Elevated Plasma Prothrombin Levels And An Increase In Venous Thrombosis”, Blood, vol. 88(10): 3698-3703, (1996).

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Method for locating defects in the clotting system does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Method for locating defects in the clotting system, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method for locating defects in the clotting system will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-2615368

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.