Describes how Factor V Leiden mutation and PT 20210 mutation tests are used, when Factor V Leiden mutation and PT 20210 mutation tests are ordered, and what the results of Factor V Leiden mutation and PT 20210 mutation tests might mean
Describes how Factor V Leiden mutation and PT 20210 mutation tests are used, when Factor V Leiden mutation and PT 20210 mutation tests are ordered, and what the results of Factor V Leiden mutation and PT 20210 mutation tests might mean
A 27-year-old man was admitted to our hospital with the complaints of swelling of his face and lower limbs. Echocardiography showed minimal pericardial effusion accompanied by disordered diastolic function. Cardiac catheterization was performed to rule out constrictive pericarditis. Normal pressure tracings of the right heart rule out constrictive pericarditis, however, a. narrowing of the inferior vena cava was observed. Venographies of the inferior and superior vena cavae showed extensive thrombotic involvement of these great veins. Protein C, protein S, anticardiolipin antibodies, fibrinogen, antithrombin-III, activated protein C resistance, and factor V levels were in normal limits. Heterozygosity for factor V Leiden mutation was detected. We conclude that factor V Leiden mutation can cause extensive thrombotic involvement of major veins and should be considered in idiopathic thrombosis of them. ...
Factor V Leiden is a common inherited genetic disorder in which your blood has an increased tendency to form clots (thrombophilia), usually in your veins.. Although blood clots can form at any age, for most people the increased risk of clotting doesnt begin until adulthood. Most people with factor V Leiden never develop abnormal clots. However, some people with factor V Leiden develop clots that lead to long-term health problems or are life-threatening.. Both men and women can have factor V Leiden, but women may have an increased tendency to develop blood clots during pregnancy or when taking the hormone estrogen.. If you have factor V Leiden, medications can lessen your risk of developing blood clots and help you avoid potentially serious complications.. Its possible to have factor V Leiden without ever developing signs or symptoms. However, the first indication that you have the disorder may be the development of a blood clot (thrombosis).. Some clots do no damage and disappear on their own. ...
Description of disease Factor V Leiden. Treatment Factor V Leiden. Symptoms and causes Factor V Leiden Prophylaxis Factor V Leiden
Background. If a thrombophilia (clotting disorder) has been identified in a patient with blood clots (venous thromboembolism = VTE), the question arises whether other family members should be tested for the same thrombophilia.. My Clinical Approach. My approach in clinical practice to thrombophilia testing in family members is summarized in table 1: Family Member Testing. If the patient has a "strong" inherited thrombophilia (i.e. homozygous factor V Leiden, homozygous prothrombin 20210 mutation, double heterozygous factor V Leiden plus prothrombin 20210 mutation, deficiency of protein C, S or antithrombin) then I consider and discuss testing of other family members. However, if the patient only has heterozygous factor V Leiden or heterozygous prothrombin 20210 mutation, I do not recommend testing of family members, as the finding of one of these "mild" thrombophilias typically has no impact on management of family members also affected by one of those "mild" thrombophilias.. Finding of a ...
Factor V Leiden (rs6025) is a variant (mutated form) of human factor V (one of several substances that helps blood clot), which causes an increase in blood clotting (hypercoagulability). With this mutation, the anticoagulant protein secreted (which normally inhibits the pro-clotting activity of factor V) is not able to bind normally to Factor V, leading to a hypercoagulable state, i.e., an increased tendency for the patient to form abnormal and potentially harmful blood clots. Factor V Leiden is the most common hereditary hypercoagulability (prone to clotting) disorder amongst ethnic Europeans. It is named after the Dutch city Leiden, where it was first identified in 1994 by Prof R. Bertina et al. Abnormal, recurrent venous thromboses. In the normal person, factor V functions as a cofactor to allow factor Xa to activate prothrombin, resulting in the enzyme thrombin. Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a ...
Six cases of congenital thrombophilia (15%) were found: 1 PC deficiency (patient 25), 1 PS deficiency (patient 34), and 4 heterozygous factor V Leiden (patients 21, 22, 28, and 30). Three patients had increased aCL antibodies, 1 with systemic lupus (patient 21) and 2 with a primary aPL syndrome (patients 8 and 22); 2 of these had also factor V Leiden mutation. There was no antithrombin or plasminogen deficiency. Cases with thrombophilia and/or aCL antibodies are briefly summarized. Treatment and outcome are not detailed because all patients received heparin followed by oral anticoagulants and made an uneventful recovery.. Patient 25 was 34 years old in 1986 when she complained of headache, seizures, and left-sided sensory symptoms in a context of uveomeningitis. No other signs of Behçets disease11 or sarcoidosis were present. Angiography and MRI showed right LS thrombosis. The patient has been well since then. While receiving oral anticoagulants, PC activity was 24%, antigen was 33%, and ...
What is factor V Leiden? The most common genetic risk factor for venous thrombosis is factor V Leiden, present in 5 percent of the general population. Factor V is one of the normal blood clotting factors. Factor V Leiden is a changed or "mutated" form of factor V that is inactivated 10 times slower than the normal factor V. This causes it to persist longer in the circulation, resulting in a hypercoagulable state. In other words, the blood continues clotting, resulting in possible obstruction.. One copy of the factor V Leiden gene increases the risk for venous thrombosis 4 to 8 times, while two copies of the gene increase the risk 80-fold.. Other coexisting coagulation defects can occur with factor V Leiden, and in general, the risk for thrombosis increases in patients with more than one genetic defect.. The factor V Leiden mutation is involved in 20 to 40 percent of venous thrombosis cases and is suspected in individuals who have a medical history of venous thrombosis or in families with a high ...
The relation between factor V mutation and risk for venous thromboembolism was confirmed in a prospective study of 14 916 men with no history of cardiovascular disease or cancer followed for a mean of 8.6 years. 11.6% of men with venous thromboembolism had the mutation compared with 6.0% of those with no thromboembolism (relative risk [RR] 2.7, 95% CI 1.3 to 5.6, P = 0.008). Risks were higher for patients with idiopathic events (RR 3.5, CI 1.5 to 8.4, P = 0.004) and for men , 60 years of age (adjusted RR 4.0, CI 1.6 to 9.7, P = 0.003). A prospective study showed that men with both factor V mutation and moderate hyperhomocystinemia had an increased risk for any form of venous thromboembolism (RR 9.7, P = 0.009) and for idiopathic venous thromboembolism (RR 21.8, P , 0.001) compared with men who had neither abnormality. In a case-control study comparing 155 premenopausal women who had deep venous thrombosis unrelated to a malignant condition with 169 women who had no history of thrombosis, the ...
Background: Activated Protein C Resistance (APCR), a poor anticoagulant response of APC in haemostasis, is the commonest heritable thrombophilia. Adverse outcomes during pregnancy have been linked to APCR. This study determined the frequency of APCR, factor V gene known and novel SNPs and adverse outcomes in a group of pregnant women. Methods:Blood samples collected from 907 pregnant women were tested using the Coatest® Classic and Modified functional haematological tests to establish the frequency of APCR. PCR-Restriction Enzyme Analysis (PCR-REA), PCR-DNA probe hybridisation analysis and DNA sequencing were used for molecular screening of known mutations in the factor V gene in subjects determined to have APCR based on the Coatest® Classic and/or Modified functional haematological tests. Glycosylase Mediated Polymorphism Detection (GMPD), a SNP screening technique and DNA sequencing, were used to identify SNPs in the factor V gene of 5 APCR subjects. Results:Sixteen percent of the study ...
Product Mouse Coagulation Factor V (F5) ELISA Kit From DL Develop - A sandwich quantitative ELISA assay kit for detection of Mouse Coagulation Factor V (F5) in samples from plasma. Should the Mouse Coagulation Factor V (F5) ELISA Kit is proven to show malperformance, you will receive a refund or a free replacement.
A young woman 38 years of age underwent Doppler ultrasonography following the spontaneous appearance of cervical pain causing loss of sleep. The examination revealed bilateral dissection of the internal carotid arteries, confirmed by supraaortic arteriography. Two successive CT scans showed no cerebral lesions. A thrombosis of the great saphenous vein was recorded as the only vascular event in her medical history. Thrombophilia was assessed following discovery of the dissection, and upon examination a heterozygotic mutation of Factor V Leiden was revealed. This observation is the second case of carotid dissection occurring in a subject presenting a factor V mutation. At the present time, however, there are no results to justify the assumption of a direct link between these two pathologies.
Factor V Leiden. If the fetus inherits the gene from a Factor V Leiden paternal carrier , the pregnancy is six times more likely to be affected by clotting which can cause miscarriages and other serious placental malfunctions. It is therefore likely that some or all of the miscarriages were caused by your husbands gene mutation. Get early placental gene testing with your next pregnancy to predict occurrence ...
The mutation G1691A (R506Q) in the human factor V gene is associated with the resistance to activated protein C (APC) that represents a major risk of development of venous thrombosis. A population...
Activated protein C (aPC), in a complex with protein S, inactivates procoagulant factors Va and VIIIa by proteolytic cleavage at specific arginine residues.7,10,11 This serves to control coagulation and limit the extent of thrombus formation. The functionality of the aPC inhibitory system in a given individual can be assessed through an in vitro clotting assay. Addition of aPC to a patients plasma serves to extend the activated partial thromboplastin time (aPTT) for individuals who are sensitive to aPC. Individuals are considered to be aPC resistant when addition of aPC fails to extend the time to clot formation in this assay. More than 95% of cases of aPC resistance are caused by a specific polymorphism in the factor V gene that is referred to as factor V Leiden.8 This single point mutation results in a substitution of glutamine for arginine at amino acid number 506 of factor V. Arginine number 506 is an aPC cleavage site of normal factor V, making factor V Leiden resistant to inactivation by ...
English-language studies were identified using MEDLINE (1993 to April 1997) with the search terms factor V, mutation, protein C, resistance, thromboembolism, prevalence, diagnosis, screening, therapy, and prevention. Bibliographies of relevant papers were also reviewed ...
Individuals who carry the Factor V Leiden mutation have a 3- to 8-fold increased risk as heterozygotes and a greater than 10-fold increased risk as homozygotes. Individuals who carry the F2 prothrombin mutation have a 2- to 5-fold increased risk as heterozygotes and up to a 10-fold increased risk as homozygotes. Individuals who carry two copies of the 677C,T mutation, or one 677C,T and one 1298A,C mutation, in the MTHFR gene have between a 2- and 8-fold increased risk. Compound heterozygotes (heterozygous for more than one of the mutations tested for) have an even higher risk of thrombophilia. For example, a person that is heterozygous for both the Factor V Leiden mutation and heterozygous for the F2 prothrombin mutation has a greater than 20-fold increased risk ...
Factor V Leiden is an autosomal dominant condition which exhibits incomplete dominance and results in a Factor V variant which cannot be as easily degraded by aPC. The gene that codes the protein is referred to as F5. Mutation of this gene-a single nucleotide polymorphism (SNP) is located in exon 10.[6] As a missense substitution it changes a proteins amino acid from arginine to glutamine. Depending on the chosen start the position of the nucleotide variant is either at position 1691 or 1746.[7] It also affects the amino acid position for the variant which is either 506 or 534. Together with the general lack of nomenclature standard it means that the SNP can be referred to in several ways such as G1691A, c.1601G,A, 1691G,A, c.1746G,A, p.Arg534Gln, Arg506Gln, R506Q or rs6025! Since this amino acid is normally the cleavage site for aPC, the mutation prevents efficient inactivation of factor V. When factor V remains active, it facilitates overproduction of thrombin leading to excess fibrin ...
Factor V antibody [5108] (coagulation factor V (proaccelerin, labile factor)) for RIA, WB. Anti-Factor V mAb (GTX79798) is tested in Human samples. 100% Ab-Assurance.
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Factor V Leiden, also known as Activated Protein C Resistance, is a hereditary blood disorder that causes hypercoagulability and an increased risk of thrombosis.
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Background: The rate of progression to cirrhosis varies among individuals chronically infected with the hepatitis C virus (HCV). Coagulation pathway activation in models of hepatic fibrosis suggests variation in coagulation pathway components may influence the rate of fibrosis. We hypothesised that polymorphisms of the coagulation factors II and V affect the rate of progression to cirrhosis in HCV infected subjects. Methods: We studied the relationship between rate of fibrosis (calculated by dividing the fibrosis stage by duration of infection) and genotypes of specific coagulation pathway genes in 352 White European patients infected with HCV. Genotyping was performed using reverse line blot hybridisation. Results: The rate of fibrosis was significantly higher in patients with the factor V Leiden genotype (Arg560Gln) (ANOVA, p=0.004). In disease association studies, o significant association was seen (Fishers exact test, p=0.029; odds ratio 3.28 for fast progression to cirrhosis (expected to reach
Factor V Leiden is not a disease, but a genetic mutation that results in thrombophilia, a blood clotting condition that increases a persons risk of developing abnormal blood clots in their blood vessels.
Care should also be exercised in patients with Factor V (five) Leiden. This is a variation in a gene that affects the clotting process, increasing coagulation. Factor V Leiden is the most common inherited blood disorder in the United States. It is present in 4 to 6 percent of Caucasians; 2 percent of Hispanic Americans; a little over 1 percent of African Americans and Native Americans and about 0.5 of one percent of Asian Americans. Treatment is typically unwarranted unless there is evidence of a blood clot, in which case warfarin or other anticoagulants are prescribed. Depending on the situation, anticoagulants may be recommended to help afford advance protection against the development of blood clots. For example, women with a Factor V Leiden mutation may be advised to take anticoagulants during pregnancy and in the postpartum period.. ...
This study describes a novel microplate assay that measures FV coagulation activity during fibrin clot formation in human plasma which...
Uncovering common genetic risk factors for Parkinsons disease Introduction. Mutations in the so called PARK genes lead to rare familial forms of Parkinsons disease (PD). However the extent to which common genetic variability around these genes alters risk for common PD remains unclear. The Australian Parkinsons Project is analysing genetic variability around the PARK loci in a large PD case-control sample recruited from three Australian states. The emphasis is on gene-gene and gene-environment interactions between commonly occurring variables. Aim. To report on a pilot PD association analysis of 87 polymorphisms around13 PARK genes in an initial case-control sample recruited during 2006. Methods. PD cases (n=326) and unaffected control subjects (n=298) of white European ancestry were recruited from three specialist clinics in Brisbane and the Australian Electoral Roll. Common genetic variables (86 SNPs genotyped on the TaqMan platform and 1 STR variable genotyped using standard methods) were ...
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owrens disease ...
A test for Factor V Leiden was positive for 1 copy of the Factor V Leiden mutation. The test results were returned to Dr Hs office, where they were reviewed and incorrectly interpreted as being all normal.
Technoclone Factor V Deficient Plasma is a lyophilized, stable, immunodepleted, human plasma with a coagulation activity | 1% of factor V.
Determination of the predisposing genetic factors for thrombosis - factor V Leiden mutation, the prothrombin mutation, and mutations of the MTHFR gene
An APTT-based kit for the screening of factor-V-related APC resistance. The high sensitivity and specificity of the test for the factor V:Q506 mutation is obtained by prediluting the sample plasma with an excess of V-DEF Plasma bioreagent. The test design makes it possible to discriminate between heterozygous and homozygous factor V genotypes. It also allows for analysis of plasma from patients on heparin or oral anticoagulant therapy. High discrimination between genotypes with 100% sensitivity for FV:Q506. Reduces need for PCR determination. Applicable to anticoagulant treated patients.. ...
The Role of APC-Resistance for Predicting Venous Thrombosis and Pregnancy Complications in Carriers of Factor V Leiden (1691) G/A Mutation. By Andrey Pavlovich Momot, Maria Gennadevna Nikolaeva, Valeriy Anatolevich Elykomov and Ksenia Andreevna Momot. This chapter presents the results of the prospective cohort study of 500 females with factor V Leiden, FVL, 1691 GA genotype, during 2008-2015. The association between FVL (regardless of its laboratory phenotype-factor Va resistance to activated protein C, APC resistance) and the development of VTEC (both outside of and during pregnancy) and gestational complications such as preeclampsia, fetal growth restriction, and miscarriage has been established. Additionally, the leading role of APC resistance degree in the clinical manifestation of FVL 1691 GA genotype as thrombotic events and pregnancy complications has been proved. Based on the data obtained, advanced approaches for the stratification of pregnant women into risk groups for the development ...
What you need to know about DVT. Definition: A thrombosis is a. however it is most useful to think of those that are provoked and those that are not provoked.WUN, Department of Medicine, UC Davis School of Medicine Search for more papers by this author B.Natural coagulation inhibitors deficiencies, homozygous factor V Leiden and prothrombin G20210A and the antiphospholipid syndrome, increase the risk of first venous thrombosis and their recurrences and require adequate prevention.The homozygous cases are very rare (less than 20 reported) and are associated with severe and early onset of the thromboembolic disease (with both venous and arterial thrombosis) and often without a family history of thrombosis.Also, considering the costs, it is recommended to begin the screening of asymptomatic relatives with the mutation found in the index case.. Characteristics of the study cohorts with venous thromboembolism (VTE).Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) Resources Learn all you can ...
Rahimi Z, Felehgari V, Rahimi M, Mozafari H, Yari K, Vaisi-Raygani A, Rezaei M, Malek-Khosravi S, Khazaie H. The frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria, Molecular Biology Reports, 2010; [Epub ahead of print]. Rezaie L, Khazaie H, Soleimani A, Schwebel DC. Is self-immolation a distinct method for suicide? A comparison of Iranian patients attempting suicide by self-immolation and by poisoning, Burns, 2010; [Epub ahead of print]. Tahmasian M, Khazaie H, Sepehry AA, Russo, MB. Ambulatory Monitoring of Sleep Disorders [Review article], Journal of Pakistan Medical Association (JPMA), 2010; 60(6) 480-487. Ahmadi A, Mohammadi R, Schwebel DC, Khazaie H, Yeganeh N, Almasi A. Demographic risk factors of self-immolation: A case-control study, Burns, 2009; 35, 580-586. Khazaie H, Rezaei L, Tahmasian M, Schwebel DC. Insomnia Treatment ...
Kendall Ann has blessed our lives in so many ways. She is truly a gift from God and has proven herself to be a fighter from the beginning. She was born with many neurological and optical abnormalities, which we now know is due to a stroke in utero...probably due to her Factor V Leiden mutation and two copies of the MTHFR gene (1-14-09). Oh, and NOW she has Type 1 Diabetes (8-19-09) And NOW (12-16-10) she has problems with her Mitochondria ... and NOW (2-11-13) a neurogenic bladder resulting in a vesicostomy. Of course there is a possibility of a Mitochondrial Disorder, and a possibility CDLK5 caused all the problems and Mito secondary...but we will never know, because weve decided no more testing! When she was born she came right home...no NICU stay...and we had no idea anything was wrong! She has undergone numerous hospital stays and a number of surgeries, but through it all, she has maintained a smile that wins the hearts of everyone who meets her. Please join us in our journey of life with a ...
Kendall Ann has blessed our lives in so many ways. She is truly a gift from God and has proven herself to be a fighter from the beginning. She was born with many neurological and optical abnormalities, which we now know is due to a stroke in utero...probably due to her Factor V Leiden mutation and two copies of the MTHFR gene (1-14-09). Oh, and NOW she has Type 1 Diabetes (8-19-09) And NOW (12-16-10) she has problems with her Mitochondria ... and NOW (2-11-13) a neurogenic bladder resulting in a vesicostomy. Of course there is a possibility of a Mitochondrial Disorder, and a possibility CDLK5 caused all the problems and Mito secondary...but we will never know, because weve decided no more testing! When she was born she came right home...no NICU stay...and we had no idea anything was wrong! She has undergone numerous hospital stays and a number of surgeries, but through it all, she has maintained a smile that wins the hearts of everyone who meets her. Please join us in our journey of life with a ...
Hi, Im Bobby and I love to write! My main passion is on invisible illnesses as Im living with my own invisible illness (Heterozygous Factor V...
The assay utilizes the Invader Plus® chemistry manufactured by Hologic for the detection of the FVL(F5) c.1601G,A, R506Q mutation in genomic DNA (NM_000130.4 transcript isoform). Invader and allele-specific probes match the mutant and the wild-type alleles and have overlapping 5-ends that are cleaved upon perfect hybridization to the amplified DNA. The cleaved 5-end of the primary probes transiently hybridize with a corresponding fluorescence resonance energy transfer (FRET) cassettes triggering the cleavage of the fluorophore from the cassette by the cleavase enzyme and allowing signal release and detection.. ...
Science & Technology, Life Sciences & Biomedicine, Immunology, Surgery, Transplantation, IMMUNOLOGY, SURGERY, TRANSPLANTATION, ACTIVATED PROTEIN-C, COAGULATION-FACTOR-V, CORONARY-ARTERY-DISEASE, VENOUS THROMBOSIS, MYOCARDIAL-INFARCTION, INHIBITOR-1 PAI-1, FIBRINOGEN LEVELS, RESISTANCE, PLASMA, THROMBOPHILIA ...
As a new feature of CNNhealth.com, our team of expert doctors will answer readers questions. Heres a question for Dr. Gupta. Asked by Sharon, Montgomery, Texas I just heard that this month is Deep Vein Thrombosis Awareness month, and that Heidi Collins has had DVT.
As a new feature of CNNhealth.com, our team of expert doctors will answer readers questions. Heres a question for Dr. Gupta. Asked by Sharon, Montgomery, Texas I just heard that this month is Deep Vein Thrombosis Awareness month, and that Heidi Collins has had DVT.
I had to stop taking oral contraceptives because of the DVT, apparently the hormones make it worse so Ive finally come on my period after being 6 weeks late! Even though I am on tramadol at the moment for my DVT Im still suffering with the period pain. My flow is also really bad, its a lot heavier than Ive been used to in a long time ...
A phone call came to me a few weeks later that shattered me. The baby (Triton) that had made it to 13 weeks was "no longer viable" and he had passed away (miscarriage # 9). I was confused - I had done everything right - I was on the progesterone, was on bed rest - everything. I was scheduled for a D&C because I did not want to deliver at home.. The OB who was going to be doing the surgery turned out to be a lifesaver to me. Another miracle that Triton brought into my life. My OB had read over my chart, talked to me for a long time about my history and pegged that I had been diagnosed with Factor V Leiden, a blood disorder that predisposes me to making blood clots.. The surgery was scheduled for April 24, 2008 and I was able to get the answer I needed. When the pathology came back it showed blood clots caught in the umbilical cord cutting off the supply to Triton. He had given me the answer and we had a new plan and a concrete diagnoses for all my losses - Factor V Leiden.. Recovering from ...
You should reduce your risk of forming clots by working on the risk factors that can be changed. You should not smoke, should exercise regularly & watch your weight. You should never take hormone supplements (birth control or hormone replacement therapies) that contain estrogen. If you are traveling or otherwise sitting for long periods of time, you should periodically take breaks to move around as much as possible. You should notify your doctor if you ever have surgery so you can be treated prophylactically with blood thinners. It is important to always stay well hydrated ...
My new addiction is House, M.D, he is my DVT kindred spirit and knows what its like to experience the pain and muscle death that goes with it. The stabbing pains that I get seem to be coming back with greater intensity and frequency. I dont if thats because of my increased mobility or whether its because the muscle is dying or if its because the clot is moving around or if its because of some increased swelling but on the other hand it could be something completely different ...
Other research groups also have found the G2385R mutation is at a higher frequency in Asian patients with Parkinsons disease, than in matched control subjects. These types of case and control genetic studies provide a powerful tool for researchers to find disease genes and risk factors in homogeneous or isolated populations where there has been little immigration. Interestingly, the present papers authors found evidence to suggest G2385R carriers share a common ancestor. They performed a genetic analysis looking at the inheritance pattern of a specific DNA sequence along chromosome 12 that includes the LRRK2 gene. Examining known genetic markers, which are short stretches of repeated DNA subject to variation in the number of times they repeat, their analysis showed a unique pattern of these DNA sequence markers is almost always passed from generation to generation along with the G2385R variant. Researchers used genetic theory to estimate the level of variation at these genetic markers between ...
The above factors can all be measured in the laboratory with specific genetic tests, coagulation or antibody-based tests. Other acquired causes (regarded as risk factors) include malignancy, OCP, HRT, immobilisation, obesity, smoking, pregnancy and major surgery. Consideration should be given to screening patients with a DVT, especially in travellers at possible risk. Referral to a haematologist if thrombophilia is proved or suspected is advisable. Of particular interest is factor V Leiden, which occurs in about 5% of Caucasians, and the risk of venous thrombosis is increased three to seven times in heterozygotes and 80 times in homozygotes.2 ...