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Factor V Leiden: more detail

Stroke after Marijuana smoking in a teenager with factor V Leiden mutation.(Brief Article): An article from: Southern Medical Journal by Mark A. Marinella, 2001-12-01
Estrogen use with factor V Leiden not advised.(Women's Health)(Clinical report): An article from: Internal Medicine News by Colin Nelson, 2006-08-15
Factor V Leiden genetic variant in an American Indian population.(COMMUNICATIONS--PROFESSIONAL): An article from: Proceedings of the North Dakota Academy of Science by Melanie Nadeau, Sheri T. Dorsam, et all 2007-04-01
Genetic Polymorphisms: Single Nucleotide Polymorphisms, 5-Httlpr, Factor V Leiden, Rs6265, Rs6313, Rs6295, Rs5569, Rs6311, Rs6314, Rs7997012
Single Nucleotide Polymorphisms: Factor V Leiden, Rs6265, Rs6313, Rs6295, Rs5569, Rs6311, Rs6314, Rs7997012, Rs1805054, Rs4680, Rs1801133
Factor V Leiden thrombophilia: An entry from Thomson Gale's <i>Gale Encyclopedia of Genetic Disorders, 2nd ed.</i> by Dawn, MS, CGC Jacob, 2005
Blood Proteins: Hemoglobin, Hemocyanin, Glycated Hemoglobin, Haptoglobin, Human Serum Albumin, Fibrin, Factor V Leiden
Factor V Leiden as a common genetic risk factor for venous thromboembolism.(Genomics to Health): An article from: Journal of Nursing Scholarship by McDonald K., III Horne, Donna Jo McCloskey, 2006-03-22
Factor V Leiden

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Factor V Leiden
The presence of Factor V (Leiden) is the most common cause of inherited thrombophilia Factor V (Leiden) has traditionally been first detected by an APTT
http://www.repromedix.com/documents/FactorVLeiden.htm

Extractions: Factor V Leiden (APC Resistance, Coagulation) Pregnancy-Induced Venous Thrombosis In normal individuals, once clotting occurs, thrombin binds thrombomodulin and activates a number of anticoagulant proteins including protein C. Activated Protein C (APC) specifically degrades and inactivates Factor Va, down-regulating the coagulation cascade. APC Resistance is associated with a point mutation in the Factor V gene (Factor V (Leiden)). The mutation results in the replacement of arginine at position 506 with glutamine in the Factor V protein. This mutation slows the inactivation of Factor Va by APC causing a hypercoagulable state. The presence of Factor V (Leiden) is the most common cause of inherited thrombophilia, accounting for 20% to 50% of cases. Factor V (Leiden) is associated with an increased risk of venous thrombosis and is estimated to occur in 20-50% of patients with family history of thrombosis. It also occurs in 37% of apparently normal individuals in white European populations. There is a 7.9 fold increase in the relative risk for thrombosis for carriers of the Factor V mutation. Thrombotic events can be triggered by surgery, trauma, pregnancy, oral contraceptive use, or infection. In one study (Kupferminc et al., 1999), 110 women with one of four pregnancy complications (severe preeclampsia, abruptio placentae, fetal growth retardation, or intrauterine fetal death) and 110 women with one or more normal pregnancies were tested for the Factor V Leiden mutation. 22 of the women with complications, compared with 7 of the women with normal pregnancies (20 percent and 6 percent respectively), were identified as carriers of the Leiden mutation by PCR-RFLP analysis. This corresponds to an odds ratio of 3.7 (95% CI 1.5-9.0, P=0.003), suggesting that women with the Factor V Leiden variant have a nearly 4 times greater risk of pregnancy complications than do women without the mutation.
FACTOR V LEIDEN (PCR/RFLP)
The presence of Factor V (Leiden) is the most common cause of inherited thrombophilia, Factor V (Leiden) is associated with an increased risk of venous
http://www.repromedix.com/documents/FVL_PCRflyer.htm

Extractions: Factor V Leiden (PCR/RFLP) In normal individuals, once clotting occurs, thrombin binds thrombomodulin and activates a number of anti-coagulant proteins including protein C. Activated Protein C (APC) specifically degrades and inactivates Factor Va, down-regulating the coagulation cascade. APC Resistance is associated with a point mutation in the Factor V gene (Factor V (Leiden)). The mutation results in the replacement of arginine at position 506 with glutamine in the Factor V protein. This mutation slows the inactivation of Factor Va by APC causing a hypercoagulable state. The presence of Factor V (Leiden) is the most common cause of inherited thrombophilia, accounting for 20% to 50% of cases. The point mutation G1691A results in a loss of a restriction enzyme cleavage site in Exon 10 of the Factor V gene. The Leiden mutation can be detected by amplifying a segment of the gene flanking nucleotide 1691 by PCR followed by restriction fragment length polymorphism (RFLP), which involves digesting the PCR product with the restriction enzyme Mnl I. Especially when used in combination with the functional coagulation screening test, this method detects the Leiden variant of Factor V with extremely high sensitivity and specificity. Pregnancy-Induced Venous Thrombosis Factor V (Leiden) is associated with an increased risk of venous thrombosis and is estimated to occur in 20-50% of patients with family history of thrombosis. It also occurs in 3-7% of apparently normal individuals in white European populations. There is a 7.9 fold increase in the relative risk for thrombosis for carriers of the Factor V mutation. Thrombotic events can be triggered by surgery, trauma, pregnancy, oral contraceptive use, or infection.
August 1995 - The Factor V Leiden Mutation
The factor V mutation, named factor v leiden after the site of its The newly described factor v leiden mutation represents a major advance in the
http://www.itxmdiagnostics.com/Archive/tmu8-95.htm

Extractions: Traditional attempts to identify an underlying cause of familial thrombosis by testing for antithrombin III, protein C, and protein S have only rarely provided an explanation for a patient's thrombotic event. Recently, studies have clearly shown that a mutation of clotting factor V is highly associated with thrombosis and may account for as much as 25% of all cases of venous thrombosis of unknown cause. In addition, knowledge that a patient carries this gene may have significant clinical implications. Pathophysiology The factor V mutation, named factor V Leiden after the site of its discovery, is due to a point mutation in the normal factor V molecule. This mutation renders the factor V molecule insensitive to the action of activated protein C, a natural anticoagulant. This in turn appears to shift the patient's overall hemostatic balance toward thrombosis, especially venous thrombosis. Incidence The incidence of the factor V Leiden mutation in both European and American populations has been repeatedly found to be surprisingly high. The best evidence from the United States indicates that 6% of the population carries the gene for the factor V mutation. The reason for its persistence at such a high level is unclear.
Varicella Purpura Fulminans Associated With Heterozygosity For Factor V Leiden A
factor v leiden, a factor V variant resulting from a single point mutation at nucleotide 1691 The factor v leiden mutation confers resistance to .
http://pediatrics.aappublications.org/cgi/content/extract/102/5/1208

Extractions: This Article Full Text Full Text (PDF) P ... Citation Map Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Cited by other online articles PubMed PubMed Citation Articles by Woods, C. R. Articles by Johnson, C. A. Related Collections Blood Varicella Purpura Fulminans Associated With Heterozygosity for Factor V Leiden and Transient Protein S Deficiency The first 300 words of the full text of this article appear below. Purpura fulminans is an acute, rapidly progressive hemorrhagic necrosis of the skin attributable to dermal vascular necrosis that is associated with disseminated intravascular coagulation. It is a rare and occasionally life-threatening disorder that occurs most commonly in the setting of acute, severe bacterial or viral infection, or as a postinfectious syndrome after infections such
Varicella Purpura Fulminans Associated With Heterozygosity For Factor V Leiden A
factor v leiden, a factor V variant resulting from a single point mutation The factor v leiden mutation confers resistance to protein C activation and
http://pediatrics.aappublications.org/cgi/content/full/102/5/1208

Extractions: This Article Extract Full Text (PDF) P ... Citation Map Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Cited by other online articles PubMed PubMed Citation Articles by Woods, C. R. Articles by Johnson, C. A. Related Collections Blood Varicella Purpura Fulminans Associated With Heterozygosity for Factor V Leiden and Transient Protein S Deficiency Purpura fulminans is an acute, rapidly progressive hemorrhagic necrosis of the skin attributable to dermal vascular necrosis that is associated with disseminated intravascular coagulation. It is a rare and occasionally life-threatening disorder that occurs most commonly in the setting of acute, severe bacterial or viral infection, or as a postinfectious syndrome after infections such as primary varicella or scarlet fever. Postinfectious purpura fulminans usually occurs 7 to 10 days after onset of symptoms of the acute infection.
Liver Information: Budd-Chiari Syndrome Associated With Factor V Leiden Mutation
Resistance to activation of protein C caused by factor v leiden mutation (FVLM), presenting as BCS syndrome was first reported in 1995 (Lancet345525) and
http://www.surgery.usc.edu/divisions/hep/livernewsletter-budd-chiarisyndromeasso
Factor V Leiden / Thrombophilia - [Support Group]
This information is provided as a resource and does not constitute an endorsement for any group. It is the responsibility of the reader to decide whether a
http://www.bchealthguide.org/kbase/shc/shc29fac.htm

Extractions: var hwPrint=1;var hwDocHWID="shc29fac";var hwDocTitle="Factor V Leiden / Thrombophilia";var hwRank="1";var hwSectionHWID="shc29fac-Header";var hwSource="en-caQ2_05";var hwDocType="Shc"; This information is provided as a resource and does not constitute an endorsement for any group. It is the responsibility of the reader to decide whether a group is appropriate for his/her needs. For evidence-based information on diseases, conditions, symptoms, treatment and wellness issues, continue searching this site. Online. The above information was "verified" as correct on the date at the end of each entry. Since American Self-Help Group Clearinghouse's database is extensive but staffing is limited and information for these organizations can change, it is not possible to keep every entry in American Self-Help Group Clearinghouse database completely current and accurate. Please check with the organizations listed for the most current information. For additional information on self-help groups, please visit the American Self-Help Group Clearinghouse web site at http://www.mentalhelp.net/selfhelp
BioMed Central | Full Text | The Relationship Of The Factor V Leiden Mutation Or
Specifically, we examined if the factor v leiden (FVL) mutation or the deletion The factor v leiden mutation was present in none of the 38 experimental
http://www.biomedcentral.com/1471-2474/2/1
Factor V Leiden Mutation
The approximately 6% with the mutant factor v leiden gene should not Heterozygosity for the Leiden mutation of the Factor V gene, a common
http://www.mdl-labs.com/factorv.htm
Genaissance - Products And Services - GLP Genotyping - Factor V Leiden
CYP3A5, DRD2, F2, factor v leiden, FLT3, MDR1, NAT2, PPAR, SDC4, UGT1A1, 5HTT factor v leiden is associated with the following complications venous
http://www.genaissance.com/pcds/capabilitiesServices_cg_factor.asp

Extractions: Available Assays Choose an Assay... APOE COMT Factor V Leiden PPAR This mutation is in the initial cleavage site of Factor Va, which disrupts the recognition by Activate Protein C. The result is a long-lived Factor Va and a hypercoaguable state. The clinical name for this condition is Activate Protein C resistance (APCR), which is the most common inherited risk factor in venous thrombosis. Heterozygosity for this mutation is associated with a 5 to 10-fold increased risk of developing a venous thrombitic episode while homozygosity for this mutation is associated with a 50 to 100-fold increased risk. Factor V Leiden is associated with the following complications: venous thrombosis (blood clots, especially with oral contraceptives); deep vein thrombosis (DVT, blood clots in veins); unexplained miscarriage; blood clots in the lungs or anywhere else; gall bladder dysfunction; preeclampsia and/or eclampsia (toxemia while pregnant); and stroke and/or heart attack. Phenotype expression: Blood clots Therapeutic significance: Cardiovascular disease What gene codes for: Clotting factor Indications for use of assay: Concern of thrombophilia
Hypercoagulability And Thrombosis: Factor V Leiden
factor v leiden Figure Inactive factor V is activated by thrombin mediated cleavage of the B domain, resulting in the formation of a dimer.
http://medicine.ucsf.edu/htc/hypernthromb/hypernthromb.fctrvldn.html

Extractions: The factor V Leiden mutation is represented by a single adenine-to-guanine point mutation in the gene coding for coagulation factor V. This results in the replacement of arginine by glutamine at a key proteolytic site on the activated factor V protein, such that the molecule cannot be cleaved by activated protein C - hence the so-called APC resistance. Factor V clotting activity is normal in coagulation assays. Rather, factor V is resistant to inactivation in vivo. The factor V Leiden mutation is found in 2% - 5% of the asymptomatic caucasian population, and is accountable for approximately 40% of patients presenting with idiopathic venous thromboembolic disease. It has also been associated with increased risks for recurrent venous thromboembolism, for venous thrombosis during use of oral contraceptives and pregnancy, and for thrombosis in the presence of other genetic and acquired abnormalities of anticoagulation, such as protein C and S deficiencies. Homozygous Leiden mutation is estimated to be 1:5,000. The overall thrombotic risk for homozygotes is estimated to be 11-fold higher than for heterozygotes and 80-fold higher than normal individuals. The probability of a thrombotic episode before the age of 33 years in a homozygous Leiden mutation is twice that for a heterozygote (40% versus 20%). Below is a diagram of the inactivation of factor V: Figure: Inactive factor V is activated by thrombin mediated cleavage of the B domain, resulting in the formation of a dimer.
Factor V Leiden - Children's Hospital Boston
Home factor v leiden. Flower factor v leiden. Programs that treat this condition or perform this procedure. Thrombophilia. Unfortunately, at this time,
http://www.childrenshospital.org/az/Site866/mainpageS866P0.html

Extractions: or find by letter: A-F G-L M-R S-Z My Child Has... Home Factor V Leiden Factor V Leiden Programs that treat this condition or perform this procedure Thrombophilia Unfortunately, at this time, we are not able to provide information about this condition or procedure. However, we will be frequently adding and updating information in Child Health A to Z. So please bookmark this site and visit us again soon. Children's Hospital Boston is the primary pediatric teaching hospital of Harvard Medical School Contact Us Privacy Accessibility Give Now Children's Hospital Boston 300 Longwood Avenue Boston MA 02115
JAMA -- Abstract: Ethnic Distribution Of Factor V Leiden In 4047 Men And Women.
Activated Protein C Resistance, factor v leiden, and Central Retinal Vein High Prevalence of Factor V Mutation (Leiden) in the Eastern Mediterranean
http://jama.ama-assn.org/cgi/content/abstract/277/16/1305

Extractions: Vol. 277 No. 16, April 23, 1997 Featured Link E-mail Alerts ARTICLE Article Options Send to a Friend Similar articles in this journal Literature Track Add to File Drawer Download to Citation Manager PubMed citation Articles in PubMed by Ridker PM Buring JE Articles that cite this article Contact me when this article is cited P. M. Ridker, J. P. Miletich, C. H. Hennekens and J. E. Buring Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA 02215-1204, USA. pmridker@bics.bwh.harvard.edu OBJECTIVE: To estimate ethnic-specific prevalence rates of factor V Leiden, an inherited defect of hemostasis associated with risk of venous thrombosis. DESIGN: Survey of 4047 American men and women participating in
Factor V Leiden
Hematology and Oncology Coagulopathy Hypercoagulable APC resistance.
http://www.fpnotebook.com/HEM27.htm

Extractions: Home About Links Index ... Editor's Choice document.write(code); Advertisement Hematology and Oncology Coagulopathy Assorted Pages Coagulation Bleeding Disorders Dysfibrinogenemia Hemophilia A Factor IX Deficiency ... Perioperative Anticoagulation Factor V Leiden Factor 5 Leiden APC Resistance Activated Protein C resistance Book Home Page Cardiovascular Medicine Dentistry Dermatology Emergency Medicine Endocrinology Gastroenterology Geriatric Medicine Gynecology Hematology and Oncology HIV Infectious Disease Jokes Laboratory Neonatology Nephrology Neurology Obstetrics Ophthalmology Orthopedics Otolaryngology Pediatrics Pharmacology Practice Management Prevention Psychiatry Pulmonology Radiology Rheumatology Sports Medicine Surgery Urology Chapter Hematology and Oncology Index Anemia Cancer Coagulopathy Cardiovascular Medicine Dermatology Endocrinology Otolaryngology Examination Gastroenterology Hemoglobin Hemolysis Histiocytosis HIV Infectious Disease Laboratory Leukemia General Pulmonology Lymph Marrow Neurology Obstetrics Orthopedics Pediatrics Pharmacology Platelet Prevention Procedure Psychiatry Rheumatology Sarcoma Surgery Symptom Evaluation Vascular Page Coagulopathy Index Bleeding Bleeding Dysfibrinogenemia Bleeding Hemophilia A Bleeding Hemophilia B Bleeding Von Willebrands Clotting Pathway Background Clotting Pathway Common Clotting Pathway Extrinsic Clotting Pathway Inhibition Clotting Pathway Intrinsic DIC Hypercoagulable Hypercoagulable Antithrombin III Hypercoagulable APC resistance Hypercoagulable Fibrinolysis Hypercoagulable Protein C-S Epidemiology
Improved Distinction Of Factor V Wild-Type And Factor V Leiden Using A Novel Pro
Key Words, factor v leiden; Activated protein C resistance; Antiphospholipid antibodies; Noscarin; Russell viper venomfactor V
http://www.ajcp.com/previews/abstracts/204232.html

Extractions: Marianne Wilmer, PhD Christoph Stocker, Brigitte Conell, MD, and Andreas Calatzis, MD Key Words: DOI: 10.1309/T8AVVH7QWGL0QTF5 Abstract A new prothrombin-based activated protein C resistance (APC-R) test is described. In this method, the patient sample is prediluted in a plasma depleted of factor V (FV). A reagent containing APC and a specific activator of FV is added. After an incubation period, clotting is initiated by the addition of the FV-dependent prothrombin activator Noscarin. We analyzed 703 samples from patients undergoing thrombophilia screening. By using a predefined cutoff ratio of 2.5, 100% sensitivity and specificity for the detection of a factor V Leiden ( FVL ) mutation was found. With a cutoff ratio of 1.2, a complete but narrow distinction of FVL heterozygous (n = 192) and FVL homozygous samples (n = 27) was determined. No interference by the international normalized ratio, activated partial thromboplastin time (aPTT), protein S activity, fibrinogen and factor VIII (FVIII) levels, or lupus anticoagulant ratio was detected. The new prothrombin-based APC-R assay provides improved distinction of FV wild-type and FVL carriers compared with the aPTT-based method. By the use of an FV-dependent prothrombin activator, the assay is not influenced by FVIII concentration or lupus anticoagulants.
Diagnostic Single Nucleotide Polymorphism Analysis Of Factor V Leiden And Prothr
Diagnostic Single Nucleotide Polymorphism Analysis of factor v leiden and Prothrombin 20210G A. A Comparison of the Nanogen Electronic Microarray With
http://www.ajcp.com/previews/abstracts/202267.html

Extractions: Iris Schrijver, MD, Marla J. Lay, and James L. Zehnder, MD Key Words: Thrombophilia; Factor V; Prothrombin; Factor II; Microarray; LightCycler; NanoChip; Restriction fragment length polymorphism; RFLP DOI: 10.1309/3VTR7TL2X7TXL0QY Abstract Roche Diagnostics , Indianapolis, IN), and microarray-based testing on the novel NanoChip electronic microarray (NanoChip Molecular Biology Workstation, Nanogen, San Diego, CA). We compared these methods for accuracy, time to results, throughput, and interpretation. Results from 789 of 800 individual amplicons analyzed on the NanoChip were in complete agreement with the other assays. Eleven were "no calls" (uninterpreted by the NanoChip system) resulting from failed polymerase chain reaction amplifications. Although the NanoChip System, when used in a low-throughput setting, requires more overall time than the LightCycler, it is nearly equivalent per genotyping call. Owing to minimal sample handling, assay results are more reliable on the NanoChip platform and on the LightCycler than with RFLP. The NanoChip assay is reliable and may be especially valuable to laboratories with a large volume of thrombophilia test requests.
Factor V Leiden Meetup Groups - Meetup.com
It s easy to join one of our groups of factor v leiden Sufferers. Look around to find the perfect Organize your own factor v leiden Meetup Group today!
http://fvl.meetup.com/groups/

Extractions: @import url("http://www.meetup.com/templates/default_v2/site.css"); @import url( http://www.meetup.com/templates/default_v2/images.css ); To organize a local Hurricane Support Meetup for free, email us All Factor V Leiden Meetup Groups What's this? Add to your site google_color_bg = 'eef6fe'; google_color_border = 'D6E3F6'; google_color_line = 'bdd0ee'; google_alternate_color = 'eef6fe'; google_hints = "Factor V Leiden"; Meetup.com is home to thousands of local interest groups that meet face-to-face every month. It's easy to join one of our groups of Factor V Leiden Sufferers . Look around to find the perfect group for you Interested in some thing else? Some where else? Explore thousands of other groups worldwide Country United States of America Canada Great Britain Australia Afghanistan Albania Algeria American Samoa Andorra Angola Anguilla Antarctica Argentina Armenia Aruba Australia Austria Azerbaijan Bahamas Bahrain Bangladesh Barbados Belarus Belgium Belize Benin Bermuda Bhutan Bolivia Bosnia-Herzegovina Botswana Brazil Brunei Bulgaria Burkina Faso Burundi Cambodia Cameroon Canada Cape Verde Cayman Islands Central Africa Chad Chile China Colombia Comoros Congo Congo (Dem. Rep.)
Factor V Leiden Meetups On The Map - Meetup.com
It s easy to join one of our groups of factor v leiden Sufferers. Meet other local people who have been diagnosed with factor v leiden (FVL).
http://fvl.meetup.com/about/

Extractions: @import url("http://www.meetup.com/templates/default_v2/site.css"); @import url( http://www.meetup.com/templates/default_v2/images.css ); To organize a local Hurricane Support Meetup for free, email us All Factor V Leiden Meetup Groups What's this? Add to your site google_color_bg = 'eef6fe'; google_color_border = 'D6E3F6'; google_color_line = 'bdd0ee'; google_alternate_color = 'eef6fe'; google_hints = "Factor V Leiden"; Meetup.com is home to thousands of local interest groups that meet face-to-face every month. It's easy to join one of our groups of Factor V Leiden Sufferers . Look around to find the perfect group for you Interested in some thing else? Some where else? Explore thousands of other groups worldwide World Cont. US
Factor V Leiden Is Not Common In Patients Diagnosed With Primary Pulmonary Hyper
An abnormal factor V (factor v leiden) may contribute to thrombosis in the pulmonary microcirculation of PPH patients. A point mutation in which adenine is
http://erj.ersjournals.com/cgi/content/abstract/12/5/1177

Extractions: This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Elliott, C. Articles by Pietra, G. Eur Respir J 1998; 12: 1177-1180 ERS Journals Ltd CG Elliott, MF Leppert, GJ Alexander, K Ward, L Nelson, and GG Pietra Substantial evidence suggests that thrombosis contributes to the pathogenesis of primary pulmonary hypertension (PPH). An abnormal factor V (factor V Leiden) may contribute to thrombosis in the pulmonary microcirculation of PPH patients. A point mutation in which adenine is substituted for guanine at nucleotide 1691 (1691A) alters factor V so that it resists cleavage by activated protein C. Heterozygosity for the 1691A mutation is more common (2-8%) in Caucasian Europeans and Americans than in Africans (1%) and Asians ( <1%). The aim of the study was to examine the prevalence of the mutation that codes for factor V Leiden in individuals with PPH. We identified 42 Caucasians diagnosed with PPH. We extracted deoxyribonucleic acid (DNA) from whole blood and assayed DNA samples for the point mutation (1691 A) that codes for factor V Leiden. One out of 42 (2.4%; 95% confidence interval=0.1-12.6) Caucasians diagnosed with PPH was heterozygous for the normal 1691G and mutant 1691A allele. All 10 individuals with familial PPH were homozygous for the normal 1691G allele. The prevalence of heterozygosity for the 1691A allele and the normal 1691G allele does not differ from that observed in reference (control) populations. The low prevalence of the 1691A mutation among individuals diagnosed with primary pulmonary hypertension provides evidence that factor V Leiden does not contribute to the pathogenesis of the disease in most patients.
YOUNG-WOMEN Messages For June, 2002: Factor V Leiden
Yesterday, i found out that I am factor v leiden. The hematologist says I shouldn t continue depo provera, but does not say that I cannot continue
http://forums.obgyn.net/young-women/YOUNG-WOMEN.0206/0263.html

Extractions: Thu, 20 Jun 2002 10:50:06 -0500 (CDT) Yesterday, i found out that I am Factor V Leiden. The hematologist says I shouldn't continue depo provera, but does not say that I cannot continue injections. Any advice? recommended search... OBGYN.net only forums endozone.org Web use when must restrict search to only the young women's forum...

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