Advice for those planing to take first time AAS

[emeric delczeg]

Before you you start taking any AAS or prohormones, have check your hormone levels, all organs, glands and for factor 5 blood disorder.

 

[PsyT]

what can happen to you?

if a person already has started should they still check for this?

also, if a person has cycled and their hormone levels never got back up to normal (did not check them before cycle so its possible they were low to start with), would you recommend getting on TRT asap? This is after trying an "aggressive" PCT (HCG followed by aromasin and clomid and also humanofort if that makes a difference).

 

[hawkmoon]

I think Emeric's advice is very wise, if not only to check for any potential issues that might be raised when/if going on, but also to establish a baseline for future reference.

I wish I had done this 20+ years ago. I have always felt I had naturally low test, but I have no numbers to back it up.

 

[emeric delczeg]

I think Emeric's advice is very wise, if not only to check for any potential issues that might be raised when/if going on, but also to establish a baseline for future reference.

I wish I had done this 20+ years ago. I have always felt I had naturally low test, but I have no numbers to back it up.

Yes, so this way you will know if you have a existing hormonal problem.

 

[royal]

Factor 5 blood disorder

Emeric,what is that?I get regular check ups and blood work every six months.
I'm not on aas but i have never heard of this.

 

[kscowboy]

Very good recommendation Emric!

 

[emeric delczeg]

what can happen to you?

if a person already has started should they still check for this?

also, if a person has cycled and their hormone levels never got back up to normal (did not check them before cycle so its possible they were low to start with), would you recommend getting on TRT asap? This is after trying an "aggressive" PCT (HCG followed by aromasin and clomid and also humanofort if that makes a difference).

Yes, you shold check you organs and glands, and factor 5 is a must.

.

 

[emeric delczeg]

Emeric,what is that?I get regular check ups and blood work every six months.
I'm not on aas but i have never heard of this.

Factor V Leiden
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factor V Leiden
Classification and external resources
ICD-9 289.81
DiseasesDB 154
Factor V Leiden (sometimes factor VLeiden) is the name given to a variant of human factor V that causes a hypercoagulability disorder. In this disorder the Leiden variant of factor V cannot be inactivated by activated protein C.[1] Factor V Leiden is the most common hereditary hypercoagulability disorder amongst Eurasians.[2][3][4] It is named after the city Leiden (The Netherlands), where it was first identified in 1994 by Prof R. Bertina et al.[5]

Contents [hide]
1 Pathophysiology
2 Epidemiology
3 Diagnosis
4 References
5 Further reading
6 External links


[edit] Pathophysiology
In the normal person, factor V functions as a cofactor to allow factor X to activate an enzyme called thrombin. Thrombin in turn cleaves fibrinogen to fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C (aPC) is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.

SNP: Factor V Leiden
Name(s) Factor V Leiden, Arg506Gln, R506Q, G1691A
Gene F5
Chromosome 1
External databases
Ensembl Human SNPView
dbSNP 6025
HapMap 6025
SNPedia 6025
HgenetInfoDB 6025
ALFRED SI001216K
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 (activated Protein C). 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 protein's 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 generation and excess clotting.

The excessive clotting that occurs in this disorder is almost always restricted to the veins, where the clotting may cause a deep vein thrombosis (DVT). If the venous clots break off, these clots can travel through the right side of the heart to the lung, where they block a pulmonary blood vessel and cause a pulmonary embolism. Women with the disorder have an increased risk of miscarriage and stillbirth. It is extremely rare for this disorder to cause the formation of clots in arteries that can lead to stroke or heart attack, though a "mini-stroke", known as a transient ischemic attack, is more common . Given that this disease displays incomplete dominance, those who are homozygous for the mutated allele are at a heightened risk for the events detailed above versus those that are heterozygous for the mutation.

[edit] Epidemiology
Studies have found that about 5% of Caucasians in North America have factor V Leiden. The disease is less common in Hispanics and African-Americans and is extremely rare in people of Asian descent.

Up to 30% of patients who present with deep vein thrombosis (DVT) or pulmonary embolism have this condition. Factor V Leiden doubles the risk that a person will have a DVT during their life, but it is unclear whether these individuals are at increased risk for recurrent venous thrombosis. While only 1% of people with factor V Leiden have two copies of the defective gene, these homozygous individuals have a more severe clinical condition. The presence of acquired risk factors for venous thrombosis—including smoking, use of estrogen-containing (combined) forms of hormonal contraception use, and recent surgery—further increase the chance that an individual with the factor V Leiden mutation will develop DVT.

Women with factor V Leiden have a substantially increased risk of clotting in pregnancy (and on estrogen-containing birth control pills or hormone replacement) in the form of deep vein thrombosis and pulmonary embolism. They also may have a small increased risk of preeclampsia, may have a small increased risk of low birth weight babies, may have a small increased risk of miscarriage and stillbirth due to either clotting in the placenta, umbilical cord, or the fetus (fetal clotting may depend on whether the baby has inherited the gene) or influences the clotting system may have on placental development.[8] Note that many of these women go through one or more pregnancies with no difficulties, while others may repeatedly have pregnancy complications, and still others may develop clots within weeks of becoming pregnant.

[edit] Diagnosis
Suspicion of factor V Leiden being the cause for any thrombotic event should be considered in any caucasian patient below the age of 45, or in any person with a family history of venous thrombosis.

There are a few different methods by which this disease can be diagnosed. Most laboratories screen 'at risk' patients with either a snake venom (e.g. dilute Russell's viper venom time) based test or an aPTT based test. In both methods, the time it takes for blood to clot is shortened in the presence of the factor V Leiden mutation. This is done by running two tests simultaneously, one test is run in the presence of activated protein C (APC) and the other, in the absence. A ratio is determined based on the two tests and the results signify to the laboratory whether APC is working or not. These are quick, three minute, automated tests that most hospital laboratories can easily perform.

There is also a genetic test that can be done for this disorder. The mutation (a 1691G→A substitution) removes a cleavage site of the restriction endonuclease MnlI, so PCR, treatment with MnlI, and then DNA electrophoresis will give a diagnosis.

[edit] References
Comparison of Russell viper venom-based and activated partial thromboplastin time-based screening assays for resistance to activated protein C. Am J Clin Pathol. 2008 Nov;130(5):796-804. Herskovits AZ, Lemire SJ, Longtine J, Dorfman DM. Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.[1][dead link]
Press, R. D., Bauer, K. A., Kujovich, J. L., Heit, J. A. (2002) Arch Pathol Lab Med 126, 1304-1318. "Clinical Utility of Factor V Leiden (R506Q) Testing for the Diagnosis and Management of Thromboembolic Disorders"
^ De Stefano V, Leone G (1995). "Resistance to activated protein C due to mutated factor V as a novel cause of inherited thrombophilia". Haematologica 80 (4): 344–56. PMID 7590506. **broken link removed**.
^ Ridker PM, Miletich JP, Hennekens CH, Buring JE (1997). "Ethnic distribution of factor V Leiden in 4047 men and women. Implications for venous thromboembolism screening". JAMA 277 (16): 1305–7. doi:10.1001/jama.277.16.1305. PMID 9109469.
^ Gregg JP, Yamane AJ, Grody WW (December 1997). "Prevalence of the factor V-Leiden mutation in four distinct American ethnic populations". Am. J. Med. Genet. 73 (3): 334–6. doi:10.1002/(SICI)1096-8628(19971219)73:3<334::AID-AJMG20>3.0.CO;2-J. PMID 9415695.
^ De Stefano V, Chiusolo P, Paciaroni K, Leone G (1998). "Epidemiology of factor V Leiden: clinical implications". Semin. Thromb. Hemost. 24 (4): 367–79. doi:10.1055/s-2007-996025. PMID 9763354.
^ Bertina RM, Koeleman BP, Koster T, et al. (1994). "Mutation in blood coagulation factor V associated with resistance to activated protein C". Nature 369 (6475): 64–7. doi:10.1038/369064a0. PMID 8164741.
^ "SNP linked to Gene F5". NCBI. SNP linked to Gene F5(geneID:2153) Via Contig Annotation.
^ Jennifer Bushwitz, Michael A. Pacanowski, and Julie A. Johnson (2006-10-11). "Important Variant Information for F5". PharmGKB. Important Variant Information for F5 [PharmGKB].
^ Rodger MA et al.Inherited Thrombophilia and Pregnancy Complications Revisited.Obstet Gynecol. 2008 Aug;112(2 Pt 1):320-4.
[edit] Further reading
Hooper WC, De Staercke C (2006). "The relationship between FV Leiden and pulmonary embolism". Respir. Res. 3: 8. doi:10.1186/rr180. PMID 11806843.
Nicolaes GA, Dahlback B (2002). "Factor V: Factor V and thrombotic disease: description of a janus-faced protein". ATVB 22 (4): 530–538. PMID 11950687.
Andreassi MG, Botto N, Maffei S (2006). "Factor V Leiden, prothrombin G20210A substitution and hormone therapy: indications for molecular screening". Clin. Chem. Lab. Med. 44 (5): 514–21. doi:10.1515/CCLM.2006.103. PMID 16681418.
Segers K, Dahlback B, Nicolaes GA (2007). "Coagulation factor V and thrombophilia: background and mechanisms.". Thrombosis Haemost. 98 (3): 530–542. PMID 17849041.
[edit] External links
MeSH factor+V+Leiden
Kujovich JL, Goodnight SH (2007-02-17). "Factor V Leiden Thrombophilia". GeneReviews. University of Washington, Seattle. **broken link removed**. Retrieved 2008-06-20.
Smith DO (2008-05-12). "Thrombophilia Awareness Project". Information for those living with factor V Leiden and other forms of thrombophilia. Retrieved 2008-06-20. "Information for those living with thrombophilia"
National Alliance for Thrombosis and Thrombophilia - National Patient organization dedicated to thrombosis and thrombophilia.]
GeneReview/NIH/UW entry on Factor V Leiden Thrombophilia
[hide]v • d • ePathology: hematology · hematologic diseases of RBCs and megakaryocytes / MEP (D50-69,74, 280-287)

Red
blood cells ↑ Polycythemia Polycythemia vera


↓ Anemia Nutritional Micro-: Iron deficiency anemia (Plummer-Vinson syndrome)


Macro-: Megaloblastic anemia (Pernicious anemia)

Hemolytic
(mostly Normo-) Hereditary enzymopathy: G6PD · glycolysis (PK, TI, HK)

hemoglobinopathy: Thalassemia (alpha, beta, delta) · Sickle-cell disease/trait · HPFH

membrane: Hereditary spherocytosis (Minkowski-Chauffard syndrome) · Hereditary elliptocytosis (Ovalocytosis) · Hereditary stomatocytosis

Acquired Autoimmune (WAHA, CAD, PCH)


membrane (PNH)

MAHA · TM (HUS)

Drug-induced autoimmune · Drug-induced nonautoimmune

Hemolytic disease of the newborn


Aplastic
(mostly Normo-) Hereditary: Fanconi anemia · Diamond-Blackfan anemia


Acquired: PRCA · Sideroblastic anemia · Myelophthisic

Blood tests MCV (Normocytic, Microcytic, Macrocytic) · MCHC (Normochromic, Hypochromic)


Other Methemoglobinemia · Sulfhemoglobinemia · Reticulocytopenia



Coagulation/
coagulopathy/
bleeding
diathesis ↑ Thrombocytosis Essential thrombocytosis

Hypercoagulability primary: Antithrombin III deficiency · Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden · Hyperprothrombinemia
acquired: DIC (Congenital afibrinogenemia, Purpura fulminans) · autoimmune (Antiphospholipid)


↓ Thrombocytopenia
and purpura Nonthrombocytopenic purpura: Henoch-Schönlein purpura

Thrombocytopenic purpura: ITP (Evans syndrome) · TM (TTP)

Heparin-induced thrombocytopenia · May-Hegglin anomaly

Platelet function adhesion (Bernard-Soulier syndrome) · aggregation (Glanzmann's thrombasthenia) · platelet storage pool deficiency (Hermansky-Pudlak syndrome, Gray platelet syndrome)

Clotting factor Hemophilia (A/VIII, B/IX, C/XI) • Von Willebrand disease • Hypoprothrombinemia/II · XIII



myeloid navs: cells/physio, disease of RBCs+megakaryocytes/monocytes+granulocytes/neoplasia, symptoms+signs/eponymous
↑ means increased, ↓ means decreased


Retrieved from "http://en.wikipedia.org/wiki/Factor_V_Leiden"
Categories: Hematology | Blood proteins | Single nucleotide polymorphisms
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[maldorf]

Yes, you shold check you organs and glands, and factor 5 is a must.

.

Yep, factor five to make sure you dont have a natural tendency for a high hematocrit. Another thing I learned of, and nobody ever tests for, is the prothrombin mutation. Testing for the prothrombin mutation is a genetic test, I think factor five might be too? They can run an INR on your blood to see how fast it clots, this would be a tip that you might have a prothrombin issue.

 

[Athlete]

Yes, I've recommended here that people take a DNA test. This is along the same lines as that. It will tell you a lot of things that are great to know before cycling.

 

[FilthyMick]

Soooo.... I go to my doctor ad tell him i would like to order a DNA test? Does insurance cover this, as well as the factor 5?
Also how do AAS affect someone with factor 5, does it cause extremely high hematocrit, what is a symptom?

 

[Athlete]

Soooo.... I go to my doctor ad tell him i would like to order a DNA test? Does insurance cover this, as well as the factor 5?
Also how do AAS affect someone with factor 5, does it cause extremely high hematocrit, what is a symptom?

For a more extensive DNA test you can use a company like 23andme.com or similar.
I know some big hospitals do them too, for example the university hospital in my neighboring city. They specialize in cardiology and said they could test me for certain hereditary traits.

Note: I don't live in the US.

 

[maldorf]

QUESTION TO EMERIC

Emeric, I am wondering if you take coumadin now.

When they test you for clotting problems, there is a thing that they call the clotting cascade. there is a whole hoast of things that can go wrong during that long chain of chemical rxns in your body. The factor 5 and prothrombin issues are 2 of them.

 

[maldorf]

Good medical article on clotting and Prothrombin mutation (Factor 2)

So we have identified factors 2 and 5 now. There is a whole lot more that can go wrong though. Steroids affect these conditions because steroids can make you hypercoagulable on their own even if youre "normal". Put them together with steroids and you can have a real problem. Women with these problems are told not have take birth control pills becuase of the hormones. It appears both the androgens and "female" hormones can lead to hypercoagulabity. If you read the warnings with these drugs you will see it in the literature.

Prothrombin 20210 Mutation (Factor II Mutation) -- Varga and Moll 110 (3): e15 -- Circulation

From the article, it lists the 3rd reason why you might get a clot "or (3) have a temporary condition that leads to an increased clotting tendency, such as recent surgery, trauma, a cast, prolonged immobility, pregnancy, or the use of oral contraceptives or hormone replacement therapy."

Also of interest, but you should read the whole thing: "Understanding the Blood Clotting Process

Normally, there is a fine balance in the body which ensures that there is not too much bleeding or blood clotting. If this balance is disrupted, a blood clot may occur.

Throughout the course of a normal day, the blood vessels sustain many minor injuries of which you are not aware. In response, the body naturally triggers the "clotting cascade"—a sequence of events that allows the blood cells (platelets) and clotting proteins to respond to the site of the injury to clog up the vessel disruption and stop you from bleeding, and then to repair it. Although the activation of this clotting process occurs normally, a problem may arise in a person with thrombophilia. This is because he or she may possess blood clotting proteins in abnormal amounts, so that the clotting overshoots and a big blood clot may form." Steroids will aggrevate this condition.

 

[maldorf]

Risks of having factor 2

YOU CAN SEE THAT IT IS RATHER COMMON, EPIDEMIALOGICALLY, BECAUSE IT OCCURS IN 2% OF WHITE POPULATION OR 2 IN EVERY 100. IF YOU EXTRAPLOATE THAT TO 2108 ACTIVE USERS I SEE ON THE SITE NOW, THERE ARE 42 PEOPLE THAT HAVE IT. THATS ASSUMING THEY ARE ALL WHITE.


What Are the Implications of Having a Prothrombin 20210 Mutation?

Heterozygous prothrombin mutations are found in about 2% of the US white population. The mutation is uncommon in African Americans (approximately 0.5%) and is rare in Asians, Africans, and Native Americans. The homozygous form is considered uncommon, with an expected occurrence of approximately 1 in 10 000 individuals. The prothrombin 20210 mutation is equally as common in men and in women. It has nothing to do with blood type.

Having the prothrombin mutation increases the risk of developing a DVT (a blood clot in the deep veins, typically the legs) and/or PE (blood clot that travels to the lungs). DVTs are dangerous because they can damage the veins, leading to pain and swelling, and sometimes to disability. PEs can damage the blood vessels in the lung, leading to chest pain and shortness of breath, and are sometimes life-threatening. Approximately 1 in every 1000 people will develop a DVT or PE each year. The risk of developing a DVT or PE increases with age, with an average risk of 1 in 10 000 for people in their twenties to 1 in 200 for people in their seventies. Having a heterozygous prothrombin mutation increases the risk of developing a first DVT by about 2 to 3 times the background (or 2 to 3 in 1000 people each year). Having homozygous prothrombin mutations increases the risk further, but it is not yet known how much the risk is increased.

It should be noted that many people with the prothrombin mutation will never develop a blood clot in their lifetime. Very often, people who have the prothrombin mutation and develop a blood clot have additional risk factors (see the Table).

YOU CAN SEE BELOW THAT MOST PEOPLE THAT HAVE THIS NEVER KNOW IT AND NEVER HAVE ANY ISSUES AT ALL, BUT YOU START ADDING IN HORMONES AND THEN PROBLEMS CAN ARISE.
Most studies indicate that prothrombin mutations are not a risk factor for heart attack and stroke in the middle-aged and elderly. However, few studies have shown that the prothrombin mutation may increase risk of heart attacks in young women, particularly those who smoke cigarettes.

 

[emeric delczeg]

Emeric, I am wondering if you take coumadin now.

When they test you for clotting problems, there is a thing that they call the clotting cascade. there is a whole hoast of things that can go wrong during that long chain of chemical rxns in your body. The factor 5 and prothrombin issues are 2 of them.

I take only 2.5mg per day, after my last check up my MD thinks that I don`t have any clottin problems, so he told me that I don`t need coumedin, I made my own decision regardion the 2.5mg. I ben taking for the last 3 years 400mg Nattokinase per day 2x200mg, and I think that the reason why I am OK.

 

[emeric delczeg]

So we have identified factors 2 and 5 now. There is a whole lot more that can go wrong though. Steroids affect these conditions because steroids can make you hypercoagulable on their own even if youre "normal". Put them together with steroids and you can have a real problem. Women with these problems are told not have take birth control pills becuase of the hormones. It appears both the androgens and "female" hormones can lead to hypercoagulabity. If you read the warnings with these drugs you will see it in the literature.

Prothrombin 20210 Mutation (Factor II Mutation) -- Varga and Moll 110 (3): e15 -- Circulation

From the article, it lists the 3rd reason why you might get a clot "or (3) have a temporary condition that leads to an increased clotting tendency, such as recent surgery, trauma, a cast, prolonged immobility, pregnancy, or the use of oral contraceptives or hormone replacement therapy."

Also of interest, but you should read the whole thing: "Understanding the Blood Clotting Process

Normally, there is a fine balance in the body which ensures that there is not too much bleeding or blood clotting. If this balance is disrupted, a blood clot may occur.

Throughout the course of a normal day, the blood vessels sustain many minor injuries of which you are not aware. In response, the body naturally triggers the "clotting cascade"—a sequence of events that allows the blood cells (platelets) and clotting proteins to respond to the site of the injury to clog up the vessel disruption and stop you from bleeding, and then to repair it. Although the activation of this clotting process occurs normally, a problem may arise in a person with thrombophilia. This is because he or she may possess blood clotting proteins in abnormal amounts, so that the clotting overshoots and a big blood clot may form." Steroids will aggrevate this condition.

Yes, this information is very important , can save many lifes.

 

[maldorf]

I take only 2.5mg per day, after my last check up my MD thinks that I don`t have any clottin problems, so he told me that I don`t need coumedin, I made my own decision regardion the 2.5mg. I ben taking for the last 3 years 400mg Nattokinase per day 2x200mg, and I think that the reason why I am OK.

I took the nattokinase like you recommended before I started in on the coumadin. Now that Im on coumadin I dont worry about it. The research of nattokinase is impressive and I recommend others consider its use when on AAS. Im glad you brought it up!
I now take 6mg coumadin/day to maintain my INR between 2-3. Its been averaging about 2.4.

 

[emeric delczeg]

I took the nattokinase like you recommended before I started in on the coumadin. Now that Im on coumadin I dont worry about it. The research of nattokinase is impressive and I recommend others consider its use when on AAS. Im glad you brought it up!
I now take 6mg coumadin/day to maintain my INR between 2-3. Its been averaging about 2.4.

I was taking 5mg coumadin per day with 400mg Nattokinase per day for 3 years, is very safe to take coumadin and Nattokinase togheter. Also you my take as high to 15g Omega 3 per day with the coumadin, it will halp to prevent vein calcification one of the side effect of the coumadin.

 

[hugga39]

Very good advice! But chances are 99% wont do it... I wish I did!