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  1. Association between isotretinoin use and central retinal vein occlusion in an adolescent with minor predisposition for thrombotic incidents: a case report An otherwise healthy 17-year-old white man who was treated with systemic isotretinoin for recalcitrant acne was referred with central retinal vein occlusion in one eye. Although a detailed investigation was negative, DNA testing revealed that the patient was a heterozygous carrier of the G20210A mutation of the prothrombin gene. Despite the fact that this particular mutation is thought to represent only a minor risk factor for thromboses, it is probable that isotretinoin treatment greatly increased the risk of a vaso-occlusive incident in this patient. the drug appears to act on the coagulation process by a still unexplained mechanism.
  2. How did I get these antibodies? Most the time, doctors do not know why some people get antiphospholipid antibodies. In a small number of people, an infection or drug caused the antibody. (im sure this could apply to numerous types of antibodies triggered by a drug) Antiphospholipid syndrome (APS) is an immune disorder that commonly manifests with a variety of CNS effects. Moderate/severe erectile dysfunction in patients with antiphospholipid syndrome. CONCLUSION: To our knowledge, this was the first study that demonstrated moderate/severe ED in almost 50% of cases of a rare autoimmune disease. This alteration was linked to arterial events and longer disease duration.
  3. looking at genes related to lupus, and there are a lot of them. I've flagged bad for quite a few in prometheus. Which some are showing as 50/50 chance basically of inheriting in the general population. But a few of mine are more rare, at least according to Snpedia or this software. I notice some keywords here possibly relating to vitamin k. I haven't done much research on lupus or categories of it. i'm not sure yet if this could be sort of silent with no skin manifesting symptoms or maybe it's overall a non-issue. I'll look into this a little more. Testing should also help or be definitive. im homozygous for this snp. 4 percent chance. SNP rs13277113 PubMedID [PMID 18204098] Condition Systemic lupus erythematosus Gene C8orf13, BLK Risk Allele A pValue 1.00E-010 OR 1.39 95% CI 1.28-1.51 OMIM 612254 Desc SYSTEMIC LUPUS ERYTHEMATOSUS, SUSCEPTIBILITY TO, 12; SLEB12 Variant Related also OMIM 191305 Desc TYROSINE KINASE, B-LYMPHOCYTE SPECIFIC; BLK
  4. Just had this blood test as well Antiphospholipid Antibody Panel Hopefully, at least with what i got going on, I'll be able to narrow this down pretty quickly. At least with what's testable. I mainly got these two tests after reading this paragraph from genetic genie, and doing some research on it. so we will see. This test alone was 900 dollars. luckily fully insurance covered. I hope lol. Acetylcholine and antiphospholipid autoantibodies are seen in various autoimmune and chronic illnesses. It is well know that with Myasthenia Gravis, patients most commonly have autoantibodies against nicotinic acetylcholine receptor (nAChR). A large number of CFS patients may have acetylcholine receptor antibodies according to a study published in the International Journal of Molecular Medicine. Dysautonomia and POTS can also be associated with autoantibodies against acetylcholine receptors. Mayo medical laboratories has a very comprehensive Autoimmune Dysautonomia Evaluation lab test that tests for autoantibodies against acetylcholine receptors and much more. Antiphospholipid Syndrome (or Hughes syndrome) is an autoimmune condition that can lead to hypercoagulation and blood clots. Conditions such as Lupus, Sjogren’s syndrome, Chronic Fatigue Syndrome, and Fibromyalgia are often associated with antiphospholipid antibodies. Antiphospholipid antibodies can even develop in presence of chronic infections such as Hepatitis C, Syphilis, Chlamydia pneumoniae, EBV, HHV-6, Lyme disease, mycoplasma, Q Fever, and many other infections. Antiphospholipid syndrome can be tested for with LabCorp’s Thrombotic Risk Profile.
  5. @mariovitali You posted this. Am I missing something here? This is vitamin k dependant. This is vitamin k stimulating. two vitamin K-dependent proteins, are ligands for the Tyro3/Axl/Mer family Increased plasma levels of the soluble Mer tyrosine kinase receptor in systemic lupus erythematosus relate to disease activity and nephritis. Increased levels of, in particular, sMer and, to some extent, sTyro3, were found in patients with SLE or RA, but not in patients with CLI. Patients with SLE demonstrated the highest sMer levels and there was a strong correlation to higher SLE disease activity score (SLEDAI). In contrast, in patients with RA, the sMer levels did not correlate with the disease activity score (DAS). In SLE, sMer levels were particularly high in those with lupus nephritis, patients who also had decreased C1q levels and increased titers of anti-DNA antibodies. After therapy, the plasma concentrations of sMer decreased in parallel to the decrease in SLEDAI score.
  6. Was just thinking back on my MRA. One drawback of MRA is that it does not depict small vessels or extremely slow blood flow as well as conventional angiography does. However, with its advantages, MRA is a good examination for many patients. WHAT SHOULD I EXPECT DURING THE PROCEDURE? MRA is a painless and noninvasive procedure in which no incisions or arterial catheters are required. With some MRA techniques, contrast agents are not necessary, so no intravenous lines are needed. With other techniques, a small amount of a gadolinium-based contrast agent is added to highlight the blood vessels and enhance the sharpness of the image. This contrast material is infused through an intravenous line placed in your arm. No other preparation is involved. - See more at:
  7. isnt this putting the cart before the horse a little bit? Im sure anyone is capable of answering this question, but I would just say lets cross that bridge when we get there. I'm sure there would be alot of people to tell if we found something concrete. I have seen there is blood testing for menaquinones, its just not widely available or standardized. Maybe sometime in the future when there is more research and understanding on its importance, it will become a standard test. Regarding Lupus I am curious if some of us would show some of the antibodies to lupus that might contribute to symptoms but not necessarily have full blown lupus. Here is kind of what im talking about. There are also associations between antiphospholipid antibodies and headaches, migraines, and oscillopsia.[5] Some studies have shown the presence of antiphospholipid antibodies in the blood and spinal fluid of patients with psychological symptoms.[6] Very few patients with primary APS go on to develop SLE. If testing did reveal this to be a autoimmunity issue triggered by accutane, it sounds like there are some people on your forum that might have some good knowledge of this. There is also this for digestive issues. Some of these tests are the exact tests I just got, being tested by Mayo Clinic. Serological Profiles Aiding the Diagnosis of Autoimmune Gastrointestinal Dysmotility Autoimmune gastrointestinal dysmotility is a limited autoimmune dysautonomia occurring idiopathically or in the context of an anatomically remote neoplasm, previously documented or unsuspected. Here we report 24 Mayo Clinic patients in whom the profile of serum autoantibodies aided this diagnosis. Recorded motility abnormalities included: esophageal dysmotility 8 (6 had achalasia), delayed gastric emptying 12, slow small intestinal transit 7, slow colonic transit 4, and pelvic floor dyssynergia 4. Four patients underwent abdominal surgery; 2 commenced total parenteral nutrition. Plasma membrane cation channel autoantibodies were detected in 23 patients: neuronal voltage-gated calcium channel (5 N-type and 1 P/Q-type), acetylcholine receptor (11 ganglionic-type and 4 muscle-type) and neuronal voltage-gated potassium channel autoantibodies (4). Two patients had anti-neuronal nuclear autoantibody, type 1. Approximately half of the patients had other antibody markers of organ-specific autoimmunity (including skeletal muscle, striational, GAD65, thyroid or gastric parietal cell specificities). Neoplasia was diagnosed in 11 patients (9 recent, 2 remote): lung, breast and endometrial, gastrointestinal and thymoma. Moderate to dramatic improvement in gastrointestinal symptoms was reported following immunotherapy in 4 of 4 patients treated, and following pyridostigmine in 2 of 2 patients treated.
  8. Just got this blood test in. Ammonia, Plasma 54 ug/dL reference 27 - 102 Still waiting on the osteocalcin results, they might have messed something up and I might need to retake it.
  9. I prefer to use aspirin alternatives like nattokinase, fish oil, garlic, ginger, and turmeric instead. They are useful and safe natural blood thinners. So here is a thought. Just for one time purposes you take 2 full strength Aspirin 325mg each. Do you feel better? More color in your skin? clearer thoughts? Nice Warm sensation in your head? Im not looking at this for anti-headache. im looking at this for powerful blood thinning properties you might notice pretty quick. (i would caution this for people with gastritis or serious heartburn, maybe try lower dose or safe alternatives first) If you notice a big difference. This could explain alot. Then we would go from here. id substitute fish with Krill btw. This could still all tie together with liver/cardiovascular/neurological/Digestive It could have started with methyl donor loss via loss of PC (choline) or systemic reduction in b12 levels (also methyl donor loss) that starts to dispose you to some of these conditions. how can you correct this? maybe a combination of k2 and natural blood thinner? not sure. While continuing to detox the liver. (ie. lecithin) or supply methyl donors like b12. Just a thought, but id try the aspirin. Because what your feeling or not feeling in your head might be from lack of blood flow. What they are showing for blood thinners would probably also be the most powerful and safe anti inflammatories. You could maybe include vitamin e in that as well.
  10. you can check these genes. It might be good to know this. Thrombotic Risk Profile, DNA Analysis This assay detects the R506Q (Leiden) mutation in the factor V gene, the G20210A mutation in the factor II (prothrombin) gene, and the C677T and A1298C mutations in the MTHFR gene. factor is f5, f2 you can find all of this on 23andme. I just checked. I already knew I was heterozygous for c677t and a1298c, but normal for r506q and g20210a
  11. One of my favorite artists ever. tighter and tighter from down on the upside. Yea the drugs to keep him off the drugs is what might have killed him. Such a loss. Saw him live once, best show ever. He was a rock God, had the coolest friends, a wife and kids, and goes out like that. More then tragic and yea you wonder if he never took those pills...
  12. Here is some more info on k2 safety or thickening the blood. It is often postulated that excessive vitamin K may result in overcoagulation, i.e. increased thrombosis risk. However, vitamin K-dependent proteins have a limited number of Glu residues capable of g-carboxylation per molecule, beyond which there can be no further g-carboxylation or excessive coagulation. Despite this, it is critical to demonstrate that a high intake of menaquinones does not increase thrombosis risk. It was shown in rats that thrombosis risk is not increased at doses up to 250 mg/kg of MK-4(104). In human subjects, the endogenous thrombin potential, which is the most sensitive marker to evaluate thrombosis risk in plasma(105), was not affected by MK-7 intakes as high as 360mg/d for 6 weeks(70). The only exception to this is observed in individuals on coumarin-based oral anticoagulants, for whom dietary sup- plementation with vitamin K can influence the stability of the international normalised ratio(59,106). MK-7 has the poten- tial to interfere with oral anticoagulants at doses greater than 50mg/d(13). However, there is little collective experience on the potential toxicity or adverse events associated with sustained menaquinone supplementation among individuals with normal coagulation.
  13. CHRONIC FATIGUE SYNDROME: STUDIES ON CLINICAL PRESENTATION, so this is kind of interesting. Floats around alot of things that have been discussed on here. Myalgic encephalomyelitis: A highly prevalent debilitating disease • Persistent, debilitating fatigue associated with numerous physical and neurocognitive symptoms Disease severity can range from moderate to extremely severe: • Prevalence estimates: 0,3 to 0,6%; one million patients in the USA, two million patients in Europe This may just be the tip of the iceberg • High socio-economic cost Cost to the society estimated as approximately $16 billion in the USA, €20 billion in Europe • Patients usually present with multiple intestinal symptoms including: Nausea Abdominal pain Poor appetite Abnormal bowel motility Gastric reflux Bloating • Inflammation of the gastrointestinal tract • Marked alteration of the intestinal microbial flora Immune alterations resulting from intestinal dysfunction CHRONIC FATIGUE SYNDROME: STUDIES ON CLINICAL ... Persistent, debilitating fatigue associated with numerous physical and .... Heavy metals interfere directly with energy production. Oxidase. Cu2+. H. S. S. S. S. H.
  14. here is a study referencing mk7 did not induce any type of hypercoagulation. I'd still like to look more into this though. Low-dose menaquinone-7 supplementation improved extra-hepatic vitamin K status, but had no effect on thrombin generation in healthy subjects.
  15. Here is a study linking vitamin k to bile salt metabolism Vitamin K and thrombosis. Merli GJ1, Fink J. Author information Abstract Vitamin K was discovered in the 1930s during cholesterol metabolism experiments in chickens. It is a fat-soluble vitamin which occurs naturally in plants as phylloquinone (vitamin K1) and is produced by gram-negative bacteria in the human gastrointestinal tract as menaquinone (vitamin K2). This vitamin was found to be essential for normal functioning of hemostasis. In addition, a number of clinical conditions in which vitamin K deficiency was found to be the underlying pathophysiologic problem were discovered. These conditions include hemorrhagic disease of the newborn, obstructive jaundice, and malabsorption syndromes. The importance of this vitamin has become more apparent with the discovery of the anticoagulant warfarin which is a vitamin K antagonist. There are millions of patients on this therapy for a variety of thrombogenic conditions such as atrial fibrillation, deep vein thrombosis, pulmonary embolism, and prosthetic cardiac valves. The wide use of this narrow therapeutic index drug has resulted in significant risk for major bleeding. Vitamin K serves as one of the major reversing agent for patients over-anticoagulated with warfarin. In the past few years, research has focused on new areas of vitamin K metabolism, which include bone and endovascular metabolism; cell growth, regulation, migration, and proliferation; cell survival, apoptosis, phagocytosis, and adhesion. These new areas of research highlight the significance of vitamin K but raise new clinical questions for patients who must be maintained on long-term warfarin therapy.
  16. A low-oxalate diet is a meal plan that is low in oxalate.Oxalate is a chemical found in plant foods Ha I think im already on this diet. No salads? no problem. So that guy didn't realize accutane might have been the source of his problems after all these years. Unfortunately that's nothing new. Just looking at that forum, I can come to one conclusion, that southpark looking girl is a real B. But seriously, I think we can have the most elaborate, in-depth theories in the world, (it's easy to get lost in this too) but it really comes down to what can we test? and what can we do about this, or how do we treat and gage things? In other words what's medically viable that applies to the real world? Hopefully some of this will all come together.
  17. here is just looking at one side of things, but it goes to show how potent k2 in the form of mk7 can be. Obviously there are alot of health benefits to k2 as well, putting calcium in the bones ,decreasing heart disease risk, and blood vessel health. Maybe that osteocalcin blood test will reveal something. Effect of low-dose supplements of menaquinone-7 (vitamin K2 ) on the stability of oral anticoagulant treatment: dose-response relationship in healthy volunteers. CONCLUSIONS: MK-7 supplementation at doses as low as 10 μg (lower than the usual retail dose of 45 μg) significantly influenced anticoagulation sensitivity in some individuals. Hence, the use of MK-7 supplements needs to be avoided in patients receiving VKA therapy
  18. what your saying has been similar with me. Ive been getting alot of blood test recently, and its like my blood clots so fast i dont even need a bandaid after getting blood drawn. Its a drop or two of blood, then it quickly dries up and thickens. id keep this in mind as well. Natto as the food is very high in k2. Which maybe there could be a balancing effect. There could be more info then just this on the subject as well. Will Nattokinase and K-2 Work Against Each Other If Taken Together? By Vitamins and Supplements FAQs Question: I am a bit confused. I've read that nattokinase can be a good supplement to take for cardio issues as it has blood thinning properties, and at the same time read that K-2 can be a good supplement to take for cardio issues, but doesn't K-2 assist in coagulation? It seems to me that if both of these supplements are taken that they will work against each other? One of the major reasons people take Vitamin K-2 for cardiovascular support is because it supports the formation of Osteocalcin, a protein carrier which helps to transfer calcium into the bone. Nattokinase helps breaks down fibrin, which is the webby structure that forms the basis of clots to help support circulation. Vitamin K-2 does support the formation of clotting factors in the liver, which under ideal circumstances will simply remain on stand-by until the body has a legitimate need to initiate the clotting process, leading to production of fibrin. The two could actually be considered as “balancing” one another. Generally, there is a cycle going on for most substances in the body with the substance being built up or formed and then being broken down. In other words, Nattokinase and Vitamin K-2 have very different effects on the body, but like many other supplements can have some overlapping areas of benefits. They don’t exactly work against each other because the clotting factors will allow your blood to clot when needed, but won’t force it to clot. If you have any history of blood clots or anything which might compromise the integrity of the blood vessels and contribute to abnormal clotting, you wouldn’t want to take either product without consulting your health care practitioner. If you have a tendency to clotting, K-2 could aggravate this since something is activating the clotting process when it isn’t desirable instead of just having the clotting factors sitting around on stand-by. If you take any prescription blood-thinners like Warfarin, Coumadin, Plavix, etc you certainly wouldn’t want to take either Nattokinase or K-2 without consulting health care practitioner.
  19. Nattokinase improves blood flow by inhibiting platelet aggregation and thrombus formation Im thinking there could be issues of reduced blood flow to the brain. Natural blood thinners could maybe help.
  20. Hatetane posted about spinal cord degeneration possibly being associated with accutane. anyone seem to develop bad posture post tane? From a nutritional standpoint, there arent many factors that cause this, but b12 deficiency is one of them. Im going to get a intrinsic factor test on monday to see if this comes back showing antibodies. Oral vitamin B12 therapy: a cautionary note Although absorption of dietary vitamin B12 requires gastric intrinsic factor and an intact terminal ileum, pharmacologic doses of the vitamin can be absorbed by passive diffusion throughout the small intestine.1(pp96-97) Indeed, an oral dose of 2000 μg per day of cyanocobalamin was found to be effective treatment for clinically significant vitamin B12 deficiency even in subjects with classic pernicious anemia.2Ease of administration and low cost make oral vitamin B12 a more attractive option than traditional intramuscular therapy. However, over-the-counter vitamin B12preparations are not subject to regulation and standardization. When one subject was noted to be using vitamin B12 tablets labeled as a “timed release” preparation, pharmacies in the New Haven, CT, area were surveyed. In the 9 pharmacies visited, 10 of 12 brands of tablets containing 1000 μg or 2000 μg of vitamin B12 were found to be “timed release” preparations. Dissolution times were indicated on the labels of 4 of these preparations and ranged from 3 hours to 6 hours. Only “timed release” preparations were available in 5 of 6 major chain discount pharmacies visited. The most recent study of therapy with oral vitamin B12 used two 1000-μg tablets of the Nature's Bounty brand (Bohemia, NY) which is not labeled as a “timed release” preparation.2 Thus, the effectiveness of “timed release” tablets has not been established. Since prompt treatment of vitamin B12-deficient subjects is required to prevent progressive, irreversible neurologic and cognitive impairment,1(pp287-290),3caution is warranted in the use of oral vitamin B12 therapy particularly with “timed release” tablets, and particularly in the setting of pernicious anemia or disorders of the terminal ileum.
  21. Phosphatidylcholine is not the same as polyenylphosphatidylcholine (PPC). PPC is actually listed in the Physician’s Desk Reference of the United States and it is an approved treatment in many European countries for chronic liver disease. Others who would benefit from PPC include those who have Hepatitis C (but not Hepatitis B), liver cirrhosis or impaired liver function, pancreatitis or NSAID-induced gastritis and ulceration. Research suggests that PPC’s protection may extend from the liver to the stomach, pancreas and cardiovascular system. Looking into this^ I hopefully doubt you have this, but I believe we can experience very similar types of symptoms. I would def get tested for this though( MRI,Spinal MRI) if you are concerned. the longer you wait without treatment, the worse it can get. Random. These findings identify an LRH-1 dependent phosphatidylcholine signalling pathway that regulates bile acid metabolism
  22. here is just one study showing lecithin being a good thing, and possibly even a causative factor in lupus through methyl donor loss. Metabolic Disturbances Associated with Systemic Lupus Erythematosus Abstract The metabolic disturbances that underlie systemic lupus erythematosus are currently unknown. A metabolomic study was executed, comparing the sera of 20 SLE patients against that of healthy controls, using LC/MS and GC/MS platforms. Validation of key differences was performed using an independent cohort of 38 SLE patients and orthogonal assays. SLE sera showed evidence of profoundly dampened glycolysis, Krebs cycle, fatty acid β oxidation and amino acid metabolism, alluding to reduced energy biogenesis from all sources. Whereas long-chain fatty acids, including the n3 and n6 essential fatty acids, were significantly reduced, medium chain fatty acids and serum free fatty acids were elevated. The SLE metabolome exhibited profound lipid peroxidation, reflective of oxidative damage. Deficiencies were noted in the cellular anti-oxidant, glutathione, and all methyl group donors, including cysteine, methionine, and choline, as well as phosphocholines. The best discriminators of SLE included elevated lipid peroxidation products, MDA, gamma-glutamyl peptides, GGT, leukotriene B4 and 5-HETE. Importantly, similar elevations were not observed in another chronic inflammatory autoimmune disease, rheumatoid arthritis. To sum, comprehensive profiling of the SLE metabolome reveals evidence of heightened oxidative stress, inflammation, reduced energy generation, altered lipid profiles and a pro-thrombotic state. Resetting the SLE metabolome, either by targeting selected molecules or by supplementing the diet with essential fatty acids, vitamins and methyl group donors offers novel opportunities for disease modulation in this disabling systemic autoimmune ailment.
  23. here is this test right here. I'll try to get this as well. Antiphospholipid Antibody Panel Overview Ordering Info Algorithms Related Guides CPT Code(s) 86146 (x3), 86147 (x3), 86148 (x3) Includes Beta-2-Glycoprotein I Antibodies (IgG, IgA, IgM), Phosphatidylserine Antibodies (IgG, IgA, IgM), Cardiolipin Antibodies (IgA, IgG, IgM) Methodology Immunoassay Antiphospholipid syndrome is an autoimmune disease characterized by antiphospholipid antibodies and at least 1 clinical manifestation, the most common being venous or arterial thrombosis and recurrent fetal loss.1,2,3,4,5,6,7,8 The syndrome occurs in isolation (primary antiphospholipid syndrome)9,10,11 or in association with connective tissue diseases (secondary antiphospholipid syndrome), particularly systemic lupus erythematosus.12 Antiphospholipid antibodies are heterogeneous and may be detected by immunoassays or functional coagulation assays. Current treatment strategies focus on anticoagulation,13whereas traditional forms of immunosuppression are unhelpful I did have the coagulation test already. I take that back there might be another one more exclusive to lupus. anyone had lupus type testings? That actually has been mentioned in accutane lawsuits, or at least a law firm's website. There was a study relating to reduced blood flow in the brain and accutane.
  24. I wouldnt supplement Methionine , it can actually harm the methylation cycle. excess is harmful in other ways as well. Id supplement lecithin over choline. Unfortunately all of this has been done and thought of to death since day 1, so idk what's new?