IndigoRush

Repairing the long-term damage from Accutane

12,542 posts in this topic

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: http://www.asnr.org/patientinfo/procedures/mrangiography.shtml#sthash.fwutECbD.dpuf

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@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.

 

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1 hour ago, guitarman01 said:
@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.

Actually it gets interesting when Professor Jonathan Edwards who was responsible for using Rituximab on patients of Lupus, starts saying that the method being used for Research using machine learning will be "Garbage In", "Garbage out"

http://forums.phoenixrising.me/index.php?threads/machine-learning-assisted-research-on-cfs.51283/page-4#post-853554

I specifically ask him if References in the paper are also considered Garbage and he fails to answer this. I believe that this fact is quite interesting.

http://forums.phoenixrising.me/index.php?threads/machine-learning-assisted-research-on-cfs.51283/page-4#post-853658


I recall very vividly that when i crashed with Propecia, i had autoimmune-like symptoms for months including Urticaria ,Joint Pains, dysphagia and dyspepsia. Edited by mariovitali

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4 hours ago, guitarman01 said:

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: http://www.asnr.org/patientinfo/procedures/mrangiography.shtml#sthash.fwutECbD.dpuf

Is a MRA similar to MRI in procedure?

you lie down and go back into machine etc, I got claustrophobic with an MRI and had to get out. They gave me the option next time to be sedated during procedure. 

Does this procedure measure brain inflammation? Which is what I need to address first and foremost.

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Guys, just want to write a quick sappy post.. 

Very thankful for the community that we have here. If it weren't for the constant research, love (maybe not all the time lol) and support I truly believe a lot of us wouldn't keep pushing through today. We WILL find a way out. So much respect for all of you. 

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Just had this blood test as well
http://www.questdiagnostics.com/testcenter/TestDetail.action?ntc=14890

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.





  Edited by guitarman01
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1 hour ago, guitarman01 said:

Just had this blood test as well
http://www.questdiagnostics.com/testcenter/TestDetail.action?ntc=14890

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.





 
Keep us updated sir! I think we're getting closer

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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



 

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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.





  Edited by guitarman01

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Association between isotretinoin use and central retinal vein occlusion in an adolescent with minor predisposition for thrombotic incidents: a case report

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649144/

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.
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This is quite interesting too i believe.

You will recall that one of the Genes selected by the Network Analysis i provided has selected MERTK.  I added to string-db the term MERTK in order to find associated Genes :


screen1.png


You may also see GAS6 (also selected by the Network Analysis i provided)


Next we have the following :

screen2.png





Notice the lines having as entries :

1) Biotin
2) acetyl-coa Metabolic Process
3) Fatty acid biosynthesis
4) Fatty acid Metabolism
5) Pyruvate Metabolism (...!!!)


Then we have the CFS Study by Fluge mentioning impaired Pyruvate Dehydrogenase function!
 

Quote

Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161229/


  Edited by mariovitali
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@mariovitali  Good stuff. I've been following the gist of your recent posts and wanted to mention that I went years believing I may have CFS before making a solid connection to using Accutane when the nightmare began. ...Main reason was simply that I was chronically fatigued and in pain from the time I went on the drug until a few years ago, when these symptoms lifted. There didn't seem to be the large subgroup of CFS patients with sexual symptoms and severe depression, as there are with post-Accutane, but I may have missed them. Either way, thanks for enlightening some of the post-Accutane folks on the CFS forums.

Have been thinking of collecting sets of differentially expressed genes from studies of Accutane, SSRI, and 5-ari drugs, and running them through pathway analysis tools to find possible overlapping effects:
https://david.ncifcrf.gov/
http://pantherdb.org/index.jsp

Have you tried this yet, or have  you been focused on starting with symptomatology of the patient groups you are looking at?
Is the software you have been using available as a web-based application?

 
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@Dubya_B

Thank you for your post. I haven't tried this because -in full honesty- i have no idea how to do it. The tool i use basically generated Hypotheses on the most likely aetiologies of these syndromes. Yet one more tool i use, reads 23andme Data and identifies all relevant SNPs that need to be looked at. As an example , if SUOX/CDO1 SNPs are found then we most likely need to support Sulfation with Low dose Molybdenum and B2.

I strongly believe that the software #1 repeatedly was able to identify important information (relevant Genes and Pathways) and all results are reproducible. Unfortunately it is not available as a Web-based application.

Also in full knowledge of what i am saying here, the latest case is a 37- year old woman having a mixture of CFS/Fibro, Depression, Constipation, Loss of Libido and many other neurological symptoms and hormonal symptoms (including premature menopause which was slowly reversed) being 90% well after 25 years of disease (Post-Accutane). This happened within 10 weeks. This is why i asked if there is some organization of the Post-Accutane sufferers so we may readily start (=evaluate these Hypotheses by Medical Personnel). Needless to say that this patient does not believe on what she experiences and believes that there may be a relapse. 

Very soon i will disclose the main node of the Network Analysis on my Blog so all of this is somehow documented. I wil also post some excerpts from-probably- one of the most interesting Papers i've ever read.

I will help in any way i can, no compensation involved, but this effort has to be properly evaluated by Medical researchers. Unfortunately this is easier said than done as over and over i hit a wall when it comes to having *any* researcher evaluate the findings of my Research.

  Edited by mariovitali
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@Dubya_B @tanedout

I was in shock to see this. The OMF has appointed Fluge and Mella (both trying to use Rituximab) for CFS/ME patients.


Excerpts from a site i found on Rituximab :
 
Quote
Rituximab is marketed with black box warnings about a number of serious side effects that can cause death and disability. It is given intravenously; infusion reactions are common, and severe infusion reactions have been fatal. Infusions require premedication and special safety precautions. Infusion reactions occur in up to 50% of patients, usually with the first dose; they typically develop within 30 minutes to 2 hours but can be delayed for up to 24 hours. Severe mucocutaneous reactions can also be fatal. Hepatitis B virus can be reactivated. Fatal bacterial, fungal, and viral infections can occur. It can cause cardiac arrhythmias, renal toxicity, bowel obstruction and perforation, and many other side effects.


<SNIP>
 
Quote
At the time I wrote, there were two more studies pending, both open label and without a control group. One of those is still ongoing. The other has been completed. It found an improvement in self-reported fatigue scores in 64% of patients. It took an average of 23 weeks to see improvement. 14 patients had a “major response” lasting an average of 105 weeks; 4 had a “moderate response” lasting 69 weeks. 18 of the 28 subjects were the same individuals who had participated in the 2008 randomized study. Adverse events included two allergic reactions, two episodes of neutropenia, and eight transient symptom flares. One major responder dropped out after 32 months when he experienced a full relapse. Since there was no control group, it’s hard to judge what these results mean.


<SNIP>
 
Quote
Whitney is featured in a video that also features Dr. Kogelnik and his Open Medicine Institute.  He posts as “Whit” on the Phoenix Rising forum. In December 2012 he was able to write an articulate, coherent post. He apparently was started on rituximab by Dr. Kogelnik in January 2013 and rapidly went downhill. By April he posted “Can’t read much now…”


The treatment costs $40K



https://sciencebasedmedicine.org/chronic-fatigue-syndrome-rituximab-revisited/
  Edited by mariovitali

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7 hours ago, mariovitali said:
Also in full knowledge of what i am saying here, the latest case is a 37- year old woman having a mixture of CFS/Fibro, Depression, Constipation, Loss of Libido and many other neurological symptoms and hormonal symptoms (including premature menopause which was slowly reversed) being 90% well after 25 years of disease (Post-Accutane). This happened within 10 weeks. This is why i asked if there is some organization of the Post-Accutane sufferers so we may readily start (=evaluate these Hypotheses by Medical Personnel). Needless to say that this patient does not believe on what she experiences and believes that there may be a relapse. 

What protocol did she follow Mario? Is there a thread on PR where she has posted the details of what she did to recover? Great to hear she is 90% better! 
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@tanedout

Her regimen is personalised. This means that if a person is given -say- Molybdenum for supporting Sulfation, for another individual it may be toxic.

This is why i insist that this Research should be investigated under controlled conditions and under the supervision of Medical Personnel. My Goal is to gather around 20 people that became symptom-free and then -as a group- ask for Research done on the specific kind of regimen and Hypothesis on what is going on.

She is not on PR but she is ready to talk to a Research team with her real name if i ask her to do so.

Edited by mariovitali

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