blood vessel pathology suggested in sepsis

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby 1eye » Sun Jun 26, 2011 6:41 pm

Well, from the sound of it: 1 of 3 things. Either H pylori doesn't have those effects. Or it has those effects and the damage does not stop after the H pylori is gone. Or the treatment you had got rid of the stomach infection but didn't touch the endothelial one.

Take your pick. I have no clue. Heat is a wicked problem, isn't it?
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Postby 1eye » Mon Jun 27, 2011 8:56 am

How can somebody be born without a jugular or some other major vein and not know it? In them, how can there be any onset of disease, if they were born with it and lived happily without it until the onset, when the onset is caused by equipment that they have never had?

Some of the MRIs I have seen look like damage that has taken a long time, not something that either happened at birth or overnight. Certainly collateral growth can happen over time in response to environment, pathogens, or injury. Maybe fully formed veins can atrophy and eventually disappear?
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Postby Shannon » Mon Jun 27, 2011 9:13 am

Or, an alternative explaination, such as that described here: http://discovermagazine.com/2011/apr/16 ... :int=2&-C= Perhaps we have spirochetes DNA in our genomes which interacts with subsequent bacterial infections in ways that we do not yet understand. Our very DNA may be altered by bacterial infections, with the evolutionary benefit being that further bacterial invasions in the body have to compete. This could be the process that we see when we have "exacerbations" of MS. Also, H. Pylori might have already incorporated human DNA into its own, the way gonorrhea was found to have human DNA in it when sequenced. If that were the case, then I suppose it would make H.Pylori even more a dangerous fugitive than once thought. I do not think that the H. Pylori genome has yet been decoded. I think it should be next on the list!
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Postby 1eye » Mon Jun 27, 2011 10:34 am

I'm sorry, I think my brain is very seriously overloaded and I'm sure many would agree underpowered. I cannot for the life of me imagine what this person or you or somebody is proposing is happening in exacerbation or is happening to damaged or missing veins. I am really very serious. I tried. I read the interview you linked to and it was great, but my mind is tabula rasa. I have a massive headache and I really can't cope anymore with this train of thought. If you can help me with some kind of a more simple-minded explanation, great, but otherwise I am afraid I may have to leave further elaboration to the experts, who are more capable than I. It really does sound fascinating, and I regret terribly to have had this melt-down. Sorry.
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Postby Shannon » Mon Jun 27, 2011 11:28 am

I was suggesting that it could possibly explain how infections, whether bacterial or viral, can exacerbate symptoms of MS. My last exacerbation, the worst I've had thus far, came following being exposed to a child who turned out to have had Hand Foot and Mouth Disease when visiting my house. Others that I have had seemed to be triggered by flu. Who knows if maybe E.coli infections, or something else, may also trigger exacerbations? That was my only point. As to the endothelium of veins or the vein structure that we see in CCSVI, I have nothing to add to what has already been theorized earlier. I doubt that what I posted was even helpful in that regard. I was only giving another possible avenue as to how H. Pylori may play it's role in MS, not CCSVI specifically. If that is what you were looking for in my post, then i'm really sorry, too. I certainly believe that CCSVI exists, also, but how it relates to anything else I really have no clue. So many unknowns, so many possible causes, so many possible triggers, so many questions.
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Postby 1eye » Mon Jun 27, 2011 3:18 pm

Me, I think all it takes for a bacterium or virus to trigger an exacerbation is for the host to be ready for the next big push of infection: to be in a weakened state. Personally I associate all my attacks with stress brought on by a state of mortal fear. I am a prime candidate for the nocebo effect. There was always a reason for fear: it was not irrational. But it also weakened me. The other key event that seemed connected was the removal of the fear or stress. I don't know if I am allergic to cortisol, or if withdrawal from it is what is bad for me: I had a course of oral steroids where it was such a high dose the pharmacist had to double-check. I went off it cold-turkey with no problems. Same when I had IV steroids. But when I used low-dose oral cortisone to titrate myself down from an IV course, I thought I was gonna die.
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Postby Shannon » Mon Jun 27, 2011 7:07 pm

That's bad news. :( I get oral prednisone to come down from the IV steroids. Is this the same as cortisol, or similar? I know you're in Canada, so maybe just another name for the same thing? I know that steroids and prednisone lower the immune system and make us prone to infection, too. The thing about our genome, and portions of it coming from bacteria and viruses, is that they find it in RNA, or protein producing bodies, therefore they make viral proteins and bacterial proteins for the immune system to play with. This cannot be good, and when new infections arise, there must be something that happens. I agree about stress, boy do I ever! And saturated fats, too. I had one episode directly after Christmas, when I consumed all sorts of deviled eggs, sour cream dips, cocktail weenies, and you name it. This in another reason that I believe in the role that is played by CCSVI. It fits perfectly with why the Swank Diet worked so well for many PWMS. Almost no saturated fat and the right combination of vitamin supplements. That has to be due to vascular issues, in my humble, non-academic, opinion. If you happen to be interested in DNA and genetics, as I am, here is an article that I came across today. Interesting trivia about DNA for all: http://discovermagazine.com/2011/apr/20 ... -about-dna
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Postby Johnson » Mon Jun 27, 2011 11:14 pm

Shannon wrote:That's bad news. :( I get oral prednisone to come down from the IV steroids. Is this the same as cortisol, or similar?


Cortisol is a natural steroidal hormone produced and released by the adrenal glands as a response to stress. Cortisone is a chemical synthesized in the laboratory, and used to reduce inflammation. Both are toxic in the long term. Both cause the loss of bone mass, inhibit the immune system, insulin production - amongst other not-so-good things.
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Postby Shannon » Wed Jun 29, 2011 1:48 pm

So, why give Cortisone instead of Prednisone? I assume they must have a similar purpose, in titrating down the steroid dose and reducing inflammation? Is Prednisone the same as Cortisone under a different name? I am just wondering, because 1eye had such a bad response to Cortisone, but I do pretty good on Prednisone. I know that Prednisone lowers the immune system though. I thought it was the IV Solumedrol that wore down bone mass over time? Thanks for answering!
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Postby Johnson » Wed Jun 29, 2011 4:21 pm

Shannon wrote:So, why give Cortisone instead of Prednisone? I assume they must have a similar purpose, in titrating down the steroid dose and reducing inflammation? Is Prednisone the same as Cortisone under a different name? I am just wondering, because 1eye had such a bad response to Cortisone, but I do pretty good on Prednisone. I know that Prednisone lowers the immune system though. I thought it was the IV Solumedrol that wore down bone mass over time? Thanks for answering!


Question: What are the differences between hydrocortisone, cortisone acetate, prednisone, and dexamethasone? Are there any guidelines as to when one is used versus another?

Answer: These compounds are all adrenal steroid analogs; specifically, they are called glucocorticoids. Glucocorticoids affect carbohydrate, protein, and fat metabolism, bone metabolism, and immune and inflammatory functions. In contrast, the mineralocorticoid aldosterone, also secreted by the adrenal, regulates sodium and potassium metabolism and fluid balance. The glucocorticoid that is produced by the body is cortisol, also known as hydrocortisone. Cortisone acetate is the glucocorticoid cortisone with an ester group attached that makes it soluble in water. Cortisone is biologically inactive and is rapidly converted to cortisol by the liver so that it can exert its effects. Hydrocortisone and cortisone acetate are both short-acting glucocorticoids. They are given once daily, in the early morning, to patients who are recovering from Cushing's syndrome or are being tapered off pharmacological dosages of glucocorticoids to allow their hypothalamic -pituitary-adrenal axis to recover. These are the only circumstances in which I prescribe hydrocortisone, and I do not use cortisone acetate.

Prednisone and dexamethasone are also synthetic glucocorticoids. Prednisone is 4 to 5 times more potent than hydrocortisone and has a longer duration of action, perhaps 12 hours or more. Dexamethasone is 40 to 50 times more potent than hydrocortisone and even longer-acting, 18 to 24 hours. Both of these glucocorticoids are given when a prolonged action is desired. This includes replacing cortisol in patients with permanent adrenal insufficiency (Addison's disease) or suppressing ACTH secretion in patients with congenital adrenal hyperplasia. In such cases, the medication is taken at bedtime, thus the patient awakens with appropriate levels of steroid. Very rarely, these medications cause insomnia if taken at night. These longer acting glucocorticoids are also used to suppress inflammation or immune rejection, and both are less expensive than hydrocortisone.

If a patient with permanent adrenal insufficiency is doing well on hydrocortisone replacement, usually split between two or three doses, the largest taken in the morning, I usually do not change the medication. However, if the patient is not doing well, I will change the medication to dexamethasone or prednisone. Some of my patients have reported remarkable improvements in their quality of life on these longer acting medications. The longer acting glucocorticoids have been reported to have greater catabolic activity on bone, but there is no evidence that they act differently than cortisol. Rather, it is probably because they are used in inappropriately high dosage.

The usual replacement dosages of these glucocorticoids are : hydrocortisone about 25 mg/day, cortisone acetate about 37.5 mg/day, prednisone about 5 mg/day, and dexamethasone about 0.5 mg/day. Glucocorticoid replacement in any patient must be carefully monitored and individualized.

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Cortico-steroids do have a deleterious effect on bones (besides inhibiting the immune system, insulin synthesis, etc.). I am not familiar with Solumedrol.

I do not believe that "MS" is an auto-immune dis-ease, but that one of it's antagonsts is actually a compromised immune system. This is why Vitamin D3 can be beneficial in "MS", as it has an Abx effect, and boosts the immune system (provided that Vit. D receptors are not clogged by bio-films).

Neurology offered IV cortico-steroids to me in the event of a major relapse and I refused on the basis of immune inhibition. The neuro said that that was a good thing as my immune system was attacking my brain, and was stunned/annoyed when I told him that "MS" is not auto-immune. I believe that research will eventually vindicate me in my position.
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Postby Shannon » Wed Jun 29, 2011 7:40 pm

Thanks so much for clarifying that Johnson (or whatever your name is)! I see the answer to one of my questions is that Cortisone and Prednisone are in the same group of drugs, which I should have known by looking at the suffix -sone- in both. The trouble for me is how incredibly good I feel when I have the Solumedrol/Prednisone treatments. I've had them only twice, but I feel like I would do it again, if needed. I really do feel normal again, for a time, and it is a good feeling. I have known that the treatment comes with risks, however.

My brother was just diagnosed with Hyperesinophilic Syndrome, so I understand that corticosteroids have been used with him several times during flare ups. He is a 25 yr. old male. He presents with urticaria to the feet and dangerously high white blood cell levels. I was told that his levels when admitted recently were as high as 2,700 cells/microL, with 3,000 often being fatal. We do not know yet what the treatment plan will be for him going forward, until he sees many more doctors. The information that you've posted will be on my mind as we hear more.
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