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!
Quote:
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.
linkyCortico-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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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: 
