CFS, celiac, Addison's and orthostatic intolerance

xchocoholic

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Hi there ...

Has anyone here looked at this ?

I hadn't looked at this yet and was surprised at how many of the symptoms and treatments for POTS / NMH / OI are the same as the treatments for Addison's disease. I appear to meet the diagnostic criteria for Addison's. I haven't been tested yet though. I know salt loading helps my OI and I need it to keep my BP up. And I know that my DHEA is low. And I have feelings of hypoglycemia every couple of hours at least, that respond to eating a healthy snack and/or sometimes a quick sugar fix.

My doc told me to try taking DHEA so I started taking 5 mg yesterday. So far all I noticed is that I still feel the need to lay down every few hours. But when I do, my body doesn't want to stay there ... lol ... Normally, I feel a huge sense of relief throughout my body when I lay down. GRANTED ... it is way too early to tell how this is going to work. The RDA from my doc was 25 - 50 mg a day too. I'm one of those who sometimes responds to tiny dosages of meds or supplements though ...

It's interesting and a little disappointing that the NIH considers digestive problems common for Addison's yet doesn't mention being tested for celiac disease. I wonder if I googled it, if I'd find a study by the NIH saying that Addison's and celiac disease are linked ...

For those who aren't up on gluten intolerance versus celiac disease, studies are showing that you don't have to have celiac disease to be gluten intolerant or suffer from the autoimmune problems that celiacs are known for ...


http://endocrine.niddk.nih.gov/pubs/addison/addison.htm


What do adrenal hormones do?

Cortisol

Cortisol belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body. Cortisols most important job is to help the body respond to stress. Among its many vital tasks, cortisol helps

maintain blood pressure and cardiovascular function
slow the immune systems inflammatory response
maintain levels of glucosea form of sugar used for energyin the blood
regulate the metabolism of proteins, carbohydrates, and fats

The amount of cortisol produced by the adrenals is precisely balanced. Like many other hormones, cortisol is regulated by the brains hypothalamus and the pituitary gland. First, the hypothalamus releases a trigger hormone called corticotropin-releasing hormone (CRH) that signals the pituitary gland. The pituitary responds by sending out ACTH, which in turn stimulates the adrenal glands. The adrenal glands respond by producing cortisol. Completing the cycle, cortisol then signals back to both the pituitary and hypothalamus to decrease these trigger hormones.


The hypothalamus sends CRH to the pituitary, which responds by sending out ACTH. ACTH then causes the adrenals to release cortisol into the bloodstream.

Aldosterone

Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. Aldosterone helps maintain blood pressure and water and salt balance in the body by helping the kidneys retain sodium and excrete potassium. When aldosterone production falls too low, the kidneys are not able to regulate water and salt balance, leading to a drop in both blood volume and blood pressure.

From the same article ...



QUOTE
How is adrenal insufficiency treated?

Treatment of adrenal insufficiency involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced with a synthetic glucocorticoid such as hydrocortisone, prednisone, or dexamethasone, taken orally once to three times each day, depending on which medication is chosen. If aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid, called fludrocortisone acetate (Florinef), taken once or twice a day. Doctors usually advise patients receiving aldosterone replacement therapy to increase their salt intake. Because people with secondary adrenal insufficiency normally maintain aldosterone production, they do not require aldosterone replacement therapy. The doses of each medication are adjusted to meet the needs of the individual.

During an Addisonian crisis, low blood pressure, low blood glucose, and high levels of potassium can be life threatening. Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose, a type of sugar. This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.
Article that shows link between celiac disease and Addison's ...




http://jcem.endojournals.org/cgi/content/s.../jc.2007-0960v1

QUOTE
This version published online on June 26, 2007

Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2007-0960


Submitted on April 30, 2007
Accepted on June 18, 2007


Risk of primary adrenal insufficiency in patients with celiac disease

Peter Elfstrm*, Scott M. Montgomery, Olle Kmpe, Anders Ekbom, and Jonas F. Ludvigsson
Department of Pediatrics, rebro University Hospital, Sweden; Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Sweden; Clinical Research Centre, rebro University Hospital, Sweden; Department of Medical Sciences, Uppsala University, University Hospital, Uppsala, Sweden; and Harvard School of Public Health, Boston, Massachusetts, United States

* To whom correspondence should be addressed. E-mail: peter.elfstrom@orebroll.se.


Objectives: Earlier research has suggested a positive association between Addison's disease (AD) and celiac disease (CD). We have here investigated the risk of AD in individuals with CD from a general population cohort.

Methods: Through the Swedish national registers we identified 14,366 individuals with a diagnosis of CD (1964-2003) and 70,095 reference individuals matched for age, sex, calendar year and county of residence. We used Cox regression to estimate hazard ratios (HRs) for subsequent AD. Analyses were restricted to individuals with more than one year of follow-up and without AD prior to study entry or within one year after study entry. Conditional logistic regression estimated the odds ratio (OR) for CD in individuals with prior AD.

Results: There was a statistically significantly positive association between CD and subsequent AD (HR = 11.4; 95% CI = 4.4-29.6). This risk increase was seen in both children and adults, and did not change with adjustment for diabetes mellitus or socioeconomic status. When we restricted reference individuals to inpatients, the adjusted HR for AD was 4.6 (95% CI = 1.9-11.4). Individuals with prior AD were at increased risk of CD (OR = 8.6; 95% CI = 3.4-21.8).

Conclusions: This study found a highly increased risk of AD in individuals with CD. This relationship was independent of temporal sequence. We therefore recommend that individuals with AD should be screened for CD. We also suggest an increased awareness of AD in individuals with CD.