For about two years, I've been low in Vitamin D 25-Hydroxy, and abnormal high for Vitamin D 1,25-Dihydroxy. My Vitamin D 1,25-Dihydroxy were over 100ng/mL, both first noticed in July & Sept 2010.
My Vitamin D 25-Hydroxy was under 15 ng/mL I took Vitamin D3 supplemental, 1000IU daily, start Sept 2010.
Jan 2011, it is still under 15 ng/ML, and 1,25-Dihydroxy is still over 100 ng/mL. Finally, Sept 2011, 25-Hydroxy rises to 35 ng/mL, before drops to 21 ng/mL this month.
I haven't had Vitamin D 1,25-Dihydroxy tested again since Jan 2011. I will try to have it tested at next visit.
By the way I am supposedly to be hypothyroid too, I am still trying to verify the dx, and determine if it is primary or secondary, because I am not feeling better since being on thyroid medications, and now have myraid of symptoms.
Clearly, I need to increase Vitamin D supplemental dosages, to raise my Vitamin D 25-Hydroxy level. But how much? I am really perplexed by my 1,25-Dihydroxy level from , because supposedly 25-Hydroxy convert to 1,25-Dihydroxy.
1,25-D is usually well above a healthy range in patients with autoimmune diseases due to the inability of CYP24A1 to break down the active metabolite. In one study, of the 100 autoimmune disease patients, 85 had high 1,25-D. However no patients had signs of hypercalcemia (high calcium).
Pathogens (infectious organisms) generate substances which bind and inactivate the vitamin D nuclear receptor (VDR), blocking 1,25-D's ability to activate the VDR. Eg: lyme disease, tuberculosis, candida infection, epstein-barr virus, HIV, cytomegalovirus, Hepatitis C virus.
1,25-D is elevated by systemic inflammation. Under most normal conditions,1,25-D levels are constant throughout the year (no variability due to sun exposure), but there is no such tight biochemical regulation in some chronic inflammatory diseases. Eg: obesity, sarcoidosis, rheumatoid arthritis.
Production of 1,25-D is controlled by parathyroid hormone (PTH) and by serum phosphate concentration: a rise in PTH or a fall in serum phosphate increases 1,25-D synthesis. Eg: hyperparathyroidism
Hashimoto's Thyroiditis (autoimmune disease) is the most common cause of hypothyroidism. Tests to confirm - elevated TPOAb and/or TgAb antibodies.
Thanks for explanation. For me, the question is which autoimmune or pathogens. I am negative for TPOAb, TgAb, Lymes ( borrelia burgdorferi ), sarccoidiosis, tuberculous, HIV, Hepatitis.
I was tested weak positive for anti ccp antibody, thus are on plaquenil for RA, since July 2010. I no longer have morning stiffness in my fingers, it was the only sign I have. My anti ccp antibody has been in negative range on the recent tests.
I had blood culture done recent, I am waiting to hear the results. I will see endocrinologist at university hospital setting in January, in additional to see a
neurologist. A Local endocrinologist seems to not know what he is doing, couldn't answer my questions or come up explanation.
Do i have to get underlying condition under control first before vitamin d level return to normal level, so effects of vitamin deficenc
If you experience a worsening of symptoms when starting thyroid medication, adrenal insufficiency needs to be ruled out. Thyroid hormone preparations are generally contraindicated (a reason to withhold a medical treatment) in patients with diagnosed but as yet uncorrected adrenal cortical insufficiency. Testing for adrenal insufficiency includes cortisol (24 hour saliva cortisol test recommended), ACTH (adrenocorticotropic hormone), aldosterone, renin, potassium and sodium, ACTH stimulation test.
TPOAb and TGAb may be negative in approx 10 - 15% with Hashimoto's Thyroiditis. A fine needle aspiration (FNA) biospy may be done alone or in addition to a thyroid ultrasound to help with a diagnosis. Hashimoto's Thyroiditis has a fairly characteristic pattern of lymphocytes, hurthle cells, and minimal or no colloid on an FNA smear. Hashimoto's Thyroiditis and Graves' disease show moderately heterogeneous, reduced echogenicity on a thyroid ultrasound.
Inflammation of any type reduces the utilization of vitamin D. In this case, addressing the inflammation will help increase vitamin D levels. As stated, high 1,25-D levels can be due to inflammation.
Causes of vitamin D deficiency include:
* Lack of sunlight
* Living north of 35° latitude (eg: Europe, Canada, two thirds of the US). There are no UVB rays (that create vitamin D) between the months of November through March due to the angle of the sun
* Dark or black skin needs up to 10 times the amount of sun than light skin to absorb vitamin D in their skin
* Wearing sunscreen - prevents absorption of UVB rays
* Lack of vitamin D co-factors - magnesium (most important co factor), zinc, vitamin K2, boron, and a tiny amount of vitamin A
* Magnesium and calcium compete for absorption so excessive consumption of calcium can cause a magnesium deficiency (most important co factor for vitamin D absorption).
* Low cholesterol - cholesterol is the precursor to vitamin D. Vitamin D3 is made in the skin when 7-dehydrocholesterol absorbs UVB ultraviolet light at wavelengths between 270 - 300 nm
* Kidney and liver disease - vitamin D is processed (metabolized) by the liver and kidneys into an active form of vitamin D
* Hashimoto's Thyroiditis - genetic defects in the receptor site for vitamin D. More vitamin D is needed than the average person
* Parathyroid conditions (parathyroid - glands in front of the thyroid). PTH (parathyroid hormone) regulates calcium in the blood. As the calcium level increases, the level of vitamin D decreases
* Malabsorption problems like Celiac's disease, Crohn's disease
* Very large or obese body, as a larger body requires more vitamin D
* Very low fat diet - in order to absorb vitamin D the body needs to have fat (vitamin D is fat soluble)
* Conditions that impair fat absorption such as Cystic Fibrosis, IBS, IBD, gall bladder, liver disease
* Older adults - the skin converts less vitamin D from sunlight
* High cortisol levels (caused by stress, medications like steroids or medical conditions such as Cushing's Disease). When the body is in an active stress response, most of the cholesterol is used to make cortisol and not enough is left over for vitamin D production
* Inflammation of any type reduces the utilization of vitamin D
* Lacking vitamin D in the diet or a strict vegetarian diet - natural food sources of vitamin D are animal based
* Hereditary disorders
- Renal 1 alpha-hydroxylase deficiency (also called type I hereditary vitamin D-dependent rickets)
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