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Question (08/06/2012):

Title: Treatment of very low levels of Vitamin D-25 hydroxy caused by hypothyroidism.

I have hypothyroidism sarcoidosis and peripheral neuropathy.

My Vit.D-25 hydroxy levels were 12.5 so my endocrinologists put me on 50,000 units once weekly.

He rechecked my levels 6 months later and the level was 13.

So he changed the dose to 50,000 twice weekly.

After 6 months he rechecked the levels and they were 5.9 ng/ml.

Any ideas on why they keep dropping or what to do about it?

What kind of disease would cause this?

This is more than just deficiency

Help please


Thank you very much for your question.

It was thought that one of two mechanisms may explain the low levels of vitamin D in patients with hypothyroidism, 1) the low levels of vitamin D may be due to poor absorption of vitamin D from the intestine or 2) the body may not activate vitamin D properly.

Vitamin D itself is inactive and needs to get converted to the liver to 25-hydroxy vitamin D (25-OH vitamin D) and then in the kidney to 1, 25-hydroxy vitamin D

It is only the 1, 25- OH vitamin D which is biologically active.

Patients that are vitamin D deficient usually have a low 25-OH vitamin D level

The conclusion of a 2011 study of Tamer G, Arik S, Tamer I and Coksert D., was that Vitamin D insufficiency (defined as serum levels of 25-hydroxyvitamin D [25(OH)D3] lower than 30 ng/mL)is associated with HT or Hashimoto's thyroiditis.

Further studies are needed to determine whether vitamin D insufficiency is a casual factor in the pathogenesis of Hashimoto's thyroiditis or rather a consequence of the disease.

Hashimoto's thyroiditis is the most common cause of hypothyroidism.

Vitamin D deficiency is common in sarcoidosis patients.

The conclusion of a 2011 study of D. Shehab, K. Al-Jarallah, O. A. Mojiminiyi, H. Al Mohamedy and N. A. Abdella, was that Vitamin D deficiency is an independent risk factor for diabetic peripheral neuropathy, and further studies are required to confirm if Vitamin D supplementation could prevent or delay the onset.

The following study regarding the substitution therapy with thyroid hormone may be helpful:

Barsony J, Lakatos P, Foldes J, Feher T - "Effect of vitamin D3 loading and thyroid hormone replacement therapy on the decreased serum 25-hydroxyvitamin D level in patients with hypothyroidism" Acta Endocrinol (Copenh) 113(3):329-34 (1986)

Twelve hypothyroid subjects, 13 healthy and 12 healthy women with a slight deficiency of vitamin D were studied to distinguish seasonal changes from the thyroxine-dependent ones.

Serum 25-hydroxyvitamin D levels of hypothyroid patients were lower than those of healthy individuals when the sera were obtained in the autumn.

In hypothyroid patients a single oral dose of 100,000 IU vitamin D3 resulted in a smaller increase in 25-hydroxyvitamin D concentration than in controls having subclinical exogenous vitamin D deficiency.

Substitution therapy with thyroid hormone, started in our study always in autumn, increased the 25-hydroxyvitamin D concentration in hypothyroid patients, which was opposite to the autumn-to-spring variation of this hormone observed in healthy controls.

The increase of 25-hydroxyvitamin D, dehydroepiandrosterone and its sulphate values following substitution therapy in the hypothyroid patients may indicate that thyroid hormone(s) is (are) involved in the regulation of steroid hormone synthesis.

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