I’m interested to know if anyone is aware of research associated with hypercalcemia in patient's with long standing Hashimoto’s disease such that the thyroid has atrophied. I
It is my thought that
Calcitonin is produced in the Thyroid C cells are considered as the primary origin of circulating calcitonin.
An atrophied thyroid to the point that it is non-resectable will therefore not produce calcitonin at a normal level if at all.
(what is the effect of an atrophied thyroid on C cell production of calcitonin?)
The three main functions of calcitonin are: i) To absorb calcium into the bones; ii) to inhibit calcium reuptake in the kidneys; and iii) to inhibit calcium reuptake in the small intestine.
If this is the case, then my thought is that I have an underproduction of Calcitonin, which have contributed to the non-absorption of Calcium into the bones, leading to the osteopenia and consequently high end normal and/or high serum calcium levels.
Calcitonin is currently FDA-approved for treating postmenopausal osteoporosis, provided the patient has been in the postmenopausal phase for a minimum of 5 years. It inhibits osteoclasts activity.(Aug 17, 2023
what if any are the current clinical recommendations for hypercalcemia secondary to Hashimotis thyroiditis ( if in fact an association/cause/effect) has been found.
Thank you for your time and assistance with this query.
The atrophy of the thyroid gland in Hashimoto's Thyroiditis can potentially lead to a decrease in the number of C cells present in the gland. As a result, there may be a reduction in the production of calcitonin by these C cells. Calcitonin is a hormone that helps regulate calcium levels in the body by promoting calcium deposition in bones and inhibiting calcium absorption in the intestines.
Therefore, if the thyroid gland is atrophied due to Hashimoto's Thyroiditis, there may be a decrease in calcitonin production, which could potentially impact calcium metabolism and bone health.
I appreciate this. Could this potentially lead to hypercalcemia and consequent osteopenia (Or visa versa)?
Would you know if there is any clinical treatment indicated for patients with the above DX?
Thank you.
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