Internally, the gland consists of follicles, which produce thyroxine and triiodothyronine hormones. These hormones contain iodine. About 95 percent of the active thyroid hormone is thyroxine, and most of the remaining 5 percent is triiodothyronine.
Both of these require iodine for their synthesis. Thyroid hormone secretion is regulated by a negative feedback mechanism that involves the amount of circulating hormone , hypothalamus , and adenohypophysis. When bone is broken down, the calcium contained in the bone is released into the bloodstream. Therefore, the inhibition of the osteoclasts by calcitonin directly reduces the amount of calcium released into the blood.
However, this inhibition has been shown to be short-lived. It can also decrease the resorption of calcium in the kidneys , again leading to lower blood calcium levels. How is calcitonin controlled? What happens if I have too much calcitonin? What happens if I have too little calcitonin? Last reviewed: Feb Prev. Related Endocrine Conditions.
Osteoporosis Hypercalcaemia Thyroid cancer Rickets Paget's disease Multiple endocrine neoplasia type 2A Multiple endocrine neoplasia type 2B Familial medullary thyroid cancer View all Endocrine conditions. In rats with hypercalcemia from NH 4 Cl-induced metabolic acidosis, CT administration decreased the serum calcium concentration [ 28 ]. In the CT receptor knockout mouse, 1,25D-induced hypercalcemia was greater than in the control mouse [ 29 ].
In a mouse study consisting of PTH knockout, PTH and calcium-sensing receptor CaSR double knockouts, and wildtype mice, it was shown that both CaSR-mediated CT secretion and enhanced renal calcium excretion were important for preventing the development of hypercalcemia while inhibition of PTH secretion was not required for a robust defense against hypercalcemia [ 30 ]. In summary, strong evidence exists that CT is an important modifier of the hypercalcemic effect of acute calcium loading.
Reprinted with permission from Kidney International. The mechanisms for the opposite effects downstream from the CaSR are still poorly understood. The CT response to hypercalcemia is a sigmoidal curve opposite in direction to the sigmoidal curve of the PTH response to hypocalcemia [ 32 — 34 ]. In one animal study, a rapid induction of hypercalcemia resulted in a greater CT response than a slow induction of hypercalcemia of similar magnitude [ 35 ].
Also, as PTH secretion is suppressed by the induction of hypercalcemia, CT secretion in both control and CKD patients is suppressed by the induction of hypocalcemia [ 34 ]. In a study of normal and CKD subjects, a maximal CT response was seen after an increase in ionized calcium of 0.
Many more studies of the PTH response to hypocalcemia have been performed than of the CT response to hypercalcemia. Interestingly, while every normal and azotemic subject in studies of PTH secretion has shown a sigmoidal response to hypocalcemia, studies in normal and azotemic humans and animals have shown that some patients and animals fail to increase CT secretion in response to hypercalcemia induced by a calcium infusion [ 34 , 36 ]. In a study in cats, a strong correlation was found between the number of CT-positive cells in the thyroid gland and the plasma CT concentration induced by hypercalcemia [ 36 ].
Finally, both in azotemic patients and rats, baseline CT values have been shown to be increased compared with normal [ 32 , 34 , 37 ] and also to stimulate more during the induction of hypercalcemia [ 34 ]. Similar to PTH secretion, CT secretion also appears to adapt to the ambient or existing serum calcium concentration [ 38 ]. In Deftos et al. CT values were shown to increase before hypercalcemia developed.
In a subsequent study in normal young male subjects, oral calcium loading that increased serum calcium to higher, but still normal values resulted in increases in serum CT that correlated with the increase in serum calcium [ 22 ]. In a study in normal, parathyroidectomized, and azotemic rats with the latter divided by a serum calcium less or greater than 8.
Finally, Messa et al. When hypocalcemia was present PTX and RF a , the calcitonin response to an increase in serum calcium began before hypercalcemia developed shifting the set point for calcitonin secretion to the left [ 32 ].
The adapting of PTH and CT secretion to the existing serum calcium concentration is an interesting phenomenon that may reflect a broader concept of physiologic adaptation. For example, adaptation to cold and hot weather as well as oxygen adaptation to high altitude in Himalayan mountain climbers is well known. However, adaptation of hormonal effects and secretion is less well appreciated. In type 1 diabetic patients, an unawareness of hypoglycemia is associated with prolonged insulin therapy and frequent episodes of hypoglycemia [ 39 ].
After resection of the insulinoma, these same responses became similar to those in normal subjects. Besides adaptation to hypercalcemia, other causes for changes in CT secretion are also possible. Raue and associates have shown that chronic hypercalcemia resulted in a decrease in CT content of the thyroid gland and a diminished CT response to acute calcium stimulation while basal serum CT levels remained unchanged [ 40 ].
Also, it was shown that 1,25D-induced hypercalcemia failed to stimulate CT secretion [ 40 ] which may be related to the presence of 1,25D receptors on C cells [ 41 ] and a 1,25D decrease in CT gene transcription [ 14 , 15 , 42 ]. In an in vitro study with rat C cells, repetitive calcium stimulation led to a decline in CT release, but 2 h after reversing the calcium concentration in the media to basal values, the CT response to a calcium stimulus was restored [ 43 ].
In the cat, the CT response to hypercalcemia correlated with the number of CT-positive cells in the thyroid [ 36 ]. Also, it was shown that several cats failed to increase CT in response to hypercalcemia.
Chronic hypocalcemia induced by parathyroidectomy in rats has resulted in increased thyroidal CT content after 50 days and longer, but interestingly not at 32 days [ 44 , 45 ]. Such a finding could explain an enhanced CT response to calcium loading in chronic hypocalcemia [ 23 ]. However, in the study by Torres et al. Several studies have evaluated CT secretion in primary hyperparathyroidism which is characterized by chronic hypercalcemia.
In one study, a gender difference was observed. Males, but not females had elevated baseline CT values and a further increase in CT values during a calcium infusion [ 46 ].
In a subsequent study, men and women with primary hyperparathyroidism had normal serum CT levels and the CT response to a calcium infusion was indistinguishable between men and women with primary hyperparathyroidism and normal men and women [ 47 ].
In another study performed in post-menopausal women with primary hyperparathyroidism, all the patients had normal serum CT levels and a blunted response to a calcium stimulus as compared with normal women [ 48 ].
In a study in horses, the rapid induction of hypercalcemia increased CT values by 6-fold, but CT values returned to baseline values before hypercalcemia resolved [ 49 ]. Thus, the question remains whether the lack of a CT response to hypercalcemia in primary hyperparathyroidism is due to a depletion of CT stores or a reset of the set point for CT secretion.
When dogs were subjected to hypocalcemia, repetitive cycles of the induction of and recovery from hypocalcemia done without pause, whether for 30 or 60 min, produced the same PTH response on the second as the first cycle Figure 3 A and B [ 38 ]. Also, the PTH value for the same serum calcium concentration was greater during the induction of than the recovery from hypocalcemia Figure 3 C and greater during the recovery from than the induction of hypercalcemia not shown [ 38 ].
This phenomenon, known as hysteresis, is not unique to PTH secretion, but is seen with other physiologic phenomenon [ 38 ]. But for PTH secretion, hysteresis may be important in preventing an overcorrection during the restoration of a normal serum calcium concentration [ 38 ]. Another interesting observation has been that an episodic versus a linear induction of hypocalcemia of the same magnitude over the same time period resulted in differences in PTH secretion [ 50 ].
Finally, it was shown that metabolic acidosis stimulates and metabolic alkalosis inhibits PTH secretion in the rat and dog [ 51 — 54 ]. Moreover, because calcium suppresses PTH secretion and stimulates CT secretion, the effects of acidosis and alkalosis may be reversed from that of PTH with alkalosis stimulating and acidosis suppressing CT secretion. The PTH response to the sequential induction of and recovery from hypocalcemia is shown for 30 min A and 60 min B cycles in the dog.
PTH values were similar during the first and second cycles both in the 30 and 60 min groups. C The lower PTH value for the same serum calcium concentration during the recovery from hypocalcemia than during the induction of hypocalcemia is shown and is known as hysteresis.
Results of PTH hysteresis from dogs in the 60 min cycle were similar data not shown. Besides being stimulated by calcium, CT secretion has been shown to be stimulated by gastrointestinal hormones such as gastrin. An infusion of pentagastrin, a synthetic peptide with gastrin-like effects, has been used to evaluate CT stimulation [ 55 ].
In one study of oral calcium loading, the increase in serum CT correlated with the increase in serum calcium, but not that of gastrin [ 22 ]. Moreover, the CT response to pentagastrin was absent in 12 of 25 women and 4 of 25 men, while the CT response to calcium, was absent only in 2 of 18 women and none of the men. Because gastrin and other gastrointestinal hormones potentially stimulate CT secretion, interest developed in the concept that postprandial CT secretion acted to facilitate calcium deposition in bone and potentiate bone mass [ 21 ].
However, in studies in children with congenital hypothyroidism and in thyroidectomized patients, bone loss has been attributed to inadequate thyroid replacement and not to the absence of CT [ 24 , 57 ]. Also, skeletal changes have not been observed in patients with elevated CT values in medullary thyroid carcinoma [ 31 ]. Potentially, there may be different challenges among species in defending against hypercalcemia.
CT is an older hormone phylogenetically than PTH dating back to fish in the ocean with a need to protect against hypercalcemia while PTH developed in land-dwelling animals to protect against hypocalcemia. As such, this may be an explanation why salmon CT is more potent than CT from mammals [ 7 , 58 ]. Not often discussed is that the need to protect against hypercalcemia may be different among land-dwelling animals.
Humans and domesticated animals eat meals on a regular basis throughout the day. Conversely, carnivorous animals in the wild eat large meals consisting of a high percent of their body mass at irregular intervals. Besides a large protein load, the ingestion of calcium and phosphate is also great. Serum calcium did not change, but serum phosphorus increased from 6.
Serum bicarbonate increased from 11 mM fasting to 20 mM and remained significantly elevated for 6 days. Blood pH which was 7. Whether similar physiologic adaptations occur in infrequently feeding carnivorous mammals in the wild and whether CT secretion plays a role and is possibly stimulated by gastrin secretion or the calcium load is an interesting question.
Also, the possibility exists that post-prandial alkalemia could be an additional stimulus for CT secretion. Gender and age differences in serum CT values have been reported. Deftos and associates reported that in normal adult subjects, basal CT values were similar between men and women, but basal CT values decreased with age in both groups and the response to a calcium or pentagastrin challenge was less in women than in men [ 25 , 60 ].
If you are already being treated for this thyroid cancer, high levels may mean the treatment is not working or that cancer has returned after treatment. Other types of cancer, including cancers of the breast , lung , and pancreas , can also cause high levels of calcitonin.
If your levels were high, you will probably need more tests before your health care provider can make a diagnosis. A thyroid scan is an imaging test that uses sound waves to look at the thyroid gland. A biopsy is a procedure where a health care provider removes a small piece of tissue or cells for testing. If your calcitonin levels were low, it may mean your cancer treatment is working, or you are cancer free after treatment.
Learn more about laboratory tests, reference ranges, and understanding results. If you are or have been treated for medullary thyroid cancer, you will probably be tested regularly to see if treatment was successful.
You may also get regular calcitonin tests if you have a family history of multiple endocrine neoplasia type 2. Testing can help find C-cell hyperplasia or medullary thyroid cancer as early as possible. When cancer is found early, it's easier to treat. The information on this site should not be used as a substitute for professional medical care or advice.
Contact a health care provider if you have questions about your health. Calcitonin Test. What is a calcitonin test? These include: C-cell hyperplasia , a condition that causes abnormal growth of cells in the thyroid Multiple endocrine neoplasia type 2 MEN 2 , a rare, inherited disease that causes the growth of tumors in the thyroid and other glands in the endocrine system.
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