Most of us have 4 tiny parathyroid glands (2 on each side) behind the thyroid gland. In healthy state, they are very small (weighing ~30 mg; for comparison, the thyroid gland weighs almost 500 to 1,000 times that). Hence, normal-sized parathyroid glands are difficult to see in any kind of scan.
The 'chief cells' in parathyroid glands produce and release into the blood a hormone called 'parathormone' (PTH). In a healthy state, PTH is released in response to reduced calcium level in the blood. Function of PTH is to increase calcium level in the blood. It also very marginally reduces the blood level of phosphate. PTH increased blood calcium level through actions on following organs:
Parathyroid glands handle short durations of low calcium ('hypocalcaemia') by just increasing the synthesis and release of PTH into the blood. However, if hypocalcaemia is long term, there is increase in number of parathyroid chief cells, which is a largely irreversible process.
An abnormally high level of PTH in the blood is known as 'hyperparathyroidism', which is because of increased function of parathyroid gland(s). Hyperparathyroidism is almost always accompanied by increase in gland size.
Nowadays most of the patients of hyperparathyroidism do not have specific symptoms and are diagnosed because of altered laboratory test results (i.e., increased blood calcium and PTH levels). However, in the past when reliable methods to estimate blood PTH level were less accessible, the symptoms used to be severe, and were related to high blood calcium, reduced bone density and increased urine concentration of phosphate, and had commonly included the following.
'Adenoma' is a kind of non-cancerous tumour usually arising from glands ('gland' is any organ that specializes in producing one or few types of substances and releasing them into the blood or surroundings). 'Hyperplasia' means increase in number of cells performing a specific task.
In context of hyperparathyroidism, it is difficult to distinguish between an adenoma versus hyperplasia. Hyperplasia is usually in response to a sustained stimulus. Whereas, an adenoma develops because of random unprovoked mutations in genes of a (single) cell after birth (i.e., not inherited but acquired), which in turn makes the mutated cell and its daughter cells survive longer and divide at faster rate. Adenoma cells also tend to be autonomous, i.e., they secrete PTH even when blood calcium level is adequate or high. However, what complicates distinction between adenoma and hyperplasia is that hyperplastic cells could also develop autonomy, and risk of adenoma-causing mutations increases in hyperplastic cells.
Parathyroid hyperplasia develops in response to sustained stimuli that are most commonly encountered with chronic kidney disease (CKD), wherein the function of both kidneys is impaired and results in reduced blood calcium, increased blood phosphate and reduced blood vitamin D (healthy kidneys are involved in activation of vitamin D). This is known as 'secondary hyperparathyroidism'.
While it is not a rule, but adenoma tends to develop as an 'accident' without pre-existing provocation, and the resulting condition is called 'primary hyperparathyroidism'.
Thus, removal of only the affected parathyroid adenomas (most commonly involving a single parathyroid gland) completely cures hyperparathyroidism. However, if hyperparathyroidism is in background of long-standing CKD (i.e., if it is 'secondary'), there is a risk of incomplete cure with removal of single parathyroid gland or there could be recurrence of hyperparathyroidism after initial cure.
In mild forms of hyperparathyroidism, especially in who surgery is deemed risky, medical therapy could be an acceptable treatment option. In all other cases, only surgical removal of the parathyroid gland(s) / adenoma(s) (known as 'parathyroidectomy') is the only definitive treatment. In past, surgery used to involve removal of all the 4 parathyroid glands without trying to identify the adenomatous / hyperplastic ones; while this approach had excellent cure rates, it needed a relatively extensive and morbid surgery. MIBI parathyroid scan (discussed here) localizes the culprit parathyroid gland(s) with high certainty, which allows for a less invasive and more precise surgery. Most surgical techniques also involve taking small parts of parathyroid tissue and transplanting them elsewhere (e.g., forearm or neck), which are expected to secrete PTH normally after the recovery from surgery.
As repeat surgery after initial parathyroidectomy is challenging, it is highly desirable to remove all adenomatous, hyperplastic or supernumerary parathyroid glands in the first attempt itself.
MIBI stands for methoxyisobutylisonitrile, and is also known as 99mTc-sestamibi when complexed with radioactive technetium-99m. It is a fat-soluble positively charged molecule.
Normal parathyroid glands accumulate very little MIBI. Normal thyroid glands accumulate relatively high amount of MIBI, but lose it over next few hours ('washout'); this is relevant because parathyroid and thyroid glands are next to each other. Hyperplastic parathyroid glands and parathyroid adenomas contain abnormally increased number of overactive mitochondria. Functioning mitochondria tend to be negatively charged from within, and hence attract and retain the positively charged MIBI.
There are no remarkable expected risks or side effects.
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