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Hungry bone syndrome (HBS) is actually a calcium retention disorder by bones that have been demineralized. This is normally found after the acute onset of suppression of the thyroid’s functioning, and thus creates a less than calcified bone, causing the name of ‘hungry’ bone syndrome or HBS. This syndrome is characterized as a state of hypocalcaemia where there are large calcium deposits to a bone, and the effects can be short lived or last years depending on treatment. Hypocalcaemia often is seen after the removal of the thyroid and causes a severe fall in the serum calcium, which in turn leads to the bones being unable to reabsorb calcium and the intestines are also unable to absorb. For those patients with the end stage of renal diseases, there is a drastic increase in calcium excretions and therefore causes more calcium to be released into the bloodstream. When the bones and intestines are unable to reabsorb the calcium, the deficiency begins.
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Symptoms of HBS
Primarily the HBS is found in cases where hyperparathyroidism is a problem, and must be removed via parathyroidectomy. This treatment is deemed the most efficient way of dealing with the disease, and therefore is widely accepted. Transient hypocalcaemia or HBS is rarely life threatening, but can develop after this surgery. HBS can be severe and long lived, where according to The Society for Endocrinology BES says a patient will be requiring massive amounts of calcium to prevent symptoms of neuromuscular irritability, tetany.
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Causes of HBS
Some cases of hungry bone syndrome are caused by postoperative hypocalcaemia where the long case of normal or elevated level of PTH or parathyroid hormone has been seen. This happens normally in those who had developed the bone disease after surgery because of a major increase in the bone absorption, which is caused by the higher levels of PTH. For those with end stage renal diseases, the hyperparathyroidism can be a secondary or a primary illness due to the renal disease. Other syndromes like HBS have been found to be present in those patients with end stage renal diseases, and these are normally treated with calcimimetics. This syndrome has been found after the removal of the thyroid in patients that have hyperthyroidism as well. These patients generally have the bone disease because of a high turnover caused by too much thyroid hormone or estrogen therapy found in those with metastatic prostate cancer.
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Treatment of HBS
According to the Journal of Clinical Endocrinology and Metabolism, calcimimetics are drugs used to reduce the PTH that is secreted by telling the calcium receptor in the parathyroid glands to stop making so much calcium. Hungry bone syndrome causes the parathyroid cells to change when the calcium concentration outside of the cells are concentrated. So the extracellular calcium or calcium outside of the cells is considered the first responder to the bones. So the homeostatic controls the mineral calcium that is controlled by calcimimetics, and is used for all cases of HBS that have had the need of surgical interventions.
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Journal of Clinical Endocrinology and Metabolism from the article Calcimimetics—New Drugs with the Potential To Control Hyperparathyroidism publication date Feb. 05, 1998.
Society for Endocrinology BES from the article Case of parathyroid carcinoma with severe hungry bone syndrome published 2007.