Some medical conditions can cause long-term (chronically) low levels of calcium in the bloodstream (hypocalcaemia). When calcium levels are low, parathyroid hormone is appropriately produced in order to try and raise blood calcium levels to normal. Long-term excess parathyroid hormone secretion due to a chronic hypocalcaemic stimulus is called secondary hyperparathyroidism.
There are many causes of secondary hyperparathyroidism and it can occur in any condition that causes chronic hypocalcaemia. The commonest cause is chronic kidney disease but may also include vitamin d deficiency from lack of sunlight exposure or malabsorption of vitamin D (small bowel disease, pancreatic disease etc).
Vitamin D is an important hormone controlling calcium levels in the blood and, like parathyroid hormone, can raise blood calcium levels. It does this by increasing calcium absorption from the gut and increasing the release of stored calcium from bone. In vitamin D deficiency, less calcium from food is absorbed in the gut and this causes more parathyroid hormone to be produced.
In the case of kidney disease, several factors contribute to increasing parathyroid hormone production:
When parathyroid hormone cannot correct the level of calcium in blood, either as a result of organ failure or reduced calcium available to the body, a condition of too little calcium (hypocalcaemia) can develop along with the hyperparathyroidism. Unlike primary hyperparathyroidism, in secondary hyperparathyroidism, calcium levels may be normal or low so the symptoms are different. Almost all patients with long-term, dialysis-dependent kidney failure have some degree of secondary hyperparathyroidism, so the signs of the condition appear as part of kidney failure itself. In secondary hyperparathyroidism, as a result of vitamin D deficiency, the symptoms are mainly from the lack of the vitamin itself. The symptoms may be a lack of bone mineralisation (osteomalacia), an increased risk of bone fractures and muscle weakness. In severe cases of secondary hyperparathyroidism, bone pain or deformity may occur.
Secondary hyperparathyroidism can affect anyone with kidney disease, a malabsorption problem, a lack of calcium or vitamin D in their diet or too little exposure to sunlight, which will reduce the body's ability to make vitamin D. It is not known how common this endocrine disorder is, but vitamin D insufficiency is common in the UK given the latitude of the UK and relative lack of sunlight, and so it is believed that many less severe cases of secondary hyperparathyroidism remain undiagnosed, particularly in patients with vitamin D deficiency. The consequences or risk from this for otherwise healthy people remain unproven.
Secondary hyperparathyroidism is not inherited.
Secondary hyperparathyroidism can be diagnosed with simple blood tests and these will reveal low or normal blood calcium, raised parathyroid hormone and either low or high phosphate levels, depending on the cause of the secondary hyperparathyroidism. For example, in kidney disease, levels of phosphate will be high, but in vitamin D deficiency levels will be low. X-rays may show evidence of bone disease. These tests can all be carried out as an outpatient.
Secondary hyperparathyroidism is often initially treated medically rather than surgically. Typically, the underlying cause of the condition needs to be treated, rather than the hyperparathyroidism itself, by correcting vitamin D deficiency or treating chronic kidney disease, for example.
For those patients who do not respond to the first level of medical treatment, a type of medication called calcimimetics, for example, Cinacalcet, may be used. However, in the UK, their use is only recommended for people in the final stages of kidney disease whose hyperparathyroidism does not respond to medical treatment and who are unable to have surgery.
Surgical removal of the parathyroid glands can be considered in severe cases where medical treatment has been ineffective.
Secondary hyperparathyroidism is usually treated with calcium and/or vitamin D supplements, which have no noted side-effects if taken as directed by a doctor or pharmacist.
Secondary hyperparathyroidism can increase the risk of broken bones because of the excess parathyroid hormone secretion. Patients with kidney disease can develop a bone disease (renal osteodystrophy) which, may cause bone pain, weakness and fractures resulting from the failure of the kidneys to maintain normal phosphate and calcium levels.
A good diet with plenty of vitamin D and calcium and safe sunlight exposure is recommended along with daily exercise, which will help to protect against bone loss. Hyperparathyroidism, if left untreated, can cause loss of bone mass and increase the risk of fractures.
Last reviewed: Mar 2015