There are four parathyroid glands, situated in the front of the neck and they are normally about the size of a grain of rice. The main action of parathyroid hormone is to keep blood calcium levels in a set range by trying to increase calcium levels if they are too low.
Some medical conditions can cause low levels of calcium in the bloodstream (hypocalcaemia). When calcium levels are low, parathyroid hormone (PTH) is produced to try and raise blood calcium levels back up to normal. Increased parathyroid hormone (PTH) secretion in response to low calcium levels (hypocalcaemia) is called secondary hyperparathyroidism.
There are many causes of secondary hyperparathyroidism and it can occur in any condition that causes low blood calcium levels (hypocalcaemia). The commonest causes are vitamin D deficiency from lack of sunlight exposure or malabsorption of vitamin D (small bowel disease, pancreatic disease, etc.), and chronic kidney disease (due to an inability to activate vitamin D in the kidney).
Vitamin D is necessary to absorb dietary calcium from the gut. In vitamin D deficiency, less calcium from food is absorbed in the gut, so blood calcium levels are low. This low calcium level is sensed by the parathyroid glands, which secrete more parathyroid hormone (PTH) in order to bring calcium levels back up to normal.
In chronic kidney disease, several factors contribute to increasing parathyroid hormone production. The kidney’s ability to appropriately excrete phosphate levels is reduced. Also, vitamin D is activated in the kidney, so kidney disease reduces the effectiveness of vitamin D.
Most of the symptoms of secondary hyperparathyroidism are due to the underlying cause. People with vitamin D deficiency may notice muscle aching and weakness, or aching bones. In severe cases, they can develop osteomalacia (soft bones) which can cause fractures and bone deformity (in children this is called rickets).
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. 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. The consequences or risk from this for otherwise healthy people are not clear.
Secondary hyperparathyroidism is not inherited.
Secondary hyperparathyroidism can be diagnosed with simple blood tests and these will reveal low or normal blood calcium and raised parathyroid hormone. Bone density scans (DXA) and X-rays may be used to look for osteomalacia. These tests can all be carried out as an outpatient.
Secondary hyperparathyroidism is treated medically by restoring vitamin D and calcium levels if deficient, or preventing excess phosphate levels in patients with chronic kidney disease, rather than needing surgical treatment.
Secondary hyperparathyroidism is usually treated with calcium and/or vitamin D supplements, which usually have minimal side-effects if taken as directed by a doctor or pharmacist. Calcium tablets can cause gastrointestinal symptoms such as constipation.
Untreated secondary hyperparathyroidism can increase the risk of brittle bones (osteoporosis). Patients with chronic kidney disease can affect their bones (called 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 to help protect against bone loss.
Parathyroid UK may be able to provide advice and support to patients and their families dealing with secondary hyperparathyroidism.
Last reviewed: May 2021