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.
Some medical conditions can cause long-term (chronically) low levels of calcium in the bloodstream (hypocalcaemia). When calcium levels are low, parathyroid hormone is produced to try and raise blood calcium levels to normal. Long-term high parathyroid hormone secretion due to chronic hypocalcaemia is called secondary hyperparathyroidism.
There are many causes of secondary hyperparathyroidism and it can occur in any condition that causes chronic 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.
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 and this causes more parathyroid hormone to be produced.
In chronic kidney disease, several factors contribute to increasing parathyroid hormone production. The kidney’s ability to control blood calcium 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 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, 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. 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 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.
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.
Untreated secondary hyperparathyroidism can increase the risk of broken bones. 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.
Last reviewed: Feb 2018