Secondary hyperparathyroidism

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Secondary hyperparathyroidism
Classification and external resources
Illu thyroid parathyroid.jpg
Thyroid and parathyroid.
ICD-10 E21.1
ICD-9 252.02, 588.81
DiseasesDB 6301
MedlinePlus 000318
MeSH D006962

Secondary hyperparathyroidism refers to the excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and associated hypertrophy of the glands. This disorder is especially seen in patients with chronic renal failure. It is often—although not consistently—abbreviated as SHPT in medical literature.

Signs and Symptoms[edit]

Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on blood, immune system and neurological system.

Diagnosis[edit]

The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. It is usually seen in cases of chronic renal disease or defective calcium receptors on the surface of parathyroid glands.

Etiology[edit]

Chronic renal failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active form, and they do not adequately excrete phosphate. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes lead to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from malabsorption (chronic pancreatitis, small bowel disease, malabsorption-dependent bariatric surgery) in that the fat soluble vitamin D can not get reabsorbed. This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum calcium levels.

Treatment[edit]

If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In patients with chronic renal failure, treatment consists of dietary restriction of phosphorus, supplements with an active form of vitamin D such as calcitriol, Hectorol, Zemplar(paricalcitol), etc. and phosphate binders which can be divided into calcium-based and non-calcium based. A newer class of medications is calcimimetics, one of which is commercially available as Sensipar (cinacalcet) in the US and Australia, and as Mimpara in the EU. Calcimimetics have achieved positive responses[1] and are FDA approved for use in patients on dialysis, but have not been approved for use in chronic kidney disease pre-dialysis because, among other concerns, they can increase phosphorus levels. Most patients with hyperparathyroidism secondary to chronic kidney disease will improve after renal transplantation, but many will continue to have a degree of residual hyperparathyroidism (tertiary hyperparathyroidism) post-transplant with associated risk of bone loss, etc.

Prognosis[edit]

If left untreated, the disease will progress to tertiary hyperparathyroidism, where correction of the underlying cause will not stop excess PTH secretion, i.e. parathyroid gland hypertrophy becomes irreversible.

See also[edit]

References[edit]

External links[edit]