Hypoparathyroidism describes a condition in which there are low circulating levels of parathyroid hormone (PTH) or insensitivity to its action.  The causes of hypoparathyroidism vary; however, they all share a common feature of hypocalcemia. The presentation of hypoparathyroidism also varies depending on the chronicity of the resultant hypocalcemia. Muscle spasms/tetany, paresthesias, and seizures may occur in an acute onset, whereas chronic hypoparathyroidism may only be evidenced by visual impairment due to cataract formation.
See Hypocalcemia for more information.
Many underlying pathologic etiologies of hypoparathyroidism exist.
The most common causes are neck surgery and autoimmune processes. Hypoparathyroidism resulting from thyroid or parathyroid surgery can become clinically apparent 1-2 days after the procedure or follow the operation by many years. The incidence of permanent hypoparathyroidism varies with the extent of the procedure, the surgeon’s experience, and the underlying disease process being treated. Rarely, hypoparathyroidism can be a complication of radioactive iodine treatment of external localized radiotherapy. 
Autoimmune insult to the parathyroid gland can be isolated or associated with a variety of polyglandular syndromes. Antibodies to the parathyroids have been detected in up to 30% of patients with isolated hypoparathyroidism and 40% of patients with polyglandular disease.  The calcium sensor-receptor is another target of autoantibodies in hypoparathyroidism. In patients with polyglandular autoimmune syndrome type 1, more than 50% will have this antibody. See Polyglandular Autoimmune Syndrome, Type I.
Both hypermagnesemia and hypomagnesemia can result in decreased PTH secretion. In the case of hypermagnesemia, elevated magnesium levels result in stimulation of a calcium-sensing receptor on the pituitary. This, in turn, attenuates PTH secretion. In the case of chronic alcoholics with hypomagnesemia, there is diminution of PTH secretion levels and a resistance to hormone activity. [7, 8] See Hypermagnesemia and Hypomagnesemia.
This condition is characterized by thymus and parathyroid dysgenesis, cardiac malformation, and facial dysmorphogenesis.  Other complex syndromes associated with hypoparathyroidism have been described and include Sanjat-Sakati syndrome, HDR syndrome, Kenny-Caffey syndrome, Kearns-Sayre syndrome, and Pearson marrow-pancreas syndrome.  See DiGeorge Syndrome and Kearns-Sayre Syndrome.
PTH functions to maintain plasma calcium levels by withdrawing calcium from bone tissue, glomerular filtrate reabsorption, and indirectly through increased intestinal absorption of calcium by activation of vitamin D-1,25. Insufficient production of PTH is known as true hypoparathyroidism, while decreased action on target tissues is called pseudohypoparathyroidism.  See Pseudohypoparathyroidism.
Primary hypoparathyroidism is rare. Familial cases occur with autosomal dominant, autosomal recessive, and X-linked transmission.
Acute hypocalcemia can be treated with good outcome. The mortality rate of hypoparathyroidism depends on the underlying cause.
With the exception of X-linked transmitted syndromes, no sex predilection exists.
See the list below:
Patients with DiGeorge syndrome present for clinical evaluation between birth and 3 months of age with a variety of symptoms.
Patients with polyglandular autoimmune syndrome type I present early in life. These patients typically have candidiasis by age 5 years and hypoparathyroidism by age 10 years.
For other forms of hypoparathyroidism, no age predilection is noted.
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