Hypoparathyroidism may be a primary disorder due to surgery, autoimmunity, or genetic abnormalities or it may be a functional and reversible phenomenon resulting from medications or hypomagnesemia.
Postsurgical hypoparathyroidism
Postsurgical hypoparathyroidism is a rare (1–2%) but devastating complication of total thyroidectomy. It may also result from exploration of the parathyroid glands or following radical neck dissection for cancers of the head and neck. Hypocalcemia in this setting may be intermittent or permanent.
Autoimmune mechanisms
Hypoparathyroidism induced by autoimmune mechanisms may be associated with other endocrine deficiencies termed polyglandular autoimmune syndrome type I. This condition is associated with adrenal insufficiency and mucocutaneous candidiasis, which reflect defects in thymic development. Patients may also develop anemia due to vitamin B12 deficiency as a result of autoantibodies to gastric parietal cells and subsequent achlorhydria. In some patients, there may be autoantibodies to the calcium-sensing receptor on the surface of parathyroid cells. These antibodies may activate the receptor and mimic the effects of calcium, thereby reducing PTH secretion.
Hypoparathyroidism on a genetic basis is a rare condition that is the result of mutations of the gene for the calcium-sensing receptor that activate the receptor at low levels of calcium, which thereby leads to reduced PTH secretion despite hypocalcemia. The condition is associated with normal but inappropriately low PTH secretion, hypercalciuria, and nephrolithiasis and nephrocalcinosis. DiGeorge's syndrome, a genetic disorder leading to maldevelopment of the third and fourth branchial pouches, is associated with absence of parathyroid glands and an associated aplasia of the thymus as well as cardiac malformations.
Hypoparathyroidism induced by autoimmune mechanisms may be associated with other endocrine deficiencies termed polyglandular autoimmune syndrome type I. This condition is associated with adrenal insufficiency and mucocutaneous candidiasis, which reflect defects in thymic development. Patients may also develop anemia due to vitamin B12 deficiency as a result of autoantibodies to gastric parietal cells and subsequent achlorhydria. In some patients, there may be autoantibodies to the calcium-sensing receptor on the surface of parathyroid cells. These antibodies may activate the receptor and mimic the effects of calcium, thereby reducing PTH secretion.
Hypoparathyroidism on a genetic basis is a rare condition that is the result of mutations of the gene for the calcium-sensing receptor that activate the receptor at low levels of calcium, which thereby leads to reduced PTH secretion despite hypocalcemia. The condition is associated with normal but inappropriately low PTH secretion, hypercalciuria, and nephrolithiasis and nephrocalcinosis. DiGeorge's syndrome, a genetic disorder leading to maldevelopment of the third and fourth branchial pouches, is associated with absence of parathyroid glands and an associated aplasia of the thymus as well as cardiac malformations.
Most people with pyelonephritis do not have complications if appropriately treated with bacteria-fighting medications called antibiotics.
In rare cases, pyelonephritis may cause permanent kidney scars, which can lead to chronic kidney disease, high blood pressure, and kidney failure. These problems usually occur in people with a structural problem in the urinary tract, kidney disease from other causes, or repeated episodes of pyelonephritis.
Infection in the kidneys may spread to the bloodstream—a serious condition called sepsis—though this is also uncommon.
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