TY - JOUR
T1 - Presentation of hypoparathyroidism: Etiologies and clinical features
AU - Shoback, Dolores M.
AU - Bilezikian, John P.
AU - Costa, Aline G.
AU - Dempster, David
AU - Dralle, Henning
AU - Khan, Aliya A.
AU - Peacock, Munro
AU - Raffaelli, Marco
AU - Silva, Barbara C.
AU - Thakker, Rajesh V.
AU - Vokes, Tamara
AU - Bouillon, Roger
PY - 2016
Y1 - 2016
N2 - Context: Understanding the etiology, diagnosis, and symptoms of hypoparathyroidism may help to improve quality of life and long-term disease outcomes. This paper summarizes the results of the findings and recommendations of the Working Group on Presentation of Hypoparathyroidism. Evidence Acquisition: Expertsconvenedin Florence, Italy, inMay2015andevaluated the literatureand recent data on the presentation and long-term outcomes of patients with hypoparathyroidism. Evidence Synthesis: The most frequent etiology is surgical removal or loss of viability of parathyroid glands. Despite precautions and expertise, about 20-30% of patients develop transient and 1-7% developpermanentpostsurgicalhypoparathyroidismafter totalthyroidectomy.Autoimmunedestruction is the main reason for nonsurgical hypoparathyroidism. Severe magnesium deficiency is an uncommon but correctable cause of hypoparathyroidism. Several genetic etiologies can result in the loss of parathyroid function or action causing isolated hypoparathyroidism or a complex syndrome with other symptoms apart from those of hypoparathyroidism or pseudohypoparathyroidism. Neuromuscular signs or symptoms due to hypocalcemia are the main characteristics of the disease. Hyperphosphatemia can contribute to major long-term complications such as ectopic calcifications in the kidney, brain, eye, or vasculature. Bone turnover is decreased, and bone mass is increased. Reduced quality of life and higher risk of renal stones, renal calcifications, and renal failure are seen. The risk of seizures and silent or symptomatic calcifications of basal ganglia is also increased. Conclusions: Increased awareness of the etiologyandpresentation of the diseaseandnewresearch efforts addressing specific questions formulated during the meeting should improve the diagnosis, care, and long-term outcome for patients.
AB - Context: Understanding the etiology, diagnosis, and symptoms of hypoparathyroidism may help to improve quality of life and long-term disease outcomes. This paper summarizes the results of the findings and recommendations of the Working Group on Presentation of Hypoparathyroidism. Evidence Acquisition: Expertsconvenedin Florence, Italy, inMay2015andevaluated the literatureand recent data on the presentation and long-term outcomes of patients with hypoparathyroidism. Evidence Synthesis: The most frequent etiology is surgical removal or loss of viability of parathyroid glands. Despite precautions and expertise, about 20-30% of patients develop transient and 1-7% developpermanentpostsurgicalhypoparathyroidismafter totalthyroidectomy.Autoimmunedestruction is the main reason for nonsurgical hypoparathyroidism. Severe magnesium deficiency is an uncommon but correctable cause of hypoparathyroidism. Several genetic etiologies can result in the loss of parathyroid function or action causing isolated hypoparathyroidism or a complex syndrome with other symptoms apart from those of hypoparathyroidism or pseudohypoparathyroidism. Neuromuscular signs or symptoms due to hypocalcemia are the main characteristics of the disease. Hyperphosphatemia can contribute to major long-term complications such as ectopic calcifications in the kidney, brain, eye, or vasculature. Bone turnover is decreased, and bone mass is increased. Reduced quality of life and higher risk of renal stones, renal calcifications, and renal failure are seen. The risk of seizures and silent or symptomatic calcifications of basal ganglia is also increased. Conclusions: Increased awareness of the etiologyandpresentation of the diseaseandnewresearch efforts addressing specific questions formulated during the meeting should improve the diagnosis, care, and long-term outcome for patients.
KW - Biochemistry
KW - Biochemistry (medical)
KW - Clinical Biochemistry
KW - Endocrinology
KW - Endocrinology, Diabetes and Metabolism
KW - Biochemistry
KW - Biochemistry (medical)
KW - Clinical Biochemistry
KW - Endocrinology
KW - Endocrinology, Diabetes and Metabolism
UR - http://hdl.handle.net/10807/93389
UR - http://press.endocrine.org/doi/pdf/10.1210/jc.2015-3909
U2 - 10.1210/jc.2015-3909
DO - 10.1210/jc.2015-3909
M3 - Article
SN - 0021-972X
VL - 101
SP - 2300
EP - 2312
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
ER -