Do we overtreat post-thyroidectomy hypocalcemia? 2012

Shih-Ming Huang
Department of General Surgery, College of Medicine and Hospital, National Cheng-Kung University, No. 138, Sheng Li Road, 704, Tainan, Taiwan, R.O.C. smhuang@mail.ncku.edu.tw

BACKGROUND Calcium and calcitriol supplements are standard for patients with post-thyroidectomy serum calcium <2.0 mmol/L; however, we wondered whether we overtreat post-thyroidectomy hypocalcemia with intraoperative parathyroid hormone (PTH). We examined quick-intraoperative intact PTH (QiPTH) assay results to find a suitable treatment for post-thyroidectomy hypocalcemia. METHODS We studied 197 bilateral thyroidectomy patients. Post-thyroidectomy hypocalcemia was defined as serum calcium <2.0 mmol/L. A QiPTH assay was done 15 min after the thyroidectomy (QiPTH(15)), and hypoparathyroidism was defined as PTH <15 ng/L. The QiPTH(15) assay was used to determine the effects of the thyroidectomy on postoperative PTH levels and serum calcium levels. The natural course and medical response of hypocalcemia was observed in patients with a QiPTH(15) ≥ 15 ng/L. RESULTS None of the 187 patients with a QiPTH(15) ≥ 15 ng/L developed postoperative hypoparathyroidism. However, 79 patients developed transient hypocalcemia, and those with Graves' disease (47/94) had significantly (p < 0.05) higher hypocalcemia than those with non-Graves' thyroid disease (32/93). The serum calcium of these 79 patients declined to its lowest level within the first postoperative 18 h. Seven patients with serum calcium <1.75 mmol/L were successfully treated using a calcium supplement only, and the others recovered spontaneously without treatment. CONCLUSIONS When post-thyroidectomy QiPTH(15) was ≥ 15 ng/L, postoperative hypoparathyroidism was excluded, but more than one-third of the patients developed post-thyroidectomy hypocalcemia. However, most of them recovered without treatment, and a few recovered after taking only a calcium supplement. We believe that using QiPTH(15) results as a guide will prevent overtreatment of post-thyroidectomy hypocalcemia.

UI MeSH Term Description Entries
D006996 Hypocalcemia Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed) Hypocalcemias
D007011 Hypoparathyroidism A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone. Idiopathic Hypoparathyroidism,Hypoparathyroidism, Idiopathic
D007432 Intraoperative Period The period during a surgical operation. Intraoperative Periods,Period, Intraoperative,Periods, Intraoperative
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D010281 Parathyroid Hormone A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates. Natpara,PTH (1-84),PTH(1-34),Parathormone,Parathyrin,Parathyroid Hormone (1-34),Parathyroid Hormone (1-84),Parathyroid Hormone Peptide (1-34),Hormone, Parathyroid
D002117 Calcitriol The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption. 1 alpha,25-Dihydroxycholecalciferol,1 alpha,25-Dihydroxyvitamin D3,1, 25-(OH)2D3,1,25(OH)2D3,1,25-Dihydroxycholecalciferol,1,25-Dihydroxyvitamin D3,1 alpha, 25-dihydroxy-20-epi-Vitamin D3,1,25(OH)2-20epi-D3,1,25-dihydroxy-20-epi-Vitamin D3,20-epi-1alpha,25-dihydroxycholecaliferol,Bocatriol,Calcijex,Calcitriol KyraMed,Calcitriol-Nefro,Decostriol,MC-1288,MC1288,Osteotriol,Renatriol,Rocaltrol,Silkis,Sitriol,Soltriol,Tirocal,1 alpha,25 Dihydroxyvitamin D3,1,25 Dihydroxycholecalciferol,1,25 Dihydroxyvitamin D3,1,25 dihydroxy 20 epi Vitamin D3,Calcitriol Nefro,D3, 1 alpha,25-Dihydroxyvitamin,D3, 1,25-Dihydroxyvitamin,D3, 1,25-dihydroxy-20-epi-Vitamin,KyraMed, Calcitriol,MC 1288
D002118 Calcium A basic element found in nearly all tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. Coagulation Factor IV,Factor IV,Blood Coagulation Factor IV,Calcium-40,Calcium 40,Factor IV, Coagulation
D002120 Calcium Channel Agonists Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture. Calcium Channel Activators,Calcium Channel Agonists, Exogenous,Calcium Channel Agonist,Exogenous Calcium Channel Agonists,Activators, Calcium Channel,Agonist, Calcium Channel,Agonists, Calcium Channel,Channel Activators, Calcium,Channel Agonist, Calcium,Channel Agonists, Calcium
D005260 Female Females

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