Hungry bone syndrome after thyroidectomy for thyroid storm

Abstract

A 39-year-old man was admitted to our hospital with the diagnosis of thyroid storm due to Graves’ disease. Near-total thyroidectomy was performed after 1 month’s pharmacological treatment, and he presented with tetany next morning. Serum corrected calcium value was 5.7 mg/dL. Procollagen type 1 N-terminal propeptide increased considerably, while tartrate-resistant acid phosphatase 5b decreased. These changes indicated that bone formation exceeded bone resorption in reverse after thyroidectomy. Calcium gluconate was administered intravenously for 14 days, before the patient was discharged. Oral administration of calcium and active forms of vitamin D was continued for 4 months. Rapid skeletal uptake of calcium from blood caused severe and persistent hypocalcaemia, which is called hungry bone syndrome. When patients with Graves’ disease have severe thyrotoxicosis, high serum alkaline phosphatase levels and low bone mineral densities, they are at high risk for hungry bone syndrome after thyroidectomy, and should be educated for the symptoms of hypocalcaemia.

Significant Role of 1,25-Dihydroxyvitamin D on Serum Calcium Levels After Total Thyroidectomy: A Prospective Cohort Study

“…In such areas, preoperative identi cation of patients with SHPT and targeting these patients for treatment to improve SHPT would be more e cient than treating all patients uniformly. Patients with Graves' disease differ signi cantly from those with other thyroid diseases in terms of preoperative thyroid hormone status and the bone-and Ca-related effects of thyroid hormones and thyroid-stimulating antibodies [3,29,30,31]. Most surgical indications for our patients with tumors were peritracheal or lateral neck malignancies requiring lymph node dissection, which tend to have decreased postoperative PTH levels compared with Graves' disease.…”

“…It is thought that the high preoperative PTH and 1,25(OH)2D levels lead to a hypercatabolic state of 1,25(OH)2D, which is further aggravated by the postoperative PTH decrease (PTH is known to inhibit 24-hydroxylase activity) (Fig. 3) [30], while the Ca-elevating effect of 1,25(OH)2D is severely suppressed. Prescribing high doses of active VD for such a condition may further activate 1,25(OH)2D catabolism-promoting 24-hydroxylase; therefore, it would be appropriate to provide intravenous Ca infusion therapy during this period and then wait for PTH recovery and a decrease in bone hypermetabolism.…”

Post-thyroidectomy hypocalcemia and related complications

“…Prolonged untreated hyperthyroidism can lead to osteodystrophy and, consequently, to post-total thyroidectomy hypocalcemia, due to rapid recalcification (bone starvation) due to the loss of hormone stimulus from thyroid (Delitala et al, 2020;Lademann et al, 2020;Shi et al, 2020;Tsourdi et al, 2018). This situation is confirmed by the high levels of alkaline phosphatase resulting from osteoblastic activity and bone formation in patients with postoperative tetany (Delitala et al, 2020;Ibrahim & Anumahb, 2021;Kusuki & Mizuno, 2019;Lademann et al, 2020;Shi et al, 2020;Tsourdi et al, 2018).…”

Significant role of 1,25-dihydroxyvitamin D on serum calcium levels after total thyroidectomy: a prospective cohort study

“…First, we discuss the “hungry bone syndrome” in postoperative patients with Graves’ disease and hyperparathyroidism who have hyperdynamic bone disease. It is often observed that prescribing high doses of active VD and Ca in these patients does not result in the expected increase in serum Ca ( 29 , 30 ). It is thought that the high preoperative PTH and 1,25(OH) 2 D levels lead to a hypercatabolic state of 1,25(OH) 2 D, which is further aggravated by the postoperative PTH decrease (PTH is known to inhibit 24-hydroxylase activity) ( Figure 3 ) ( 31 ), while the Ca-elevating effect of 1,25(OH) 2 D is severely suppressed.…”