A teenage boy with hypocalcemia after radioablation for Graves’ disease

Lazareva, O. V.; Panayiotopoulos, Aristotle; Kazachkova, Irina; Jacobson-Dickman, Elka

doi:10.1515/jpem-2013-0322

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…One mechanism of serum calcium fall, especially if the patient experienced thyrotoxicosisassociated hypercalcemia, is increased osteoblastic activity, bone formation being more exacerbated than bone resorption after normalization of thyroid status. Excessive thyroid hormones cause an elevation of osteoblast-derivate bone turnover favoring the resorption while acute drop of these hormones causes a prompt reversal of bone resorption, newly synthesized osteoid being "hungry" to deposit calcium which leads to hypocalcemia [167][168][169][170][171]. Lazareva et al reported a teenager with Basedow's disease who developed HBS after radioiodine ablation [171].…”

Section: Integrating Ptx-related Hbs To Non-ptx Causes Of Hbsmentioning

confidence: 99%

“…Excessive thyroid hormones cause an elevation of osteoblast-derivate bone turnover favoring the resorption while acute drop of these hormones causes a prompt reversal of bone resorption, newly synthesized osteoid being "hungry" to deposit calcium which leads to hypocalcemia [167][168][169][170][171]. Lazareva et al reported a teenager with Basedow's disease who developed HBS after radioiodine ablation [171]. Post-thyroidectomy hypocalcemia, on the other hand, may be caused by transitory or permanent hypoparathyroidism, being described with a much more important epidemiological impact than other complications [172].…”

Section: Integrating Ptx-related Hbs To Non-ptx Causes Of Hbsmentioning

confidence: 99%

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Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism

Cârșote

Nistor

2023

Diagnostics

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Hungry bone syndrome (HBS), severe hypocalcemia following parathyroidectomy (PTX) due to rapid drop of PTH (parathormone) after a previous long term elevated concentration in primary (PHPT) or renal hyperparathyroidism (RHPT), impairs the outcome of underlying parathyroid disease. Objective: overview HBS following PTx according to a dual perspective: pre- and post-operative outcome in PHPT and RHPT. This is a case- and study-based narrative review. Inclusion criteria: key research words “hungry bone syndrome” and “parathyroidectomy”; PubMed access; in extenso articles; publication timeline from Inception to April 2023. Exclusion criteria: non-PTx-related HBS; hypoparathyroidism following PTx. We identified 120 original studies covering different levels of statistical evidence. We are not aware of a larger analysis on published cases concerning HBS (N = 14,349). PHPT: 14 studies (N = 1545 patients, maximum 425 participants per study), and 36 case reports (N = 37), a total of 1582 adults, aged between 20 and 72. Pediatric PHPT: 3 studies (N = 232, maximum of 182 participants per study), and 15 case reports (N = 19), a total of 251 patients, aged between 6 and 18. RHPT: 27 studies (N = 12,468 individuals, the largest cohort of 7171) and 25 case reports/series (N = 48), a total of 12,516 persons, aged between 23 and 74. HBS involves an early post-operatory (emergency) phase (EP) followed by a recovery phase (RP). EP is due to severe hypocalcemia with various clinical elements (<8.4 mg/dL) with non-low PTH (to be differentiated from hypoparathyroidism), starting with day 3 (1 to 7) with a 3-day duration (up to 30) requiring prompt intravenous calcium (Ca) intervention and vitamin D (VD) (mostly calcitriol) replacement. Hypophosphatemia and hypomagnesiemia may be found. RP: mildly/asymptomatic hypocalcemia controlled under oral Ca+VD for maximum 12 months (protracted HBS is up to 42 months). RHPT associates a higher risk of developing HBS as compared to PHPT. HBS prevalence varied from 15% to 25% up to 75–92% in RHPT, while in PHPT, mostly one out of five adults, respectively, one out of three children and teenagers might be affected (if any, depending on study). In PHPT, there were four clusters of HBS indicators. The first (mostly important) is represented by pre-operatory biochemistry and hormonal panel, especially, increased PTH and alkaline phosphatase (additional indicators were elevated blood urea nitrogen, and a high serum calcium). The second category is the clinical presentation: an older age for adults (yet, not all authors agree); particular skeleton involvement (level of case reports) such as brown tumors and osteitis fibrosa cystica; insufficient evidence for the patients with osteoporosis or those admitted for a parathyroid crisis. The third category involves parathyroid tumor features (increased weight and diameter; giant, atypical, carcinomas, some ectopic adenomas). The fourth category relates to the intra-operatory and early post-surgery management, meaning an associated thyroid surgery and, maybe, a prolonged PTx time (but this is still an open issue) increases the risk, as opposite to prompt recognition of HBS based on calcium (and PTH) assays and rapid intervention (specific interventional protocols are rather used in RHPT than in PHPT). Two important aspects are not clarified yet: the use of pre-operatory bisphosphonates and the role of 25-hydroxyitamin D assay as pointer of HBS. In RHPT, we mentioned three types of evidence. Firstly, risk factors for HBS with a solid level of statistical evidence: younger age at PTx, pre-operatory elevated bone alkaline phosphatase, and PTH, respectively, normal/low serum calcium. The second group includes active interventional (hospital-based) protocols that either reduce the rate or improve the severity of HBS, in addition to an adequate use of dialysis following PTx. The third category involves data with inconsistent evidence that might be the objective of future studies to a better understanding; for instance, longer pre-surgery dialysis duration, obesity, an elevated pre-operatory calcitonin, prior use of cinalcet, the co-presence of brown tumors, and osteitis fibrosa cystica as seen in PHPT. HBS remains a rare complication following PTx, yet extremely severe and with a certain level of predictability; thus, the importance of being adequately identified and managed. The pre-operatory spectrum of assessments is based on biochemistry and hormonal panel in addition to a specific (mostly severe) clinical presentation while the parathyroid tumor itself might provide useful insights as potential risk factors. Particularly in RHPT, prompt interventional protocols of electrolytes surveillance and replacement, despite not being yet a matter of a unified, HBS-specific guideline, prevent symptomatic hypocalcemia, reduce the hospitalization stay, and the re-admission rates.

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Section: Integrating Ptx-related Hbs To Non-ptx Causes Of Hbsmentioning

confidence: 99%

Section: Integrating Ptx-related Hbs To Non-ptx Causes Of Hbsmentioning

confidence: 99%

Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism

Cârșote

Nistor

2023

Diagnostics

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“…There are case reports about patients appearing hypocalcemia after RAI treatment as well. Oksana Lazareva [81] reported 16-year-old young male patients with Graves' disease was given 15mCi RAI for treatment. After 11 weeks, he had paralysis, muscle spasms, fatigue and discomfort.…”

Section: Effect Of Rai Treatment On Parathyroid Function For Benign Thyroid Diseasementioning

confidence: 99%

Effect of Parathyroid Function After Thyroidectomy and Radioactive-Iodine Therapy for Thyroid Disease

Xiao¹,

Zhang²,

Li³

2019

BJSTR

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Objective: Thyroidectomy and radioactive-iodine (RAI) treatment are two important methods for benign and malignant thyroid diseases. Thyroidectomy and RAI treatment may influence parathyroid gland function. This paper systematically reviewed the literatures on the effect of thyroidectomy and RAI on parathyroid gland function in patients with benign and maligant thyroid disease. Subjective and Methods:We searched PubMed for English literautres by using terms of "thyroidectomy" or "radioactive iodine" and "hyperthyroidism" or "Graves' disease" or "toxic multinodular goiter" or "toxic adenoma" or "differentiated thyroid carcinoma" and "parathyroid gland" or "calcium" or "parathyroid hormone" to review the effect of thyroidectomy and RAI on parathyroid gland function.Result: Thyroidectomy may lead to hypocalcaemia and hypoparathyroidism both for benign thyroid disease and DTC. For benign thyroid disease, RAI treatment may cause increasing PTH in the short term and may induce parathyroid adenoma or hyperplasia in the long term. For DTC patients, parathyroid gland function may transiently decline after RAI treatment. Conclusion:Thyroidectomy and RAI treatment may influence the parathyroid function in both benign and DTC patients. Thus, it is important to monitor PTH and blood calcium regularly in order to detect early abnormal parathyroid function for those patients.

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Pediatric thyroidectomy in a high volume thyroid surgery center: Risk factors for postoperative hypocalcemia

Chen

Masiakos

Gaz

et al. 2015

Journal of Pediatric Surgery

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A teenage boy with hypocalcemia after radioablation for Graves’ disease

Cited by 3 publications

References 8 publications

Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism

Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism

Effect of Parathyroid Function After Thyroidectomy and Radioactive-Iodine Therapy for Thyroid Disease

Pediatric thyroidectomy in a high volume thyroid surgery center: Risk factors for postoperative hypocalcemia

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