Endocrinology and Metabolism

Review Articles

Mineral, Bone & Muscle
Roles of Parathyroid Hormone and Fibroblast Growth Factor 23 in Advanced Chronic Kidney Disease: Yosuke Nakagawa, Hirotaka Komaba; Endocrinol Metab. 2024;39(3):407-415. Published online May 16, 2024; DOI: https://doi.org/10.3803/EnM.2024.1978

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Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) each play a central role in the pathogenesis of chronic kidney disease (CKD)-mineral and bone disorder. Levels of both hormones increase progressively in advanced CKD and can lead to damage in multiple organs. Secondary hyperparathyroidism (SHPT), characterized by parathyroid hyperplasia with increased PTH secretion, is associated with fractures and mortality. Emerging evidence suggests that these associations may be partially explained by PTH-induced browning of adipose tissue and increased energy expenditure. Observational studies suggest a survival benefit of PTHlowering therapy, and a recent study comparing parathyroidectomy and calcimimetics further suggests the importance of intensive PTH control. The mechanisms underlying the regulation of FGF23 secretion by osteocytes in response to phosphate load have been unclear, but recent experimental studies have identified glycerol-3-phosphate, a byproduct of glycolysis released by the kidney, as a key regulator of FGF23 production. Elevated FGF23 levels have been shown to be associated with mortality, and experimental data suggest off-target adverse effects of FGF23. However, the causal role of FGF23 in adverse outcomes in CKD patients remains to be established. Further studies are needed to determine whether intensive SHPT control improves clinical outcomes and whether treatment targeting FGF23 can improve patient outcomes.

Citations

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Molecular and Cellular Endocrinology.2027; 623: 112909. CrossRef
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Pre-Parathyroidectomy PTH as an Integrated Biomarker of Glandular Remodeling and Skeletal Turnover in Secondary Hyperparathyroidism
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Combination therapy with nutritional vitamin D and calcimimetics in secondary hyperparathyroidism: a mechanism-based approach to restoring PTH regulation
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Frontiers in Nutrition.2026;[Epub] CrossRef
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O.I. Nishkumai, O.B. Iaremenko, V.E. Kondratiuk, Mike K.S. Chan, M.B. Dzhus, I.V. Rudenko, A.B. Bezrodnyi
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Guoying Cao, Xiaomeng Mao, Xiaojie Wu, Nanyang Li, Haijing Yang, Jingjing Wang, Jicheng Yu, Jingqiu Hu, Lingli Zhang, Jingyun Chen, Jing Zhang
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Journal of Clinical Medicine.2026; 15(14): 5519. CrossRef
Role of fibroblast growth factor-23 in renal disease activity and bone density involvement in patients with lupus nephritis
Nashwa M Azoz, Ammar A Ammar, Howaida A Nafady, Rabea A Gadelkareem, Essam M Abdel Aziz, Randa A Elzohne
World Journal of Nephrology.2026;[Epub] CrossRef
Headache across the spectrum of kidney disease: epidemiology, clinical patterns, pathophysiological mechanisms, and management-a narrative review
Amin Roshdy Soliman, Rabab Mahmoud Ahmed, Ahmed Fayed
The Egyptian Journal of Internal Medicine.2026;[Epub] CrossRef
Bone turnover markers associated with cognitive dysfunction in patients undergoing hemodialysis: a cross-sectional study
Kazuhiko Kato, Akio Nakashima, Chiharu Aizawa, Arisa Kobayashi, Shunichiro Shinagawa, Ichiro Ohkido, Mitsuyoshi Urashima, Takashi Yokoo
JBMR Plus.2026;[Epub] CrossRef
Gene expression and hormonal signaling in osteoporosis: from molecular mechanisms to clinical breakthroughs
Gurinderdeep Singh, Ronald Darwin, Krishna Chandra Panda, Shaikh Amir Afzal, Shashwat Katiyar, Ram C. Dhakar, Sangeetha Mani
Journal of Biomaterials Science, Polymer Edition.2025; 36(10): 1466. CrossRef
Correlation linking fibroblast growth factor 23 in circulation (FGF-23) and serum aldosterone levels in different stages of chronic kidney disease
Amira Hassan Elsaid Dohuim, Medhat Abd El Megeid Ghazy, Nahla Abdel Aziz Nosair, Amr Khalifa Hussien
The Egyptian Journal of Internal Medicine.2025;[Epub] CrossRef
Effects of Blood Flow Restriction Training and Possible Applications in Chronic Kidney Disease: A Narrative Review
Shen Liu, Zhuo Wang, Jia-fu Tang, Yong-long Yang, Wei-xiu Ji, Da-qi Xu
Current Physical Medicine and Rehabilitation Reports.2025;[Epub] CrossRef
Correlation Between Fibroblast Growth Factor 23 and Biochemical Parameters in Hemodialysis Patients With End-Stage Renal Disease
Barat Yusubov, Mirkhalig Javadov, Khanbaba Huseynov, Muradali Bakhshiyev
Cureus.2025;[Epub] CrossRef
Serum FGF-23 and Vitamin D Deficiency as Predictors of Metabolic Syndrome in Chronic Kidney Disease

Pakistan Journal of Medicine and Dentistry.2025; : 334. CrossRef
Efficacy of Different Doses of Sodium in the Dialysis Fluid on the Levels of Calcium, Phosphorus and Parathyroid Hormone in Patients Undergoing Chronic Hemodialysis
Asieh Aref, Ladan Mirzaei, Ali Ghorbani, Samaneh Tirom, Elham Farhadi
Nephro-Urology Monthly.2025;[Epub] CrossRef
Skeletal Health in Youth with Type 2 Diabetes
Hanine AlArab, Anna Zenno, Melinda Pierce
Current Osteoporosis Reports.2025;[Epub] CrossRef
Capture the superior anti-osteoporotic innovative multi-component complex from Ligustri Lucidi Fructus based on Component Recombination strategy
Jun Jiang, Baixiu Zhao, Yuwen Ma, Yichen Zeng, Yusong Zeng, Jin Fang, Wenjiao Kang, Tong Chen
Phytomedicine.2025; 146: 157116. CrossRef
Serum Calcium as a Determinant of Fibroblast Growth Factor 23 Levels in Patients With Primary Hyperparathyroidism and Graves’ Disease
Hiroyuki Yamashita, Yusuke Mori, Yasuo Imanishi, Hisakazu Shindo, Daisuke Tatsushima, Seigo Tachibana, Takashi Fukuda, Hiroshi Takahashi, Yuji Nagayama, Shinya Satoh
Cureus.2025;[Epub] CrossRef
Immune mechanisms in chronic kidney disease-mineral and bone disorder: current insights and therapeutic implications
Bin Xu, Rui Ma, Yuqiang Wu, Chi Liu, Xiangrong Song
Frontiers in Medicine.2025;[Epub] CrossRef
Treatment outcomes and determinants of combined hemodialysis-hemoperfusion therapy in chronic glomerulonephritis
Xiaotong Yuan
American Journal of Translational Research.2025; 17(11): 8612. CrossRef

Mineral, Bone & Muscle
Treatment of Hypoparathyroidism by Re-Establishing the Effects of Parathyroid Hormone: Lars Rejnmark; Endocrinol Metab. 2024;39(2):262-266. Published online April 4, 2024; DOI: https://doi.org/10.3803/EnM.2024.1916

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The conventional treatment of hypoparathyroidism (HypoPT) includes active vitamin D and calcium. Despite normalization of calcium levels, the conventional treatment is associated with fluctuations in calcium levels, hypercalciuria, renal impairment, and decreased quality of life (QoL). Replacement therapy with parathyroid hormone (PTH)(1-84) is an option in some countries. However, convincing beneficial effects have not been demonstrated, which may be due to the short duration of action of this treatment. Recently, palopegteriparatide (also known as TransCon PTH) has been marketed in Europe and is expected also to be approved in other countries. Palopegteriparatide is a prodrug with sustained release of PTH(1-34) designed to provide stable physiological PTH levels for 24 hours/day. A phase 3 study demonstrated maintenance of normocalcemia in patients with chronic HypoPT, with no need for conventional therapy. Furthermore, this treatment lowers urinary calcium and improves QoL. Another long-acting PTH analog with effects on the parathyroid hormone receptor (eneboparatide) is currently being tested in a phase 3 trial. Furthermore, the treatment of autosomal dominant hypocalcemia type 1 with a calcilytic (encaleret) is also being tested. All in all, improved treatment options are on the way that will likely take the treatment of HypoPT to the next level.

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Construction of a predictive model for postoperative hypoparathyroidism in papillary thyroid cancer based on the Inflammatory Load Index
Xiangdong ZHAO, Yakun ZHANG, Yang PEI, Kewen LU, Shuaichong JI, Yuexin WANG
Chirurgia.2026;[Epub] CrossRef
Long-Term Morbidity after Postoperative Hypoparathyroidism in Thyroid Cancer Patients: A Nationwide Population-Based Cohort Study
Seong Hee Ahn, Sung-Hyo Seo, Chai Young Jung, Dong Han Yu, Ki-Pyo Kim, Youngjoon Kim, Yongin Cho, Da Hea Seo, So Hun Kim, Jun-Il Yoo, Seongbin Hong
Thyroid®.2026; 36(3): 320. CrossRef
First Reported Use of Recombinant Parathyroid Hormone in Kenny–Caffey Syndrome Type 2: A Case Report and Literature Review
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Combination therapy with nutritional vitamin D and calcimimetics in secondary hyperparathyroidism: a mechanism-based approach to restoring PTH regulation
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Frontiers in Nutrition.2026;[Epub] CrossRef
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Gene expression and hormonal signaling in osteoporosis: from molecular mechanisms to clinical breakthroughs
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Original Article

Mineral, Bone & Muscle
Protein Signatures of Parathyroid Adenoma according to Tumor Volume and Functionality: Sung Hye Kong, Jeong Mo Bae, Jung Hee Kim, Sang Wan Kim, Dohyun Han, Chan Soo Shin; Endocrinol Metab. 2024;39(2):375-386. Published online March 21, 2024; DOI: https://doi.org/10.3803/EnM.2023.1827

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Background
Parathyroid adenoma (PA) is a common endocrine disease linked to multiple complications, but the pathophysiology of the disease remains incompletely understood. The study aimed to identify the key regulator proteins and pathways of PA according to functionality and volume through quantitative proteomic analyses.
Methods
We conducted a retrospective study of 15 formalin-fixed, paraffin-embedded PA samples from tertiary hospitals in South Korea. Proteins were extracted, digested, and the resulting peptides were analyzed using liquid chromatography-tandem mass spectrometry. Pearson correlation analysis was employed to identify proteins significantly correlated with clinical variables. Canonical pathways and transcription factors were analyzed using Ingenuity Pathway Analysis.
Results
The median age of the participants was 52 years, and 60.0% were female. Among the 8,153 protein groups analyzed, 496 showed significant positive correlations with adenoma volume, while 431 proteins were significantly correlated with parathyroid hormone (PTH) levels. The proteins SLC12A9, LGALS3, and CARM1 were positively correlated with adenoma volume, while HSP90AB2P, HLA-DRA, and SCD5 showed negative correlations. DCPS, IRF2BPL, and FAM98A were the main proteins that exhibited positive correlations with PTH levels, and SLITRK4, LAP3, and AP4E1 had negative correlations. Canonical pathway analysis demonstrated that the RAN and sirtuin signaling pathways were positively correlated with both PTH levels and adenoma volume, while epithelial adherence junction pathways had negative correlations.
Conclusion
Our study identified pivotal proteins and pathways associated with PA, offering potential therapeutic targets. These findings accentuate the importance of proteomics in understanding disease pathophysiology and the need for further research.

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Aberrant Histone Methylation Profile in Patients with Sporadic Primary Hyperparathyroidism
Poonam Kumari, Sanjay Kumar Bhadada, Ashutosh Kumar Arya, Jyotdeep Kaur, Naresh Sachdeva, Uma Nahar Saikia, Divya Dahiya, Anoop Kumar, Chirag Kharbanda, Sudhaker D Rao
The Journal of Clinical Endocrinology & Metabolism.2026; 111(6): 1680. CrossRef
Stearoyl-CoA desaturase 5 (SCD5) in lipid remodeling: From molecular control to pathophysiology
Veronika Zámbó, Gabriella Orosz, Miklós Csala, Éva Kereszturi
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Review Articles

Mineral, Bone & Muscle
New Insights into Calorie Restriction Induced Bone Loss: Linyi Liu, Clifford J. Rosen; Endocrinol Metab. 2023;38(2):203-213. Published online April 27, 2023; DOI: https://doi.org/10.3803/EnM.2023.1673

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Caloric restriction (CR) is now a popular lifestyle choice due to its ability in experimental animals to improve lifespan, reduce body weight, and lessen oxidative stress. However, more and more emerging evidence suggests this treatment requires careful consideration because of its detrimental effects on the skeletal system. Experimental and clinical studies show that CR can suppress bone growth and raise the risk of fracture, but the specific mechanisms are poorly understood. Reduced mechanical loading has long been thought to be the primary cause of weight loss-induced bone loss from calorie restriction. Despite fat loss in peripheral depots with calorie restriction, bone marrow adipose tissue (BMAT) increases, and this may play a significant role in this pathological process. Here, we update recent advances in our understanding of the effects of CR on the skeleton, the possible pathogenic role of BMAT in CR-induced bone loss, and some strategies to mitigate any potential side effects on the skeletal system.

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Mineral, Bone & Muscle
Normocalcemic Primary Hyperparathyroidism: Need for a Standardized Clinical Approach: Guido Zavatta, Bart L. Clarke; Endocrinol Metab. 2021;36(3):525-535. Published online June 1, 2021; DOI: https://doi.org/10.3803/EnM.2021.1061

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Since normocalcemic primary hyperparathyroidism (NHPT) was first defined at the Third International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism in 2008, many papers have been published describing its prevalence and possible complications. Guidelines for the management of this condition are still lacking, and making the diagnosis requires fulfillment of strict criteria. Recent studies have shown that intermittent oscillations of serum calcium just below and slightly above the normal limits are very frequent, therefore challenging the assumption that serum calcium must be consistently normal to make the diagnosis. There is debate if these variations in serum calcium outside the normal range should be included under the rubric of NHPT or, rather, a milder form of classical primary hyperparathyroidism. Innovative approaches to define NHPT have been proposed that still need to be validated in prospective studies. Non-classical complications, especially cardiovascular complications, have been associated with NHPT, indicating that hyperparathyroidism may be a cardiovascular risk factor. New associations between parathyroid hormone (PTH) and several other comorbidities have also been reported from observational studies, suggesting that excessive PTH secretion might cause tissue dysfunction independent of serum calcium. Heterogeneous studies using different definitions of NHPT, however, make it difficult to draw definitive conclusions regarding the role of PTH excess when complications other than osteoporosis or kidney stones are described. This review will focus on clinical aspects and suggest an approach to NHPT.

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Original Article

Clinical Study
Radioactive Parathyroid Adenomas on Sestamibi Scans: Low Parathyroid Hormone Secretory Potential and Large Volume: Sung Hye Kong, Jung Hee Kim, Sang Wan Kim, Chan Soo Shin; Endocrinol Metab. 2021;36(2):351-358. Published online April 6, 2021; DOI: https://doi.org/10.3803/EnM.2020.823

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Background
We investigated the clinical characteristics of parathyroid adenomas according to radioactivity on ^99mTc-methoxyisobutylisonitrile (^99mTc-MIBI) single-photon emission computed tomography/computed tomography (SPECT/CT) in primary hyperparathyroidism (PHPT) patients.
Methods
The study included 217 patients diagnosed with PHPT from 2000 to 2019 at Seoul National University Hospital who underwent ^99mTc-MIBI SPECT/CT scans. On SPECT/CT, the radioactivity of parathyroid adenomas was measured as the ratio of the mean radioactivity count of the parathyroid adenoma to that of the contralateral thyroid.
Results
Tumors were localized by MIBI scans in 190 patients (MIBI [+] group) and by ultrasound or parathyroid four-dimensional CT in 27 patients (MIBI [–] group). The mean age was 55 years, and mean body mass index was 23.4 kg/m². Patients in the MIBI (+) group had higher parathyroid hormone (iPTH) and lower 25-hydroxy vitamin D levels than those in the MIBI (–) group (168.0 pg/mL [interquartile range, IQR, 111.0 to 250.7] vs. 134.7 pg/mL [IQR, 98.2 to 191.2], P=0.049; 15.4 ng/mL [IQR, 11.1 to 20.8] vs. 21.2 ng/mL [IQR, 13.9 to 24.8], P=0.012, respectively). Patients in the MIBI (+) group had larger tumor volumes, but lower iPTH/volume ratios than those in the MIBI (–) group (1,216.66 [IQR, 513.40 to 2,663.02], 499.82 mm³ [IQR, 167.77 to 1,229.80], P=0.002; 0.18 [IQR, 0.08 to 0.46], 0.40 pg/mL/mm³ [IQR, 0.16 to 1.29], P=0.016, respectively). Adenoma radioactivity was positively correlated with calcium, iPTH, and volume (r=0.180, P=0.020; r=0.208, P=0.006; r=0.288, P<0.001, respectively), but not with iPTH/volume.
Conclusion
Parathyroid adenomas with positive MIBI scans had larger volumes and higher iPTH than adenomas with negative scans, but lower iPTH per unit volume.

Citations

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Review Articles

Miscellaneous
Rare PTH Gene Mutations Causing Parathyroid Disorders: A Review: Joon-Hyop Lee, Munkhtugs Davaatseren, Sihoon Lee; Endocrinol Metab. 2020;35(1):64-70. Published online March 19, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.1.64

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Since parathyroid hormone (PTH) was first isolated and its gene (PTH) was sequenced, only eight PTH mutations have been discovered. The C18R mutation in PTH, discovered in 1990, was the first to be reported. This autosomal dominant mutation induces endoplasmic reticulum stress and subsequent apoptosis in parathyroid cells. The next mutation, which was reported in 1992, is associated with exon skipping. The substitution of G with C in the first nucleotide of the second intron results in the exclusion of the second exon; since this exon includes the initiation codon, translation initiation is prevented. An S23P mutation and an S23X mutation at the same residue were reported in 1999 and 2012, respectively. Both mutations resulted in hypoparathyroidism. In 2008, a somatic R83X mutation was detected in a parathyroid adenoma tissue sample collected from a patient with hyperparathyroidism. In 2013, a heterozygous p.Met1_Asp6del mutation was incidentally discovered in a case-control study. Two years later, the R56C mutation was reported; this is the only reported hypoparathyroidism-causing mutation in the mature bioactive part of PTH. In 2017, another heterozygous mutation, M14K, was detected. The discovery of these eight mutations in the PTH gene has provided insights into its function and broadened our understanding of the molecular mechanisms underlying mutation progression. Further attempts to detect other such mutations will help elucidate the functions of PTH in a more sophisticated manner.

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Miscellaneous
Intraoperative Parathyroid Hormone Monitoring in the Surgical Management of Sporadic Primary Hyperparathyroidism: Zahra F. Khan, John I. Lew; Endocrinol Metab. 2019;34(4):327-339. Published online December 23, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.4.327

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Intraoperative parathyroid hormone monitoring (IPM) has been shown to be a useful adjunct during parathyroidectomy to ensure operative success at many specialized medical centers worldwide. Using the Miami or “>50% intraoperative PTH drop” criterion, IPM confirms the complete excision of all hyperfunctioning parathyroid tissue before the operation is finished, and helps guide the surgeon to identify additional hyperfunctioning parathyroid glands that may necessitate further extensive neck exploration when intraoperative parathyroid hormone (PTH) levels do not drop sufficiently. The intraoperative PTH assay is also used to differentiate parathyroid from non-parathyroid tissues during operations using fine needle aspiration samples and to lateralize the side of the neck harboring the hypersecreting parathyroid through differential jugular venous sampling when preoperative localization studies are negative or equivocal. The use of IPM underscores the recognition and understanding of sporadic primary hyperparathyroidism (SPHPT) as a disease of function rather than form, where the surgeon is better equipped to treat such patients with quantitative instead of qualitative information for durable long-term operative success. There has been a significant paradigm shift over the last 2 decades from conventional to focused parathyroidectomy guided by IPM. This approach has proven to be a safe and rapid operation requiring minimal dissection performed in an ambulatory setting for the treatment of SPHPT.

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Stefan Janičić, Kristina Stepanović, Mia Manojlović, Dean Bjelajac, Slađana Pejaković, Milan Mirković, Dragana Tomić-Naglić, Ivana Bajkin, Tijana Ičin
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Bradley A. Richards, Robert A. Vierkant, Benzon M. Dy, Trenton R. Foster, Travis J. McKenzie, Melanie L. Lyden
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Alessio Imperiale, Jacob Bani, Gianluca Bottoni, Adrien Latgé, Céline Heimburger, Ugo Catrambone, Michel Vix, Giorgio Treglia, Arnoldo Piccardo
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Grant N Schalet, Luke Vincent, Carl Eguez, Gerardo Diaz, Mark S Shachner
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Sophie Dream, Tina W. F. Yen, Kara Doffek, Douglas B. Evans, Tracy S. Wang
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Dongbin Ahn, Ji Hye Kwak
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Shikha Mahajan, Alka Kumar, Vivek Aggarwal, Vikas Jain, Vipul Baweja, Ajay Ajmani, Diplomate CBNC, Fellow EBNM LNU
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Klaas Van Den Heede, Amélie Bonheure, Nele Brusselaers, Sam Van Slycke
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Ismail Ethem Akgün, Mehmet Taner Ünlü, Nurcihan Aygun, Mehmet Kostek, Mehmet Uludag
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Murilo Catafesta das Neves, Rodrigo Oliveira Santos, Monique Nakayama Ohe
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Original Articles

Adrenal gland
Effects of Altered Calcium Metabolism on Cardiac Parameters in Primary Aldosteronism: Jung Soo Lim, Namki Hong, Sungha Park, Sung Il Park, Young Taik Oh, Min Heui Yu, Pil Yong Lim, Yumie Rhee; Endocrinol Metab. 2018;33(4):485-492. Published online November 30, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.4.485

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Background

Increasing evidence supports interplay between aldosterone and parathyroid hormone (PTH), which may aggravate cardiovascular complications in various heart diseases. Negative structural cardiovascular remodeling by primary aldosteronism (PA) is also suspected to be associated with changes in calcium levels. However, to date, few clinical studies have examined how changes in calcium and PTH levels influence cardiovascular outcomes in PA patients. Therefore, we investigated the impact of altered calcium homeostasis caused by excessive aldosterone on cardiovascular parameters in patients with PA.

Methods

Forty-two patients (mean age 48.8±10.9 years; 1:1, male:female) whose plasma aldosterone concentration/plasma renin activity ratio was more than 30 were selected among those who had visited Severance Hospital from 2010 to 2014. All patients underwent adrenal venous sampling with complete access to both adrenal veins.

Results

The prevalence of unilateral adrenal adenoma (54.8%) was similar to that of bilateral adrenal hyperplasia. Mean serum corrected calcium level was 8.9±0.3 mg/dL (range, 8.3 to 9.9). The corrected calcium level had a negative linear correlation with left ventricular end-diastolic diameter (LVEDD, ρ=−0.424, P=0.031). Moreover, multivariable regression analysis showed that the corrected calcium level was marginally associated with the LVEDD and corrected QT (QTc) interval (β=−0.366, P=0.068 and β=−0.252, P=0.070, respectively).

Conclusion

Aldosterone-mediated hypercalciuria and subsequent hypocalcemia may be partly involved in the development of cardiac remodeling as well as a prolonged QTc interval, in subjects with PA, thereby triggering deleterious effects on target organs additively.

Citations

Citations to this article as recorded by

Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis
Anning Wang, Yuhan Wang, Hongzhou Liu, Xiaodong Hu, Jiefei Li, Huaijin Xu, Zhimei Nie, Lingjing Zhang, Zhaohui Lyu
Frontiers in Endocrinology.2022;[Epub] CrossRef

Miscellaneous
Novel Mutation in PTHLH Related to Brachydactyly Type E2 Initially Confused with Unclassical Pseudopseudohypoparathyroidism: Jihong Bae, Hong Seok Choi, So Young Park, Do-Eun Lee, Sihoon Lee; Endocrinol Metab. 2018;33(2):252-259. Published online June 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.2.252

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Background

Autosomal-dominant brachydactyly type E is a congenital abnormality characterized by small hands and feet, which is a consequence of shortened metacarpals and metatarsals. We recently encountered a young gentleman exhibiting shortening of 4th and 5th fingers and toes. Initially, we suspected him having pseudopseudohypoparathyroidism (PPHP) because of normal biochemical parameters, including electrolyte, Ca, P, and parathyroid hormone (PTH) levels; however, his mother and maternal grandmother had the same conditions in their hands and feet. Furthermore, his mother showed normal biochemical parameters. To the best of our knowledge, PPHP is inherited via a mutated paternal allele, owing to the paternal imprinting of GNAS (guanine nucleotide binding protein, alpha stimulating) in the renal proximal tubule. Therefore, we decided to further analyze the genetic background in this family.

Methods

Whole exome sequencing was performed using genomic DNA from the affected mother, son, and the unaffected father as a negative control.

Results

We selected the intersection between 45,490 variants from the mother and 45,646 variants from the son and excluded 27,512 overlapping variants identified from the father. By excluding homogenous and compound heterozygous variants and removing all previously reported variants, 147 variants were identified to be shared by the mother and son. Variants that had least proximities among species were excluded and finally 23 variants remained.

Conclusion

Among them, we identified a defect in parathyroid hormone like hormone (PTHLH), encoding the PTH-related protein, to be disease-causative. Herein, we report a family affected with brachydactyly type E2 caused by a novel PTHLH mutation, which was confused with PPHP with unclassical genetic penetrance.

Citations

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PTHLH gene variant in an Indian boy with brachydactyly type E: A case report and literature review
Anjana Hulse, Priya Ranganath
Clinical Pediatric Endocrinology.2026; 35(3): 266. CrossRef
Case Report: A novel PTHLH nonsense variant in a mother–son pair with brachydactyly type E and short stature, with a genotype–stature review
Hui Huang, Binyang Zhu, Zaisheng Wang, Zhuqiang Wu, Jinqiu Rao, Yu Yang, Xiangyu Xiong
Frontiers in Endocrinology.2026;[Epub] CrossRef
Human diseases caused by homozygous PTH1R mutations
Ignacio Portales-Castillo, Jakob Höppner, Harald Jüppner, Thomas J. Gardella
Frontiers in Endocrinology.2025;[Epub] CrossRef
A novel heterozygous mutation in PTHLH causing autosomal dominant brachydactyly type E complicated with short stature
Jian Sun, Nian Yang, Zhengquan Xu, Hongbo Cheng, Xiangxin Zhang
Molecular Genetics & Genomic Medicine.2024;[Epub] CrossRef
A novel mutation in PTHLH in a family with a variable phenotype with brachydactyly, short stature, oligodontia and developmental delay
Mirjam E.A. Scheffer-Rath, Hermine E. Veenstra-Knol, Annemieke M. Boot
Bone Reports.2023; 19: 101699. CrossRef
Bioactive phytoconstituents as potent inhibitors of casein kinase-2: dual implications in cancer and COVID-19 therapeutics
Farah Anjum, Md Nayab Sulaimani, Alaa Shafie, Taj Mohammad, Ghulam Md. Ashraf, Anwar L. Bilgrami, Fahad A. Alhumaydhi, Suliman A. Alsagaby, Dharmendra Kumar Yadav, Md. Imtaiyaz Hassan
RSC Advances.2022; 12(13): 7872. CrossRef
Characterization and expression profiling of G protein-coupled receptors (GPCRs) in Spodoptera litura (Lepidoptera: Noctuidae)
Yanxiao Li, Han Gao, Hui Zhang, Runnan Yu, Fan Feng, Jing Tang, Bin Li
Comparative Biochemistry and Physiology Part D: Genomics and Proteomics.2022; 44: 101018. CrossRef
Genes with specificity for expression in the round cell layer of the growth plate are enriched in genomewide association study (GWAS) of human height
Nora E. Renthal, Priyanka Nakka, John M. Baronas, Henry M. Kronenberg, Joel N. Hirschhorn
Journal of Bone and Mineral Research.2020; 36(12): 2300. CrossRef
Search for Novel Mutational Targets in Human Endocrine Diseases
So Young Park, Myeong Han Seo, Sihoon Lee
Endocrinology and Metabolism.2019; 34(1): 23. CrossRef
A Heterozygous Splice-Site Mutation in PTHLH Causes Autosomal Dominant Shortening of Metacarpals and Metatarsals
Monica Reyes, Bert Bravenboer, Harald Jüppner
Journal of Bone and Mineral Research.2019; 34(3): 482. CrossRef
A 3.06-Mb interstitial deletion on 12p11.22-12.1 caused brachydactyly type E combined with pectus carinatum
Jia Huang, Hong-Yan Liu, Rong-Rong Wang, Hai Xiao, Dong Wu, Tao Li, Ying-Hai Jiang, Xue Zhang
Chinese Medical Journal.2019; 132(14): 1681. CrossRef
Parathyroid Hormone-Related Protein in the Hand or Out of Hand?
Sang Wan Kim
Endocrinology and Metabolism.2018; 33(2): 202. CrossRef

Miscellaneous
Effects of Serum Albumin, Calcium Levels, Cancer Stage and Performance Status on Weight Loss in Parathyroid Hormone-Related Peptide Positive or Negative Patients with Cancer: Ji-Yeon Lee, Namki Hong, Hye Ryun Kim, Byung Wan Lee, Eun Seok Kang, Bong-Soo Cha, Yong-ho Lee; Endocrinol Metab. 2018;33(1):97-104. Published online March 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.1.97

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Background

A recent animal study showed that parathyroid hormone-related peptide (PTHrP) is associated with cancer cachexia by promoting adipose tissue browning, and we previously demonstrated that PTHrP predicts weight loss (WL) in patients with cancer. In this study, we investigated whether prediction of WL by PTHrP is influenced by clinical factors such as serum albumin, corrected calcium levels, cancer stage, and performance status (PS).

Methods

A cohort of 219 patients with cancer whose PTHrP level was measured was enrolled and followed for body weight (BW) changes. Subjects were divided into two groups by serum albumin (cutoff value, 3.7 g/dL), corrected calcium (cutoff value, 10.5 mg/dL), cancer stage (stage 1 to 3 or 4), or PS (Eastern Cooperative Oncology Group 0 to 1 or 2 to 4), respectively. Clinically significant WL was defined as either percent of BW change (% BW) <−5% or % BW <−2% plus body mass index (BMI) <20 kg/m².

Results

After a median follow-up of 327 days, 74 patients (33.8%) experienced clinically significant WL. A positive PTHrP level was associated with a 2-fold increased risk of WL after adjusting for age, baseline BMI, serum albumin, corrected calcium level, cancer stage, and PS. The effect of PTHrP on WL remained significant in patients with low serum albumin, stage 4 cancer, and good PS. Regardless of calcium level, the effect of PTHrP on WL was maintained, although there was an additive effect of higher calcium and PTHrP levels.

Conclusion

Early recognition of patients with advanced cancer who are PTHrP positive with hypercalcemia or hypoalbuminemia is needed for their clinical management.

Citations

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Targeting of HIF2-driven cachexia in kidney cancer
Muhannad Abu-Remaileh, Laura A. Stransky, Nikita Bhalerao, Nitin H. Shirole, Qinqin Jiang, Eddy Saad, Marc Machaalani, Sean M. Vigeant, Hilina Woldemichael, Charles Xu, Jing Lu, Hairong Wei, Zhihong Liu, William Sun, Kei Enomoto, Toni K. Choueiri, Jason R
Nature Medicine.2026; 32(1): 245. CrossRef
Cancer knocks you out by fasting: Cachexia as a consequence of metabolic alterations in cancer
Salvatore Cortellino, Margherita D'Angelo, Massimiliano Quintiliani, Antonio Giordano
Journal of Cellular Physiology.2025;[Epub] CrossRef
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Cohn May, Gueron Or, Segal Gad, Zubli Daniel, Hakim Hila, Fizdel Boris, Liber Pninit, Amir Hadar, Barkai Galia
Journal of Clinical Medicine.2024; 13(5): 1409. CrossRef
Parathyroid hormone related protein (PTHrP) in patients with pancreatic carcinoma and overt signs of disease progression and host tissue wasting
Britt-Marie Iresjö, Serkan Kir, Kent Lundholm
Translational Oncology.2023; 36: 101752. CrossRef
Development and Characterization of a Cancer Cachexia Rat Model Transplanted with Cells of the Rat Lung Adenocarcinoma Cell Line Sato Lung Cancer (SLC)
Eiji Kasumi, Miku Chiba, Yoshie Kuzumaki, Hiroyuki Kuzuoka, Norifumi Sato, Banyu Takahashi
Biomedicines.2023; 11(10): 2824. CrossRef
Role of Parathyroid Hormone and Parathyroid Hormone-Related Protein in Protein-Energy Malnutrition
Praopilad Srisuwarn, Sinee Disthabanchong
Frontiers in Bioscience-Landmark.2023;[Epub] CrossRef
Inhibition of epidermal growth factor receptor suppresses parathyroid hormone‐related protein expression in tumours and ameliorates cancer‐associated cachexia
Bahar Zehra Camurdanoglu Weber, Samet Agca, Aylin Domaniku, Sevval Nur Bilgic, Dilsad H. Arabaci, Serkan Kir
Journal of Cachexia, Sarcopenia and Muscle.2022; 13(3): 1582. CrossRef
Metabolic Reprogramming in Adipose Tissue During Cancer Cachexia
Bahar Zehra Camurdanoglu Weber, Dilsad H. Arabaci, Serkan Kir
Frontiers in Oncology.2022;[Epub] CrossRef

Site-Specific Difference of Bone Geometry Indices in Hypoparathyroid Patients: Hye-Sun Park, Da Hea Seo, Yumie Rhee, Sung-Kil Lim; Endocrinol Metab. 2017;32(1):68-76. Published online February 6, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.1.68

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Background

Hypoparathyroid patients often have a higher bone mineral density (BMD) than the general population. However, an increase in BMD does not necessarily correlate with a solid bone microstructure. This study aimed to evaluate the bone microstructure of hypoparathyroid patients by using hip structure analysis (HSA).

Methods

Ninety-five hypoparathyroid patients >20 years old were enrolled and 31 of them had eligible data for analyzing bone geometry parameters using HSA. And among the control data, we extracted sex-, age-, and body mass index-matched three control subjects to each patient. The BMD data were reviewed retrospectively and the bone geometry parameters of the patients were analyzed by HSA.

Results

The mean Z-scores of hypoparathyroid patients at the lumbar spine, femoral neck, and total hip were above zero (0.63±1.17, 0.48±1.13, and 0.62±1.10, respectively). The differences in bone geometric parameters were site specific. At the femoral neck and intertrochanter, the cross-sectional area (CSA) and cortical thickness (C.th) were higher, whereas the buckling ratio (BR) was lower than in controls. However, those trends were opposite at the femoral shaft; that is, the CSA and C.th were low and the BR was high.

Conclusion

Our study shows the site-specific effects of hypoparathyroidism on the bone. Differences in bone components, marrow composition, or modeling based bone formation may explain these findings. However, further studies are warranted to investigate the mechanism, and its relation to fracture risk.

Citations

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Vertebral fractures, trabecular bone score and their determinants in chronic hypoparathyroidism
S. Saha, V. Mannar, D. Kandasamy, V. Sreenivas, R. Goswami
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Epidemiology and Financial Burden of Adult Chronic Hypoparathyroidism
Sigridur Bjornsdottir, Steven Ing, Deborah M Mitchell, Tanja Sikjaer, Line Underbjerg, Zaki Hassan-Smith, Jad Sfeir, Neil J Gittoes, Bart L Clarke L
Journal of Bone and Mineral Research.2020; 37(12): 2602. CrossRef
Effect of Endogenous Parathyroid Hormone on Bone Geometry and Skeletal Microarchitecture
A Ram Hong, Ji Hyun Lee, Jung Hee Kim, Sang Wan Kim, Chan Soo Shin
Calcified Tissue International.2019; 104(4): 382. CrossRef
Bone responses to chronic treatment of adult hypoparathyroid patients with PTH peptides
Sofie Malmstroem, Lars Rejnmark, Dolores M. Shoback
Current Opinion in Endocrine and Metabolic Research.2018; 3: 51. CrossRef

Review Articles

Adrenal gland
Hypoparathyroidism: Replacement Therapy with Parathyroid Hormone: Lars Rejnmark, Line Underbjerg, Tanja Sikjaer; Endocrinol Metab. 2015;30(4):436-442. Published online December 31, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.4.436

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Hypoparathyroidism (HypoPT) is characterized by low serum calcium levels caused by an insufficient secretion of parathyroid hormone (PTH). Despite normalization of serum calcium levels by treatment with activated vitamin D analogues and calcium supplementation, patients are suffering from impaired quality of life (QoL) and are at increased risk of a number of comorbidities. Thus, despite normalization of calcium levels in response to conventional therapy, this should only be considered as an apparent normalization, as patients are suffering from a number of complications and calcium-phosphate homeostasis is not normalized in a physiological manner. In a number of recent studies, replacement therapy with recombinant human PTH (rhPTH(1-84)) as well as therapy with the N-terminal PTH fragment (rhPTH(1-34)) have been investigated. Both drugs have been shown to normalize serum calcium while reducing needs for activated vitamin D and calcium supplements. However, once a day injections cause large fluctuations in serum calcium. Twice a day injections diminish fluctuations, but don't restore the normal physiology of calcium homeostasis. Recent studies using pump-delivery have shown promising results on maintaining normocalcemia with minimal fluctuations in calcium levels. Further studies are needed to determine whether this may improve QoL and lower risk of complications. Such data are needed before replacement with the missing hormone can be recommended as standard therapy.

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Mineral, Bone & Muscle
Emerging Therapies for Osteoporosis: Michael R. McClung; Endocrinol Metab. 2015;30(4):429-435. Published online December 31, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.4.429

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Although several effective therapies are available for the treatment of osteoporosis in postmenopausal women and older men, there remains a need for the development of even more effective and acceptable drugs. Several new drugs that are in late-stage clinical development will be discussed. Abaloparatide (recombinant parathyroid hormone related peptide [PTHrP] analogue) has anabolic activity like teriparatide. Recent data from the phase 3 fracture prevention trial demonstrate that this agent is effective in reducing fracture risk. Inhibiting cathepsin K reduces bone resorption without decreasing the numbers or activity of osteoclasts, thereby preserving or promoting osteoblast function. Progressive increases in bone mineral density (BMD) have been observed over 5 years. Early data suggest that odanacatib effectively reduces fracture risk. Lastly, inhibiting sclerostin with humanized antibodies promotes rapid, substantial but transient increases in bone formation while inhibiting bone resorption. Marked increases in BMD have been observed in phase 2 studies. Fracture prevention studies are underway. The new therapies with novel and unique mechanisms of action may, alone or in combination, provide more effective treatment options for our patients.

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Original Article

Preoperative Localization and Intraoperative Parathyroid Hormone Assay in Korean Patients with Primary Hyperparathyroidism: Eirie Cho, Jung Mi Chang, Seok Young Yoon, Gil Tae Lee, Yun Hyi Ku, Hong Il Kim, Myung-Chul Lee, Guk Haeng Lee, Min Joo Kim; Endocrinol Metab. 2014;29(4):464-469. Published online December 29, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.4.464

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Background

The intraoperative parathyroid hormone (IOPTH) assay is widely used in patients with primary hyperparathyroidism (PHPT). We investigated the usefulness of the IOPTH assay in Korean patients with PHPT.

Methods

We retrospectively reviewed the data of 33 patients with PHPT who underwent parathyroidectomy. Neck ultrasonography (US) and ^99mTc-sestamibi scintigraphy (MIBI scan) were performed preoperatively and IOPTH assays were conducted.

Results

The sensitivity of neck US and MIBI scans were 91% and 94%, respectively. A 50% decrease in parathyroid hormone (PTH) levels 10 minutes after excision of the parathyroid gland was obtained in 91% (30/33) of patients and operative success was achieved in 97% (32/33) of patients. The IOPTH assay was 91% true-positive, 3% true-negative, 0% false-positive, and 6% false-negative. The overall accuracy of the IOPTH assay was 94%. In five cases with discordant neck US and MIBI scan results, a sufficient decrease in IOPTH levels helped the surgeon confirm the complete excision of the parathyroid gland with no additional neck exploration.

Conclusion

The IOPTH assay is an accurate tool for localizing hyperfunctioning parathyroid glands and is helpful for evaluating cases with discordant neck US and MIBI scan results.

Citations

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The Economics of Intraoperative Parathyroid Hormone Monitoring for Parathyroid Surgery: A Scoping Review of Cost Analyses and Economic Evaluations
Phillip Staibano, Mohit Bhandari, Ankit Parmar, Jackie Han, Samyan Shahid, Michael Au, Jesse D. Pasternak, Catlin Yeo, Feng Xie, Martin Almquist, Sameer Parpia, Alexander Rogers, Jason W. Busse, Lisa Orloff, Carolyn Seib, Nhu‐Tram Nguyen, Alex Thabane, Ty
Laryngoscope Investigative Otolaryngology.2026;[Epub] CrossRef
Intraoperative Parathyroid Hormone Monitoring Criteria in Primary Hyperparathyroidism
Phillip Staibano, Michael Au, Han Zhang, Sheila Yu, Winnie Liu, Jesse D. Pasternak, Xing Xing, Carolyn D. Seib, Lisa Orloff, Nhu-Tram Nguyen, Michael K. Gupta, Eric Monteiro, Sameer Parpia, Tyler McKechnie, Alex Thabane, J. E. M. (Ted) Young, Mohit Bhanda
JAMA Otolaryngology–Head & Neck Surgery.2025; 151(3): 190. CrossRef
Single-Center Experience of Parathyroidectomy Using Intraoperative Parathyroid Hormone Monitoring
Seong Hoon Kim, Si Yeon Lee, Eun Ah Min, Young Mi Hwang, Yun Suk Choi, Jin Wook Yi
Medicina.2022; 58(10): 1464. CrossRef
The natural history and hip geometric changes of primary hyperparathyroidism without parathyroid surgery
Kyong Yeun Jung, A. Ram Hong, Dong Hwa Lee, Jung Hee Kim, Kyoung Min Kim, Chan Soo Shin, Seong Yeon Kim, Sang Wan Kim
Journal of Bone and Mineral Metabolism.2017; 35(3): 278. CrossRef
The utility of the radionuclide probe in parathyroidectomy for primary hyperparathyroidism
MS Lim, M Jinih, CH Ngai, NM Foley, HP Redmond
The Annals of The Royal College of Surgeons of England.2017; 99(5): 369. CrossRef
Articles in 'Endocrinology and Metabolism' in 2014
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Endocrinology and Metabolism.2015; 30(1): 47. CrossRef

Case Reports

1-34 PTH Could Reverse Impaired Bone Mineralization Induced By the Overdose of Bisphosphonate.: Kyeong Hye Park, Kwang Joon Kim, Han Seok Choi, Kyoung Min Kim, Eun Young Lee, Seonhui Han, Hyun Sil Kim, Daham Kim, Hannah Seok, Eun Yeong Choe, Yumie Rhee, Sung Kil Lim; Endocrinol Metab. 2012;27(3):247-250. Published online September 19, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.3.247

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Abstract PDF: Bisphosphonates are the mainstay of osteoporosis treatment. Despite the fact that bisphosphonates have a relatively good safety record and are tolerated well by the majority of patients, serious adverse events have been associated with their use. A 41-year-old man had been diagnosed with osteoporosis and had taken etidronate 200 mg/day daily for 2 years due to the judgmental error. He was referred for the management of refractory bone pain and generalized muscle ache. Serum calcium, phosphate, 25-hydroxy-vitamin D (25(OH)D), and immunoreactive parathyroid hormone (iPTH) were within normal range. Plain X-ray showed multiple fractures. Whole body bone scan confirmed multiple sites of increased bone uptakes. Tetracycline-labeled bone biopsy showed typical findings of osteomalacia. He was diagnosed with iatrogenic, etidronate-induced osteomalacia. The patient received daily parathyroid hormone (PTH) injection for 18 months. PTH effectively reverses impaired bone mineralization caused by etidronate misuse. Currently, he is doing well without bone pain. Bone mineral density significantly increased, and the increased bone uptake was almost normalized after 18 months. This case seems to suggest that human PTH (1-34) therapy, possibly in association with calcium and vitamin D, is associated with important clinical improvements in patients with impaired bone mineralization due to the side effect of bisphosphonate.

A Case of CATCH22 Syndrome with Normal Parathyroid Function.: Min Jeong Lee, So Yeon An, Chang Bum Bae, Young Bae Sohn, Yoon Sok Chung; Endocrinol Metab. 2012;27(2):151-154. Published online June 20, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.2.151

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Abstract PDF

CATCH 22 is a medical acronym for cardiac defects, abnormal faces, thymic hypoplasia, cleft palate, and hypocalcemia, and a variable deletion on chromosome 22. It includes DiGeorge syndrome, conotruncal anomaly face syndrome, and velo-cardio-facial syndrome. It has a prevalence estimated at 1:3,000-1:6,000. Most deletions occur at de novo, but autosomal dominant inheritance is observed in 6-10% of cases. Hormonal disorders are common in patients with CATCH22 syndrome. While hypoparathyroidism was the predominant endocrine disturbance that has been documented in the DiGeorge syndrome, other hormonal defects, such as growth hormone deficiency, hypothyroidism, and hyperthyroidism have been occurred in patients with CATCH22 syndrome. The spectrum of parathyroid gland dysfunction in this syndrome ranges from severe neonatal hypocalcemia to normal parathyroid function. Most patients are usually diagnosed in young age, but a few patients with mild abnormality are presented later in life. We report a case of CATCH22 syndrome with normal parathyroid hormone and calcium level in an adult. The diagnosis of CATCH22 syndrome was confirmed by fluorescence in situ hybridization analysis.

Citations

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A Case of CATCH22 Syndrome Diagnosed in Postmenopausal Woman
Seung Kyung Lee, Min Jeong Lee, Hyo Jin Lee, Bu Kyung Kim, Young Bae Sohn, Yoon-Sok Chung
Journal of Bone Metabolism.2013; 20(1): 57. CrossRef

Original Article

The Effects of Combination Therapy of Cathepsin K Inhibitor and PTH on Change in Bone Mineral Density in an Animal Model of Osteoporosis.: Seung Hun Lee, Jung Min Koh, Young Sun Lee, Beom Jun Kim, Je Yong Choi, Ghi Su Kim; Endocrinol Metab. 2011;26(4):303-309. Published online December 1, 2011; DOI: https://doi.org/10.3803/EnM.2011.26.4.303

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BACKGROUND
We hypothesized that combination therapy of cathepsin K inhibitor (CTKi) and human parathyroid hormone (1-34) (teriparatide, PTH) would overcome the coupling phenomenon of bone resorption and formation and thus may rapidly increase bone mass. METHODS: We selected a dose of zoledronic acid (ZA) that had shown similar effects with CTKi on body bone mineral density (BMD) change during the preliminary experiment. Female mice were subjected to ovariectomized (OVX control) or a sham operation (SHAM group). The mice were treated with CTKi (CTKi group), ZA (ZA group), PTH (PTH group) or with a combination of PTH with ZA (ZA + PTH group) or CTKi (CTKi + PTH group) for 8 weeks. Total BMD was measured before the operation and at 4 and 8 weeks. RESULTS: In the preliminary results, 10 microg/kg of ZA showed similar BMD changes with CTKi. Compared with the OVX control, BMD in the SHAM, ZA, CTKi, PTH, ZA + PTH, and CTKi + PTH groups was significantly increased after treatment. BMD in the CTKi + PTH group, but not in the ZA + PTH group increased more significantly than in the PTH group at the end of treatment. Compared with the OVX control, changes in BMD in the SHAM, ZA, CTKi, PTH, ZA + PTH, and CTKi + PTH groups increased significantly after 8 weeks of treatment. The change in BMD in the CTKi + PTH group, but not in the ZA + PTH group was more significantly increased than the change in BMD in the PTH group. CONCLUSION: When combined with PTH, CTKi augmented the anabolic action of PTH. Therefore, combination therapy with CTKi and PTH might be a new therapeutic modality capable of overcoming the coupling phenomenon, thereby markedly and rapidly increasing bone mass.

Citations

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The Effects of Combination Therapy of Cathepsin K Inhibitor and PTH on Change of Bone Mineral Density in Animal Model of Osteoporosis
Yumie Rhee
Endocrinology and Metabolism.2011; 26(4): 295. CrossRef

Case Report

Successful Localization of Distant Metastasis in Parathyroid Carcinoma Using Intraoperative Parathyroid Hormone Assay.: Ho Cheol Hong, Sun Won Kim, Tae Hyung Kim, In Hye Cha, Jae Hee Ahn, Hye Jin Yoo, Hee Young Kim, Ji A Seo, Hyun Koo Kim, Sin Gon Kim, Nan Hee Kim, Kyung Mook Choi, Jae Bok Lee, Sei Hyun Baik, Dong Seop Choi; Endocrinol Metab. 2011;26(1):92-96. Published online March 1, 2011; DOI: https://doi.org/10.3803/EnM.2011.26.1.92

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Abstract PDF

Intra-operative parathyroid hormone (IOPTH) assay is a useful tool to confirm complete excision of all hyper-functioning parathyroid gland tissue. In this report, we describe a case with successful localization of distant metastasis in a patient with parathyroid carcinoma using the IOPTH assay. A 53-year-old man presented to our clinic with a serum calcium level of 11.8 mg/dL and an intact PTH level of 233.3 pg/mL. He had been treated for parathyroid carcinoma eleven years ago. Two suspected metastatic lesions were detected on the chest computed tomography. Due to the vastly different surgical field necessary to excise each lesion, we preferentially removed only one lesion and we monitored the other remaining suspected lesion without resection via IOPTH assay. Six months later, the patient's serum calcium and intact PTH levels remained within their normal ranges. To the best of our knowledge, this is the first case to effectively utilize IOPTH assay for the management of metastatic parathyroid carcinoma.

Citations

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The association of abdominal obesity, obesity and parathyroid hormone in Korean adults (aged≥50 years): The Korea National Health and Nutrition Survey, 2011
Kyu Su Lee, Yo Sang Yoon, Hyun Yoon
Journal of the Korea Academia-Industrial cooperation Society.2015; 16(6): 3882. CrossRef

Original Article

Identification and Validation of the Relationship of the Anabolic Effect of Parathyroid Hormone with the Wnt/beta-catenin Canonical Pathway.: Se Hwa Kim, Juan Ji An, Yumie Rhee, Sung Kil Lim; J Korean Endocr Soc. 2007;22(6):411-418. Published online December 1, 2007; DOI: https://doi.org/10.3803/jkes.2007.22.6.411

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Abstract PDF

BACKGROUND
It has been well established that daily injections of low dose parathyroid hormone (PTH) increase bone mass in animals and humans. However, the precise mechanisms by which PTH exerts its anabolic action on bone are incompletely understood. The canonical Wnt-b-catenin signaling pathway has recently been demonstrated to have an important role in bone cell function. In the present study, we have examined the interaction between the PTH and Wnt signaling pathways in mouse osteoblastic MC3T3-E1 cells. METHODS & RESULTS: MC3T3-E1 cells were treated with 0.01-0.84 micrometer recombinant PTH. beta-catenin expression was significantly increased after 30 minutes of exposure to PTH and reached a maximum 2.7 fold increase at 1 hr and expression then faded at 6 hrs. In addition, treatment with PTH increased nuclear accumulation of activated beta-catenin; the ratio between the nuclear to cytoplasmic protein was more than three fold at 30 minutes and beyond. Moreover, PTH stimulated T-cell factor/lymphoid enhancer factor (TCF/LEF) reporter gene activity in MC3T3-E1 cells. Confocal microscopy revealed nuclear translocation of beta-catenin by PTH as compared with a glycogen synthase kinase-3beta (GSK-3beta) inhibitor. CONCLUSION: These results suggest that the anabolic mechanism of PTH might be partially associated with the Wnt-canonical pathway. The appropriate target of another anabolic agent should be determined through further studies of this pathway.

Citations

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Effects of N-acetyl-l-cysteine on fish hepatoma cells treated with mercury chloride and ionizing radiation
Jin Kyu Kim, Min Han, Mohammad Nili
Chemosphere.2011; 85(10): 1635. CrossRef
Bone Forming Effect of PTH through Wnt/β-catenin Signaling System
Dong Jin Chung, Min Young Chung
Journal of Korean Endocrine Society.2007; 22(6): 407. CrossRef

Case Report

A Case of Primary Hyperparathyroidism Caused by Cystic Parathyroid Adenoma, Diagnosed during Intra-Operative PTH Monitoring.: Hye Jin Yoo, Nan Hee Kim, Soo Yeon Park, Dong Jin Kim, Sae Jeung Yang, Ju Ri Park, Hee Young Kim, Ji A Seo, Kye Won Lee, Sin Gon Kim, Kyung Mook Choi, Jae Bok Lee, Young Seok Lee, Sei Hyun Baik, Dong Seop Choi; J Korean Endocr Soc. 2005;20(3):278-282. Published online June 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.3.278

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Abstract PDF: Primary hyperparathyroidism is the most frequent cause of hypercalcemia, and its prevalence is increasing due to the routine examination of serum calcium levels. Primary hyperparathyroidims is most commonly caused by an adenoma or hyperplasia of the parathyroid gland. A cystic parathyroid adenoma is an extremely rare cause of primary hyperparathyroidism. In our case, a-79-year old female presented with lower back pain and constipation. Her serum calcium, phosphate and immunoreactive parathyroid homone levels were 15.6, 1.8mg/dL and 371.8pg/mL, respectively. Neck CT revealed a cystic mass and a contour bulging heterogeneous mass in the left inferior right thyroid gland, respectively. These mass lesions were removed, and the intra-operative parathyroid hormone levels monitored, to confirm the complete resection. After removing the left cystic mass to the inferior thyroid, the serum calcium and immunoreactive parathyroid hormone levels quickly returned to normal. We report a case of primary hyperparathyroidism, caused by a cystic parathyroid adenoma, with a brief review of the literature

Original Article

Anabolic Effects of Recombinant Human Parathyroid Hormone (1-84) on Bone Histomorphometry in Overiectomized Rats.: Young Jun Won, Du Hong Park, Jae Hyun Nam, Jong In Yook, Jin Kim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh, Sung Kil Lim; J Korean Endocr Soc. 1999;14(1):81-90. Published online January 1, 2001

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Abstract PDF: To evaluate the anabolic effects of human recombinant parathyroid hormone [hrPTH(1-84)], we examined effect of low-dose and high-dose of [hrPTH(1-84)] and estradiol on bone histomorphometry in ovariectomized rats. Sixty Sprague-Dawley female rats aged 8~10 weeks were used. Eight weeks after ovariectomy, or sham operation, rats were given daily sc injection of hrPTH (1-84), 30 pg/kg (OVX+L group), 150 pg/kg (OVX+H group), 17-estradiol (30 pg/kg, OVX+E group) or vehicle (OVX+V group) for 4 weeks. After double tetracycline labeling, all rats were killed at day 84. We completed the histomorphometric analysis of distal femoral metaphyseal cancellous bone for trabecular bone volume (TBV), mean trabecular plate thickness (MTPT), mean trabecular plate density (MTPD), mean trabecular plate separation (MTPS), mean osteoid seam width (OSW) and appositional rate (AR). The histomorphometric parameters (TBV, MTPT, OSW and AR) of trabecular bone mass in (OVX+E) group were higher than those in (OVX+V) group. The TBV of trabecular bone in PTH treated groups were higher than that in sham operated, (OVX+V) and (OVX+E) group. The histomorphometric parameters (TBV, MTPD, OSW and AR) of trabecular bone mass in (OVX+H) group showed a tendency to be higher than those in (OVX+L) group, but statistically not significant. In conclusion, Low dose (30 mg/kg) hrPTH (1-84) also shows a sufficient anabolic effect on trabecular bone.

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