Parathyreoid Glands and Their Diseases

*Mineral Deficiencies - Electrolyte Disturbances, Genes, Diet and Disease Interface*

[55] Ohe MN, Santos RO, Kunii IS, Carvalho AB, Abrahão M, das Neves MC, et al. Intraoperative PTH cutoff definition to predict successful parathyroidectomy in secondary and tertiary hyperparathyroidism. Brazilian Journal of Otorhinolaryngology.

[56] Vulpio C, Bossola M, Di Stasio E, Pepe G, Nure E, Magalini S, et al. Intra-

operative parathyroid hormone monitoring through central laboratory is accurate in renal secondary hyperparathyroidism. Clinical Biochemistry [Internet]. 2016;**49**(7-8):538-543. DOI: 10.1016/j.

clinbiochem.2016.01.012

2013;**79**(4):494-499

Paricio P. Primary hyperparathyroidism associated with MEN 1: Experience in 71 cases. Cirugía Española.

2018;**96**(10):627-633

(Basel). 2019;**11**(11):1-16

2013;**398**(1):121-130

[49] Machado NN, Wilhelm SM. Parathyroid cancer: A review. Cancers

[50] Riss P, Asari R, Scheuba C, Niederle B. Current trends in surgery for renal hyperparathyroidism (RHPT)—An international survey. Langenbeck's Archives of Surgery.

Yamamoto T, Kobayashi T. A retrospective study of the impact of intraoperative intact parathyroid hormone monitoring during total parathyroidectomy for secondary hyperparathyroidism. Medicine (United

States). 2015;**94**(29):1-6

articles/srep26841

[53] Bover J, Ureña P, Ruiz-

[54] Dulfer RR, Franssen GJH,

2017;**104**(7):804-813

Hesselink DA, Hoorn EJ, van Eijck CHJ, van Ginhoven TM. Systematic review of surgical and medical treatment for tertiary hyperparathyroidism. The British Journal of Surgery.

García C, da Silva A, Lescano P, del Carpio J, et al. Clinical and practical use of calcimimetics in dialysis patients with secondary hyperparathyroidism. Clinical Journal of the American Society of Nephrology. 2016;**11**(1):161-174

[52] Zhang L, Xing C, Shen C, Zeng M, Yang G, Mao H, et al. Diagnostic accuracy study of intraoperative and perioperative serum intact PTH level for successful parathyroidectomy in 501 secondary hyperparathyroidism patients. Scientific Reports [Internet]. 2016;**6**(May):26841. Available from: http://www.nature.com/

[51] Hiramitsu T, Tominaga Y, Okada M,

**82**

**85**

**Chapter 6**

**Abstract**

fractures.

**1. Introduction**

Disorders

*and David Da Rocha-Afodu*

Calcium and Metabolic Bone

Calcium homeostasis has a pivotal role in regulating many biological processes. The interplay of calcium-regulating hormones, including parathyroid hormone (PTH), vitamin D, and calcitonin, is crucial in tightly maintaining serum calcium levels. Deregulation of calcium homeostasis has clinical implications resulting in hypercalcemia or hypocalcemia, which can lead to metabolic bone disease (MBD). MBD is a group of multifactorial bone diseases, caused by bone demineralization and characterized by an increased susceptibility to fracture risk. This chapter aims to provide an overview of associated risk factors and diagnostic, prevention, and recent treatment methods for MBD. The diagnosis of MBD is based on the assessment of clinical signs, radiological findings, quantitative ultrasonography, and biochemical evaluation of serum calcium, phosphate, PTH, alkaline phosphatase, and vitamin D. Current pharmacological treatments include antiresorptive and anabolic conventional therapies. Additionally, the efficacy of herbal extracts and nutritional supplements have been evaluated. Recent advances in the MBD management include drugs targeting calcium-sensing receptor and parathyroid hormone-related proteins, leading to the development of cathepsin K and Src tyrosine kinase inhibitors, calcilytics, and monoclonal antibodies against sclerostin or Dickkopf-1. Moreover, new nanomaterials have been used for improving the surgical treatment of vertebral

**Keywords:** calcium, parathyroid hormone, metabolic bone disease, osteoporosis,

Metabolic bone disease (MBD), the third most prevalent disorder of the endocrine system, involves any disorder that alters the phenomena of mineralization in the normal skeleton. The disorder is primarily caused by abnormalities in the structure of bone or its mass, vitamin D level as well as the presence of

The concentration of extracellular calcium is crucial for several functions at the cellular level, which needs to be retained in restricted levels. The free concentration of calcium is predominantly negatively regulated by the secretion of the parathyroid hormone (PTH) in response to calcium-sensing receptors. A substantial drop

vitamin D, anabolic drug, antiresorptive drugs

certain minerals such as calcium and phosphorus [1].

*Ayotunde Oladunni Ale, Oluwayomi Akande* 
