Endocrine Disorders, Contraception, and Hormone Therapy during Pregnancy
“Bert” Bertis Britt Little in Drugs and Pregnancy, 2022
Parathyroid glands (~4) are located along the posterior border of the thyroid gland. Their function is primarily in the regulation of bone mineral metabolism. Parathyroid hormone (PTH) maintains extracellular fluid calcium concentration. During pregnancy, calcium requirements increase to 3 to 4 times the non-pregnant daily requirement, especially during the latter half of gestation when most of the fetal bone mineral is deposited. Calcium and phosphorus are actively transported across the placenta, resulting in lower maternal serum calcium concentration, an increase in PTH secretion, and decreased calcitonin production (Schedewie and Fisher, 1980). During gestation, 1,25 dihydroxy vitamin D levels and intestinal absorption of calcium increase strikingly (Bouillon and Van Assche, 1982; Heany and Skillman, 1971; Kumar et al., 1979).
Radiopharmaceuticals for Diagnostics
Michael Ljungberg in Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
The parathyroid glands, located adjacent to the thyroid, regulate the body’s use of calcium. Parathyroid adenoma is a benign condition causing hyperparathyroidism, usually resulting in elevated blood calcium levels, which is best treated by minimally invasive surgery. Imaging plays an important role in guiding surgery. Most commonly used now is the myocardial perfusion agent, 99mTc-sestamibi, which accumulates in both the thyroid and parathyroid glands but is only retained in the parathyroid glands. The mechanism of accumulation of 99mTc-sestamibi is not fully understood but is believed to be related to high mitochondrial activity. Two imaging approaches are taken. One uses early and late imaging (15 min and 2 h) following injection of 99mTc-sestamibi. Relative focal increase in the parathyroid glands (as the tracer washes out of the thyroid) is indicative of adenoma. An alternative approach uses a second, thyroid-specific tracer, such as 99mTc-pertechnetate or 123I-iodide, to allow subtraction of thyroid activity for better definition of the parathyroid glands. In either case, SPECT or SPECT/CT imaging is useful to provide the surgeon with a roadmap [29].
Endocrine System
David Sturgeon in Introduction to Anatomy and Physiology for Healthcare Students, 2018
Another hormone produced by the thyroid gland is the peptide hormone calcitonin which helps to maintain and regulate bone mineral density and the concentration of calcium and phosphate in the blood plasma. It is secreted in response to high plasma levels of calcium (Ca++) and encourages the uptake of calcium and phosphate into the bone matrix. Calcitonin also increases calcium excretion in the urine and inhibits the reabsorption of spongy bone by osteoclasts (see Chapter 4). Calcitonin works collaboratively with another peptide hormone called parathyroid hormone (PTH). PTH is produced and secreted by four small parathyroid glands situated on the posterior surface of the thyroid gland. It is secreted in response to low levels of plasma calcium and increases the number and activity of osteoclasts in order to liberate calcium and phosphate from the bone. It also promotes the reabsorption of calcium (and magnesium) from the nephrons of the kidney and converts biologically inert vitamin D3 into calcitriol (also in the kidney). Consequently, parathyroid hormone is indirectly responsible for the absorption of dietary calcium from the gastrointestinal tract. Both hormones are controlled by negative feedback.
Formulation optimization and pharmacokinetics evaluation of oral self-microemulsifying drug delivery system for poorly water soluble drug cinacalcet and no food effect
Published in Drug Development and Industrial Pharmacy, 2018
Mengyuan Cao, Xu Xue, Xixi Pei, Yiwen Qian, Lan Liu, Lili Ren, Guoguang Chen
Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease (CKD) [1]. Cinacalcet, N-[(1R)-1-(1-naphthyl)ethyl]-3-[3-(trifluoromethyl)phenyl]propan-1-amine, was FDA-approved first calcimimetic for the treatment of SHPT in patients with CKD on dialysis [2]. Cinacalcet mimiced calcium at the parathyroid hormone receptor. The calcium outside the cells had become sensitized to the calcium-sensing receptors in the parathyroid gland because of this binding, and reducing the secretion of parathyroid hormone directly [3]. At the same time, cinacalcet overcome the side effect of traditional agents such as phosphate binders and vitamin D sterols in the risk of hypercalcemia and hyperphosphatemia [4]. Cinacalcet had poor aqueous solubility. Therefore, cinacalcet was designed as nonconventional formulations to promote the absorption and enhance bioavailability of oral administration.
Genetic variants of FGFR family associated with height, hypertension, and osteoporosis
Published in Annals of Human Biology, 2023
Hye-Won Cho, Hyun-Seok Jin, Yong-Bin Eom
Additionally, FGFRs were involved in the calcium signalling pathway, which is essential for endothelial control of cardiovascular and osteoclast activity. Calcium signals at myoendothelial projections are a fundamental factor in endothelial control of vascular tone (Wilson et al. 2019). One study demonstrated disruption in calcium signalling mediated by inositol trisphosphate (IP3), which results in release of calcium and creates microdomains that are essential to the balance of vascular function, in hypertensive rats (Yuan et al. 2016; Lin et al. 2019; Wilson et al. 2019). In addition, from the bone homeostasis point of view, it is well-known that calcium is essential for activating proliferation of osteoclast precursors and suppressing the resorption of mature osteoclasts (Kajiya 2012). Calcium homeostasis in bone is monitored by parathyroid hormone (PTH). The parathyroid gland has calcium-sensing membrane receptors, and a low level of calcium releases PTH, followed by stimulation of osteoclasts (Teitelbaum 2000).
Efficacy and safety of US-guided thermal ablation for primary hyperparathyroidism: a systematic review and meta-analysis
Published in International Journal of Hyperthermia, 2020
Jieyi Ye, Weijun Huang, Guangliang Huang, Yide Qiu, Weiwei Peng, Ninghui Lan, Xiaoyan Xie, Baoxian Liu
Primary hyperparathyroidism (PHPT) is a primary disease of the parathyroid, with a prevalence of 0.1%∼0.4%, being more frequently in female patients. It is caused by excessive synthesis and secretion of parathyroid hormone (PTH) by one or more of the four parathyroid glands and characterized by hypercalcemia and elevated or inappropriately normal concentrations of PTH [1]. The most common manifestation of PHPT is asymptomatic hypercalcemia detected during routine biochemical testing [2]. However, the disease has the potential to become symptomatic, resulting in complications that are mainly presented as skeletal, kidney and gastrointestinal involvement [3]. It has been reported that PHPT is responsible for renal, skeletal and cardiovascular damage and increased risk of nephrolithiasis, osteoporosis, bone fractures, hypertension, arrhythmias, ventricular hypertrophy, vascular calcification, and mortality [4–11].
Related Knowledge Centers
- Bone REModeling
- Epithelium
- Hyperparathyroidism
- Internal Jugular Vein
- Parathyroid Hormone
- Thyroid
- Endocrine Gland
- Pharyngeal Pouch
- Hypoparathyroidism
- Lentil