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Metabolic Bone Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Hypocalcaemia usually results from chronic renal failure or other vitamin D-dependent causes (see Table 5.6). Alternatively, it may be caused by hypoparathyroidism, which is most frequently seen as a postoperative complication of parathyroidectomy. There are a number of rare hypocalcaemic disorders characterized by hypoparathyroidism or PTH resistance.
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Calcium: It is an essential element, which plays important roles in the formation of strong bones and teeth, and participates in skeletal muscle mobilization and blood pressure stabilization.135 An imbalance in calcium can lead to either hypercalcemia or hypocalcemia.136 Calcium mostly remains in a neutral state but carries a positive electrical charge (Ca2+) when dissolved in blood. As indicated earlier, an excessive amount of calcium in the blood leads to hypercalcemia and ultimately leads to diverse diseases, including kidney diseases, hyperparathyroidism, tuberculosis, sarcoidosis, and lung and breast cancers.136 Hypercalcemia can result from an excessive use of antacids, calcium plus vitamin D supplements, or structurally diverse medications such as lithium, theophylline, or selected water pills that are reported to induce hypercalcemia.135–137 Similarly, inadequate calcium in the bloodstream leads to hypocalcemia, which can lead to kidney failure, hypoparathyroidism, pancreatitis, prostate cancer, and malabsorption.135,136
Body fluids and electrolytes
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Symptomatic hypocalcaemia occurs when there is a decrease in the percentage of calcium which is ionised (although the total serum calcium level is normal). Common causes are listed in Table 4.8.
US-guided percutaneous radiofrequency ablation of secondary hyperparathyroidism as a bridge to renal transplantation
Published in International Journal of Hyperthermia, 2023
Wenwen Yue, Tingting Jiang, Erya Deng, Huihui Chai, Ning Weng, Hongfeng He, Zhengxian Zhang, Dong Xu, Chengzhong Peng
All patients with ESRD tolerated the ablation procedure well. Hoarseness occurred in two of the treatments and all recovering within three months spontaneously. Four patients presented with mild to moderate hypocalcemia after treatment, which slowly disappeared with oral calcium supplements during the subsequent period. Serious hypocalcemia occurred in one patient requiring intravenous calcium supplementation. No serious adverse events such as local infection, skin burning, or damage to the vital structures of the neck were observed. No mortality was directly associated with RFA treatment. The median interval from RFA to RTP was 22 months (range 2.5–79 months), and none of the patients was excluded from transplant operation because of PTH values while on the waiting list following RFA treatment.
Insights into the possible impact of COVID-19 on the endocrine system
Published in Archives of Physiology and Biochemistry, 2023
Adel Abdel-Moneim, Ahmed Hosni
Furthermore, endocrine disorders, such as reduced PTH level or resistance to PTH action, calcitonin dysregulation, and vitamin D deficiency may be the cause of hypocalcaemia (Lind et al. 2000, Ardehali et al.2018). Chronic vitamin D deficiency is known to alter calcium metabolism and SARS-CoV-2 infection could exacerbate the incidence of hypocalcaemia in COVID-19 patients in severe cases (Bilezikian et al. 2020). COVID-19 infection can influence bone-metabolism via mechanisms, such as ACE2-dependent bone resorption, inflammatory cytokines storm, immunosuppression, and hypoxaemia. All these factors may affect one or more key elements of the activation process leading to increased osteoporosis and bone resorption (Zheng et al.2020). On the other hand, de Martinis et al. (2020) suggested a mechanism implicated in stimulating osteoclastogenesis. Interleukin-1, known as “osteoclast activating factor”, increases osteoclast vitality and resorptive activity by independent and RANKL-dependent pathways. Moreover, SARS-CoV-2 may have enhanced cytokine activity that induces bone resorption, but the virus may also act directly on osteoclastic activation (Salvio et al. 2020). Meanwhile, if patients with hypo/hyperparathyroidism become infected with SARS-CoV-2, special precautions should be taken in order to maintain optimal concentrations of plasma calcium, magnesium, phosphate, and vitamin D. Notably, patients with hypoparathyroidism are at-risk for hypocalcemic crisis which is exaggerated by SARS-CoV-2 infection (Chatterjee et al. 2020).
Biosimilarity of HS-20090 to Denosumab in healthy Chinese subjects: a randomized, double-blinded, pharmacokinetics/pharmacodynamics study
Published in Expert Opinion on Investigational Drugs, 2022
Yaqi Lin, Heng Yang, Xiaoyan Yang, Can Guo, Shuang Yang, Guoping Yang, Qiong Wu, Chao Pan, Changan Sun, Chuan Li, Liangliang He, Jie Huang, Qi Pei
Denosumab binds to RANKL, thereby modulating calcium release from bone. Normal serum calcium levels are 8–10 mg/dL (2.0–2.5 mmol/L), although the exact range can vary among laboratories [13]. In this study, normal serum calcium levels are 2.2–2.7 mmol/L. When the total serum calcium level is at concentrations of 2.1 mmol/L or less, it was considered hypocalcemia. Hypercalcemia is judged by our research doctor if the total serum calcium level is higher than 2.8 mmol/L. Both of them are graded according to the CTCAE. Reduced release of calcium from the bone eventually leads to hypocalcemia. However, several subjects had the hypercalcemia during the study, which might be the rebound-linked phenomenon after Denosumab discontinuation [14]. In addition, Denosumab could also affect the parathyroid gland function. Increased blood parathyroid hormone was observed in this study, which might be a compensatory response to the transient dose-dependent decrease in serum calcium levels [15]. The increased PTH levels might lead to an increased phosphorus excretion in the absence of osteoclastic liberation of bone phosphorus, consequently resulting in a hypophosphatemia [16].