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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.
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.
The locomotor system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Parathyroid hormone is important in the regulation of calcium metabolism and bone turnover. It has effects on both osteoblastic and osteoclastic activity. Overactivity of the parathyroid glands is classified as primary, secondary, or tertiary (see Chapter 18). Primary hyperparathyroidism is usually due to the presence of a parathyroid adenoma but in <5% of cases there is diffuse hyperplasia of all four glands, or a parathyroid carcinoma. Primary hyperparathyroidism affects 1 in 1,000 people and is the most common cause of hypercalcaemia in asymptomatic individuals. Early diagnosis due to routine measurement of serum calcium means that bone disease is now found in <5% of cases. In secondary hyperparathyroidism there is parathyroid gland hyperplasia and increased PTH secretion which occurs as a physiological response to hypocalcaemia. The most common cause of hypocalcaemia is chronic renal failure. Tertiary hyperparathyroidism may occur in longstanding secondary hyperparathyroidism when an autonomous nodule develops in a hyperplastic gland, resulting in hypercalcaemia.
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).
Prolonged QTc Interval in Nigerian Children with Sickle Cell Anemia
Published in Hemoglobin, 2021
Maxwell U. Anah, Anthony C. Nlemadim, Chigozie I. Uzomba, Egorp O. Ineji, Friday A. Odey
There are other established causes of prolonged QTc interval, the majority of which have been excluded in the subjects of this study [8]. One of them is hypocalcemia, which appears to be a constant factor in sickle cell anemia, and together with myocardial ischemia, may be the fundamental reason for the occurrence of prolonged QTc interval in sickle cell anemia unlike in non sickle cell anemia patients with anemia due to other hematological diseases [3,4,21]. Hypomagnesemia also causes prolonged QTc interval by impairing release of parathormone and tissue response to parathormone that leads to secondary hypocalcemia [22]. Therefore, if serum calcium levels were measured in this study, one may have found hypocalcemia in both clinical states similar to that obtained in previous studies [3–7].
Correlations of neck ultrasound and pathology in cervical lymph node of papillary thyroid carcinoma
Published in Acta Chirurgica Belgica, 2020
Bassam Abboud, Tarek Smayra, Hicham Jabbour, Claude GHORRA, Gerard Abadjian
Overall, 47 patients (23%) had transient postoperative hypocalcaemia resolving within 6 months following surgery. During follow-up, four patients required Calcium and Vitamin D supplementation with no clinical symptoms of hypocalcaemia at 12 months postoperatively. The incidence of permanent hypoparathyroidism was 2%. Fourteen patients (7%) had transient postoperative hoarseness and two had permanent vocal cord paralysis (1%). The overall postoperative length of stay was 1 day in 187 patients (91%), 2 days in 11 patients (5%), and more than 2 days in 8 patients (4%). Asymptomatic hypocalcemic patients were discharged from the hospital the day after surgery. Mean duration of hospitalization for hypocalcaemia patients was 2 days (1–3 days). A total of 11 patients (5%) developed postoperative hematoma and/or seroma. There were no major bleeding; that is, all the patients had minor bleeding or seroma not requiring surgical intervention. Wound infection occurred in 1% of all the procedures. Therapeutic radioactive iodine had been given to 188 patients. During follow-up, lymph nodes recurrence, local recurrence and distant metastasis occurred in 12 patients, 2 patients, and 2 patients, respectively.