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Related Concept Videos

Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Updated: May 21, 2025

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Does Lactation Predispose to Severe Hypocalcemia Post Total Thyroidectomy? A Case Series.

Remya Rajan1, Jino Johns Lalitha2, Natarajan Ramalingam2

  • 1Department of Endocrinology, Diabetes and Metabolism, Christian Medical College, Vellore, Tamil Nadu 632004 India.

Indian Journal of Surgical Oncology
|March 21, 2025
PubMed
Summary

Lactation may be an unrecognized risk factor for severe hypocalcemia after thyroidectomy. Breastfeeding women experiencing hypocalcemia post-surgery may require aggressive treatment for hypoparathyroidism.

Keywords:
HypocalcemiaLactationTotal Thyroidectomy

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Investigation of the Electrophysiological and Thermographic Safety Parameters of Surgical Energy Devices During Thyroid and Parathyroid Surgery in a Porcine Model
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Area of Science:

  • Endocrinology
  • Surgical Oncology
  • Women's Health

Background:

  • Post-thyroidectomy hypocalcemia is a known complication.
  • The role of lactation as a specific risk factor remains under-recognized.

Purpose of the Study:

  • To highlight lactation as a potential risk factor for severe post-thyroidectomy hypocalcemia.
  • To emphasize the need for aggressive management in affected patients.

Main Methods:

  • Case series describing three lactating women with severe hypocalcemia post-thyroidectomy.
  • Review of treatment protocols including intravenous calcium, oral calcium, and calcitriol.

Main Results:

  • All three patients experienced severe hypocalcemia requiring intensive treatment.
  • Lactation was identified as a common factor in this cohort.

Conclusions:

  • Lactation may represent an unrecognised risk factor for severe post-thyroidectomy hypocalcemia.
  • Lactating mothers undergoing thyroidectomy may need prompt and aggressive management for hypoparathyroidism.
  • Screening for and correcting pre-existing risk factors like hypomagnesemia and vitamin D deficiency is recommended.