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Related Concept Videos

Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
The Parathyroid Glands00:59

The Parathyroid Glands

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.
Oxyphil cells, whose functions remain elusive, emerge during late puberty, adding a layer of complexity to the parathyroid gland's intricacies. In contrast, principal parathyroid cells undertake a vital role by producing...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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Related Experiment Video

Updated: Jun 29, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
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Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

Published on: July 14, 2023

Long-term changes in parathyroid function after subtotal thyroidectomy for graves' disease.

Yukiko Yano1, Mitsuji Nagahama, Kiminori Sugino

  • 1Ito Hospital, 4-3-6 Jinngumae, Shibuya, Tokyo, 150-8308, Japan. geka@ito-hospital.jp

World Journal of Surgery
|October 7, 2008
PubMed
Summary

Postoperative hypocalcemia after Graves

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Area of Science:

  • Endocrinology
  • Surgical Complications
  • Thyroid Surgery

Background:

  • Transient hypocalcemia is a common complication following thyroidectomy for Graves' disease.
  • Parathyroid hormone (PTH) assays are utilized to predict postoperative hypocalcemia.
  • Long-term parathyroid function changes after Graves' disease surgery require evaluation.

Purpose of the Study:

  • To assess long-term parathyroid function in patients who experienced hypocalcemia after thyroidectomy for Graves' disease.
  • To investigate the recovery patterns of parathyroid hormone (PTH) levels post-surgery.

Main Methods:

  • Serum intact parathyroid hormone (iPTH) levels were measured on postoperative day 1 in 275 Graves' disease patients undergoing subtotal thyroidectomy.
  • Patients with transient hypocalcemia received calcium and vitamin D supplementation.
  • Serum iPTH levels were monitored during a follow-up period.

Main Results:

  • On postoperative day 1, PTH levels were normal in 18 patients, low in 22, and high in 2.
  • During follow-up, iPTH normalized in 21 patients, remained normal in 12, and increased in 9.
  • All patients eventually achieved normal serum iPTH levels.
  • A significant difference in preoperative serum alkaline phosphatase was noted between high-iPTH and normocalcemic groups.

Conclusions:

  • Elevated serum PTH levels were observed in 21% of hypocalcemic patients post-thyroidectomy for Graves' disease.
  • Normal serum calcium levels were maintained with supplementation despite elevated PTH.
  • Parathyroid function eventually normalized in all studied patients.