Tear function and ocular surface changes in multinodular goiter patients

Turgut Cavusoglu1, Ayse Burcu Nurozler, Cengiz Titiz

  • 1General Surgery Clinic, Ankara Training and Research Hospital, TR-06550 Oran, Ankara, Turkey. turgutcavusoglu@gmail.com

Abstract

Insights

Multinodular goiter (MNG) surgery can significantly impact ocular surface health, leading to reduced tear function and goblet cell density. Postoperative monitoring for these eye changes is recommended.

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Surgical Research

Background:

  • Multinodular goiter (MNG) is a common endocrine disorder.
  • Thyroidectomy is a standard surgical treatment for MNG.
  • Ocular surface changes following thyroidectomy are not well-documented.

Purpose of the Study:

  • To assess conjunctival surface and tear function changes in MNG patients.
  • To compare pre- and postoperative ocular findings with healthy controls.

Main Methods:

  • Tear function tests (Schirmer, BUT, Rose Bengal staining) and conjunctival impression cytology were performed.
  • Twenty MNG patients undergoing near-total thyroidectomy were evaluated preoperatively and at 3 months and 1 year postoperatively.
  • Fifteen healthy volunteers served as the control group.

Main Results:

  • Postoperative tear function (Schirmer, BUT) decreased, while Rose Bengal staining increased significantly by the 1st year (p < 0.001).
  • Goblet cell density significantly decreased postoperatively (p < 0.001).
  • MNG patients showed significant differences in ocular findings compared to controls, both pre- and postoperatively.

Conclusions:

  • Thyroidectomy for MNG significantly alters ocular surface parameters.
  • Ocular surface changes in MNG patients differ from healthy individuals.
  • Regular ophthalmological follow-up is advised for MNG patients post-thyroidectomy.

Related Concept Videos

Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
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...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...