EUTHYROID (NONTOXIC) GOITER

Definition and Overview

• Euthyroid (Nontoxic) Goiter: Enlargement of the thyroid gland without clinical signs of hyperthyroidism or hypothyroidism.
• Common in areas with low dietary iodine, but also seen elsewhere.
• Early stage often diffuse enlargement; later can become nodular (multinodular).

Clinical Presentation

1. Age and Timing
   • Often noted around puberty in both sexes when iodine intake is low.
   • Gradual enlargement over many years, leading to various nodular patterns.
2. Goiter Characteristics
   • Diffuse Goiter initially; later may develop nodularity (hard areas, cystic areas).
   • May be symmetric or asymmetric; can extend intrathoracically (substernal goiter).
3. Obstructive Symptoms
   • Tracheal Compression → dyspnea on exertion, stridor (in advanced cases).
   • Esophageal Compression → dysphagia.
   • Recurrent Laryngeal Nerve compression → vocal cord palsy.
   • Cervical Sympathetic Chain compression → Horner syndrome.
   • Pemberton Maneuver (raising arms) can elicit facial plethora, cyanosis, or stridor if thoracic inlet obstruction is present.
4. Sudden Enlargement/Pain
   • May be due to hemorrhage into a nodule or cyst.
   • Pain can radiate to ear, shoulder, or neck structures.
5. Possibility of Hyperfunction (“Hot Nodule”)
   • Some nodules may become autonomously functioning → hyperthyroidism (toxic multinodular goiter).
   • Cancer is rare but possible within a multinodular goiter.

Evaluation and Diagnosis

1. Exclude Hyperthyroidism
   • Measure serum thyrotropin (TSH).
2. Thyroid Ultrasound
   • Defines structure of nodules and extent of suprasternal goiter.
3. CT/MRI
   • Useful for substernal (intrathoracic) extension.
4. Fine-Needle Aspiration Biopsy (FNA)
   • If suspicious or prominent nodules are present to rule out malignancy.

Indications for Surgery

1. Cosmetic Reasons
   • Large, unsightly goiter size.
2. Sudden Enlargement
   • Rapid growth or a suspiciously hard area suggesting neoplastic change.
3. Obstructive Symptoms
   • Significant compression of trachea or esophagus, or thoracic inlet obstruction causing breathing/swallowing difficulties. (Review Pemberton Sign)
4. Malignancy suggested by Fine Needle Biopsy

GROSS PATHOLOGY OF GOITER

Types and Frequency

• Goiter: Enlargement of thyroid, often related to dietary iodine intake.
• Nontoxic (Euthyroid) Goiters: Typically do not produce hypo- or hyperthyroidism, often appear during adolescence or pregnancy.
• Early Diffuse → eventually can become multinodular.

Physical Examination and Growth

• Gland can be 2–3× normal size or larger; patients may notice neck fullness, tight collars, difficulty swallowing.
• Compression of trachea → stridor; venous engorgement if thoracic inlet is narrowed.
• Gland feels firm (not hard). Over time, becomes asymmetric and nodular; nodules can differ in size and consistency.

Gross Appearance

• Large, nodular thyroid with possible hemorrhages, cysts, fibrosis, calcifications.
• Amber, translucent colloid on cut section.
• Some nodules are partially or fully encapsulated, mimicking follicular neoplasms.
• Rarely, cancer (e.g., papillary carcinoma) arises within a multinodular goiter.

Cytology and Histology

• Fine-Needle Aspiration from colloid nodules usually shows:
  • Abundant colloid, mixed cell populations (follicular cells with uniform nuclei, inflammatory cells, Hürthle cells).
• Microscopy of multinodular goiter may show:
  • Variable follicle size, some large (2 mm), coalescing into cystic areas.
  • Rarely, malignant changes.

ETIOLOGY OF NONTOXIC GOITER

General Mechanism

• Often due to partial deficiency in thyroid hormone synthesis → increased TSH → thyroid hyperplasia/enlargement.
• Iodine Deficiency: Main environmental factor worldwide. About 1 billion people live in iodine-deficient regions.
• Dietary: The most important source of iodine (75 µg daily needed by thyroid; typical North American intake ~150–300 µg/day).

Inherited Defects (Dyshormonogenetic Goiters)

• Congenital enzyme defects in hormone synthesis (e.g., in NIS transporter, thyroglobulin, thyroid peroxidase, THOX2).
• Pendred Syndrome: Thyroid iodide transport defect + sensorineural deafness (pendrin protein abnormality).
• Thyroid Hormone Resistance: Mutations in thyroid receptor β can cause euthyroid goiter with elevated T4/T3.

Evolution of Nontoxic Goiter

1. Early: Diffuse hyperplasia.
2. Prolonged TSH Stimulation: Nodule formation, partial encapsulation, hemorrhage, cystic change, calcification.
3. Involution: Epithelium flattens, colloid accumulates → large follicles and possible cysts.
4. Rarely, carcinoma may arise.