Simple goiter occurs when certain factors lead to a reduction in thyroid hormone levels, causing a compensatory overproduction of thyroid-stimulating hormone (TSH), which in turn results in compensatory enlargement of the thyroid gland. This enlargement may manifest as diffuse or nodular changes.
Etiology
Iodine Deficiency
Environmental iodine deficiency is the primary cause of simple goiter. In some regions, residents experience higher rates of this condition due to insufficient iodine intake from water and food, making it also known as "endemic goiter." Inadequate iodine intake prevents the synthesis of sufficient thyroid hormones, leading to feedback-induced TSH hypersecretion by the pituitary gland, which stimulates thyroid gland hyperplasia and compensatory enlargement. In the early stages of iodine deficiency, when the duration is relatively short, proliferating and dilated follicles are evenly distributed throughout the gland, resulting in diffuse goiter. Over time, with prolonged iodine deficiency, the condition progresses, and the dilated follicles cluster into single or multiple nodules, forming nodular goiter. Degenerative changes, such as the development of cysts, fibrosis, calcification, or impaired blood supply to nodules, may also occur. The supplementation of iodized salt has become a key preventive measure for endemic goiter.
Increased Thyroid Hormone Requirement
Temporary increases in thyroid hormone demand, such as during adolescence, pregnancy, or menopause, may lead to mild diffuse goiter, also referred to as physiological goiter. This type of goiter often regresses on its own after adulthood or pregnancy.
Thyroid Hormone Synthesis and Secretion Disorders
Disorders, such as the use of certain medications (e.g., thiourea drugs) or congenital enzyme deficiencies that interfere with thyroid hormone synthesis, may also lead to goiter.
Clinical Manifestations
Simple goiter is more commonly observed in women and typically does not present with systemic symptoms. The thyroid gland exhibits varying degrees of enlargement and moves up and down with swallowing. In the early stages of the disease, the gland is symmetrically and diffusely enlarged, with a smooth surface and soft texture. As the condition progresses, one or more nodules may be palpable on one or both sides of the enlarged gland. These nodules often persist for years and grow slowly. Rapid enlargement of a cystic nodule may occur in the case of intranodular hemorrhage, which can sometimes be accompanied by neck pain or discomfort.
The primary clinical features of simple goiter include various degrees of thyroid gland enlargement and associated compression symptoms on surrounding structures. Manifestations may include compression of the trachea, esophagus, and recurrent laryngeal nerve. Tracheal compression may lead to tracheal bending, displacement, airway narrowing, respiratory difficulty, or even cartilage degeneration and softening of the trachea. Recurrent laryngeal nerve compression may result in hoarseness, while esophageal compression may cause a sensation of a foreign body during swallowing or difficulty swallowing. In cases where thyroid nodules grow retrosternally, forming substernal goiter, compression of deep cervical veins can impair head and neck vein drainage, leading to symptoms such as facial cyanosis, swelling, and distended superficial veins in the neck and chest. Additionally, nodular goiter may occasionally result in secondary hyperthyroidism or undergo malignant transformation.
Diagnosis
The diagnosis of endemic goiter can be made based on regional epidemiology and the characteristic movement of the thyroid mass during swallowing. All patients should undergo thyroid function testing and neck ultrasound to evaluate thyroid function and to determine the characteristics and extent of the goiter.
Treatment
Physiological goiter does not require pharmacological treatment, and increased dietary iodine intake is recommended.
Patients under the age of 20 with diffuse simple goiter may receive low doses of levothyroxine sodium to suppress TSH secretion, reducing thyroid gland hyperplasia and enlargement.
Surgical treatment is considered in the following situations:
- Clinical symptoms caused by compression of the trachea, esophagus, or recurrent laryngeal nerve.
- Substernal goiter.
- Large goiters that significantly impact daily life and work.
- Nodular goiter with secondary hyperthyroidism.
- Nodular goiter suspected or confirmed to exhibit malignant transformation.
Surgical Techniques
Depending on the extent of the pathology, options include partial lobectomy, lobectomy, subtotal thyroidectomy, or near-total/total thyroidectomy.