Background: A thyroid adenoma is a benign (non-cancerous) tumor of the thyroid gland. Thyroid adenoma can be classified into active or inactive depending on the amount of thyroid hormone produce. hereas a Colloid goitre, also known as nontoxic goitre, simple goitre, or adenomatous nodular goiter, is a benign, non-cancerous enlargement of the thyroid gland. It is characterized by the accumulationof colloid material within the thyroid tissue, often forming nodules. Thyroid adenomas and colloid goitres can occur simultaneously in the same patient and the presence of both conditions may lead to a more complex clinical picture, requiring careful evaluation and management. So, here we report a case of anterior midline neck swelling having a rare diagnosis patient having co-existing thyroid adenoma and colloid goitre.
Adenomatous goitre, commonly referred to as multinodular goitre (MNG), is a benign, non-neoplastic enlargement of the thyroid gland, characterized by multiple nodules of varying size. It typically arises from long-standing diffuse goitre, which undergoes repeated cycles of hyperplasia and involution, leading to structural and functional heterogeneity of the gland [1,2].
One of the major etiological factor is iodine deficiency, which impairs thyroid hormone synthesis, resulting in chronic TSH stimulation. This persistent stimulation leads to follicular hyperplasia, nodular formation, and degenerative changes such as hemorrhage, fibrosis, and calcification. Somatic mutations in TSH receptor genes may also contribute to the autonomous growth of some nodules [3].
Clinically, multinodular goiter presents as a slowly progressive, painless swelling in the anterior neck. It is more common in middle-aged and elderly women, particularly in areas with iodine deficiency. Most patients are euthyroid, but some may develop toxic multinodular goitre with symptoms of hyperthyroidism (Plummer’s disease). Large goitres can cause compressive symptoms like dysphagia, dyspnea, or hoarseness [4].
Diagnosis involves Thyroid function tests, Ultrasound, FNAC of dominant or suspicious nodules, and radionuclide scans to assess function. CT or MRI may be required in cases with retrosternal extension [5].
Management depends on size, symptoms, function, and malignancy risk. Options include observation, radioactive iodine therapy, or thyroidectomy in symptomatic or suspicious cases [6].
A 20 Year old female Patient presented to ENT OPD with a complaint of midline neck swelling since 6 months. Swelling was insidious in onset and progressive in nature. The swelling increased in size since last 2 months . On examination, a solitary swelling of 5*5cm was present, 2cm above sternal notch, non-tender, mobile, soft to firm in consistency and move with deglutition. Swelling does not move with protrusion of tongue and is not associated with difficulty in swallowing and shortness of breath.
Ultrasound revealed –enlarged right lobe of thyroid showing a oval shaped solid lesion with central cystic/necrotic with no vascularity on colour Doppler flow imaging (CDFI). The left lobe of thyroid was normal in size.
FNAC SWELLING showed benign follicular epithelial cells present in singly scattered as well as group of follicles in a microfollicular pattern. A stromal fragment is also seen. Background shows scanty colloid and pigment laden macrophages suggestive of Adenomatous Goitre.
The thyroid function tests were normal. Patients preanaesthetic checkup was done and was posted for Right Hemithyroidectomy. Recurrent Laryngeal nerve and parathyroid gland was preserved.
Sample was sent for histopathological examination.
HPE revealed follicular adenoma, encapsulated tumour with no capsular invasion and features of colloid changes.
Margins- all resection margin are microscopically free of tumor. Lymphatic invasion was not identified. There were colloid changes seen.
Adenomatous goitre, also known as multinodular goitre (MNG) or nodular hyperplasia, is a benign enlargement of the thyroid gland characterized by multiple nodules with variable histologic and functional profiles. It is among the most common thyroid disorders globally. According to epidemiological data, the prevalence of goitre ranges from 5% to 15% in iodine-sufficient areas and can rise to >30% in iodine-deficient regions, particularly affecting women and the elderly [1]. It evolves from diffuse hyperplasia of the thyroid due to prolonged TSH stimulation—often secondary to iodine deficiency—which leads to nodule formation over time. These nodules result from cycles of hyperplasia, involution, hemorrhage, and fibrosis, producing the characteristic irregular thyroid enlargement seen clinically.
The most significant etiological factor remains iodine deficiency, which affects more than 1.88 billion people worldwide, contributing to endemic goitre in many parts of South Asia, Africa, and the mountainous regions of South America and Europe (WHO, 2020). Iodine deficiency reduces thyroid hormone synthesis, which in turn elevates TSH levels and promotes glandular hyperplasia and hypertrophy. Additional contributing factors include dietary goitrogens (e.g., cassava, cabbage), smoking (thiocyanate exposure), selenium and zinc deficiency, and environmental pollutants. On a genetic level, somatic mutations in TSH receptor and GNAS genes have been associated with autonomous nodule formation, especially in toxic multinodular goitre [2]. MNG is more prevalent in females (female-to-male ratio ≈ 4:1) and typically presents after the third decade of life.
Clinically, patients often present with a slowly enlarging neck mass, typically painless and nodular. Most patients are euthyroid, but about 10–20% may develop subclinical or overt hyperthyroidism, particularly in the elderly due to autonomous functioning nodules. In contrast, hypothyroidism may develop in late-stage disease or in cases with autoimmune thyroiditis overlap. Large goitres can cause compressive symptoms such as dyspnea, dysphagia, and hoarseness due to tracheal or esophageal compression or recurrent laryngeal nerve involvement. Retro-sternal extension occurs in 5–15% of cases and can result in superior mediastinal compression or venous congestion[3].
Evaluation begins with thyroid function tests (TFTs), which usually show normal T3, T4, and TSH levels in euthyroid patients. In toxic MNG, TSH is suppressed while T3/T4 are elevated. Ultrasonography is the cornerstone of imaging, revealing nodules with mixed echogenicity, calcifications, cystic changes, or increased vascularity[4]. The prevalence of incidental thyroid nodules on ultrasound is high, affecting up to 67% of adults in iodine-sufficient populations (Gharib et al., 2016). Fine-needle aspiration cytology (FNAC) is the most important diagnostic tool for evaluating suspicious nodules and differentiating benign from malignant lesions. FNAC has a sensitivity of 65–98% and specificity of 72–100% for detecting thyroid cancer (Cibas & Ali, 2017) . According to data from Bethesda classification studies, the risk of malignancy in MNG is 5–15%, with papillary thyroid carcinoma being the most common [5]. Radionuclide scans are helpful in toxic cases to identify hot (functioning) versus cold (non-functioning) nodules—the latter having a higher probability of malignancy[6].
Histologically, adenomatous goitre shows nodular follicular hyperplasia with variable follicle size, colloid accumulation, and absence of a capsule. Areas of hemorrhage, fibrosis, cystic degeneration, calcification, and occasionally osseous metaplasia are commonly observed [7]. Unlike follicular adenomas, these nodules lack encapsulation, and despite their clonal expansion, they remain benign. The main histopathological challenge is distinguishing adenomatous nodules from follicular neoplasms or low-grade malignancies, particularly when architectural atypia or cellularity is present [8].
The Differential diagnosis of adenomatous goitre can be Colloid goitre,
Follicular adenoma, Papillary thyroid carcinoma, Hashimoto’s thyroiditis
Thyroid cyst and Thyroid lymphoma [9].
Management depends on the size of the goitre, symptomatology, functional status, and malignancy risk. Asymptomatic, small, and euthyroid goitres may be monitored with periodic ultrasound and clinical evaluation. The role of thyroxine suppression therapy is now limited due to the potential risk of subclinical hyperthyroidism, especially in the elderly[10]. In toxic nodular goitre, anti-thyroid drugs such as methimazole or propylthiouracil may be initiated, especially for short-term symptom control. Radioactive iodine (RAI) therapy is a non-surgical option, particularly in elderly patients, with studies showing 30–60% reduction in goitre size after 6–12 months. However, larger goitres may require higher doses or multiple sessions and may not adequately resolve compressive symptoms [4].
Surgery remains the definitive treatment in patients with large goitre, pressure symptoms, cosmetic concerns, or malignancy risk[11]. Surgical options include total or near-total thyroidectomy, especially in bilateral disease or suspected malignancy. Subtotal thyroidectomy, once common, has fallen out of favor due to recurrence rates of 10–30% over a 10-year period. Postoperative complications include transient hypocalcemia (20–30%), permanent hypoparathyroidism (1–3%), and recurrent laryngeal nerve injury (1–2%) [12]. Lifelong levothyroxine replacement is required following total thyroidectomy[12].
Recent developments include the use of ultrasound elastography to assess nodule stiffness and stratify malignancy risk. Molecular testing for mutations such as BRAF, RAS, RET/PTC, and PAX8/PPARγ is increasingly applied to indeterminate cytology (Bethesda III and IV), aiding in surgical decision-making. These tests have shown promising predictive value, with BRAF mutations highly specific for papillary carcinoma. Surgical innovation, such as robot-assisted and endoscopic thyroidectomy, has been introduced to improve cosmetic outcomes, particularly in young female patients with benign nodular disease.
Adenomatous goitre, also known as multinodular goitre, is a benign thyroid enlargement characterized by multiple nodules. It commonly results from chronic TSH stimulation due to iodine deficiency or hormonal dysregulation. Patients may present with a neck swelling, and occasionally with compressive symptoms. Diagnosis involves ultrasound and FNAC to rule out malignancy. Treatment includes observation, thyroxine therapy, or surgery, depending on the goitre’s size, symptoms, and functional or suspicious features.
In our study, we encountered a patient 20year/female, who presented with midline neck swelling, was diagnosed with adenomatous goitre, and treated by right Hemithyroidectomy. Patient is on regular 6 monthly follow up