Iodine deficiency is the main cause of endemic thyromegaly, mostly found in inlands and mountain areas with a high altitude far away from oceans. Increased demand for thyroxin in periods of puberty, pregnancy, lactation and menopause as well as a result of mental stimulation and traumas can lead to relative iodine deficiency. In cases of environmental iodine deficiency or decreased serum inorganic iodine concentration, hyperplasia of the thyroid tissues occurs to boost its function of iodine intake. Therefore, the thyroid can take in enough iodine from blood under low iodine condition to ensure synthesis of enough thyroid hormones for physiological demand of the body tissues. However, in cases of severe deficiency of iodine, this compensation mechanism can not maintain normal thyroid functions so the thyroid preferably synthesizes and secretes T3 which needs less iodine but has stronger activity and T4 synthesis decreases. Moreover, as T4 concentration is an essential cause for pituitary stimulation to produce TSH, decreased T4 concentration increases the pituitary stimulation to produce more TSH which further aggravates thyroid hyperplasia and enlargement. Contrarily, for cases with long-term excessive intake of iodine, excessive inorganic iodine ions in the thyroid tissues can impede iodine organizing process, resulting in decreased synthesis of thyroxin. Additionally, thyroxin release inhibition by abundant iodine contributes to further deficiency of blood thyroxin, which increases TSH synthesis and secretion and causes thyromegaly.

Clinical observation reveals that blood T3 and T4 levels decrease significantly with accompanying decrease of sex hormones. According to the above-mentioned mechanism, decreases of T3 and T4 levels can likewise lead to thyromegaly. Moreover, T3 and T4 level are associated with the survival rate of AIDS patients. The decreases of T3 and T4 levels are the accurate predictor for occurrence of death in AIDS patients.

It has been demonstrated that some food and drugs may be of certain relations with thyromegaly. For instances, long-term intake of cabbages in a large quantity can result in thyromegaly. It has been found by researchers that organic cyanides in cabbages can interfere in iodide oxidation to affect the synthesis of the thyroid hormones, therefore leading to compensatory thyroid enlargement. Prolonged oral administration of some medicines as potassium cyanide, potassium perchlorate, Aminosalicylic acid, phenyl-butazone, Sulfanilamide and Thioureas can hinder the synthesis of thyroid hormones and inhibit their releases. Consequently, thyroxin in blood decreases and TSH level increases, lead to thyromegaly. AIDS patients are commonly treated with various combinations of drugs. It cannot be excluded that some medicines have impacts on synthesis and release of thyroxin, leading to thyromegaly.

Synthesis of thyroid hormones cannot be completed without the catalyses of various specialized enzymes. AIDS patients probably have congenital defects in thyroid hormone synthesis. The related symptoms are prone to be clinically manifested in the stage of AIDS.

It has been reported that AIDS patients may be complicated by hyperthyroidism or hypothyroidism. Observation of thyroid hormone level and immunity suggests that immunological damages to the thyroid tissues may occur but its underlying mechanism has not be definitively reported.

Nuclear imaging demonstrates homogeneous radioactive distribution of the bilateral lobes that are similar to the normal thyroid or homogeneous increase of radioactive concentration. For cases with nodules, the demonstrations include local defects of radioactive distribution in the thyroid parenchyma, being worm-eaten liked.

Ultrasound demonstrates homogeneous enlargement of thyroid parenchyma, with its severity being related to the course and severity of the illness. The interior echo is normal, moderate and homogeneous, with occasionally scattering cystic nodules in homogeneous non-echo areas with smooth borderlines. CDFI generally demonstrates no obvious abnormalities.

CT scanning demonstrates diffuse enlargement of the thyroid with symmetric enlargement of the bilateral lobes and isthmus. The tissues density may be normal but commonly decreases. It is likely to be diffuse scattering spot liked lower density shadows in the thyroid. By enhanced scanning, there is obvious homogeneous enhancement with clearly defined borderlines. The highly enlarged thyroid can compress its surrounding tissues for their morphological changes. The compressed trachea can be narrowed and prolonged. For cases with nodular thyromegaly, there are multiple round shaped low density areas in the thyroid parenchyma, with different sizes and clearly defined borderlines. Enhanced scanning demonstrates the lower enhancement of the thyroid than its surrounding parenchyma. No obvious enhancement of the foci indicates formation of cysts.

MR imaging demonstrates the same morphological changes. Enlarged thyroid parenchyma shows homogeneous moderate high signal by T2WI and homogenous equal or slightly high signal by T1WI based on the varying protein concentrations in the parenchyma. The cysts show regional higher signal by T2WI and relatively lower signal by T1WI with smooth borderlines. The enlarged nodules are demonstrated as moderate high signal that is slightly lower than the peripheral parenchyma by T2WI, and regional high signal by T1WI with smooth borderlines.

Hyperplasia may be caused by dietary iodine deficiency or hyperthyroidism or inflammation. The diffusely enlarged thyroid commonly extends to retrosternal or other areas. CT scanning demonstrates CT values of the thyroid tissues mostly above 70 Hu due to abundant contents of iodine. Tracheas and brachiocephalic blood vessels are compressed for migration and deformation and the superior vena cava is compressed for secondary venectasia. For cases with degeneration, it may demonstrate flaky calcification and cystic changes. By enhanced scanning, the thyroid tissues show enhancement, with no enhancement of cysts and rare enhancement of the degenerating lesions. Differential diagnosis of HIV/AIDS related thyromegaly from simple thyromegaly is difficult. For cases with diffuse thyromegaly complicating HIV/AIDS, the common causes of simple thyromegaly should be firstly excluded for the diagnosis of HIV/AIDS related thyromegaly.

It has manifestations of diffuse enlargement of the thyroid with infiltration toward the peripheral area. The enlargement is lobulated with unclearly defined borderlines and a density generally lower than normal thyroid tissues but close to the peripheral muscular tissues. It can be complicated by calcification and cystic changes. After intravenous injection of reagent, there is heterogeneous enhancement. Generally, the illness course is long. Based on the clinical manifestations and case history, its diagnosis can be made. Only by CT scanning, the differential diagnosis from neoplasms is difficult.

Differential diagnosis of obvious thyroid carcinoma is not necessary. Thyroid carcinoma initially shows local nodules in thyroid parenchyma, which should be differentiated from nodules manifested in cases of HIV/AIDS related thyromegaly.

Thyroid carcinoma can be divided into five types: papillary, follicular, encephaloid, giant cell and Hürthle cell. CT scanning can define the range of the lesions as well as lymphoid metastases. In terms of thyroid masses, there are no reliable signs to differentiate the benign from the malignant. For cases with regional lymphadenectasis, recurrent laryngeal nerve paralysis and injuries of thyroid cartilage or other laryngeal cartilages, it is facilitative for the diagnosis of malignancy. Calcification is not the evidence for the differentiation of the benign from the malignant because calcification occurs in cases of benign tumors. Nuclear imaging can roughly evaluate the biological activity of thyroid nodules, which facilitates the differential diagnosis. Thyroid carcinoma commonly shows cold nodules, mostly common with adenoma hyperplasia which can be cystic or parenchymal. Only 20 % nodules are malignant.

Cervical lymphoid tuberculosis is a part of primary tuberculosis infection. Primary infection foci can be caused by invasion of M. Tuberculosis via upper respiratory tract or the oral cavity and nasopharynx. The most common location of the primary infection is the tonsil. The infection further spreads to the cervical superficial or deep lymph nodes or submandibular lymph nodes along lymph vessels, with possible involvement of preauricular and retroauricular lymph nodes. At this time of infection, the primary foci may have been absorbed gradually. But lymphoid tuberculosis may progress into cold abscess or ulcer.

After the primary tuberculosis or during the progression of secondary tuberculosis, tuberculosis invades the cervical lymph nodes via blood-borne transmission. The involved cervical lymph nodes are extensive, with bilateral involvements. Alternatively, deep cervical lymph nodes may be infected by tuberculosis that primarily invades the thoracic or abdominal lymph nodes and spreads via lymph vessels.