Thyroid nodules are not expression of a single disease but are the clinical manifestation of a wide range of different diseases. Non-neoplastic nodules are the result of glandular hyperplasia arising spontaneously or following partial thyroidectomy; rarely, thyroid hemiagenesia may present as hyperplasia of the existing lobe, mimicking a thyroid nodule. Non-neoplastic thyroid diseases, such as Hashimoto’s thyroiditis or subacute thyroiditis may appear as thyroid lumps which are not true nodules but just the expression of the underlying thyroid disease.
Benign neoplastic nodules are divided into embryonal, fetal, follicular, Hurthle, and possibly papillary adenomas on the basis of their characteristic pattern . Examples appear in Figure 18-1 (above). The adenomas usually exhibit a uniform orderly architecture and few mitoses, and show no lymphatic or blood vessel invasion. They are characteristically enveloped by a discrete fibrous capsule or a thin zone of compressed surrounding thyroid tissue. All types of nodules may become partially cystic, presumably through necrosis of a portion of the growth. Cyst formation is very common in colloid nodules.
Whether papillary adenoma is a real entity is debatable; most observers believe that all papillary tumors should be considered as carcinomas. Others consider that some papillary tumors are benign adenomas. It is our impression that papillary tumors are best thought of as carcinomatous, although the degree of invasive potential may be very slight in some instances. The same confusion extends to Hurthle cell adenomas. Many pathologists consider all of these tumors as low-grade carcinomas in view of their frequent late recurrences. For this reason, the nondefinitive term Hurthle cell tumor is commonly used. Pathologists usually grade them on the probability of being malignant, based on factors such as invasion of the thyroid tumor capsule or blood vessels, without differentiation into benign and malignant. Hurthle cell tumors are found on electron microscopy to be packed with mitochondria, which accounts for their special eosinophilic staining quality.
Nearly half of all single nodules have on gross inspection a gelatinous appearance, are composed of large colloid-filled follicles, and are not completely surrounded by a well-defined fibrous capsule. These nodules are listed as colloid variants of follicular adenomas in our classification. Many pathologists report these as colloid nodules, and suggest that each is a focal process perhaps related to multinodular goiter rather than a true adenoma. These tumors are usually not surrounded by a capsule of compressed normal tissue, and often show degeneration of parenchyma, hemosiderosis, and colloid phagocytosis (Fig. 18-2). Recent studies indicate that most adenomas, as well as carcinomas, are truly clonal — derived from one cell — whereas colloid nodules, at least in multinodular goiters, tend to be polyclonal (2).