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oncocytic thyroid nodule

Wednesday 3 May 2017


Hürthle cell nodules are diagnosed when more than 75% of a lesion is composed of this cell type. Needle biopsy of Hürthle cell tumours may cause partial or total infarction.

This probably occurs because of the high metabolic activity of these cells and the delicate blood supply of these lesions, which may readily become inadequate after direct trauma.

A solitary tumour of the thyroid occurring in a patient without thyroiditis, which is purely or predominantly composed of Hürthle cells on fine needle aspiration (FNA), should be excised because Hürthle cell tumours show an average 30% malignancy rate based on histology.

The differential diagnosis of the thyroid nodule includes a large number of lesions.

In the absence of oncocytic change, the criteria used for the diagnosis of each of these lesions is widely accepted, perhaps with the exception of papillary carcinoma, which remains one of the most controversial areas in pathology.

The criteria for the diagnosis of lesions that are composed predominantly of Hürthle cells are the same as those applied to follicular lesions that do not contain Hürthle cells.

Encapsulated lesions with no evidence of capsular or vascular invasion and no nuclear features of papillary carcinoma are diagnosed as Hürthle cell adenomas, and those that have penetrated their capsule to invade surrounding tissues are diagnosed as Hürthle cell carcinomas.

The diagnosis of Hürthle cell papillary carcinoma is possible when the cytological criteria for papillary carcinoma are present.

An oncocytic nodule in the setting of chronic lymphocytic thyroiditis may be completely encapsulated and show no evidence of capsular or vascular invasion. In the absence of nuclear features of papillary carcinoma, this would be considered an thyroid oncoytic adenoma.

Solid cellular proliferations of oncocytic thyroid cells that invade surrounding parenchyma are diagnosed as Hürthle cell carcinoma.

As with non-oncocytic lesions, the distinction between hyperplasia and neoplasia can be difficult. In patients with multinodular hyperplasia, dominant nodules are considered by some to be hyperplastic, whereas some pathologists diagnose them as follicular adenomas. Clonality studies have clearly shown that many if not most of the large nodules are indeed monoclonal, so that the second approach is biologically correct. This changes the approach to the pathobiology of neoplasia because we know (from many other examples in gut, breast, and other sites) that malignant transformation involves a stepwise progression of molecular changes. Therefore, it should not be surprising that malignancy occurs in nodular hyperplasia. The difficulty is in recognising the criteria and the clinical relevance of these changes. In the case of pure follicular proliferations, invasion can be difficult to ascertain in the setting of nodular hyperplasia. In the case of papillary transformation, the threshold for nuclear features is controversial.

If indeed oncocytic change is a metaplastic process, the criteria that apply to oncocytic lesions should be identical to those applied to non-oncocytic lesions. The only possible exception to that argument may be the diagnosis of papillary carcinoma, because the criteria are now accepted to be nuclear, and there may be difficulty identifying nuclear changes of papillary carcinoma in oncocytes that traditionally have large, hyperchromatic nuclei with prominent cherry red nucleoli.

In fact, this is not usually the case. The morphological features identified in papillary carcinoma are usually seen in a large proportion of Hürthle cell papillary carcinomas. The nuclei are enlarged, elongated, irregular in shape, crowded, and overlapping, with prominent grooves and inclusions.

There is clearing of nucleoplasm and peripheral margination of chromatin.

The threshold for these alterations varies among experts. For example, the identification of irregularity of nuclear contours is sufficient for some pathologists (including myself) when it results in a ragged nuclear outline that resembles “crumpled paper”.

Others require more florid features, such as linear grooves; these are usually present in association with the first finding. Some investigators do not recognise the morphology until the grooves become so pronounced that they fill with cytoplasm and form pseudoinclusions.

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