Evaluating an AMM in the setting of GD can be challenging for the clinician. There is no systematic, formal evaluation of how best to manage AMM in the setting of GD . There is substantial variability in the rate of thymic involution as well as thymic size, shape and density even between individuals of the same age . A retrospective study of 109 patients with AMM treated with thymectomy found that all cases with malignancy had either symptoms referable to the thymus or a discrete mass rather than a diffusely enlarged thymus gland . The utility of this information is partially limited by the finding that a “discrete mass” was seen in 32% of thymic hyperplasias and 66% of histologically normal thymus glands . Also, symptoms anatomically referable to enlargement of the thymus (chest discomfort, chest pain and shortness of breath)  can frequently also be seen in GD . Prevailing wisdom from several recent case reports of thymic hyperplasia in GD is that caution should be used in evaluating AMM in the setting of GD given the known association with thymic hyperplasia [2–5]. Clinicians are urged to wait until after resolution of hyperthyroidism to follow up AMM in the absence of features concerning for malignancy (invasion, calcifications, cysts or septations) on imaging [2–5]. Reduction of thymic enlargement after achieving a euthryoid state can vary from 2 months up to 2 years  which could complicate following up a possibly neoplastic mediastinal mass.
These cases represent two examples of mediastinal neoplasms seen in association with GD. While the first patient represents the first documented case of T-LBL/L seen in association with GD, there are two prior case reports of thymoma occuring with GD [8, 9]. On the other hand, occurance of T-LBL/L with other autoimmune diseases is well documented [10–17].
Autoimmunity alters the environment of the immune system with positive selection/expansion of autoreactive T-cells in the thymus. Thymic hyperplasia is a representation of how GD, in particular, alters the microenvironment of the thymus. This is thought to be due to the hyperthyroidism associated with active GD. It is known that thyroid hormones (TH) are able to induce thymic epithelial cell (TEC) proliferation which produces cytokines (including IL-1) . T3 also enhances thymic hormone thymulin secretion by TECs . In turn, cytokines (e.g. IL-1) and thymulin stimulate and enhance thymocyte (immature T-cell precursor) proliferation. Thymocyte differentiation occurs as the cells migrate within thymic lobules interacting with microenvironment . In active GD, thymic microenvironment may be altered due to increased proliferation of TECs driven by TH. It is unclear if thymic environment altered by the state of sustained hyperthyroidism, including increased proliferative drive on maturing thymocytes and, possibly, abnormal differentiation, may contribute to the development of genetic lesions resulting in T LBL/L in susceptible individuals. Likewise it is not unreasonable to postulate that TH driven TEC proliferation may contribute to the pathogenesis of thymoma, which is a neoplasm of thymic epithelial cells. The two patients illustrated not only raise the possibility of association between GD and mediastinal neoplasms but represent a possible reason for caution in using a watch-and-wait approach to anterior mediastinal masses in patients with GD.