The most common association of lymphofollicular thymic hyperplasia is myasthenia gravis (seen in 50% of patients with myasthenia gravis), but lymphofollicular thymic hyperplasia is also seen in other conditions, such as thyrotoxicosis, systemic lupus erythematosus, Hashimoto's thyroiditis and Addison's disease. Thymic hyperplasia is rarely severe enough to cause visible enlargement of the thymus. When it does enlarge the thymus, both lobes are enlarged, usually uniformly (Fig. 1). Only rarely, hyperplasia may mimic a thymic mass.
The thymus may atrophy because of stress or as a consequence of steroid or antineoplastic drug therapy.
The gland usually returns to its original size on recovery or cessation of treatment, but it may become larger than its original size (rebound thymic hyperplasia). Such rebound hyperplasia may be difficult to distinguish from neoplastic involvement. The diagnosis depends on a known reason for thymic rebound, the absence of clinical features to indicate tumour recurrence and the presence of an enlarged, normally shaped thymus. In patients over 15 with an enlarged thymus, chemical shift MR and fat-suppressed T2-weighted or short tau inversion recovery (STIR) imaging can diagnose thymic hyperplasia by detecting fatty infiltration or fat in the thymus, helping to differentiate from a neoplastic process. In thymic hyperplasia there is a drop in signal intensity at opposed phase images, while in thymic tumours there is no such reduction in signal. Chemical shift MR can depict physiological fatty infiltration of the thymus in 50% of persons aged between 11 and 15, in 100% of those >15 but in none of those <15 years.
FIGURE 1 ■ Thymic hyperplasia with Graves'disease (thyrotoxicosis). A 35-year-old woman with dysphagia, palpitations, tremors, exophthalmos and weight loss and elevated serum thyroid hormone. Contrast medium-enhanced CT demonstrates (A) enlarged thyroid and (B) thymus. Following treatment with I-131, (C) the thyroid gland and (D) thymus became much smaller.
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