Key Clinical Message:
In cases of pituitary lesions with elevated TSH, a comprehensive
diagnostic approach that includes biochemical, clinical, and
radiological assessment is essential. Not all pituitary masses are
adenomas. Pituitary hyperplasia secondary to primary hypothyroidism can
mimic adenomas, particularly prolactinomas, due to associated
hyperprolactinemia. Thyroxine replacement therapy often reduces
pituitary hyperplasia, making hormonal profiling essential to avoid
unnecessary surgical interventions. Patient compliance with hormone
therapy is also a key factor, as non-compliance can lead to persistent
symptoms and impact outcomes. Early specialist involvement and a
multidisciplinary approach are beneficial in these complex cases to
ensure accurate diagnosis and timely intervention.
Introduction :
The pituitary gland, often called the ”master gland” of the body,
regulates numerous essential functions by releasing various hormones.
Structurally, the gland is divided into an anterior and a posterior
lobe. The anterior lobe produces several vital hormones, including human
growth hormone (HGH or GH), thyroid-stimulating hormone (TSH),
adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH),
luteinizing hormone (LH), and prolactin. The posterior lobe produces
oxytocin and antidiuretic hormone (ADH). The hypothalamus controls all
these hormones, which regulate their release through specific signaling
chemicals.
Pituitary adenomas, or benign tumors of the pituitary gland, can be
classified by size—macroadenomas are more significant than 10 mm,
while microadenomas are smaller. They are also categorized as either
secreting or non-secreting, depending on whether they actively release
hormones. The most common secreting adenoma is prolactinoma, which
overproduces prolactin (1). Pituitary hyperplasia, on the other hand,
involves the overgrowth of pituitary cells and may affect either
specific hormone-producing cells or the entire gland. Both adenomas and
hyperplasia can present as a pituitary mass on imaging, which can
complicate diagnosis.
In primary hypothyroidism, inadequate thyroid hormone production can
result in elevated TSH levels and pituitary hyperplasia due to loss of
negative feedback in the hypothalamic-pituitary-thyroid axis. Studies
indicate that 25-81% of hypothyroid patients present with pituitary
hyperplasia (2). Additionally, thyroid-stimulating hormone
(TSH)-secreting adenomas, or TSHomas, are rare, accounting for only
0.5% to 3% of all pituitary tumors (3). These tumors are typically
characterized by elevated levels of free thyroid hormones (FT4 and FT3)
in the presence of non-suppressed TSH, often presenting clinically with
symptoms of hyperthyroidism (4). Differentiating between TSHomas,
thyroid hormone resistance, and other causes of elevated TSH can be
challenging.
This case series presents three patients with elevated TSH and pituitary
lesions, each with a unique clinical outcome and treatment pathway.
Although their initial symptoms were similar varying diagnoses led to
distinct management strategies. This series highlights the diverse
presentations of pituitary lesions with elevated TSH and underscores the
importance of systematic evaluation to avoid misdiagnosis and
unnecessary surgical interventions.