The thyroid gland is our largest endocrine organ. It is located in our neck, in the lower region of the trachea, close to the breastbone. It stimulates the secretion of thyroid hormones. Thyroid hormones are T4, which is inactive, and T3, which is the active form. The thyroid gland also secretes the hormone calcitonoin.
TRH hormone is secreted from the hypothalamus when the level of thyroid hormone in the blood decreases or in the hours when it needs to be increased. This hormone stimulates the pituitary gland in the brain to secrete TSH hormone. TSH hormone, on the other hand, stimulates the thyroid gland to secrete thyroid hormones from the thyroid follicles into the blood.
In cases where the thyroid gland does not secrete thyroid hormone for inflammatory or other reasons, the level of thyroid hormone in the blood drops. This condition is called hypothyroidism. This may be due to the inactivation of thyroid hormones in the circulation, suppression of hormone-secreting cells for some reason, or the inability of these cells to function. The most common causes are chronic autoimmune thyroiditis.
In the case of hypothyroidism, TRH secretion is increased by the hypothalamus in the brain. With the TRH hormone, the pituitary gland is stimulated more frequently, increasing TSH secretion. Thanks to TSH, the thyroid gland is stimulated more frequently and it is requested to secrete more thyroid hormone. The frequently stimulated pituitary gland begins to enlarge. This condition is called pituitary hyperplasia.
The incidence of pituitary hyperplasia is increased in patients with hypothyroidism. Pituitary hyperplasia occurs with enlargement, especially in the anterior part of the pituitary. Prolactin hormone levels also increase.
If pituitary hyperplasia is caused by hypothyroidism, symptoms of hypothyroidism may be seen in patients. Patients may experience symptoms such as weight gain, fatigue, cold intolerance, constipation, dry skin and irregular menstruation. Delayed growth, short stature, obesity and rarely precocious puberty can be seen in children.
Patients with pituitary hyperplasia may also develop symptoms caused by enlargement of the pituitary gland. Problems such as amenorrhea and galactorrhea may occur, especially due to the increase in prolactin hormone. In addition, when the pituitary gland grows excessively, it can press on the optic nerves, and headaches and vision problems may develop.
Diagnosis of pituitary hyperplasia:
Hypothyroidism and other thyroid disorders are investigated in patients at risk of developing pituitary hyperplasia. In addition, visual fields and the base of the eye are examined with biomicroscopy. The patient may also have elevated prolactin levels and symptoms.
Thyroid hormone profile is examined in all patients with suspected thyroid disease. TSH, T3 and T4 levels are evaluated. Patients with low T3 and T4 levels and high TSH levels have primary hypothyroidism. In most of these patients, an enlarged pituitary gland can be detected by MRI imaging.
If TSH levels are high and T3 and T4 levels are also high, then the probability of a problem arising from the pituitary increases. This may occur in pituitary adenomas. Thyroid hormone levels are decreased in pituitary hyperplasia caused by primary hypothyroidism.
In patients with abnormalities in pituitary hormones, all links of the chain should be examined. TSH levels and TRH levels are checked. In addition, adrenocorticotropic hormone (ACTH) and testosterone levels are checked in men. In women, morning cortisol, follicle stimulating hormone (FSH) and luteinizing hormone (LH) are examined. In women, menstrual cycle, estradiol level, insulin-like growth factor-1 (IGF-1) and prolactin are also examined.
In suspected patients, the pituitary gland is evaluated with MRI imaging.
Treatment of pituitary hyperplasia:
The main treatment for pituitary hyperplasia resulting from primary hypothyroidism is the replacement of low-level thyroid hormones. With the improvement of the blood thyroid hormone level, less TSH is expected to be secreted from the pituitary gland.
Along with thyroid hormone replacement therapy, regular follow-up of these patients and evaluation of the pituitary gland with MRI imaging from time to time are required. A shrinkage in the pituitary gland is expected within 2-4 months. Shrinkage occurs in 85% of patients.
If the pituitary gland does not shrink and TSH levels do not decrease despite thyroid hormone replacement therapy, it is thought that there may be a condition originating from the pituitary gland, such as a pituitary adenoma.
Surgical treatment can be considered in patients with increased pituitary gland enlargement despite drug therapy and who have vision problems by feeding the optic nerves.
If the pituitary hyperplasia lasts for a long time or if it is present for a long time, the pituitary gland’s pressure on its own tissues may cause disruption in the other hormone series produced by the pituitary gland itself and in relation to it.