Central hypothyroidism is the consequence of anatomical or functional disorders of the pituitary or the hypothalamus. Several of the causes reported in Box 1 may affect both the pituitary and the hypothalamus, and in many instances the main anatomical site of the dysfunction cannot be identified. Thus, the former terms of secondary hypothyroidism (of pituitary origin) and tertiary hypothyroidism (of hypothalamic origin) are no longer recommended. Central hypothyroidism is rarely isolated, being part of a generalized disorder involving the secretion of other pituitary hormones. Permanent central hypothyroidism is rare, its prevalence ranging from 1:20 000 to 1:80 000 in the general population. However, transient functional abnormalities of TSH secretion are relatively common, and often pass unrecognized due to rapid recovery of the normal thyroid hormone balance.

Box1. Causes of central hypothyroidism

Pituitary adenomas represent the most common cause of central hypothyroidism. Reduced secretion of TSH is usually a con sequence of mechanical compression of non- tumorous cells and of adenohypophyseal blood vessels by the adenoma. The pituitary stalk and the hypothalamus may also be involved by suprasellar extension of the tumour. The tumour may be non- functioning or secrete other hormones. Thus, the resulting syndrome will depend on the extent of hypopituitarism and on the particular hormone secreted by the adenoma. A sudden enlargement of pituitary adenomas may occur as a result of haemorrhage within the tumour, leading to pituitary apoplexy.

Several other causes may produce central hypothyroidism, by acting at the hypothalamic or pituitary level. Primary extrasellar brain tumours or metastatic tumours originating from other sites may produce a variable degree of hypopituitarism, depending on the location and the extension of their mass. Among brain tumours, craniopharyngiomas should be suspected when central hypothyroidism is diagnosed in young people. Craniopharyngiomas are usually extrasellar but they may extend inferiorly causing destruction of the bony margins of the sella. Pituitary infarction may develop postpartum following excessive blood loss during delivery (Sheehan’s syndrome), or in patients with severe shock or during systemic anticoagulation therapy. Various degrees of pituitary in sufficiency may be observed in these cases. Traumatic head injuries can lead to central hypothyroidism because of hypothalamic or pituitary infarction or haemorrhage. Iatrogenic causes of central hypothyroidism include external radiation and surgery for pituitary or brain tumours. The empty sella syndrome is caused by a defect of the sellar diaphragm leading to cisternal herniation within the pituitary fossa and flattening of the pituitary. Hypopituitarism develops slowly along with expansion of the cisternal herniation caused by transmission of cerebrospinal fluid pressure. Hypothalamic or pituitary lesions may derive from any of the infectious or granulomatous diseases listed in Box1.

Autoimmune (primary) hypophysitis is an increasingly recognized disease that can cause central hypothyroidism, isolated or associated with other tropin defects, in up to 45% of the cases. However, when an appropriate treatment with immunosuppressive drugs is started, TSH deficiency can considerably improve with no need of hormone replacement therapy with L- thyroxine in the long term. Another emerging disorder, first described in 2003, is hypophysitis secondary to checkpoint inhibitors immunotherapy. In this condition, observed in approximately 10% of cancer patients treated, various degrees of hypopituitarism, including isolated central hypothyroidism, have been described.

A high prevalence of hypothyroidism following traumatic brain injury or subarachnoid haemorrhage has been demonstrated, although TSH deficiency is less common than growth hormone, luteinizing hormone/ follicle- stimulating hormone, and adrenocorticotropic hormone deficiencies. Pituitary aplasia or hypoplasia is a rare congenital defect, usually associated with other severe mal formations. In most instances these patients die shortly after birth.

Genetic abnormalities in TSH synthesis may cause central hypothyroidism characterized by inherited isolated TSH deficiency. A number of mutations in genes involved in pituitary function have been described, leading to isolated central hypothyroidism or combined pituitary hormone defects, with variable clinical phenotypes and degrees of severity. In some patients no demonstrable pathology can be found to explain TSH deficiency, and the term idiopathic central hypothyroidism is still applied.

Transient impairment of TSH secretion is commonly observed and may depend on a variety of causes, including the use of several drugs (see Box1). The recognition of these conditions is essential to avoid unnecessary and expensive diagnostic procedures. In most instances, replacement therapy is not necessary or is contraindicated.

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