Hypopituitarism which is defined as partial or complete deficiency/deficiencies of anterior and/or posterior pituitary hormones results from the altered production of these hormones or their respective hypothalamic releasing hormones. There are several causes leading to hypopituitarism such as pituitary adenomas, their surgical treatments, infections, genetic disorders, Sheehan’s syndrome, cancer immunotherapy etc [1], [2]. During the last two decades traumatic brain injury (TBI) was also found as an important cause of hypopituitarism. Traumatic brain injury consists of non-specific external injuries to the calvarium, face or scalp caused by external mechanical force. Traumatic brain injury is an important cause of morbidity and mortality particularly in young people and in non-fatal cases it is associated with behavioural, cognitive and social sequela in addition to neuroendocrine alterations. It has been reported that 43.1 % of Americans have TBI-related long-term problems after they discharged from hospital [3]. Although the most common causes of TBI are traffic accidents and falls, others such as blast-related injuries, acts of violence and combative sports are also considered in the etiology *[4], [5], [6], [7], [8].

Traumatic brain injury may lead to transient or permanent pituitary dysfunction where the clinical picture is consist of large spectrum due to the number of affected hormones. There are several pathogenetic mechanisms leading to TBI-induced hypopituitarism such as direct trauma to the sellar/parasellar region, compression of surrounding structures and an interplay of ongoing process triggered by trauma such as autoimmunity [9], [10], *[11], [12]. For a long time the possibility of pituitary dysfunction due to TBI was neglected by health care professionals and although TBI is now considered as an important cause of hypopituitarism, possibly there are many unrecognized patients due to vague symptoms. Here, TBI-induced hypopituitarism is reviewed from epidemiological aspects and also the risk factors making patients vulnerable to hypopituitarism after TBI is discussed.