Abstract
The understanding of hypopituitarism has increased over the last three years. This review provides an overview of the most important recent findings. Most of the recent research in hypopituitarism has focused on genetics. New diagnostic techniques like next-generation sequencing have led to the description of different genetic mutations causative for congenital dysfunction of the pituitary gland while new molecular mechanisms underlying pituitary ontogenesis have also been described. Furthermore, hypopituitarism may occur because of an impairment of the distinctive vascularization of the pituitary gland, especially by disruption of the long vessel connection between the hypothalamus and the pituitary. Controversial findings have been published on post-traumatic hypopituitarism. Moreover, autoimmunity has been discussed in recent years as a possible reason for hypopituitarism. With the use of new drugs such as ipilimumab, hypopituitarism as a side effect of pharmaceuticals has come into focus. Besides new findings on the pathomechanism of hypopituitarism, there are new diagnostic tools in development, such as new growth hormone stimulants that are currently being tested in clinical trials. Moreover, cortisol measurement in scalp hair is a promising tool for monitoring cortisol levels over time.
Highlights
Hypopituitarism is defined as a diminished function of the pituitary gland
Conclusion and future perspective In patients with acquired pituitary insufficiency, understanding of the pathomechanisms has increased in recent years
A more profound understanding of the underlying causes leading to secondary hypopituitarism may lead to recommendations for rational screening of hypopituitarism in more precisely defined risk populations and may prevent under- or overdiagnosis
Summary
Hypopituitarism is defined as a diminished function of the pituitary gland. First described in 1914 by Simmonds, it is known as Simmonds’ disease[1]. A homozygous point mutation in the promotor region of the human growth hormone gene (GH1) was firstly described as causative for isolated GHD in siblings with normal pituitary imaging[11]. These two studies demonstrate the possibility of familial heredity that is either autosomal dominant or autosomal recessive. Acidophil growth hormone-producing cells are located mainly at the periphery of the pituitary gland, making them sensitive to perfusion deficits and hypoxia This fact contributes to the finding that somatotropic insufficiency is the most frequent hormonal deficit after brain injury[37,38,39], especially in chronic patients[40,41]. New growth hormone stimulants for oral application are currently being validated in clinical trials[77,78]
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