Hacioglu, A. | Kelestimur, F. | Tanriverdi, F.
Review | 2019 | Pituitary22 ( 3 ) , pp.322 - 331
Purpose: After traumatic brain injury was accepted as an important etiologic factor of pituitary dysfunction (PD), awareness of risk of developing PD following sports-related traumatic brain injury (SR-TBI) has also increased. However there are not many studies investigating PD following SR-TBIs yet. We aimed to summarize the data reported so far and to discuss screening algorithms and treatment strategies. Methods: Recent data on pituitary dysfunction after SR-TBIs is reviewed on basis of diagnosis, clinical perspectives, therapy, screening and possible prevention strategies. Results: Pituitary dysfunction is reported to occur in a . . . range of 15–46.6% following SR-TBIs depending on the study design. Growth hormone is the most commonly reported pituitary hormone deficiency in athletes. Pituitary hormone deficiencies may occur during acute phase after head trauma, may improve with time or new deficiencies may develop during follow-up. Central adrenal insufficiency is the only and most critical impairment that requires urgent detection and replacement during acute phase. Decision on replacement of growth hormone and gonadal deficiencies should be individualized. Moreover these two hormones are abused by many athletes and a therapeutic use exemption from the league’s drug policy may be required. Conclusions: Even mild and forgotten SR-TBIs may cause PD that may have distressing consequences in some cases if remain undiagnosed. More studies are needed to elucidate epidemiology and pathophysiology of PD after SR-TBIs. Also studies to establish screening algorithms for PD as well as strategies for prevention of SR-TBIs are urgently required. © 2019, Springer Science+Business Media, LLC, part of Springer Nature
Sav, A. | Rotondo, F. | Syro, L.V. | Serna, C.A. | Kovacs, K.
Review | 2019 | Pituitary , pp.322 - 331
Purpose: Traumatic brain injury most commonly affects young adults under the age of 35 and frequently results in reduced quality of life, disability, and death. In long-term survivors, hypopituitarism is a common complication. Results: Pituitary dysfunction occurs in approximately 20–40% of patients diagnosed with moderate and severe traumatic brain injury giving rise to growth hormone deficiency, hypogonadism, hypothyroidism, hypocortisolism, and central diabetes insipidus. Varying degrees of hypopituitarism have been identified in patients during both the acute and chronic phase. Anterior pituitary hormone deficiency has been show . . .n to cause morbidity and increase mortality in TBI patients, already encumbered by other complications. Hypopituitarism after childhood traumatic brain injury may cause treatable morbidity in those survivors. Prospective studies indicate that the incidence rate of hypopituitarism may be ten-fold higher than assumed; factors altering reports include case definition, geographic location, variable hospital coding, and lost notes. While the precise pathophysiology of post traumatic hypopituitarism has not yet been elucidated, it has been hypothesized that, apart from the primary mechanical event, secondary insults such as hypotension, hypoxia, increased intracranial pressure, as well as changes in cerebral flow and metabolism may contribute to hypothalamic-pituitary damage. A number of mechanisms have been proposed to clarify the causes of primary mechanical events giving rise to ischemic adenohypophysial infarction and the ensuing development of hypopituitarism. Conclusion: Future research should focus more on experimental and clinical studies to elucidate the exact mechanisms behind post-traumatic pituitary damage. The use of preventive medical measures to limit possible damage in the pituitary gland and hypothalamic pituitary axis in order to maintain or re-establish near normal physiologic functions are crucial to minimize the effects of TBI. © 2019, Springer Science+Business Media, LLC, part of Springer Nature
Temizkan, S. | Kelestimur, F.
Review | 2019 | Pituitary22 ( 3 ) , pp.220 - 228
Purpose: This review aimed to evaluate the data underlying the pathophysiology of TBI-induced hypothalamo-pituitary dysfunction. Methods: Recent literature about the pathophysiology of TBI-induced hypothalamo-pituitary dysfunction reviewed. Results: Traumatic brain injury (TBI) is a worldwide epidemic that frequently leads to death; TBI survivors tend to sustain cognitive, behavioral, psychological, social, and physical disabilities in the long term. The most common causes of TBI include road accidents, falls, assaults, sports, work and war injuries. From an endocrinological perspective, TBIs are important, because they can cause pi . . .tuitary dysfunction. Although TBI-induced pituitary dysfunction was first reported a century ago, most of the studies that evaluate this disorder were published after 2000. TBI due to sports and blast injury-related pituitary dysfunction is generally underreported, due to limited recognition of the cases. Conclusion: The underlying pathophysiology responsible for post-TBI pituitary dysfunction is not clear. The main proposed mechanisms are vascular injury, direct traumatic injury to the pituitary gland, genetic susceptibility, autoimmunity, and transient medication effects. © 2019, Springer Science+Business Media, LLC, part of Springer Nature
Karaca, Z. | Hacioglu, A. | Kelestimur, F.
Review | 2019 | Pituitary22 ( 3 ) , pp.305 - 321
Introduction: The prevalence of pituitary dysfunction is high following aneurysmal subarachnoid hemorrhage (aSAH) and when occurs it may contribute to residual symptoms of aSAH such as decreased cognition and quality of life. Hypopituitarism following aSAH may have non-specific, subtle symptoms and potentially serious consequences if remained undiagnosed. Methods: We reviewed the literature on epidemiology, pathophysiology, diagnostic methods and management of neuroendocrine changes after aSAH as well as on the impact of pituitary dysfunction on outcome of the patient. Results: The prevalence rates of pituitary dysfunction after aSA . . .H varies greatly across studies due to different diagnostic methods, though growth hormone deficiency is generally the most frequently reported followed by adrenocorticotropic hormone, gonadotropin and thyroid stimulating hormone deficiencies. Pituitary deficiency tends to improve over time after aSAH but new onset deficiencies in chronic phase may also occur. There are no clinical parameters to predict the presence of hypopituitarism after aSAH. Age of the patient and surgical procedures are risk factors associated with development of hypopituitarism but the effect of pituitary dysfunction on outcome of the patient is not clear. Replacement of hypocortisolemia and hypothyroidism is essential but treatment of other hormonal insufficiencies should be individualized. Conclusions: Hypopituitarism following aSAH necessitates screening despite lack of gold standard evaluation tests and cut-off values in the follow up, because missed diagnosis may lead to untoward consequences. © 2019, Springer Science+Business Media, LLC, part of Springer Nature