Sports-related chronic repetitive head trauma as a cause of pituitary dysfunction

Abstract

<jats:p>Traumatic brain injury (TBI) is recognized as a cause of hypopituitarism even after mild TBI. Although over the past decade, a growing body of research has detailed neuroendocrine changes induced by TBI, the mechanisms and risk factors responsible for this pituitary dysfunction are still unclear. Around the world, sports—especially combative sports—are very popular. However, sports are not generally considered as a cause of TBI in most epidemiological studies, and the link between sports-related head trauma and hypopituitarism has not been investigated until recently. Thus, there is a paucity of data regarding this important concern. Because of the large number of young sports participants with near-normal life expectancy, the implications of undiagnosed or untreated postconcussion pituitary dysfunction can be dramatic. Understanding the pathophysiological mechanisms and risk factors of hypopituitarism caused by sports injuries is thus an important issue that concerns both medical staff and sponsors of sports. The aim of this paper was to summarize the best evidence for understanding the pathophysiological mechanisms and to discuss the current data and recommendations on sports-related head trauma as a cause of hypopituitarism.</jats:p>

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“…Relatively few studies have addressed the association between sports-related mTBI and hypopituitarism. 47 Small case series in boxing and kickboxing have shown a high rate of GHD, and one case report highlighted the association between repeat concussion in an adolescent athlete and subsequent anterior hypopituitarism. 15,19,[21][22][23]48 Quality of life, erectile dysfunction, metabolic syndrome, and obesity…”

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“…1 In the US, each year 1.4 million people sustain TBIs, 235,000 patients are hospitalized and 50,000 die. 2 Furthermore, mild-TBI has recently attracted increasing attention due to its rising incidence after concussions in contact sports, 3 and after blast injury in military conflicts. 4 Although various anti-inflammatory and anti-apoptotic modalities have shown neuroprotective effects in experimental models of TBI, to date, no specific pharmacological agent aimed at blocking the progression of secondary brain damage has been approved for clinical use.…”

On Treating Athletes with Banned Substances: The Relationship Between Mild Traumatic Brain Injury, Hypopituitarism, and Hormone Replacement Therapy

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