Traumatic Brain Injury and Hypopituitarism

Results of recent and ongoing studies have made it clear that brain injuries like traumatic brian injury (TBI) pose substantial risk to pituitary function, perhaps even greater risk than previously believed. Patients with TBI should be screened both prospectively and retrospectively for isolated, multiple, and even total pituitary deficits. It is well known that patients with "classical" hypopituitarism (due to primary hypothalamic-pituitary pathologies) do benefit from hormonal replacement therapy. It has been suggested that patients with TBI-induced hypopituitarism may benefit with appropriate hormonal replacement receiving replacement therapy such as antidiuretic hormone (ADH), glucocorticoid, and thyroid hormones when needed. Gonadal and recombinant human growth hormone (rhGH) replacement therapy should also be introduced if there are deficiencies demonstrated and even reconfirmed in a second step. The signs and symptoms of post-TBI hypopituitarism may be masked by what has been assumed to be merely the post-traumatic syndrome. By increasing awareness among physicians of the risks of brain injuries-induced endocrinopathies and the need for appropriate endocrinological testing, it may be possible to improve the quality of life and enhance the rehabilitation prospects for these patients. In most instances, these patients are first seen and treated by trauma surgeons and neurosurgeons, and subsequently by rehabilitation physicians; they must be knowledgeable about the risks of hypopituitarism so that they can determine which patients are candidates for screening for hypopituitarism. In addition, endocrinologists and internists must be educated about TBI-induced hypopituitarism and encouraged to actively share their expertise with other physicians. KEYWORDS: traumatic brain injury (TBI), hypopituitarism, pituitary deficits INTRODUCTION The first report of traumatic brain injury (TBI)-induced hypopituitarism was published in 1918 EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY A wide range of scientific studies have attempted to evaluate the epidemiology of TBI. Because of differences in study inclusion criteria, a valid indicator of the incidence of TBI could be the rate of hospitalizations for TBI. These ranged from 91 per 100,000 patients in Cantabria, Spain[6] to upwards of 300 per 100,000 hospital admissions in Italy (Emilia Romagna and Trentino), South Africa (Johannesburg), southern Australia, and Scotland TRAUMATIC BRAIN INJURY AND HYPOPITUITARISM: REVIEW OF RECENT SCIENTIFIC LITERATURE In 1986, Edwards and Clark reviewed the topic of post-traumatic hypopituitarism and found that the typical patient was a young adult male who had experienced a severe form of head trauma and who presented with endocrine abnormalities within months to years after the accident. These patients could have reported temporary or permanent diabetes insipidus or other clinical symptoms such as weight loss, fatigue, faintness, loss of libido, and impotence. The ensuing hypopituitarism was usually ascribed to depression or the "postconcussion syndrome" with inappropriate treatment and rehabilitation often recommended. Following these observations, the authors recommended that patients with major head injury (defined by post-traumatic amnesia greater than 24 h) and, in particular, those with fractures of the base of the skull or diabetes insipidus, be closely monitored for signs and symptoms of endocrine dysfunction and appropriate dynamic pituitary-function tests performed In 2000 and 2001, Kelly et al. and Lieberman et al. found a high prevalence of anterior pituitary dysfunction in patients with a previous history of moderate and severe TBI The high risk for TBI-induced hypopituitarism and, particularly, for anterior pituitary dysfunction, was also clear in our studies (performed under the auspices of the Italian Society of Endocrinology) where we evaluated pituitary function 3 and 12 months after TBI (n = 100) or SAH (n = 40) POSSIBLE PATHOGENESIS OF TBI-INDUCED HYPOPITUITARISM The pathogenesis of brain injury-induced anterior pituitary dysfunction is not fully understood. Older studies in patients with fatal TBI demonstrated that various degrees of pituitary hemorrhagic infarction were present in more than 70% of patients CONCLUSIONS 1. Brain injuries like TBI and SAH pose high risk to pituitary function. 2. Patients with TBI should be screened both prospectively and retrospectively for isolated, multiple, and total pituitary deficits. 3. Patients with TBI-induced hypopituitarism may benefit with appropriate hormonal replacement receiving replacement therapy when needed. 4. The signs and symptoms of TBI-induced hypopituitarism may be masked by what has been assumed to be the classical post-traumatic syndrome. 5. It is indicated to increase awareness among physicians of the risks of brain injuries-induced endocrinopathies and the need for appropriate endocrinological testing and substitutive therapies. These patients are first seen and treated by trauma surgeons and neurosurgeons, and subsequently by rehabilitation physicians who must be knowledgeable about the risks of hypopituitarism, in order so that they can determine which patients are candidates for screening for hypopituitarism. Endocrinologists and internists must be educated about TBI-induced hypopituitarism and encouraged to actively share their expertise with other physicians ACKNOWLEDGMENT

NNALS A A critique of the literature on etiology of eating disorders

AbstRACt The development of eating disorders including anorexia nervosa, bulimia nervosa, binge eating disorder, and atypical eating disorders that affect many young women and even men in the productive period of their lives is complex and varied. While numbers of presumed risk factors contributing to the development of eating disorders are increasing, previous evidence for biological, psychological, developmental, and sociocultural effects on the development of eating disorders have not been conclusive. Despite the fact that a huge body of research has carefully examined the possible risk factors associated with the eating disorders, they have failed not only to uncover the exact etiology of eating disorders, but also to understand the interaction between different causes of eating disorders. This failure may be due complexities of eating disorders, limitations of the studies or combination of two factors. In this review, some risk factors including biological, psychological, developmental, and sociocultural are discussed

Cardiovascular complications in patients with PHEO: A mini-review

Phaeochromocytomas are rare neuroendocrine tumours secreting high levels of catecholamines, able to exert serious metabolic and cardiovascular effects. The serious and potentially lethal cardiovascular complications of these tumours are due to the potent effects of secreted catecholamines, especially noradrenaline, the main transmitter released from sympathetic nerve terminals. Hypertension, tachycardia, pallor, headache and anxiety, usually dominate the clinical presentation. Occasionally, patients with predominantly epinephrine-secreting tumours present hypotension or even shock. Other cardiovascular complications of pheochromocytoma include ischaemic heart disease, acute myocardial infarction, cardiac arrhythmias, heart failure due to toxic cardiomyopathy, or pulmonary edema. Catecholamines have been shown to influence the extracellular matrix with collagen deposition and subsequent fibrosis in the arterial wall and in the myocardium. These morphofunctional changes of the myocardium and of arterial wall can be emphasized by ultrasound imaging. Indeed, ultrasound imaging of the myocardium and arterial wall not only identifies wall thickness but also contains information on texture that may be revealed by acoustic tissue characterization. The latter can be quantified through videodensitometric analysis of echographic images or through ultrasonic integrated backscatter signal analysis. This paper reviews cardiovascular complications in patients with pheochromocytoma and utility of the new ultrasound technique as backscatter signal. It is useful for evaluating preclinical pathological morphofunctional changes of the myocardium and arterial wall, characterized by increased collagen content in pheochromocytoma patients. The recognition of early catecholamine-induced alterations in patients with pheochromocytoma, is important to prevent at least morbidity and mortality, before surgical treatment