Psychiatric sequelae of traumatic brain injury — future directions in research

One of the most devastating chronic consequences of traumatic brain injury (TBI) is cognitive impairment. One of the possible underlying causes is growth hormone deficiency (GHD) caused by TBI-indu...

Effect of Growth Hormone on Neuropsychological Outcomes and Quality of Life of Patients with Traumatic Brain Injury: A Systematic Review.

Abstract Traumatic brain injury (TBI) incurs substantial health and economic burden, as it is the leading reason for death and disability globally. Endocrine abnormalities are no longer considered a rare complication of TBI. The reported prevalence is variable across studies, depending on the time frame of injury, time and type of testing, and variability in hormonal values considered normal across different studies. The present review reports evidence on the endocrine dysfunction that can occur after TBI. Several aspects, including the pathophysiological mechanisms, clinical consequences/challenges (in the acute and chronic phases), screening and diagnostic workup, principles of therapeutic management, and insights on future directions/research agenda, are presented. The management of hypopituitarism following TBI involves hormonal replacement therapy. It is essential for health care providers to be aware of this complication because at times, symptoms may be subtle and may be mistaken to be caused by brain injury itself. There is a need for stronger evidence for establishing recommendations for optimum management so that they can be incorporated as standard of care in TBI management. 

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Endocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome?

Hypopituitarism is defined as a complete or partial deficiency in one or more pituitary hormones. Anterior hypopituitarism includes secondary adrenal insufficiency, central hypothyroidism, hypogonadotropic hypogonadism, growth hormone deficiency and prolactin deficiency. Patients with hypopituitarism suffer from an increased disability and sick days, resulting in lower health status, higher cost of care and an increased mortality. In particular during adulthood, isolated pituitary deficits are not an uncommon finding; their clinical picture is represented by vague symptoms and unclear signs, which can be difficult to properly diagnose. This often becomes a challenge for the physician. Aim of this narrative review is to analyse, for each anterior pituitary deficit, the main related etiologies, the characteristic signs and symptoms, how to properly diagnose them (suggesting an easy and reproducible step-based approach), and eventually the treatment. In adulthood, the vast majority of isolated pituitary deficits are due to pituitary tumours, head trauma, pituitary surgery and brain radiotherapy. Immune-related dysfunctions represent a growing cause of isolated pituitary deficiencies, above all secondary to use of oncological drugs such as immune checkpoint inhibitors. The diagnosis of isolated pituitary deficiencies should be based on baseline hormonal assessments and/or dynamic tests. Establishing a proper diagnosis can be quite challenging: in fact, even if the diagnostic methods are becoming increasingly refined, a considerable proportion of isolated pituitary deficits still remains without a certain cause. While isolated ACTH and TSH deficiencies always require a prompt replacement treatment, gonadal replacement therapy requires a benefit-risk evaluation based on the presence of comorbidities, age and gender of the patient; finally, the need of growth hormone replacement therapies is still a matter of debate. On the other side, prolactin replacement therapy is still not available. In conclusion, our purpose is to offer a broad evaluation from causes to therapies of isolated anterior pituitary deficits in adulthood. This review will also include the evaluation of uncommon symptoms and main etiologies, the elements of suspicion of a genetic cause and protocols for diagnosis, follow-up and treatment.

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Isolated anterior pituitary dysfunction in adulthood

Growth hormone (GH) is known to exert several roles during development and function of the nervous system Initially, GH was exclusively considered a pituitary hormone that regulates body growth and metabolism, but now its alternative extrapituitary production and pleiotropic functions are widely accepted Through excess and deficit models, the critical role of GH in nervous system development and adult brain function has been extensively demonstrated Moreover, neurotrophic actions of GH in neural tissues include pro-survival effects, neuroprotection, axonal growth, synaptogenesis, neurogenesis and neuroregeneration The positive effects of GH upon memory, behavior, mood, sensorimotor function and quality of life, clearly implicate a beneficial action in synaptic physiology Experimental and clinical evidence about GH actions in synaptic function modulation, protection and restoration are revised in this chapter

Growth hormone (GH) and synaptogenesis

Traumatic brain injury (TBI) is fairly common and annually affects millions of people worldwide. Post traumatic hypopituitarism (PTHP) has been increasingly recognized as an important and prevalent clinical entity. Growth hormone deficiency (GHD) is the most common pituitary hormone deficit in long-term survivors of TBI. The pathophysiology of GHD post TBI is thought to be multifactorial including primary and secondary mechanisms. An interplay of ischemia, cytotoxicity, and inflammation post TBI have been suggested, resulting in pituitary hormone deficits. Signs and symptoms of GHD can overlap with those of TBI and may delay rehabilitation/recovery if not recognized and treated. Screening for GHD is recommended in the chronic phase, at least six months to a year after TBI as GH may recover in those with GHD in the acute phase; conversely, it may manifest in those with a previously intact GH axis. Dynamic testing is the standard method to diagnose GHD in this population. GHD is associated with long-term poor medical outcomes. Treatment with recombinant human growth hormone (rhGH) seems to ameliorate some of these features. This review will discuss the frequency and pathophysiology of GHD post TBI, its clinical consequences, and the outcomes of treatment with GH replacement.

https://www.mdpi.com/1422-0067/20/13/3323/pdf

Growth Hormone Deficiency Following Traumatic Brain Injury

Abstract Background Fine needle aspiration (FNA) cytology is the preferred method for assessing thyroid nodules for malignancy. Concern remains about the rate of false negative results. The primary aim of this study is to investigate the malignancy rate of thyroid nodules initially classified as benign (Thy 2). Methods We retrospectively examined 658 nodules in 653 (429 female) patients between January 2013 to December 2017. All FNA biopsies (FNABs) were performed under ultrasound (US) guidance by a radiologist with expertise in thyroid pathology. Nodules were cytologically classified according to the UK Royal College of Pathologists guidelines. Decisions about further management were made at a regular thyroid multidisciplinary meeting. Follow up of the Thy 2 nodules was determined based on clinical and radiological criteria. Results The mean age (± SD) was 53.2 (14.6) years. Five hundred out of 658 (76.0%) nodules were classified as Thy 2 (benign) after the first FNAB. Of these thyroid nodules initially classified as benign, 208 (41.6%) underwent repeat FNAB and 9 (1.8%) were surgically removed without repeat FNAB. The remainder were followed up clinically and/or radiologically. Seven (1.4%) of nodules initially classified as Thy 2 were later shown to be or to harbor malignancy after a follow-up of 74.5 (± 19.7) months. Papillary thyroid microcarcinomas were found co-incidentally in two thyroid glands of benign nodules, giving a true prevalence of 5/500 (1.0%). Conclusions With a well targeted FNAB, the false negative rate of an initial benign thyroid FNA is very low thus routine second FNAB is not required in patients with a thyroid nodule initially deemed benign. Multidisciplinary input is imperative in informing decision making. 

/pdf/is-repeat-fine-needle-aspiration-required-in-thyroid-nodules-2ayr402t.pdf

Is repeat fine needle aspiration required in thyroid nodules with initial benign cytology? Results from a large Irish series

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Growth Hormone Deficiency Following Traumatic Brain Injury

Is repeat fine needle aspiration required in thyroid nodules with initial benign cytology? Results from a large Irish series