Growth hormone deficiency in the neurocritical patient

Abstract

Growth hormone (GH) is synthesized in the anterior pituitary, but its production and release are controlled by two neurohormones found in the hypothalamus: somatostatin and growth hormone-releasing hormone (GHRH). GH supports bone growth, regeneration of neurons, astrocytes, endothelial cells, oligodendrocytes, and even neuronal myelination. It is also responsible for stimulating the growth and differentiation of cells from different tissues and cell types, thereby contributing to protein synthesis. Original research papers, case reports, and case series on GH deficiency among neurocritical patients were thoroughly examined in this review. After extensive study, 13 articles were selected for the analysis. Traumatic lesions are defined by distortion of the brain tissue and subsequent biochemical modifications, which can affect GH secretion. The majority of researchers identified fractures, trauma, and bleeding as the mechanical causes of GH deficiency, and subarachnoid haemorrhage (SAH) or traumatic brain injury (TBI) as the etiology. The dysregulation of certain other hormones, including ACTH, Cortisol, Gonadotropin, Prolactin, FSH, TSH, Testosterone, and Hydrocortisone is also related to GH insufficiency. Growth hormone deficiency can cause complications such as hypothyroidism, hypotension, hypoxia, adrenal insufficiency, electrolyte imbalance, hyperprolactinemia, depression, anxiety, concussions, seizures, vomiting, and loss of consciousness. According to previous studies, GH insufficiency is significantly affected by age, body mass index (BMI), pituitary dysfunction, and hypogonadism. GH treatment is widely used in patients with GH deficiency, as it has more benefits than harm. The GH dose should be individualized to minimize side effects and maximize clinical efficacy.