Neuroendocrine alterations in systemic disease.
Systemic disorders clearly may exert a significant influence on neuroendocrine function. Disorders that cause significant stress to the body, either physical or psychological, may cause a resetting upward of the HPA axis to provide sufficient cortisol to counteract the stress and to help sustain energy substrate levels. GH levels also increase in many of these situations, again promoting sufficient energy substrate levels. In some circumstances the concomitantly low somatomedin activity may be speculated to be adaptative to prevent the insulin-like agonist activity of these substances as well as to prevent energy expenditure in body growth. However, in other situations such as chronic renal failure and cirrhosis, the decreased somatomedin activity may be primary, causing decreased feedback at the hypothalamic-pituitary level and increased GH levels. The stress-induced rise in PRL may also play a minor role in preserving energy substrate since high levels may promote insulin resistance. In most illnesses the 'euthyroid sick syndrome' develops. Whether such patients are 'euthyroid' or mildly hypothyroid is a matter of controversy. The fact that protein losses are increased during fasting when the lowered T3 levels are returned to normal with exogenous T3 supplementation suggests that these patients are indeed hypothyroid and this hypothyroidism serves to conserve energy substrate by decreasing the metabolic rate. The reproductive axis is often impaired with systemic illness. Again, teleologically this may be viewed as an inactivation of non-essential functions in times of stress. It would appear that the changes that occur with systemic illness, in general, are favourable to the organism in that they promote survival. The detailed neurotransmitter and hypophyseotrophic hormone changes resulting in the alteration in pituitary function remain to be elucidated for the most part.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D003863:Depression / Q000503:physiopathology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000503:physiopathology; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D001523:Mental Disorders / Q000503:physiopathology*; D008659:Metabolic Diseases / Q000503:physiopathology*; D010908:Pituitary Hormones, Anterior / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism; D012559:Schizophrenia / Q000503:physiopathology; D013312:Stress, Physiological / Q000503:physiopathology*; D013315:Stress, Psychological / Q000503:physiopathology*; D013972:Thyrotropin / Q000378:metabolism
D010908:Pituitary Hormones, Anterior; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone