Pathophysiological implications of increased brain burden of histamine in protein malnutrition.
The complex syndrome of protein-energy malnutrition (PEM) in weanling children, usually complicated by concurrent presence of numerous adverse environmental factors, is a chronic stressful situation which elicits a number of neuroendocrine and metabolic adjustments. Histidine metabolism is severely impaired in PEM in children and in experimental animals, and evidence from the latter indicate markedly increased body burden of histamine. The brain is the organ most prominently affected. Although data are still incomplete, histamine conforms with most criteria required of a neurotransmitter. Histamine interacts with other neuroregulatory substances in modulating many neuroendocrine and vegetative processes. Some of the prominent pathophysiological features associated with PEM in children such as increased circulating cortisol, defective thermoregulation, fluid/electrolyte imbalance, impaired immunity, reduced cardiac output with prolongation of systemic recirculation time, and apathy bordering on a clinical state of depression are consistent with the known effects of histamine as determined by neurochemical and neuropharmacological studies. It is suggested that studies of histamine status in human PEM, and the functional relationships between markedly elevated level of this amine with other neuroregulatory substances, will shed more light on the complex pathogenesis of the nutritional syndrome.
D002001:Adipose Tissue, Brown / Q000502:physiology; D000818:Animals; D001833:Body Temperature Regulation; D001921:Brain / Q000378:metabolism*; D006632:Histamine / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D009490:Neurosecretory Systems / Q000502:physiology; D011502:Protein-Energy Malnutrition / Q000378:metabolism* / Q000503:physiopathology
D006632:Histamine