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Pathophysiological implications of increased brain burden of histamine in protein malnutrition
Insights
Protein-energy malnutrition (PEM) impairs histidine metabolism, increasing body histamine. This may explain key symptoms in children with PEM, like altered cortisol and apathy.
Area of Science:
- Neuroscience
- Nutritional Science
- Biochemistry
Background:
- Protein-energy malnutrition (PEM) in weanling children presents a complex syndrome often exacerbated by environmental factors.
- PEM triggers significant neuroendocrine and metabolic adaptations.
- Histidine metabolism is notably impaired in PEM, leading to increased histamine levels, particularly in the brain.
Purpose of the Study:
- To investigate the role of histamine in the pathophysiology of protein-energy malnutrition (PEM).
- To explore the potential of histamine as a neurotransmitter influencing neuroendocrine and vegetative functions in PEM.
- To correlate histamine's effects with observed clinical features of PEM in children.
Main Methods:
- Review of existing neurochemical and neuropharmacological studies on histamine.
- Analysis of pathophysiological features in human PEM cases.
- Comparison of experimental animal models of PEM with human data.
Main Results:
- Histamine exhibits characteristics of a neurotransmitter and modulates key physiological processes.
- Elevated histamine levels in PEM are linked to increased circulating cortisol.
- PEM-associated symptoms like impaired thermoregulation, immune dysfunction, and apathy align with histamine's known neurological effects.
Conclusions:
- Histamine may play a significant role in the pathogenesis of protein-energy malnutrition (PEM).
- Further research into histamine status and its interactions with other neuroregulatory substances in human PEM is warranted.
- Understanding histamine's role could illuminate the complex mechanisms underlying this nutritional syndrome.
Abstract:
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.