Title: Pain and Child: A Translational Hypothesis on the Pathophysiology of a Mild Type-2 Diabetes Model
Volume: 11
Issue: 1
Author(s): S. Loizzo, A. Capasso, A. L. Loizzo, S. Spampinato, G. Campana, A. Di Giannuario, S. Pieretti and A. Loizzo
Affiliation:
Keywords:
Pain, child, stress, behaviour, metabolism, Type-2 Diabetes, polymodal nociceptors, corticotropin-releasing hormone, oligonucleotide phosphorothioate, ACTH-corticosterone
Abstract: Pediatric pain management underwent many changes since the undertreatment of pain in children was reported in the literature in 1980. Increasing data also suggest that long-term behavioural effects can be observed in children, following pain episodes as early as in the neonatal period. Therefore, the knowledge about safe and effective management of pain in children should be applied with greater effectiveness into clinical practice. Other advances in the field include the findings of long-term residual behavioural and metabolic effects induced by pain experienced during the critical periods of development in laboratory animals. Recent data in laboratory animals and clinical data in children suggest that early repeated and/or severe pain and other stressful procedures applied in the perinatal periods may produce not only behavioral, but also important hormonal, immune and metabolic long-term effects. In this paper we shall report data on some metabolic conditions described in adult humans following disruption of hormonal-metabolic programming produced in the peri-natal period. Quite similar signs can be found between animal models and human conditions, most of them being connected with hypothalamus-pituitary-adrenal hormones (HPA) dysfunction. In addition, some signs in animal models, such as overweight and abdominal overweight are prevented by treatment with the μ- and δ-opioid receptor antagonist naloxone during the lactating period. This indicates that some long-term consequences following stress received during the early phases of life in mammals may be bound to the HPA system dysregulation, whereas others are bound to different (e,g., opioid) endogenous brain receptors and/or neuromediators alteration.
