Psychosocial dwarfism: Psychopathological aspects and putative neuroendocrine markers
Autor: | Antonio Molina-Carballo, Francisco Contreras-Chova, Ana Naranjo-Gómez, Antonio Muñoz-Hoyos, José Uberos, Fuensanta Justicia-Martínez, María-del-Carmen Augustin-Morales |
---|---|
Rok vydání: | 2011 |
Předmět: |
Male
Serotonin medicine.medical_specialty Kynurenine pathway Adolescent Developmental Disabilities Physiology Dwarfism Child Behavior Disorders Adrenocorticotropic hormone Melatonin Adrenocorticotropic Hormone Internal medicine medicine Humans Child Kynurenine Biological Psychiatry Analysis of Variance Chi-Square Distribution Psychopathology beta-Endorphin medicine.disease Neurosecretory Systems Circadian Rhythm Failure to Thrive Psychiatry and Mental health Endocrinology Child Preschool Failure to thrive Female medicine.symptom Psychology Psychosocial medicine.drug |
Zdroj: | Psychiatry Research. 188:96-101 |
ISSN: | 0165-1781 |
Popis: | There exists an extensive terminology for defining the situation of children who, in varying circumstances, suffer from affective deprivation (AD), within an unsatisfactory family situation or in institutions. Nevertheless, the neuroendocrine mechanisms (if they exist) determining it have yet to be identified. Our objective was to determine if specific neuroendocrine markers, all of them previously implicated in affective disorders, could be modified, and in which sense, in affective deprivation syndrome of the child. For this purpose, we studied three separate groups of children: (1) control group (CG); (2) children suffering from AD; and (3) children with non-organic failure to thrive (NOFT). In every case, we studied the serum levels of melatonin, serotonin, β-endorphins and adrenocorticotropic hormone (ACTH); and kynurenine pathway tryptophan metabolites (both during the day and at night). Significantly, there was a conspicuous reduction in the levels of each of the neuroendocrine markers (melatonin, serotonin, β-endorphins and ACTH) in the group suffering from affective deficiency, a diminution which was even more noticeable in the group of patients presenting delayed growth. Furthermore, as also occurs in other affective disorders, there were corresponding modifications in the metabolisation of tryptophan. We report the existence of neuroendocrine mechanisms that are associated with the above-mentioned clinical manifestations in these patients, mechanisms that may underlie the close connection existing between AD syndrome and the cause of NOFT. These data suggest that the AD syndrome and NOFT comprise a single process, but one with a different evolutionary continuum of psychosocial dwarfism. |
Databáze: | OpenAIRE |
Externí odkaz: |