Growth hormone deficiency and hypopituitarism in adults after complicated mild traumatic brain injury
Autor: | Antonino Belfiore, Serafina Talarico, Claudio Ceccotti, Francesco Beniamino Nicoletti, Stefania Giuliano, Lucia Bruno |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
Adult
Blood Glucose Male medicine.medical_specialty Traumatic brain injury Endocrinology Diabetes and Metabolism Poison control 030209 endocrinology & metabolism Complicated mild traumatic brain injury Hypopituitarism Gastroenterology Growth hormone deficiency 03 medical and health sciences Basal (phylogenetics) Young Adult 0302 clinical medicine Endocrinology Adrenocorticotropic Hormone Hypothyroidism Diabetes mellitus Internal medicine Brain Injuries Traumatic medicine Central hypothyroidism Humans Glasgow Coma Scale Insulin-Like Growth Factor I Adiposity Aged business.industry Human Growth Hormone Cardiovascular risk GHD Growth hormone deficiency in adults Middle Aged medicine.disease Lipids Hormones Diabetes and Metabolism Cardiovascular Diseases Female business 030217 neurology & neurosurgery |
Popis: | Traumatic brain injury is considered the main cause of hypopituitarism in adults, and GH deficiency appears to be the most frequent pituitary deficit. Most of the available studies have included all degrees of severity of trauma. We aimed to assess pituitary function and GH deficiency in adult patients at different time lengths after complicated mild TBI according to Glasgow Coma Scale. We also aimed to evaluate whether mild TBI patients with GH deficiency had developed alterations in the glycolipid profile. Forty-eight patients (34 men and 14 women) with complicated mild TBI were included in the study. Twenty-three patients were evaluated at 1 year (Group A) and 25 patients at 5 years or longer after the injury (Group B). All patients underwent basal hormonal evaluation for pituitary function. GH deficiency was investigated by the combined test (GH releasing hormone + arginine). The glycolipid profile was also evaluated. GH deficiency occurred in 8/23 patients (34.7 %) of Group A and in 12/25 patients (48 %) of Group B. In addition, two patients, one in each group, showed evidence of central hypothyroidism. Patients with GH deficiency, especially in Group A, presented a higher frequency of visceral adiposity and adverse metabolic profile as compared to no-GH deficiency patients. Patients examined at 1 year or several years from complicated mild TBI had a similarly high occurrence of isolated GH deficiency, which was associated with visceral adiposity and metabolic alterations. Our findings suggest that patients undergone complicated mild TBI should be evaluated for GH deficiency even after several years from trauma. |
Databáze: | OpenAIRE |
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