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Published on: June 2, 2018
Endocrine pancreatic dysfunction in HIV-infected children: association with growth alterations
Mariangela Rondanelli1, Desiree Caselli, Rosita Trotti
1Department of Internal Medicine and Medical Therapy, University of Pavia, Italy. nutrizione.iar@virgilio.it
Insights
Pancreatic endocrine function is altered in children with human immunodeficiency virus (HIV), showing higher insulin and glucagon levels. This dysfunction is linked to impaired growth in these children.
Area of Science:
- Endocrinology
- Pediatrics
- Infectious Diseases
Background:
- Limited data exist on pancreatic endocrine function in children with human immunodeficiency virus (HIV).
- Understanding metabolic responses is crucial for managing HIV-infected children, particularly concerning growth failure.
Purpose of the Study:
- To investigate pancreatic endocrine secretion in HIV-infected children.
- To explore the association between pancreatic endocrine function and failure to thrive in this population.
Main Methods:
- A prospective study compared 14 HIV-infected children with 16 healthy controls.
- Evaluated insulin, glucagon, C-peptide, glucose, HOMA index, and performed glucagon tests.
- Assessed hormone levels (growth hormone, TSH, ACTH, cortisol) and lipid profiles.
Main Results:
- HIV-infected children exhibited significantly higher insulin, glucagon, C-peptide, glucose, and HOMA index levels.
- Eleven HIV-infected children showed an impaired glycemic response to the glucagon test.
- A correlation was found between the insulin-to-glucagon ratio and growth velocity in HIV-infected children.
Conclusions:
- This study presents the first evidence of altered pancreatic endocrine secretion in HIV-infected children.
- Pancreatic endocrine dysfunction is associated with growth failure in HIV-infected children.
Background:
The pancreatic endocrine system normally guarantees a quick and efficient response to daily metabolic perturbations, but associated data for human immunodeficiency virus (HIV)-infected patients are lacking. A prospective study was performed to evaluate pancreatic endocrine secretion and its possible association with failure to thrive among HIV-infected children.
Methods:
Fourteen well-nourished, prepubertal, HIV-infected children (6 boys and 8 girls; age range, 5-11 years), none of whom were receiving protease inhibitors, and 16 clinically healthy sex- and age-matched children formed the patient group and the control group, respectively. At yearly follow-up examinations, insulin, glucagon, C-peptide, and glucose levels were measured; the ratio of insulin to glucose, the ratio of insulin to glucagon, and the homeostasis model assessment (HOMA) index were calculated; the glucagon test was administered; and growth hormone, thyroid-stimulating hormone, adrenocorticotropic hormone, cortisol, and lipid patterns were evaluated.
Results:
Insulin, glucagon, C-peptide, glucose, and HOMA measurements were significantly higher among patients, compared with control subjects, at all 3 follow-ups performed to date. The glucagon test revealed a normal glycemic response in all the healthy control subjects and a significantly impaired response in 11 patients. A significant correlation emerged between the ratio of insulin to glucagon and the growth velocity of HIV-infected children.
Conclusion:
To our knowledge, the present study provides the first evidence of altered pancreatic endocrine secretion and its association with growth failure among HIV-infected children.
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