Endocrine function in children with human immunodeficiency virus infection
L. J. Schwartz, Y. St Louis, R. Wu, A. Wiznia, A. Rubinstein and P. Saenger
Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY 10467.
We sought to determine if failure to thrive in pediatric patients with the
human immunodeficiency virus could be explained based on endocrine
dysfunction. Fourteen human immunodeficiency virus-infected pediatric
patients, all of whom had adequate nutritional status, underwent endocrine
evaluation. Growth hormone and cortisol responses to glucagon stimulation
were adequate. Despite this, eight of the 12 subjects had low somatomedin C
levels. Although all patients were clinically and biochemically euthyroid,
36% (5/14) demonstrated elevated baseline and peak thyrotropin levels in
response to thyroid releasing hormone, suggesting a state of compensated
hypothyroidism. Although the importance of these findings is unclear, it is
possible that subtle alterations of thyroid regulation may contribute to
failure to thrive in some pediatric patients infected with human
immunodeficiency virus and may represent a potentially correctable defect.
