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Endocrine function in children with human immunodeficiency virus infection
L J Schwartz1, Y St Louis, R Wu
1Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY 10467.
Insights
Pediatric endocrine dysfunction may contribute to failure to thrive in children with human immunodeficiency virus (HIV). Some patients showed compensated hypothyroidism, a potentially correctable issue.
Area of Science:
- Pediatric Endocrinology
- Infectious Diseases
- Human Immunodeficiency Virus (HIV) Research
Background:
- Failure to thrive (FTT) is a concern in pediatric HIV infection.
- Endocrine dysfunction is a potential, yet understudied, contributor to FTT in this population.
Purpose of the Study:
- To investigate the role of endocrine dysfunction in explaining failure to thrive (FTT) among pediatric patients with human immunodeficiency virus (HIV).
Main Methods:
- Endocrine evaluation of 14 HIV-infected pediatric patients with adequate nutritional status.
- Assessment of growth hormone, cortisol, somatomedin C, and thyroid function (thyrotropin, thyroid-releasing hormone).
Main Results:
- Adequate growth hormone and cortisol responses were observed.
- Low somatomedin C levels were found in 8 of 12 subjects.
- 36% (5/14) of patients exhibited elevated thyrotropin levels, indicating compensated hypothyroidism despite normal thyroid function.
Conclusions:
- Subtle thyroid regulation alterations, specifically compensated hypothyroidism, may contribute to FTT in some pediatric HIV patients.
- These endocrine findings represent a potentially correctable factor in managing FTT in this cohort.
Abstract:
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.