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IN SERUM LEPTIN AFTER SYSTEMIC DEXAMETHASONE THERAPY IN PRETERM INFANTS Ng PC1, Lam CWK2,
Lee CH1, Fok TF1, Wong E3, Ma KC1,
Chan IHS2 1Department of
Paediatrics and 2Department of Chemical Pathology, 3Centre
of Clinical Trials and Epidemiological Research, Prince of Wales Hospital,
Chinese University of Hong Kong Objective: To investigate the
effect of postnatal systemic dexamethasone on serum leptin in very low
birth weight (VLBW) infants. Methods: Nineteen
VLBW infants who received a 3-week course of dexamethasone, and 28 infants
who did not receive corticosteroid were studied. In the corticosteroid group, blood samples for hormone
analysis were collected immediately before the start of the dexamethasone
course (Tdexa 0), 1 (Tdexa 1) and 3 weeks (Tdexa
3) after commencement of the drug, and 2 weeks after dexamethasone
treatment (Tdexa 5) had been stopped. Similarly, blood specimens were obtained at 2 (Tcon
2), 5 (Tcon 5) and 7 (Tcon 7) weeks of
postnatal age in the non-treatment group. Results: Serum
leptin at Tdexa 3 (p < 0.0001), and serum insulin at Tdexa
1 (p < 0.0001) and Tdexa 3 (p < 0.001) were
significantly increased when compared to the pretreatment (Tdexa 0)
concentrations. In contrast,
both serum leptin and insulin at week 5 (Tcon 5) and 7 (Tcon
7) of postnatal age did not differ significantly from their
respective levels at week 2 (Tcon 2) in the non-treatment
group. When the corticosteroid
group was compared to the non-treatment group, serum leptin (p <
0.00001) and insulin (p < 0.00001) at Tdexa 3 were also
significantly increased. The
volume of oral milk intake during dexamethasone treatment (Tdexa 1
and Tdexa 3) correlated significantly with serum leptin (r =
0.53, p < 0.001). Conclusion: Systemic
corticosteroid causes a significant increase in serum leptin and
insulin. It is likely that
corticosteroid and factors associated with oral milk ingestion were
required to act synergistically to stimulate an increase in serum leptin. .