228 - Adipose Rebound in Patients with Congenital Hypothyroidism in an Urban Multiethnic Community Hospital

Publication Number: 228.4016

Nakeesha E. Longley Sands, Flushing Hospital Medical Center, new york, NY, United States; Lily Q. Lew, Flushing Hospital Medical Center, Flushing, NY, United States; Ashleigh Glowacki, Flushing Hospital Medical Center, Flushing, NY, United States; Ankita Gogineni, Flushing hospital medical center, Quaker hill, CT, United States

Background: Prevalence of obesity continues to increase worldwide, affecting all ages. Obesity is defined as a body mass index (BMI) ≥95th percentile for age and gender. Adipose rebound (AR) is the second rise in BMI that typically occurs in children aged 5-7 years and its timing may be predictive of adult obesity. Studies have demonstrated an association between higher thyroid-stimulating hormone (TSH) levels and higher BMI percentiles. There are limited data on timing of adipose rebound and thyroid function status in children with congenital hypothyroidism (CH).

Objective: To explore TSH level and timing of AR in children with CH.

Design/Methods: A retrospective chart review of patients with CH seen in the Pediatric Endocrine Clinic at Flushing Hospital Medical Center between January 1, 2013 and December 31, 2015. Data extracted from EHR included demographics (age, gender, ethnicity), birth weight (normal 2500-4000 grams), result of newborn screen, body mass index (BMI), thyroid function tests (total thyroxine (T4), TSH) and age of AR. Normal BMI is 5- < 85%ile, overweight ≥85- < 95%ile, obese is >95%ile and normal TSH is 0.47-4.68 µU/mL. Obese and non-obese children with CH were compared. A p< 0.05 was considered significant.

Results: Of 73 identified with CH, 23 (32%) were excluded as having a transient form of CH. The remaining 50 (68%) with permanent form consisted of more male (60%) with majority of reported ethnicity Asian (56%) followed by Hispanic (20%). Newborn screening (primary T4 followed by TSH) did not identify CH in all (90%). The median birth weight was 2720 (2170, 3100) for male and 2720 (2420, 3000) for female neonates. When comparing non-obese and obese children with CH, the median T4 [8.7 (7.7,11.0) vs 12.4 (11.9, 12.6), p=0.02] was lower in the non-obese and the median TSH [2.4 (1.7, 3.4) vs 4.2 (3.3, 4.6), p=0.11] was also lower in the non-obese. The age of AR [mean (years)±SD] was earlier in the obese (4.0±1.7) compared to the non-obese (5.3±1.3) children. Those with earlier AR had higher median BMI (kg/m2) [16.1 (14.9, 17.3), p=0.50] and higher TSH [4.3 (3.3,5.5), p=0.06] compared to those with normal AR, BMI [15.2 (14.7,15.7)] and TSH [2.5 (2.0, 3.4)].

Conclusion(s): In our small multiethnic sample of children with permanent CH, those who were non-obese had normal AR and lower median TSH. Children with CH and obese had earlier AR and higher TSH. A TSH in lower half of normal reference range as goal of therapy may prevent earlier AR and obesity.