Endocrine Abstracts

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Background: Pediatric and adolescent obesity is a worldwide pandemia. Since the majority of adolescents with obesity will be an adult with the same condition and its complications, a precocious identification of cardiovascular risk factors is mandatory. Our aims were to evaluate the frequency of MHO vs MUO in children and adolescents with obesity followed in our Pediatric Clinic and to compare the cardiometabolic profile.

Patients and Methods: We evaluated 149 patients (52% males) median age 13 years (range 5–18), 16% Tanner stage 1, 38% Tanner stages 2-4, and 46% Tanner stage 5. Data on body mass index (BMI), waist-to-height ratio (WHtR), and laboratory tests were collected. MHO phenotype includes HDL cholesterol (HDL-C) >40 mg/dl, fasting plasma glucose (FPG) <100 mg/dl, Systolic and Diastolic Blood Pressure (SBP and DBP) < 90° percentile by gender, height and age, triglycerides <100 mg/dl or <130 mg/dl for aged <10 or >10 years, respectively. MUO phenotype included impaired of at least one of the above parameters. As marker of cardiovascular risk was SPISE, calculated using the formula: [600 × (HDL cholesterol^0. 185)/(triglycerides^0. 2) × (BMI^1. 338)].

Results: In the whole cohort, 40% of patients had elevated BP, 34% low HDL-C, 20% elevated triglycerides, and 9% elevated FPG. MUO phenotype was in 101 (68%) patients, with Tanner stages 2-5 more represented than Tanner stage 1 (78% vs 22%, P = 0. 016). A high prevalence of elevated SBP/DBP was observed (59%, P < 0. 001). MUO phenotype showed higher levels of BMI-SDS (2. 9 [2. 3;2. 9] vs 2. 6 [2. 5;3. 5], P = 0. 004), WHtR (0. 59 [0. 55;0. 66] vs 0. 57 [0. 53;0. 62], P = 0. 029), SDP (119 [113;126] vs 109 [103;115], P < 0. 001) and DBP (68 [62;76] vs 62 [59;68], P = 0. 001), FPG (92 mg/dl [88-96] vs 89 mg/dl [85-93], P = 0. 004), Hb1Ac (5. 3 % [5. 0-5. 5] vs 5. 0 % [4. 8-5. 3], P = 0. 002), and triglycerides (90 mg/dl [65-130] vs 65 [53-85], P < 0. 001). Conversely, MUO exhibited lower HDL-C (41 mg/dl [37-47] vs 49 mg/dl [45-58], P < 0. 001) and SPISE (4. 8 [3. 9-5. 8] vs 5. 6 [4. 9-6. 5], P = 0. 003). After adjusting for pubertal status, WHtR, and hypertension, SPISE emerged as an independent predictor of MUO (Or = 0. 39 [95%CI 0. 21-0. 75], P = 0. 004). The area under the ROC curve of SPISE in predicting the MUO phenotype was 0. 65 (95%CI 0. 56-0. 74, P = 0. 003).

Conclusions: The MUO phenotype showed a worse cardiometabolic profile than the MHO phenotype; SPISE appears to effectively capture the metabolic component of the increased cardiometabolic risk. Given the high prevalence of hypertension, routine BP monitoring is crucial in optimizing risk stratification of the MUO subset.