<b><i>Background/Aims:</i></b> Studies are lacking regarding the timing of peak growth hormone (PGH) response. We aim to elucidate the timing of PGH response to arginine and levodopa (A-LD) and evaluate the influence of body mass index (BMI) and other metabolic parameters on PGH. <b><i>Methods:</i></b> During growth hormone (GH) stimulation testing (ST) with A-LD, serum GH was measured at baseline and every 30 min up to 180 min. The PGH cut-off was defined as &amp;#x3c;10 ng/mL. IGF-1, IGF BP3, BMI, and metabolic parameters were obtained in a fasting state at baseline. <b><i>Results:</i></b> In the 315 tested children, stimulated PGH levels occurred at or before 120 min in 97.8% and at 180 min in 2.2%. GH area under the curve (AUC) positively correlated with PGH in all patients and with IGF-1 in pubertal males and females. BMI negatively correlated with PGH in all subjects. GH AUC negatively correlated with HOMA-IR and total cholesterol. <b><i>Conclusion:</i></b> We propose termination of the GH ST with A-LD at 120 min since omission of GH measurement at 180 min did not alter the diagnosis of GH deficiency based on a cut-off of &amp;#x3c; 10 ng/mL. BMI should be considered in the interpretation of GH ST with A-LD. The relationships between GH AUC and metabolic parameters need further study.

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LRT was not infrequent in ill newborns. Most were premature and half were not very low birth weight. We recommend monitoring of thyroid function by serum specimen in ill newborns with prolonged ICU care regardless of birth weight.

Currently recommended screening of obese youth by FPG is normal in 91.5%, but lacks further information to detect increased risk for youth-onset T2D. Evaluation of obese youth by LCA identified one third (class 3) in whom the combination of higher levels of BMIz, HOMA-IR, and family history suggests the greatest risk for T2D and targets them for further evaluation and intensive preventative management.

Introduction: SARS-Cov-2 (severe acute respiratory distress syndrome- coronavirus 2) viral infection has a predilection for pancreatic beta cells causing insulin deficiency. Studies from the SARS-CoV outbreak in 2003 highlighted the relationship between SARS-CoV and ACE-2 (angiotensin-converting enzyme 2) receptors in pancreatic islet cells. We describe a pediatric patient who developed Diabetes Mellitus after exposure to the Sars-CoV-2 virus. Case Report: A previously healthy 13-year-old female of Mexican descent was found to be hyperglycemic at her annual visit. The patient endorsed polyuria and polydipsia for 3 weeks, and weight loss for 3months. 3 months prior to presentation, her mother became ill and tested positive for SARS-CoV-2 by PCR analysis. The patient had no SARS-CoV-2 associated symptoms. Her exam was notable for a BMI was in the 78%ile for age with no acanthosis nigricans. She had no family history of diabetes or autoimmune disease. Initial blood glucose was 729 mg/dL, with bicarbonate of 20.6 mEq/L, pH 7.45, and anion gap of 14 mEq/L. Large ketones were present in the urine. Her concomitant C-peptide level of 1.0 ng/ml was low in the setting of hyperglycemia. Her HbA1c was 14.3%. Diabetes-related autoantibodies, celiac, and thyroid antibodies were negative. Her Sars-CoV-2 antibody titer was positive with a negative PCR. The patient was treated with a basal-bolus regimen of subcutaneous insulin at a maximal total daily dose of 0.7 u/kg/day. 5 weeks later, her insulin requirement and HbA1C were both lower; at 0.5 u/kg/day and 9.3% respectively. Discussion: This patient’s symptoms of hyperglycemia started shortly after her exposure to the SARS-CoV-2 virus. She had no features consistent with Type 2 DM. She similarly had no serological evidence of DM related autoimmunity, thus being different from reports of new-onset Type 1 DM with confirmed autoimmunity presenting during the Sars-CoV-2 pandemic. Although Type 1B DM without evidence of humoral islet autoimmunity and monogenic DM could not be fully excluded, we postulate that the patient developed SARS-CoV-2 associated DM given her time course and documented exposure to SARS –CoV-2 with the presence of SARS-CoV antibodies. One similar case has previously been reported By Holstein et al. 1 While we share the lack of direct evidence of causation, we postulate that more patients with similar presentations will be reported during the current pandemic. Reference: 1.Hollstein, T et al. Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: a case report [published online ahead of print, 2020 Sep 2]. Nat Metab. 2020;10.1038/s42255-020-00281-8. doi:10.1038/s42255-020-00281-8