Context The effects of the COVID-19 pandemic on the incident cases of pediatric Type 1 (T1D) and Type 2 diabetes (T2D) are not clear. Objective To identify trends in incidence and presentation of pediatric new-onset T1D and T2D during the COVID-19 pandemic. Methods A retrospective chart review was conducted. Demographics, anthropometrics, and initial labs from patients ages 0-21 who presented with new-onset diabetes to a pediatric tertiary care center were recorded. Results During the pandemic incident cases of pediatric T1D increased from 31 in each of the prior two years to 46; an increase of 48%. Incident cases of pediatric T2D increased by 231% from 2019 to 2020. The number of incident cases of pediatric T2D increased significantly more than the number of incident cases of pediatric T1D (p-value = 0.009). Patients with T2D were more likely to present in DKA, though this was not statistically significant (p-value=0.093). Severe DKA was higher compared to moderate DKA (p-value = 0.036) in incident cases of pediatric T2D. During the pandemic, for the first time, incident cases of T2D accounted for more than half of the all newly diagnosed pediatric diabetes cases (53%). Conclusions There were more incident pediatric T1D and T2D cases as well as an increase in DKA severity in T2D at presentation during the COVID-19 pandemic. More importantly, incident T2D cases were higher than the incident T1D during the pandemic. This clearly suggests a disruption and change in the pediatric diabetes trends with profound individual and community health consequences.

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Introduction: The COVID-19 pandemic has introduced countless challenges to the medical field and has brought increased attention to pediatric patients with pre-existing diagnoses such as diabetes. While pediatric patients have lower rates of COVID-19 mortality, the presence of pre-existing conditions can heighten the severity of their clinical presentation. Here we discuss how COVID-19 may contribute to the pathophysiology of DKA. Case Presentation: Our patient is a 6-year old female with known type 1 diabetes for 6 months, with positive GAD 0.25 nmol/L, c-peptide 0.3 ng/ml, blood glucose 555 mg/dl, HbA1c 10.9, beta hydroxybutyrate (βOHB) 3.21mmol/l, pH 7.35, HCO3 21 mEq/L at her initial presentation, and insulin requirement <0.5 IU/kg/day (in honeymoon). She presented to an outside hospital due to acute onset of abnormal breathing and altered mental status. The day prior, she had one episode of emesis, diarrhea, and abdominal pain, but no fever. She was reported to be agonal breathing with a GCS of 8 and unresponsive to physical or verbal stimuli. She was intubated shortly after arrival and given mannitol. Initial labs included a glucose 486 mg/dL, pH 6.88, bicarbonate 4 mEq/L, lactate 5.8 mmol/L, βOHB 11.9 mmol/L, and anion gap 29 mEq/L, all consistent with severe DKA. With a known family member with COVID-19, she was tested and found to be COVID-19 positive. She was transferred via flight to a higher level of care. Remarkably, she was appropriate for extubation the following day with return to her baseline mental status with improved acidosis. On day three of hospitalization, she developed further COVID-19 symptoms which included sore throat, productive cough, fatigue, headache, and high fever. These symptoms persisted four more days until she was afebrile and discharged home in good condition. Conclusion: Our patient’s rapid progression and severity of illness, including the need for intubation, requires the discussion of how COVID-19 might affect diabetes and suggests opportunities for improvement in clinical practice in children with preexisting diabetes. 1) COVID-19 might change the underlying pathophysiology and cause severe metabolic complications. Possible mechanisms might include a) binding to angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, leading to insulin resistance and islet cell destruction b) enabling a proinflammatory “cytokine storm” in the setting of higher basal proinflammatory state from diabetes. Additionally, ketoacidosis and altered mental status have been discovered in patients with COVID-19 without diabetes, which could potentiate the symptoms of DKA. 2) Prompt recognition and treatment of DKA is warranted as caregivers may attribute the symptoms to COVID-19 rather than DKA and recognition could be too late if symptoms are as acute as described in this case report.

Objective:To present an unusual case of Cushing syndrome in a pediatric patient caused by a single depot triamcinolone injection.Methods: A case report followed by a literature review are presented.Results: A 13-year-old male presented with rapid weight gain, elevated blood pressure, headaches, and diffuse purplish striae. Lab results revealed a low 24-hour urinary free cortisol of <3 µg (reference range is 4.0 to 56 µg/24 hours), a low midnight salivary cortisol of <50 ng/dL (reference range is <100 ng/dL), a low adrenocorticotropic hormone of <5 pg/mL (reference range is 6 to 55 pg/mL), and a lower than expected testosterone of 86 ng/dL. The values were not consistent, and upon further questioning the family admitted the patient had received a "Jesus shot" from a practitioner which was sold as a cure all. Upon further investigation, it was determined that this injection contained both dexamethasone and depot triamcinolone. The triamcinolone in this injection was quantified and remained measureable for over 4 months following injection. Conclusion:The cause of Cushing syndrome symptoms with adrenal suppression was exogenous glucocorticoid, specifically depot triamcinolone. Exogenous glucocorticoids can create adrenal suppression, contributing to life-threatening adrenal crises with illness or stress. Recovery of our patient's adrenal axis was demonstrable within a few months. This case highlights the potentially devastating effects of glucocorticoid treatment for unclear medical indications. Further, it raises concerns about the potential unintended consequences of such therapies and the importance for providers to raise additional questions whenever the clinical presentation and laboratory investigation are inconsistent. (AACE Clinical Case Rep. 2019;5:e1-e3) Abbreviations: CS = Cushing syndrome; HPA = hypothalamic-pituitary-adrenal