A Pediatric Case of Abrupt-Onset, Autoantibody-Negative Diab
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A 12-year-old previously healthy White Hispanic boy presented with a 1-week history of abrupt-onset polyuria, polydipsia, headache, and fatigue. He had no weight loss, fever, cough, anosmia, or diarrhea. Laboratory testing revealed DKA, with a blood pH of 7.04, glucose of 381 mg/dL, C-peptide level of 0.6 ng/mL, Beta-hydroxybutyrate level of 8.2 mmol/L, A1C of 11.3%, and a positive nasopharyngeal reverse transcription-PCR (RT-PCR) test for SARS-CoV-2.

There was evidence of pancreatic inflammation (lipase 179 units/L [normal range 15–110]), but no elevation in systematic inflammatory markers, and all autoantibody tests for autoimmune diabetes were negative. On exam, he was nonobese (BMI Z-score: -0.3), without acanthosis nigricans, and pubertal (Tanner 3). His medical and family histories were noncontributory; specifically, there was no family history of diabetes or neonatal hypoglycemia.

He was treated with intravenous (IV) insulin infusion at 0.1 units/kg/hour until DKA resolved within 24 hours. He appeared well, without signs of systemic inflammatory response and with no need for respiratory support or glucocorticoid use. He was then transitioned to a subcutaneous insulin regimen starting at 1 unit/kg/day but developed persistent hyperglycemia evidenced via continuous glucose monitoring, prompting an increase of insulin dosing and eventual resumption of IV insulin. His insulin requirements continued to increase consistently with marked insulin resistance. Given his significantly elevated insulin requirements (more than 4 units/kg/day), metformin was initiated, and, 3 days later, his insulin requirements declined, allowing for discharge 9 days after initial diagnosis on an insulin regimen closer to 1.5 units/kg/day.

In the following days, the patient’s insulin requirement continued to decrease. Metformin was discontinued 20 days after diagnosis without rebound hyperglycemia. Over the next weeks after discharge, his glycemic control continued to improve, as evidenced by A1C results of 8.8 and 5% at 4 and 12 weeks respectively, with appropriate insulin requirements for his age and pubertal status (0.86–0.9 units/kg/day).

Furthermore, he had a C-peptide of 3.39 ng/mL at the time of euglycemia (102 mg/dL), which was consistent with recovery of Beta-cell function. His insulin requirement continued to decline, and, by week 14, he was only on long-acting insulin at 0.2 units/kg/day with blood glucose levels ranging from 90 to 145 mg/dL. At week 23, long-acting insulin was discontinued altogether. Finally, because of financial constraints and a very low probability of having maturity-onset diabetes of the young (around 0.7%), molecular testing was not pursued.

Source: https://clinical.diabetesjournals.org/content/39/3/333.full
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