Introduction: Drug-induced diabetes mellitus (DIDM) could be defined as a heterogenic group of diabetes caused by pharmacotherapy. The DIDM is considered to be reversible after discontinuation of diabetogenic treatment, but there is a risk of persistence, which is related to the duration of treatment, prescribed medication, and body mass index. Case presentation: A 13-year-old boy treated for nephrotic syndrome with the use of tacrolimus and prednisone was diagnosed with diabetes during a check-up visit. On admission, he showed a cushingoid appearance and complained of dry mouth, which was not accompanied by polyuria or polydipsia. Blood tests showed elevated levels of glucose, and glycated A 1c fraction of haemoglobin (HbA 1c = 10.2%). Pancreatic islet autoantibodies were negative. The fasting and postprandial C-peptide levels were within the normal range. Diabetic ketoacidosis was excluded. Intensive insulin therapy was initially introduced; the daily dose of insulin per kilogram was low (TDD/kg = 0.31 U/kg). Those findings prompted us to consider diabetes mellitus type 2 or DIDM. Moreover, the TDD/kg and HbA 1c additionally decreased after the steroid withdrawal. Because he was constantly on diabetogenic therapy and experienced periodical hyperglycaemia, DIDM could not be excluded. Therefore, our patient remained on insulin treatment. Conclusions: DIDM in children is challenging for all specialists. Diabetologists need to remember about this rare subtype of diabetes, and other specialist should perform screening on their patients who are at risk of DIDM. There is a great need for guidelines that would provide a standardized approach for diagnosing and treating DIDM in the paediatric population.
We present 2 cases of diabetic children who developed acute pancreatitis (AP) in the course of diabetic ketoacidosis (DKA). A 14-year-old girl, diagnosed with diabetes type 1 (DT1), poorly metabolically controlled so far, was admitted with DKA. Her pancreatic enzymes were increased. In ultrasound (USG), her pancreas was enlarged. This evidence indicated AP co-existing with diabetic ketoacidosis. An 8-year-old girl, suffering from DT1, was admitted with DKA, in a diabetic coma, without verbal contact. Her pancreatic enzymes were elevated. Her pancreas was hyperechoic in USG. Criteria of AP were confirmed. DKA is a frequent severe condition occurring in children with DT1. Acute pancreatitis is a life-threatening condition. Association between AP and diabetic ketoacidosis is rare. We wish to propose with this presentation the need to check the level of pancreatic enzymes in addition to the basic tests for patients with DKA.
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