Diabetic ketoacidosis induced by long-acting growth hormone in a child without preexisting diabetes.
This case indicates that initiating long-acting growth hormone therapy may lead to diabetic ketoacidosis even in children without prior diabetes, particularly in those with obesity and on glucocorticoids.
Where it sits
this study against the rest of the desmopressin corpusSummary and findings
A 13-year-old boy with hypopituitarism and obesity developed severe diabetic ketoacidosis (DKA) after starting lonapegsomatropin at 0.23 mg/kg/week. He presented with hyperglycemia, severe metabolic acidosis, and ketonuria two days post-initiation of treatment. DKA resolved with insulin and fluid therapy, and he remained normoglycemic after discontinuation of growth hormone therapy.
Abstract
Long-acting growth hormone (LAGH) formulations improve medication adherence in children with growth hormone deficiency. Although transient insulin resistance and mild hyperglycemia are recognized effects of growth hormone therapy, diabetic ketoacidosis (DKA) in patients without prior diabetes is rare. We report a case of severe DKA shortly after initiation of lonapegsomatropin in an adolescent with hypopituitarism without preexisting glucose abnormalities. A 13-year-old boy with obesity, normal fasting glucose, and hypopituitarism receiving levothyroxine, hydrocortisone, and desmopressin replacement therapies following treatment of a suprasellar nongerminomatous germ cell tumor initiated treatment with lonapegsomatropin at 0.23 mg/kg/week. Two days after the administration of the first dose, he presented critically ill with hyperglycemia, severe metabolic acidosis, and ketonuria consistent with DKA. Hemoglobin A1c was 5.7% (reference range, <5.7%), type 1 diabetes autoantibodies were negative, and C-peptide was elevated, suggesting preserved endogenous insulin secretion. Diabetic ketoacidosis resolved with insulin and fluid therapy, and the patient remained normoglycemic after discontinuation of growth hormone therapy. This case suggests that acute LAGH-induced insulin resistance, potentially compounded by glucocorticoids and obesity, may precipitate transient DKA even in patients without prior glucose abnormalities. Close glucose monitoring should be considered when initiating LAGH therapy in high-risk patients.
Background
This paper addresses the occurrence of diabetic ketoacidosis (DKA) in a child without preexisting diabetes after the initiation of long-acting growth hormone therapy. Prior knowledge indicates that growth hormone can induce insulin resistance and mild hyperglycemia, but DKA in such patients is uncommon. Understanding this case is important as it highlights potential risks associated with growth hormone therapy in vulnerable populations.
Methods
The study reports a case of a 13-year-old boy with hypopituitarism who was treated with lonapegsomatropin at a dose of 0.23 mg/kg/week. The observation period began two days after the first dose, during which the patient developed symptoms consistent with DKA. No specific control group or comparative analysis was mentioned.
Results
The patient presented with hyperglycemia, severe metabolic acidosis, and ketonuria consistent with DKA two days after starting lonapegsomatropin. Hemoglobin A1c was measured at 5.7%, with negative type 1 diabetes autoantibodies and elevated C-peptide levels, indicating preserved insulin secretion.
Interpretation
This case adds to the limited literature on the potential for DKA in patients without prior diabetes when initiating growth hormone therapy. While the findings are statistically significant, the clinical relevance may be limited due to the small sample size and nature of the report. The presence of obesity and glucocorticoid therapy may confound the results, suggesting a need for caution and monitoring in similar patient populations.
Key findings
- Hemoglobin A1c was 5.7% (reference range, <5.7%)
- Type 1 diabetes autoantibodies were negative
- C-peptide was elevated, suggesting preserved endogenous insulin secretion
- DKA occurred two days after the first dose of lonapegsomatropin at 0.23 mg/kg/week
Limitations
- Single case report with no control group
- Limited generalizability due to small n
- No long-term follow-up reported
- Potential confounding factors not fully explored