Background Type 1 diabetes (T1D) is a chronic autoimmune disorder characterized by the destruction of pancreatic beta cells, resulting in a deficiency of insulin production. T1D typically presents in childhood and requires lifelong insulin therapy. However, in some cases, patients experience a transient ‘honeymoon period’ shortly after diagnosis, during which residual beta cell function may temporarily alleviate insulin requirements. This case report describes a 7-year-old boy diagnosed with T1D who displayed a prolonged honeymoon period and an intriguing sensitivity to insulin therapy, accompanied by positive anti-GAD antibodies in his laboratory results.

Case Report(s) A 7-year-old male child presented to our pediatric endocrinology clinic with a recent diagnosis of T1D. He had been experiencing polyuria, polydipsia, and unintentional weight loss over the preceding weeks. His initial blood glucose was markedly elevated at 400 mg/dL (normal range: 70- 120 mg/dL), with a hemoglobin A1c (HbA1c) of 10% (normal range: 4-6%). Upon examination, the child was thin but appeared well. He had no family history of diabetes.

Upon admission, he was initiated on insulin therapy with basal and prandial insulin. Surprisingly, the patient exhibited remarkable sensitivity to insulin, with rapid normalization of blood glucose levels. After only a few days, his insulin requirements had dramatically decreased, and hypoglycemia became a recurrent concern. The clinical team decided to cautiously decrease and eventually halt his insulin therapy, given the potential for hypoglycemia. Despite discontinuing insulin, his blood glucose levels remained within the target range. This phenomenon was reminiscent of a prolonged honeymoon period, which is typically short-lived in T1D patients.

Laboratory results revealed an interesting finding. The patient‘s anti-glutamic acid decarboxylase (anti-GAD) antibody titer was significantly elevated at 1156 IU/mL (normal range: <5 IU/mL). Anti- GAD antibodies are associated with autoimmune destruction of beta cells in T1D. The persistence of positive anti-GAD antibodies in this case was intriguing, as it is often considered a marker of ongoing autoimmunity.

The patient‘s clinical course was closely monitored, and he continued to maintain stable blood glucose levels without insulin therapy. Regular follow-up assessments, including HbA1c, C-peptide, and anti- GAD antibody measurements, were performed to track his progress.

Conclusion(s) This case highlights a rare and fascinating scenario in pediatric T1D. The 7-year-old patient exhibited an extended honeymoon period, during which he displayed an exceptional sensitivity to insulin therapy, allowing for the discontinuation of insulin without compromising glycemic control. The presence of persistently elevated anti-GAD antibodies raises intriguing questions about the underlying immunological processes at play. Further research and long-term follow-up of this patient are warranted to better understand the mechanisms responsible for this unique presentation of T1D. This case underscores the importance of personalized management in T1D and the need for ongoing research into the immunological aspects of the disease to develop novel therapeutic approaches.