Maternal Graves' autoantibodies are well known to cause fetal and neonatal thyroid disturbances. Despite radioiodine therapy, Graves' autoantibodies are known to persist, which can cross the placenta and cause hyperthyroidism in the fetus. We present the case of a 26-year-old woman in her first pregnancy, clinically and biochemically euthyroid with history of treated Graves' disease, where the fetus showed signs of hyperthyroidism on antenatal scans. This was confirmed by amniotic fluid testing as fetal blood sampling was not feasible and successfully treated with maternal carbimazole whilst continuing thyroxine for the mother (block-replacement). We discuss the challenges in the diagnosis of fetal hyperthyroidism and treatment whilst maternal thyroid status is maintained on thyroxine.

Wong, Mimi*,1,2; Hills, Frances3; Vogler, Katrina3; Zardawi, Ibrahim4; Nandi, Nirjhar1 Author Information

ObjectiveImmunotherapy is a novel treatment that can cause autoimmune diabetes in rare cases. More cases occur following use of the inhibitor to the protein programmed cell death-1 rather than the inhibitor to programmed cell death-ligand 1.MethodsWe report a unique case of autoimmune diabetes following atezolizumab use.ResultsA 55-year-old, Aboriginal Australian female with no prior history of diabetes was commenced on atezolizumab for recurrent squamous cell lung carcinoma. Two months following its commencement, there was the onset of fatigue, polyuria, polydipsia, and new hyperglycemia. Subsequently she was found to have a borderline-low C peptide level of 0.6 nmol/L (reference range is 0.5 to 1.0 nmol/L), and positive zinc transporter-8 antibodies. Following the diagnosis of autoimmune diabetes, 5 units of glargine insulin was commenced which maintained euglycemia and resolved her symptoms of hyperglycemia.ConclusionThere are few case reports of atezolizumab-induced autoimmune diabetes. We present the first case associated with zinc transporter-8 antibodies, and a unique case of autoimmune diabetes in a patient of Aboriginal Australian background.

Objective Adult nesidioblastosis is characterized by endogenous hyperinsulinemia typically causing post-prandial hypoglycemia, and most commonly occurs post-Roux-en-Y gastric bypass. Methods We report a unique case of nesidioblastosis occurring in a 67-year-old female. Results A 5-year history of symptomatic hypoglycemia occurred in a patient with short bowel syndrome and type 2 diabetes mellitus (T2DM) managed previously with a glucagon-like peptide 1 (GLP-1) agonist, which achieved significant weight loss. Continuous glucose monitoring captured 42 hypoglycemia episodes in a 2-week period, and following an oral glucose tolerance test there was the suggestion of a hyperinsulinemia state. She was managed with an open distal pancreatectomy, and subsequently required medical therapy to maintain euglycemia. Conclusion We present the first case of nesidioblastosis occurring in a patient with short bowel syndrome, pre-existing T2DM managed with a GLP-1 agonist which achieved significant weight loss, all of which we speculate could have predisposed to hypoglycemia and development of nesidioblastosis.