Immune checkpoint inhibitor-induced diabetes mellitus with nivolumab.

Immune checkpoint inhibitors (ICIs) have been increasingly used in the treatment of various advanced cancers; however, therapy can be complicated by immune-related adverse events (irAEs). We present the case of a man in his 40s, with metastatic melanoma treated with nivolumab immunotherapy who developed ICI-induced diabetes mellitus (ICI-DM). Hyperglycaemia in the absence of ketoacidosis was incidentally noted when he presented to the emergency department for review of an urticarial rash.

Immune checkpoint inhibitor-induced diabetes mellitus with pembrolizumab.

An 81-year-old woman with a background of metastatic melanoma on pembrolizumab with no history of diabetes was brought into the emergency department with polyuria, polydipsia and weight loss. The initial assessment was consistent with severe diabetic ketoacidosis (DKA) and prerenal acute kidney injury with no clinical evidence of infection. The patient was treated with fluid resuscitation and an insulin infusion and eventually transitioned to a basal-bolus insulin regime, which was continued after discharge.

Flucloxacillin and paracetamol induced pyroglutamic acidosis.

A 75-year-old woman was admitted to a regional hospital with an acute kidney injury (AKI) and nausea on a background of recent treatment for bacteraemia secondary to pneumonia. The treatment thereof resulted in a high anion gap metabolic acidosis (HAGMA). The pneumonia was initially treated with intravenous piperacillin and tazobactam and the patient transferred to a tertiary hospital.

Acquired pyroglutamic acidosis due to long-term dicloxacillin and paracetamol use.

An 85-year-old man with a background of transfusion-dependent chronic myelomonocytic leukaemia and chronic kidney disease stage III presented with symptomatic anaemia, acute kidney injury, sepsis and high anion gap metabolic acidosis (HAGMA). Initial treatment with intravenous antibiotics and blood transfusion was complicated by transfusion-associated circulatory overload, necessitating diuresis and non-invasive ventilation. Despite gradual clinical improvement, the patient's HAGMA persisted, and no cause was identified on urine testing or renal ultrasound.