Abstract / Summary
Recurrent hypoglycaemia is an uncommon clinical problem that warrants careful evaluation for underlying systemic and paraneoplastic causes when typical etiologies are excluded. Among haematological malignancies, multiple myeloma classically presents with anaemia, renal dysfunction, lytic bone disease, and monoclonal protein excess; however, hypoglycaemia is an exceptionally rare and easily overlooked manifestation. We report a case of severe, recurrent non-insulin-mediated hypoglycaemia associated with previously undiagnosed IgG kappa multiple myeloma, underscoring the diagnostic complexity of tumour-associated hypoglycaemia and the importance of maintaining a broad differential diagnosis particularly in resource-limited settings. A 55-year-old Sri Lankan woman presented with reduced responsiveness and found her capillary glucose level is 35 mg/dL. Her hospital course was complicated by recurrent refractory hypoglycaemic seizures, and aspiration pneumonia. Investigations revealed severe anaemia, markedly elevated inflammatory markers, and multiple pathological thoracolumbar vertebral compression fractures. Serum protein electrophoresis demonstrated a monoclonal gammopathy, and immunofixation confirmed an IgG kappa paraproteinemia (20.6 g/L) with immunoparesis, consistent with multiple myeloma. During a documented hypoglycaemic episode, capillary glucose level 46 mg/dL and simultaneous laboratory plasma glucose was 38 mg/dL, with serum insulin and C-peptide concentrations appropriately suppressed. Renal, hepatic, and adrenal dysfunction were excluded, and computed tomography of the chest, abdomen, and pelvis did not identify an alternative malignancy. Hypoglycaemic episodes markedly decreased following initiation of multiple myeloma-directed therapy, which included dexamethasone, with subsequent stabilisation of glycaemic control, and the patient was referred for ongoing disease-directed haematological management. Recurrent severe hypoglycaemia is an uncommon, but important diagnostic clue to underlying systemic malignancy. Suppressed insulin and C-peptide levels during hypoglycaemia support a non-insulin-mediated mechanism. This case underscores the need for clinician vigilance in unexplained recurrent hypoglycaemia, as delayed recognition may lead to life threatening neuroglycopenic events. Identification and treatment of the underlying disorder may be important for sustained glycaemic stabilisation.