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THU388 Insulin Edema Associated With Glargine: A Case Report And Brief Review Of Literature

Disclosure: J. Wood: None. V. Samji: None. F.S. Celi: None. P. Majety: None. Introduction: Insulin edema is an uncommon and poorly understood complication of insulin therapy in patients with diabetes. We report a patient with type 1 diabetes (T1DM) who developed edema within days of initiating insul...

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Detalles Bibliográficos
Autores principales: Wood, Jessica, Samji, Varun, Celi, Francesco S, Majety, Priyanka
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10555093/
http://dx.doi.org/10.1210/jendso/bvad114.821
Descripción
Sumario:Disclosure: J. Wood: None. V. Samji: None. F.S. Celi: None. P. Majety: None. Introduction: Insulin edema is an uncommon and poorly understood complication of insulin therapy in patients with diabetes. We report a patient with type 1 diabetes (T1DM) who developed edema within days of initiating insulin glargine that resolved with discontinuation of this medication. Case Report: A 20-year-old man with no past medical history presented with nausea, vomiting, polydipsia, and a 15-pound weight loss and was noted to have a hemoglobin A1c greater than 14.0%. Diabetic ketoacidosis (DKA) was ruled out and was started on weight-based insulin therapy with glargine and lispro three units with meals. Additional diabetes workup was notable for positive Anti-IA2 antibodies. Blood glucose levels improved prior to discharge. A week after discharge, he complained of swelling of limbs. Patient denied any shortness of breath, cough, chest pain, orthopnea, or nocturnal dyspnea. He was found to have extensive 2+ pitting edema in bilateral feet extending up to his calves. Dorsalis Pedis pulses were 2+ bilaterally. No warmth or erythema of legs was noted. His weight in clinic was 70.2 kg (154.4 lbs), up 11.6 kg (25.5 lbs) ten days post discharge. Evaluation for bilateral pedal edema was performed. Labs were notable for normal liver enzymes, creatinine, glomerular filtration rate and urine albumin levels, ruling out hepatic and renal causes of edema. Thyroid function tests were normal. His presentation was discussed with cardiology and brain natriuretic peptide level was drawn which was also normal. No further cardiac workup was recommended at that time given the patient’s history and lack of other clinical signs or symptoms of heart failure. After ruling out other systemic causes of edema in our patient, a diagnosis of insulin edema was made. Based on prior case reports of glargine associated insulin edema, he was switched from insulin glargine to insulin degludec. He noted significant improvement within 24 hours of switching insulin with a 6.4-pound weight loss in just one day and complete resolution of edema within 3 days. He had no recurrence of edema once glargine was discontinued despite increasing insulin dosing for glycemic control. Conclusion: The pathophysiology of insulin edema is unclear. Insulin’s role in renal sodium handling, vasodilation, and increased vascular permeability, have been postulated as possible mechanisms. Risk factors for developing insulin edema include T1DM, high A1C, high dose of insulin, rapid correction of hyperglycemia, DKA on presentation and poor nutritional status. Additional risk factors for developing insulin edema include thiamine deficiency and an underlying genetic predisposition related to a mitochondrial mutation, although this seems to be rare. Insulin edema is a diagnosis of exclusion. Clinicians should be aware of this rare complication, and its occurrence should be documented and differentiated from other causes of edema. Presentation: Thursday, June 15, 2023