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LBODP037 Acute Foot Drop In An Adolescent With Type 1 Diabetes Mellitus At Onset: A Case Report

BACKGROUND: The incidence of type 1 diabetes (T1D) among youth is on the rise worldwide. Diabetic neuropathy is often a late manifestation of diabetes and usually results from the exposure to prolonged hyperglycemia, oxidative and inflammatory stress, and dyslipidemia. Here, we report a case of pain...

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Detalles Bibliográficos
Autores principales: Albasri, Eman Ebrahim, Al-Sofiani, Mohammed E
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9624995/
http://dx.doi.org/10.1210/jendso/bvac150.547
Descripción
Sumario:BACKGROUND: The incidence of type 1 diabetes (T1D) among youth is on the rise worldwide. Diabetic neuropathy is often a late manifestation of diabetes and usually results from the exposure to prolonged hyperglycemia, oxidative and inflammatory stress, and dyslipidemia. Here, we report a case of painless diabetic mononeuropathy as the presenting symptom of T1D that improved shortly after the improvement in glycemic control. Clinical case A previously healthy 15-year-old boy, presented to the emergency department (ED) with left foot weakness and dragging for 1 week. This was preceded by numbness over the left lateral leg and dorsum of the left foot. There was no history of trauma. The patient reported a history of polyuria, polydipsia, and significant weight loss for 3 months, for which he did not seek medical care. There was no family history of diabetes, hereditary neuropathy, or autoimmune diseases. Upon presentation to the ED, a general physical examination was unremarkable with a weight of 60 Kg (BMI= 20 Kg/m2), neurological examination revealed weakness in the dorsiflexion of the left foot (3/5), eversion (4/5), and normal sensation and reflexes. The remainder of the neurological examination including the right foot, upper extremities, cerebellar functions, cranial nerves and monofilament and vibration sensory testing was normal. Fundoscopic exam showed no evidence of retinopathy. The initial laboratory investigations revealed mild DKA (PH 7.28, HCO3 16mmol/L, Na 137 mEq/L, random blood glucose of 306 mg/dl, positive blood ketones) and normal kidney function. A nerve conduction study showed moderate left peroneal motor axonal neuropathy, with normal sensory nerve action potentials. Brain CT scan was unremarkable. Further tests to rule out secondary causes of neuropathy (ANA, B12 level, and thyroid function) were within normal. The diagnosis of diabetes-related mononeuropathy was confirmed by the neurology team and the patient underwent physiotherapy. After the resolution of DKA, the patient continued to use basal/bolus insulin therapy and was discharged home with close follow-up of blood glucose readings. His glycemic control has improved, and the patient reported a significant improvement in the foot drop 3 weeks later. A repeated examination by the neurology team 3 months later confirmed a complete recovery of the left foot drop. CONCLUSION: Acute diabetic mononeuropathy can be an unusual presenting feature of T1D and may pose a diagnostic challenge. Although diabetic mononeuropathy is often a late complication of diabetes, our patient presented with acute mononeuropathy at the onset of T1D. This case highlights the importance of early diagnosis and management of diabetes to prevent and sometimes reverse diabetic neuropathy. It also shows that a complete recovery of acute diabetic mononeuropathy can be achieved by improving glycemic control in patients with newly diagnosed T1D. Presentation: No date and time listed