ESPE Abstracts (2015) 84 P-3-757


Acute Painful Neuropathy in a Teenager with Type 1 Diabetes (T1D) and Eating Disorders

Maria Lourakia, Marina Katsaloulib, Dimitra Kallinikoua, Christina Kanaka-Gantenbeinc, Betina Kandylaa, Eirini Sakkoua & Kyriaki Karavanakia


aDiabetic Clinic, Second Pediatric Department University of Athens, “P&A Kyriakou” Children’s Hospital, Athens, Greece; bNeurologic Department, “Aghia Sophia” Children’s Hospital, Athens, Greece; cDiabetes Center, First Pediatric Department University of Athens, “Aghia Sophia” Children’s Hospital, Athens, Greece

Background: Acute painful neuropathy (APN) is a rare manifestation of diabetic neuropathy (DN) in T1D adolescents, associated with poor metabolic control. Eating disorders (ED) often present in T1D patients in association with metabolic derangement, leading to the development of diabetic complications.

Case presentation: A teenage girl aged 12 years with a recently diagnosed T1D (duration: 9 months) was admitted with diabetic ketoacidosis (DKA), also complaining of pain and numbness in the limbs. During the last 3 months she reduced food intake and insulin doses (0.3 IU/kg per day) in order to lose weight, leading to metabolic deterioration (HbA1c: 11%). On admission, her height was 150 cm (50th–75th centile), weight: 34 Kg (3rd centile), BMI: 15.1 kg/m2 (3rd centile). She had impaired vibration sensation thresholds (VPT) in upper and lower limbs and abnormal sensory peroneal nerve measurements (amplitude: 2.7 mV, velocity: 35 msec), with a marginally impaired pupillary adaptation in darkness (58.3%, normal: 54.2–78.6%). She was put under long term psychiatric support. Six months later binge eating episodes were reported, with no neurologic symptoms. Her weight (41.5 kg) (25th–50th centile) and BMI (17.7 kg/m2) (<25th centile) were increased and her metabolic control was improved (HbA1c: 7.5%), as well as her VPT measurements at all sites (index finger: 3.5 vs 10.5V, big toe: 4.0 vs 8.0V). During the following 2 years she had a progressive metabolic deterioration (HBA1c: 7.6–9.4%) and periodical symptoms of DN. Her previously abnormal peroneal nerve parameters were slightly improved (amplitude: 5.1 mV, velocity: 38.6 msec), with additional abnormal sural nerve values (amplitude: 6.5 uV, velocity: 40 msec), and no indices of other microvascular complications.

Conclusion: A teenager with a short T1D duration and eating disorders developed APN. DN symptoms and electrophysiological findings were temporarily improved after BMI and HbA1c improvement, but were subsequently deteriorated with poor metabolic control. APN may present in T1D adolescents during a period of acute weight loss and cannot be reversed unless optimal metabolic control is achieved in the long term.

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