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Immune-globulin/methylprednisolone/pembrolizumab Diabetic ketoacidosis, pancreatitis and immune-mediated cerebellar degeneration: case report

An 82-year-old man developed diabetic ketoacidosis, pancreatitis and immune-mediated cerebellar degeneration during off label treatment with pembrolizumab for Merkel cell carcinoma. Additionally, he exhibited lack of efficacy during treatment with methylprednisolone and immune-globulin for immune-mediated cerebellar degeneration [not all routes stated; duration of treatment to reactions onsets not stated]. The man, who had a history of hypertension, type 1 diabetes mellitus, alcohol and tobacco consumption, presented by the end of 2016 with progressive growth of axillary and cervical lymph nodes in the previous year. He was diagnosed with Merkel cell carcinoma with lymph node metastasis. Based on his age and comorbidities, from May 2017, he started receiving off-label therapy with pembrolizumab 2 mg/kg once every 3 weeks. After 4 cycles, he showed an objective clinical response. At that point, he was admitted to the hospital with the complaints of acute anorexia and mental confusion, he was found to be obnubilated and dehydrated. Through a blood analysis hyperglycaemia, acute kidney injury grade 3 associated with hyponatraemia, hypercalcaemia, hyperphosphataemia, and ketonuria were detected. The clinical picture rapidly evolved with respiratory arrest with bradycardia and hypotension. He underwent orotracheal intubation and mechanic ventilation, and aminergic support was started. Mixed metabolic academia was revealed by initial blood gas analysis. For advanced life support, he was transferred to ICU. Hence, progressive clinical stability was observed. An increased amylase and lipase but low C peptide were revealed by complementary examinations. Based on the presentation of inaugural insulinopenic type 1 diabetes, he was diagnosed with diabetic ketoacidosis possible pancreatitis, which were attributed to pembrolizumab. The man was started on intensive insulin therapy and subsequent support therapy. Six days after the ictus and clinical stabilization, he was transferred to the oncology ward. He was discharged after 2 weeks, under corticosteroid therapy at weaning and insulin therapy. His immune therapy was discontinued. After 6 months, basal-bolus insulin dose was reduced. Although, he was readmitted in between January and March 2018, for an insidious and progressive worsening of dysarthria and ataxia. Various laboratory examinations were performed for the reassessment of the disease, and a substantial partial response was confirmed. Electromyography showed a mild axonal sensorimotor polyneuropathy. Proteinorachia was found through lumbar puncture analysis. Despite the lack of identification of any circulating antibody in serum and cerebrospinal fluid, an immune-mediated cerebellar degeneration was hypothesized (progressive pancerebellar syndrome). He was started on methylprednisolone pulse therapy (1 g/day for 5 days). However, his neurologic deficits worsened, mainly ap