Trametinib
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Trametinib Hyponatraemia: 2 case reports
A report described a 9-year-old girl and a 7-year-old girl, who developed hyponatraemia during treatment with trametinib [route not stated]. Case 1: The 9-year-old girl presented with an optic pathway glioma since 18months of age. Her medical history included hypopituitarism, visual impairment, developmental delay and precocious puberty. She had a subtotal surgical resection at the age 2 years and had failed multiple lines of unspecified chemotherapy. The tumour had disseminated at the age of 8 years. At the age of 9 years, she had started receiving trametinib 1.25mg daily. Her other medications included desmopressin, hydrocortisone, levothyroxine sodium [levothyroxine] and leuprorelin [leuprolide]. She was adipsic and fluid balance was managed with a fixed daily total fluid intake. Her serum sodium had been in the normal range for many years. Serum sodium on day 1 of starting trametinib was 138 mmol/L. Within 1 week of starting trametinib she presented with vomiting and decreased urine output. Serum sodium was 113 mmol/L (hyponatraemia). CT scan of head did not show any new findings. She started receiving sodium chloride infusion. Her desmopressin was held. Over the following days, serum sodium increased to 135 to 140 mmol/L and desmopressin was restarted at a lower dose. Again desmopressin dose was quickly decreased further based on clinical status and to allow for a 24-hour urine output of 1 to 2 mL/kg/h. Two weeks later she was admitted with lethargy and hypotension with serum sodium of 154 mmol/L. A septic work-up was negative. A MRI of brain showed worsening hydrocephalus. She underwent a ventriculoperitoneal (VP) shunt revision. Her desmopressin was further titrated to maintain euvolemia and normal serum sodium. She was discharged home on desmopressin at 8% of the original dose required prior to starting trametinib. She was admitted again 4 days later with a serum sodium of 171 mmol/L. Over the next 3 days the sodium level decreased to 151 mmol/L. her desmopressin dose was increased. Three weeks later her parent elected to discontinue trametinib given the persistent difficulties in managing her diabetes insipidus. After discontinuing trametinib, her serum sodium levels stabilised. Over the next 3 months the desmopressin dose was increased, a similar dose she required prior to starting trametinib. Case 2: The 7-year-old girl presented with an optic-hypothalamic pilomyxoid astrocytoma diagnosed at 18 months of age. Her medical history included hypopituitarism, seizures, decreased visual acuity and neurocognitive delay. She had partial adipsia and was managed by her parents in with a fixed daily total fluid intake. She had a ventriculoperitoneal shunt. She had completed four lines of unspecified chemotherapy in the past. Dissemination of tumour became evident on scans at 7 years of age. She had started receiving trametinib 0.75mg daily after further tumour progression. Medications at the time of starting trametinib included desmopressin, hydrocortisone, levetiracet
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