Proton pump inhibitors
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Hypergastrinaemia, hyperemesis and dyspepsia: case report An approximately 46-year-old woman developed hypergastrinaemia, hyperemesis and dyspepsia during treatment with lansoprazole, esomeprazole and vonoprazan for gastric ulcer [routes and durations of treatment to reactions onset not stated]. The woman presented with a refractory gastric ulcer, was admitted to hospital due to abnormal sensation in the limb and altered level of consciousness at the age of 56 years. One month prior to presentation, she experienced mild drowsiness during the day. She required admission due to lower limb weakness 10 days prior to the current admission. Her drowsiness had worsened four days prior to the admission. Her anamnesis revealed a history of Helicobacter pylori and peptic ulcer 10 years previously and had started receiving lansoprazole 30mg daily and an unspecified antiemetic. The eradication therapy was successful, however occasional nausea and epigastric pain remained. On further investigation, a refractory gastric ulcer due to hypergastrinaemia was noted at that time (at the age of 46 years). Gastroenterological imaging studies were performed. Four years prior to admission, lansoprazole was switched to esomeprazole 20mg daily, but hyperemesis and dyspepsia did not improve. At the age of 54 years, direct sequence analysis and pancreaticoduodenectomy showed no abnormalities. Despite esomeprazole therapy, frequent vomiting and hypergastrinaemia persisted . Six months prior to admission, esomeprazole was switched to vonoprazan [vonoprazan fumarate] 20mg daily, which resulted in an elevated gastrin level and worsening of hyperemesis and dyspepsia. One month prior, she complained of abnormal sensation, disorientation and somnolence. Prior to admission, she had received treatment with mecobalamin [methylcobalamin] as prescribed by a physician. On admission, she was 155cm tall and weighed 40.4kg. Vital signs were as follows: body temperature 36.6°C, BP 114/76mm Hg, HR 61 bpm, RR 11 breaths per minute and SpO2 97% in supine position on room air. Neurological examination revealed mild clouding of consciousness with Glasgow Coma Scale score of 14 with lateral gaze evoked nystagmus and suppression of ocular movement in the upward direction. Manual muscle testing was found to be grade 3 at both the lower and upper limb, but it was difficult to evaluate due to her drowsiness. She also experienced dysesthesia in the fingertips with diminished biceps, triceps, and patellar reflexes bilaterally. A blood gas analysis showed respiratory compensation for metabolic acidosis. Laboratory investigations showed hypergastrinaemia and vitamin B1 deficiency with low vitamin B1 level. Cardiac findings were unremarkable. A nerve conduction study showed sensory polyneuropathy. Brain MRI, fluidattenuated inversion recovery (FLAIR) images revealed abnormal bilaterally symmetrical hyperintense signals in the mammillary bodies, a periaqueduct area of gray matter in the medial thalami, cerebrum and vermis suggestive of Wernicke encephalopathy. The clini
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