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Hypertriglyceridaemia and pancreatitis: case report A 46-year-old woman developed hypertriglyceridemia during treatment with mirtazapine for depression. Additionally, she developed pancreatitis during treatment with mirtazapine, lisinopril and hydrochlorothiazide [routes not stated; not all dosages and time to reactions onsets stated]. The woman presented to the emergency department with severe abdominal pain, leg and lower back pain for several days. Her medical history included gout, depression, anxiety, chronic back pain and hypertension. Three months prior to admission, she was hospitalised for similar symptoms. At that time laboratory findings revealed sodium 132 mEq/L (normal range 135–145), chloride 110 mEq/L (normal range (98–108), bicarbonate 9 mEq/L (normal range: 24–30), blood urea nitrogen 36 mg/dL (normal range: 6–20), creatinine 2.3 mg/dL (normal range: 0.5–1.5), glucose 133 mg/dL (70–115), AST 277 U/L (normal range: 0–35), ALT 70 U/L (normal range: 0–35), alkaline phosphatase 245 U/L (normal range: 30–120), total bilirubin 1.9 mg/dL (normal range: 0–1.0), albumin 3.1 g/dL (normal range: 0–0.2), total protein 7.1 g/dL (normal range: 6–8), lipase 595 U/L (normal range: 20–190), triglycerides 127 mg/dL (normal range: 50–200), which were consistent with alcohol-induced pancreatitis. She was presumed to have a similar episode the second time as well. Laboratory tests at the time of current admission revealed sodium 134 mEq/L, chloride 102 mEq/L, bicarbonate 10 mEq/L, blood urea nitrogen 29 mg/dL, creatinine 2.7 mg/dL, glucose 152 mg/dL, calcium 7 mg/dL, AST 294 U/L, ALT 77 U/L, alkaline phosphatase 253 U/L, lipase 1488 U/L, amylase 627 U/L and triglycerides 1240 mg/dL, which were suggestive of recurrent alcohol-induced pancreatitis. However, she denied recent alcohol consumption, which was confirmed by a negative toxicology screening. A lipid panel showed a severely increased triglyceride level, a new finding compared to her previous hospitalisation. She was suspected to have hypertriglyceridemia-induced pancreatitis. Upon further investigation on her medications, it was found that she started receiving mirtazapine 15mg at night, 4 months prior to the second admission and one month prior to the original episode of presumed alcohol-induced pancreatitis. She had selftitrated the dose of mirtazapine to 30mg at night within a month of her therapy. The other home medications included lisinopril and hydrochlorothiazide, which she had been receiving for several years before the initiation of mirtazapine without any episodes of pancreatitis. During the second hospitalisation, when alcohol-induced pancreatitis was ruled out, mirtazapine was suspected to be a cause of her hypertriglyceridemia-induced pancreatitis. The Naranjo Adverse Drug Reaction Probability Scale score was 5 indicating a probable association between mirtazapine and hypertriglyceridemia-induced pancreatitis. The woman’s treatment with mirtazapine, lisinopril and hydrochlorothiazide were discontinued and she started receiving IV fluid with insul