There has been scant prior research focusing on

There has been scant prior research focusing on the clinical efficiency and safety of either BV alone or in combination with chemotherapy in treating relapsed or refractory CD30+ T cell lymphoma, ALCL and HL. Although the most common and significant adverse events of BV, such as peripheral neuropathy or neutropenia, are well tolerable but rare during BV treatment, severe and life-threatening events, acute pancreatitis occurring after BV treatment had also been reported. Here, we report the case of a mortality caused by acute pancreatitis after the first course of BV treatment in a patient with ALCL. To our knowledge, this is the first report describing such fatal pancreatitis in an Asian patient after BV treatment.
Case report When the patient felt acute onset of epigastric pain with the sensation of abdominal fullness, he was sent to a metropolitan hospital where acute pancreatitis was diagnosed on July 22, 2015. Although the medical staff suggested hospitalization, the patient refused and was transferred to our ED. At our ED, he complained of persistent abdominal pain with abdominal fullness and poor appetite, yet manifested no fever, nauseas, vomiting or diarrhea. Physical examination revealed acutely ill condition and obesity, with a body temperature of 36.2 °C and a regular pulse of 139 beats per min, blood pressure of 133/89 mmHg and breath rate was 20 times per min. Pink conjunctiva, bilateral clear breathing sounds, distended and soft abdomen, normal active bowel sounds and tenderness over the epigastric area were noted. His laboratory data of peripheral blood showed leukocytosis: white blood cell count (WBC) 18,700/mm3 with an absolute neutrophil count of 14,287/mm3, hemoglobin 10.1 g/dL and platelet count 3,43,000/mm. Subsequent laboratory investigation revealed increased high sensitivity C- reactive protein (14.94 mg/dL), creatinine (2.37 mg/dL), l-alanine manufacturer (360 mg/dL), total bilirubin (1.4 mg/dL), lipase (1422 U/L), triglyceride (290 mg/dL)and lactic dehydrogenase (LDH)(482 U/L). Metabolic acidosis was fully compensated for in respiration with lactate acidosis and ketoacidosis (pH:7.3, pCO2: 23 mmHg, HCO3: 11.3 mmol/L, lactate: 25.3 mg/dL, ketone body: 6.9 mmol/L), hypocalcemia (5.6 mg/dL) and hyponatremia(130 mmol/L). The level of aspartate aminotransferase was in normal range. The patient\'s Ranson\'s Criteria score on admission was three points (WBC > 16,000/mm3, glucose > 200 mg/dL and LDH > 350 U/L). Abdominal CT without contrast was arranged in order to estimate possible causes and severity of his acute pancreatitis, which showed diffusely swelling pancreas with fat standing and surrounding fluid collection and duct dilatation (Fig. 1). After admission, although the patient was subjected to massive intravenous fluid hydration with calcium supply, regular insulin pump, empiric antibiotic treatment, shock and multiple organ failure with oliguria and acute respiratory distress syndrome, so an endotracheal tube was inserted post-sedation and mechanical ventilation support was provided. The patient\'s Ranson\'s Criteria score within 48 h was four points (hematocrit dropped > 10% from admission, Ca < 8 mg/dL within 48 h and base deficit > 4 mg/dL within 48 h, fluid requirements > 6 L within 48 h) and the total Ranson\'s Criteria score was seven points which suggested 100% predicted mortality. Due to acute kidney injury, hypotension and uncorrectable metabolic acidosis, continuous venous venous hemofiltration (CVVH) was arranged beginning in late July, 2015. Although the patient was under mechanical ventilation, vasoactive agents and CVVH support, his hypotension and hypoxia continued to progress, and he expired on July 29, 2015.
Discussion Although this patient had a habit of alcohol consumption, he had quit drinking more than a year earlier and had no history of pancreatitis. Triglyceride levels were mildly increased but not more than 1000 mg/dL, and there was no evidence of ampullary obstruction found in the abdominal CT. He denied taking any drug which could induce acute pancreatitis. However, the acute pancreatitis which occurred on the thirteenth day after administration of BV in this patient was similar to most events previously reported