although hypercalcemia of various etiologies is known to be associated with pancreatitis , most cases have been associated with hypercalcemia of primary hyperparathyroidism . few cases of pancreatitis have been reported to be secondary to the hypercalcemia of metastatic tumors or multiple myeloma . we report a second case of acute pancreatitis occurring in a patient with multiple myeloma and discuss its clinical implication . a 38-year - old male was hospitalized with a 3-week history of a painful sternal mass and low back pain . the patient also complained of generalized weakness , anorexia and occasional nausea . on physical examination , there was a 3 cm  3 cm , ill defined , hard tender mass in the lower sternal area . initial laboratory studies in the emergency room the night before admission showed that the hemoglobin was 10.1 g / dl , the hematocrit 30.7% and the white blood cell count 11,200 . the serum calcium was 12.7 mg / dl , serum phosphorus 4.2 mg / dl , total serum protein 11.7 g / dl , serum albumin 3.2 g / dl , serum urea nitrogen 15 mg / dl , and the serum creatinine was 1.4 mg / dl . there was a monoclonal igg kappa component with decreased iga and igm on the serum immunoelectrophoresis . the diagnosis of multiple myeloma was confirmed by a bone marrow examination showing a hypercellular marrow with 40% plasma cells . the day after admission , the patient developed nausea , vomiting and abdominal pain . the serum calcium level was 13.3 mg / dl and the patient was treated with iv hydration and iv furosemide 20 mg every 2 hours for 6 days . despite the treatment , the calcium level remained elevated , and was 14.0 mg / dl on the fourth hospital day . the regimen included bcnu 80 mg and cytoxan 800 mg iv on the first day , melphalan 8 mg po daily for 7 days , and prednisone 40 mg po twice daily for 7 days then in tapering doses . due to severe emesis , the patient vomited the first doses of melphalan and prednisone . an upper endoscopy was performed on the sixth hospital day , which showed multiple small erosions in the gastric antrum and a normal duodenum . the serum amylase was 120 u/ ( normal , 37117 ) , and the lipase was 311 u/ ( normal , 23208 ) . ultrasound examination of the abdomen showed no evidence of cholelithiasis or dilatation of the biliary ducts . subsequent serum lipase levels and calcium levels are shown in fig . 1 along with the date when the therapeutic agents were administered . the patient was placed on parenteral hyperalimentation until he was asymptomatic and his serum amylase and lipase had returned to normal . it is felt that the hypercalcemia of hyperparathyroidism favors the deposition of intraductal calculi in the pancreas , leading to ductal obstruction and pancreatitis . another possibility is that an increased concentration of calcium ions in pancreatic secretion and pancreatic tissue might promote activation of trypsinogen to trypsin . reports of pancreatitis secondary to the hypercalcemia of metastatic tumors or multiple myeloma are rare . in 1976 grafter reported a case of acute pancreatitis in a patient with hypercalcemia due to metastatic breast carcinoma . in this case , the diagnosis of pancreatitis was made on the postmortem examination . in another case , pancreatitis occurred in a patient with transitional cell and squamous cell carcinoma of the renal pelvis with metastasis to the bones . meltzer et al described a patient with multiple myeloma who had extensive bone disease with hypercalcemia and abdominal pain . no antemortem serum pancreatic enzyme levels or parathyroid hormone levels were available . in the present case , the possibility of coexistence of primary hyperparathyroidism is remote since the serum parathyroid hormone level was normal . although the patient received intravenous furosemide , it is not likely the cause of pancreatitis since the symptoms of pancreatitis occurred before the beginning of furosemide therapy . furosemide induced pancreatitis has been reported in patients on chronic oral therapy and the onset of the symptoms was 35 weeks after initiation of the therapy . alcohol intake , gallstones , trauma , peptic ulcer disease and hypertriglyceridemia have been ruled out as a cause of the pancreatitis by the history and appropriate tests . the chemotherapy reigmen for multiple myeloma included prednisone but the patient vomited the first dose and subsequently received no further steroids . although hypercalcemia was the suspected cause of pancreatitis , it is difficult to exclude direct involvemnt of the pancreas by multiple myeloma . primary pancreatic carcinoma and tumors metastatic to the pancreas are known to be able to initiate acute pancreatitis . in 1952 the rarity of reported cases of acute pancreatitis in patients with multiple myeloma seems surprising in view of a 3060% incidence of hypercalcemia in multiple myeloma . the possibility of pancreatitis in a patient with multiple myeloma may be overlooked since the symptoms of acute pancreatitis , such as nausea , vomiting and abdominal pain , are easily attributable to hypercalcemia itself or the side effects of chemotherapeutic agents . we believe this case represents a patient with pancreatitis secondary to hypercalcemia from multiple myeloma . pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea and vomiting .
a patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis . 
 other etiologic factors for pancreatitis were excluded . 
 hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis . in english literature , only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis . 
 pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea / vomiting , and abdominal pain .