Recurrent abdominal pain in a patient with Down syndrome.

A 34 year-old woman with Down syndrome was seen in clinic after having two episodes of acute pancreatitis over the preceding 2 months, each requiring hospital admission. The initial episode of pancreatitis was initially manifest as severe epigastric pain radiating to her back associated with loose stools. She denied having had any fevers, nausea, or vomiting. Her medical history included hypothyroidism and a coagulation disorder that had been complicated by a cerebral vascular accident, now under treatment with anticoagulants. Her family history revealed the presence of celiac disease in several family members. She denied any use of alcohol or illicit drugs. Her medication list did not reveal any medications that are considered as possible etiologic agents [1, 2]. Physical examination revealed mild tenderness to palpation in the epigastric area but no organomegaly or palpable masses. Laboratory test results included: white blood cell count of 5.7 9 10/mm, serum concentrations of aspartate aminotransferase 27 Unit/L (range 6–58 Unit/L), alanine aminotransferase of 34 Unit/L (range 14–67 Unit/L), alkaline phosphatase 89 Unit/L (range 38–150 Unit/L), total bilirubin 0.6 mg/dL (range 0.3–1.2 mg/dL), direct bilirubin 0.1 mg/dL (range 0.1–0.4 mg/dL), serum lipase 1695 Unit/L (range 66–360 Unit/L), creatinine 0.91 mg/dL (range 0.6–1 mg/ dL), serum triglycerides 95 mg/dL (range \150 mg/dL), calcium 8.2 mg/dL (range 8.4–10.4 mg/dL), and serum IgG4 22 mg/dL (range 7–89 mg/dL). A CT scan of the abdomen and pelvis with and without contrast was reported as showing mildly heterogeneous attenuation of the pancreas without frank pancreatic free fluid, no dilation of the pancreatic duct, and no pancreatic mass or pseudocyst. An abdominal ultrasound showed no cholelithiasis, pericholecystic fluid or gallbladder wall thickening, and a common bile duct that measured 4 mm with no intrahepatic bile duct dilation. An incidental note was made of a Phrygian cap of the gallbladder; the visualized portion of the pancreas appeared sonographically unremarkable. She was clinically diagnosed as having acute pancreatitis was hospitalized for 6 days of conservative management and then discharged. One month later, she was again hospitalized with similar symptoms of abdominal pain and laboratory findings of serum concentrations of lipase of 1241 Unit/L, creatinine 0.84 mg/dL, aspartate aminotransferase 23 Unit/L, alanine aminotransferase of 27 Unit/L, alkaline phosphatase 75 Unit/L, total bilirubin 0.5 mg/dL, and direct bilirubin 0.1 mg/dL. A CT scan of the abdomen and pelvis was reported as showing acute inflammatory changes in the region of the pancreatic tail and the presence of a small amount of free fluid in the left paracolic gutter. The remainder of the pancreas was without inflammatory changes or masses, although a punctate hyperattenuation was noted in the pancreatic tail that may have reflected a focus of calcification from prior pancreatitis; there was no dilation of the pancreatic duct. An abdominal ultrasound scan was unremarkable with no cholelithiasis or bile duct dilation noted. At an outpatient follow-up visit 2 weeks later, further laboratory testing revealed serum concentrations of tissue & Allison Venner AVenner@salud.unm.edu