Fatigue, Weight Loss, and Abdominal Cramping in a 70-Year-Old Man

Tomislav Dragovich, MD, PhD; Shailja B. Amin, PA-C

Disclosures

December 19, 2014

Discussion

The patient presented with unintentional weight loss and abdominal cramping. The physical examination was remarkable for hepatomegaly and abdominal ascites. CT of the abdomen and pelvis revealed a 3.7-cm mass within the body of the pancreas, which was further evaluated by esophagogastroduodenoscopy with EUS.

The EUS study confirmed the presence of a solid lesion measuring 4 cm x 3 cm (Figures 1-3). The pathologic interpretation of the EUS-guided fine-needle aspiration biopsy was consistent with atypical glandular cells suspicious for malignancy.

Because the findings were only suspicious for and not diagnostic of malignancy, the patient underwent staging laparoscopy with biopsies. Upon exploration, diffuse peritoneal and omental carcinomatosis were found. The mass from the body of the pancreas was abutting the common hepatic artery. Pathology of the peritoneum implants and omentum was consistent with metastatic adenocarcinoma. The intraperitoneal fluid that was collected for cytology was positive for malignancy. The serum level of the tumor maker CA 19-9 was elevated, at 3650 IU/mL (normal range, < 35.9 IU/mL).

Pancreatic cancer is the fourth leading cause of cancer related death in the United States and the second leading cause of digestive cancer-related death.[1] The incidence of pancreatic cancer increases at age 50 years and peaks in the seventh decade. Male sex and African American race confer higher risk and a higher mortality rate.[2] The 5-year survival rate is about 25%-30% for node-negative disease and 10% for node-positive disease.[2]

The pancreas has both endocrine and exocrine functions. Exocrine pancreatic neoplasms include pancreatic ductal, acinar cell, and stem cell neoplasms. About 85% of malignant pancreatic cancer arises as ductal adenocarcinomas. Several subtypes of ductal adenocarcinomas share a poor prognosis; the exception is colloid carcinomas, which have a better prognosis. Endocrine neoplasms include pancreatic neuroendocrine islet cell tumors, which consist of about 5% of pancreatic neoplasms.[3]

Diabetes mellitus can be both a symptom of and a risk factor for pancreatic cancer. Studies show that 1% of patients who are diagnosed with diabetes after 50 years of age develop pancreatic cancer within 3 years of being diagnosed with diabetes.[4]Chronic pancreatitis or long-term inflammation of the pancreas can be caused by greater alcohol consumption, leading to a risk for pancreatic cancer that is increased up to 16-fold.[5] Patients with chronic pancreatitis caused by hereditary pancreatitis have up to 50-fold increased risk for developing pancreatic cancer.[6]

Hereditary pancreatic cancer accounts for 2% of total pancreatic cancers. Some of these genetic conditions include familial atypical mole and melanoma syndrome (FAMMM), hereditary nonpolyposis colorectal cancer (HNPCC), Peutz-Jeghers syndrome, familial adenomatous polyposis, BRCA2 mutation, and hereditary pancreatitis.[7] Other nonhereditary factors shown to increase risk for pancreatic cancer include peptic ulcer surgery or partial gastrectomy, smoking, obesity, and physical inactivity. Occupational chemicals, such as petrochemicals, have also been linked to pancreatic cancer.[8]

The initial presentation of pancreatic cancer varies and depends on tumor location. As many as 60%-70% of tumors arise in the head of the pancreas, which causes symptoms of duct obstruction, jaundice, and pain. Jaundice is most often due to obstruction of the common bile duct by a mass in the head of the pancreas. Only 20%-25% arise in the body or tail; these are less likely to cause symptoms until metastasis has occurred.[7]

Other clinical presentations include recent onset of atypical diabetes mellitus or unexplained thrombophlebitis. Signs of metastatic disease include ascites and lymphadenopathy. Common sites of metastasis are the liver; peritoneum; lungs; and, less commonly, the bones.

Initial laboratory tests include measurement of serum aminotransferases, alkaline phosphatase, and bilirubin. Imaging should include endoscopic retrograde cholangiopancreatography and EUS to identify the extent of disease for tumor and nodal staging.[2] These techniques are also useful to detect tumor invasion of the portal vein, identify hepatic lesions, and obtain tissue samples. A fine-needle aspiration sample for pathologic diagnosis can be obtained.

Dual-phase, contrast, helical CT has a sensitivity of 67% for lesions smaller than 1.5 cm and 100% for tumors larger than 1.5 cm.[2] This scan is also used to investigate major vessel involvement, which includes the superior mesenteric artery, inferior vena cava, aorta, celiac axis, or hepatic artery. A serum CA 19-9 level is not diagnostic but can be useful in patients who are potentially cured after surgery or those who are receiving chemotherapy.[9]

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