The patient was a previously healthy 49-year-old Caucasian female who presented to the hospital with abdominal pain associated with nausea, vomiting, and weight loss. CT of her abdomen showed circumferential wall thickening of the ascending colon, highly suspicious for colonic carcinoma with associated pericolic and upper abdominal lymphadenopathy and splenomegaly with several splenic hypodensities suggestive of metastases was also noted.
The patient underwent laparotomy with hemicolectomy, histopathology revealed ascending colon adenocarcinoma. Five lymph nodes were positive for metastatic carcinoma and multiple sarcoidal noncaseating granulomas were also noted.
PET (positron emission tomography) scan following surgery revealed mediastinal bilateral hilar lymphadenopathy and splenomegaly with marked abnormally increased metabolic activity suspicious for metastasis. Prior to her presentation, there was no chest imaging available for comparison.
Splenic biopsy showed multiple granulomas with focal necrosis. Stain was negative for fungal and acid-fast microorganisms.
Blood work at the time showed Ca of 9.1 mg/dl, Cr of 0.9 mg/dl, CEA level of 9.6 ng/ml, and ACE level of 45 nmol/ml/min. CRP and ESR were not checked as they could be falsely elevated in postoperative state. Given the absence of respiratory symptoms and minimally elevated serum ACE level, no treatment was deemed necessary for asymptomatic incidental sarcoidosis and the patient was started on chemotherapy to treat cancer.
Two years later, a follow-up PET scan revealed increased lymphadenopathy in multiple areas including the left axilla and the left mammographic chain and mesenteric lymphadenopathy. Lesions were also noted in the liver and spinous processes of L3-L4. Progression of her splenic involvement was also noted (see Figures 1 and 2 ). Liver biopsy at the time showed only noncaseating granulomas with no evidence of malignancy (see Figure 3).
At that time, her CEA level had increased from 3 to 14.2 ng/ml and ACE level was >120 nmol/ml/min, ESR was>100 mm/hr, CRP was 15.5 mg/L, and Cr was 1.7 mg/dl. QuantiFERON-TB Gold and ANCA antibodies were all negative.
Given the presence of biopsy-proven sarcoidosis with elevated ACE level, compatible imaging, and the fact that serum CEA can also be elevated sarcoidosis, the patient was started on 40 mg of prednisone for treatment of sarcoidosis flare. Following two months of therapy, blood work showed significant improvement. Serum ACE level was down to normal at 35 nmol/ml/min, Cr improved to 1.01 mg/dl, and CRP decreased to 12.4 mg/L; however, CEA increased to 98 ng/ml.
Repeated PET scan showed resolution of the hilar lymphadenopathy with improvement of the left axillary and liver metabolic activity. Previously reported increased splenic and bone metabolic activity had also resolved (see Figures 4 and 5). Mesenteric lymphadenopathy, however, had progressed. Biopsy of the mesenteric lymph node showed recurrence of cancer. The patient was referred to oncology to continue treatment for colon cancer, and, finally, hospice was offered given the poor response.