scholarly journals Presumed Solitary Dissemination of Colon Cancer Mimicking Primary Cancer of the Small Intestine

2021 ◽  
pp. 1422-1428
Author(s):  
Daisuke Inoue ◽  
Shoji Oura ◽  
Tomoya Takami ◽  
Shinichiro Makimoto

A 69-year-old man with abdominal distention was referred to our hospital. The patient had undergone laparoscopic surgery for his Borrmann type 2 rectal cancer 2 years before. In addition to the re-elevation of serum CEA and CA19-9 levels, computed tomography (CT) showed intestinal dilatation, and positron emission CT showed a presumed tumor with abnormal fluorodeoxyglucose accumulation in the small intestine. We judged the small intestinal dilatation was highly due to the solitary recurrent peritoneal dissemination of rectal cancer and performed laparoscopic evaluation of the abdominal cavity followed by laparoscopic resection of the affected small intestine. The small intestinal tumor resembled the rectal cancer both on macroscopical and microscopical findings, that is, Borrmann type 2 phenotype and adenocarcinoma that was well differentiated in the part that protruded into the small intestinal lumen and whose degree of differentiation gradually decreased toward the serosa. In addition, abrupt disruption of the normal small intestinal epithelium and the lymphocytic aggregation, presumed tumor-infiltrating lymphocytes, just between the tumor and the small intestinal epithelium highly suggested the tumor originating from the colon cancer. The patient recovered uneventfully with marked decrease in tumor marker levels 1 month after the operation but did not receive colon cancer-oriented chemotherapy as adjuvant therapy for his financial reasons. Oncologists should note this type of recurrence to properly treat the patients with recurrent colorectal cancer.

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Paul Cray ◽  
Breanna J. Sheahan ◽  
Jocsa E. Cortes ◽  
Christopher M. Dekaney

AbstractEnteric bacteria and/or their products are necessary for doxorubicin (DXR)-induced small intestine mucosal damage. While DXR does not induce gross loss of epithelium, others have shown elevated serum endotoxin after DXR administration. However, the mechanism of movement is unknown. We hypothesized that DXR treatment resulted in increased paracellular translocation of bacteria or bacterial products through the small intestinal epithelium. We measured permeability after DXR administration using transepithelial resistance and macromolecular flux and assessed tight junctional gene expression and protein localization both in vitro using T84 cells and ex vivo using murine jejunum. DXR treatment increased flux of 4 kDa dextrans in mouse jejenum, but increased flux of 4, 10 and 20 kDa dextrans in T84 cells. Following DXR, we observed increased permeability, both in vitro and ex vivo, independent of bacteria. DXR induced increased expression of Cldn2 and Cldn4 in murine small intestine but increased only CLDN2 expression in T84 cells. DXR treatment induced disorganization of tight junctional proteins. We conclude that DXR increases paracellular transit of small macromolecules, including bacterial products, through the epithelium, by altering expression of tight junctional components and dynamic loosening of cellular tight junctions.


1994 ◽  
Vol 71 (5) ◽  
pp. 701-707 ◽  
Author(s):  
G. J. Van Den Berg ◽  
S. YU ◽  
A. G. Lemmens ◽  
A. C. Beynen

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.


Sign in / Sign up

Export Citation Format

Share Document