Eosinophilic colitis is a relatively rare complication of hypereosinophilic syndrome which is characterized by abdominal pain and bloody diarrhea and is usually treated with steroids and hydroxyurea. However, no standard regimen exists in cases of intractable disease despite several treatment attempts with Interferon- alpha, cyclosporin, etoposide, and vincristine, etc. We here report a case of a 43-year-old woman with recurrent eosinophilic colitis as a complication of hypereosinophilic syndrome who was successfully treated with cyclophosphamide.
Adult ; Case Report ; Colitis/*complications/*drug therapy/pathology ; Cyclophosphamide/*therapeutic use ; Eosinophilia/*complications/*drug therapy/pathology ; Female ; Human ; Hypereosinophilic Syndrome/*complications ; Recurrence

Autoimmunity is thought to play a central role in the pathogenesis of inflammatory bowel disease and associated extraintestinal manifestations. Autoimmune hemolytic anemia associated with ulcerative colitis is a rare occurrence. No more than 50 cases have been described in the international literatures, and only 2 cases reported in Korea. A 29-year-old woman who was diagnosed as ulcerative colitis two years ago was complicated with autoimmune hemolytic anemia, and did not respond to steroid therapy. Ultimately, total colectomy and splenectomy were carried out for the treatment of ulcerative colitis and hemolytic anemia. After the operation, anemia was resolved. We present the case with a review of literature.
Adult ; Anemia, Hemolytic, Autoimmune/*diagnosis/drug therapy/etiology ; Colectomy ; Colitis, Ulcerative/complications/*diagnosis/pathology ; Drug Resistance ; Female ; Humans ; Splenectomy ; Steroids/therapeutic use

Amebic colitis is a disease revealing diverse clinical manifestations and endoscopic gross features and often confused with other types of colitis. In case of misdiagnosis as an idiopathic inflammatory bowel disease or delayed recognition of intestinal amebiasis, an undesirable outcome may occur resulting from erroneous administration of steroids or delayed antiamebic treatment. To demonstrate the pitfalls in the diagnosis and treatment of intestinal amebiasis, 3 cases of amebic colitis with atypical clinical manifestations are presented in this paper. In conclusion, despite the low sensitivities of routine stool examination for parasite and histopathologic confirmation in biopsy specimen, every effort must be made to find amebic trophozoites either in fresh stool or biopsy specimens for prompt and correct diagnosis of amebic colitis when we manage patients with chronic intestinal ulcerations, even though their clinical course and endoscopic findings are not typical of amebiasis. Moreover, following initial successful anti-amebic therapy, more careful clinical, endoscopical, and parasitological follow-up should be done for the early detection of recurrence.
Adult ; Aged ; Aged, 80 and over ; Colitis, Ulcerative/diagnosis ; Diagnosis, Differential ; Diarrhea/etiology ; Dysentery, Amebic/complications/drug therapy/*pathology ; Female ; Humans ; Inflammatory Bowel Diseases/diagnosis ; Male ; Middle Aged

Segmental colitis associated with diverticular disease (SCAD) is a colonic inflammatory disorder with localized non-granulomatous inflammation at sigmoid colon, and associated with colonic diverticulosis. SCAD is an apparently uncommon disorder in Western. We experienced a rare case of SCAD in a 46-year-old woman who visited the hospital due to abdominal discomfort. Colonoscopic examination showed multiple sigmoid diverticula in association with a segment length colitis. Colonoscopic biopsies of the sigmoid colon demonstrated cryptitis and crypt abscess along with chronic inflammatory cells infiltration. The biopsies of the rectum was histologically normal. The patient was given the diagnosis of SCAD and treated with oral mesalamine. This is the first case of SCAD reported in Korea.
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Colitis/complications/*diagnosis/drug therapy ; Colon, Sigmoid/pathology ; Colonoscopy ; Diverticulitis, Colonic/complications/*diagnosis/drug therapy ; Female ; Humans ; Mesalamine/therapeutic use ; Middle Aged

Granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil trafficking and is highly expressed in multiple tumors. Myeloid derived suppressor cells (MDSCs) promote neoplastic progression through multiple mechanisms by immune suppression. Despite the findings of G-CSF function in colon cancer progression, the precise mechanism of G-CSF on MDSCs regulation and its blockade effects on tumor growth remains a worthy area of investigation. In this study we observed an overexpression of G-CSF in a mouse colitis-associated cancer (CAC) model, which was consistent with the accumulation of MDSCs in mouse colon tissues. Further in vitro studies demonstrated that G-CSF could promote MDSCs survival and activation through signal transducer and activator of transcription 3 (STAT3) signaling pathway. Moreover, compared with isotype control, anti-G-CSF mAb treatment demonstrated reduced MDSC accumulation, which led to a marked decrease in neoplasm size and number in mice. Our results indicated that G-CSF is a critical regulating molecule in the migration, proliferation and function maintenance of MDSCs, which could be a potential therapeutic target for colitis-associated cancer.
Animals ; Carcinogenesis ; Colitis ; complications ; Colorectal Neoplasms ; complications ; drug therapy ; immunology ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Granulocyte Colony-Stimulating Factor ; genetics ; metabolism ; Immunotherapy ; Mice ; Molecular Targeted Therapy ; Myeloid Cells ; immunology ; metabolism ; pathology

A case of hemophagocytic syndrome associated with ulcerative colitis is very rare. A 32-year-old man visited the hospital complaining of fever and severe abdominal pain for 7 days. He was diagnosed to have ulcerative colitis 2 years ago and had been treated with sulfasalazine. Three months ago, he had abdominal pain, weight loss, and hematochezia, so prednisolone and mercaptopurine were added to the treatment. On admission, the physical examination showed splenomegaly. Peripheral blood counts revealed pancytopenia, and bone marrow aspirate smears showed many histiocytes with active hemophagocytosis. There was no evidence of viral and bacterial infections and other neoplasms, which were commonly associated with hemophagocytic syndrome. He was successfully treated with high dose steroid. We report this case along with a review of the related literatures.
6-Mercaptopurine/therapeutic use ; Adult ; Anti-Inflammatory Agents/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Bone Marrow Cells/pathology ; Colitis, Ulcerative/complications/*diagnosis/drug therapy ; Colonoscopy ; Dexamethasone/therapeutic use ; Humans ; Immunosuppressive Agents/therapeutic use ; Lymphohistiocytosis, Hemophagocytic/complications/*diagnosis/drug therapy ; Male ; Prednisolone/therapeutic use ; Sulfasalazine/therapeutic use ; Syndrome ; Tomography, X-Ray Computed

Triptolide, a diterpenoid triepoxide from the traditional Chinese medicinal herb Tripterygium wilfordii Hook. f., is a potential treatment for autoimmune diseases as well a possible anti-tumor agent. It inhibits proliferation of coloretal cancer cells in vitro and in vivo. In this study, its ability to block progress of colitis to colon cancer, and its molecular mechanism of action are investigated. A mouse model for colitis-induced colorectal cancer was used to test the effect of triptolide on cancer progression. Treatment of mice with triptolide decreased the incidence of colon cancer formation, and increased survival rate. Moreover, triptolide decreased the incidence of tumors in nude mice inoculated with cultured colon cancer cells dose-dependently. In vitro, triptolide inhibited the proliferation, migration and colony formation of colon cancer cells. Secretion of IL6 and levels of JAK1, IL6R and phosphorylated STAT3 were all reduced by triptolide treatment. Triptolide prohibited Rac1 activity and blocked cyclin D1 and CDK4 expression, leading to G1 arrest. Triptolide interrupted the IL6R-JAK/STAT pathway that is crucial for cell proliferation, survival, and inflammation. This suggests that triptolide might be a candidate for prevention of colitis induced colon cancer because it reduces inflammation and prevents tumor formation and development.
Animals ; Cell Transformation, Neoplastic/*drug effects ; Colitis/complications ; Colonic Neoplasms/chemically induced/*drug therapy/metabolism/pathology ; Dextran Sulfate/toxicity ; Dimethylhydrazines/toxicity ; Diterpenes/*administration & dosage ; Epoxy Compounds/administration & dosage ; Humans ; Interleukin-6/biosynthesis ; Janus Kinases/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred ICR ; Mice, Nude ; Neoplasm Transplantation ; Phenanthrenes/*administration & dosage ; STAT3 Transcription Factor/metabolism ; Signal Transduction/*drug effects ; Tumor Burden/drug effects ; rac1 GTP-Binding Protein/*biosynthesis