Evaluation of the relationship between the spleen volume and the disease activity in ulcerative colitis and Crohn disease.

ABSTRACT: Inflammatory bowel disease (IBD) is caused by the activation of an abnormal immune response in the intestinal mucosa; the spleen is involved in the main immune response. Ulcerative colitis (UC) and Crohn disease (CD) have different inflammatory mechanisms; this study aimed to quantitatively measure and compare the spleen volumes between patients with UC and CD and examine the relationship between spleen volume and disease activity in both.We retrospectively analyzed 44 patients with IBD aged 30-60 years (UC group, n = 24; CD group, n = 20). The control group comprised 19 patients with pancreatic cysts that did not affect the spleen volume. All patients underwent computed tomography (CT) between April 2014 and March 2019. Using the Image J software, spleen volumes in the UC, CD, and control groups were measured accurately from the CT images and adjusted for the body weight.No significant differences in the sex, age, or body weight were noted between the UC and CD groups and the control group. The spleen volumes, adjusted for the body weight, were 2.2 ±â€Š1.0 cm3/kg, 2.0 ±â€Š1.0 cm3/kg, and 3.6 ±â€Š1.7 cm3/kg in the control, UC, and CD groups, respectively. The volumes differed significantly between the CD and control groups (P = .01), but not between the UC and control groups (P = .43). Furthermore, a significant strong correlation was found between the disease activity and the body weight-adjusted spleen volume in patients with CD (P < .01).The spleen volume, adjusted for the body weight, was significantly larger in patients with CD than in the controls and was also strongly correlated with the CD activity. These results suggest that the immune response in CD may affect the spleen volume.

Upregulation of complement C1q reflects mucosal regeneration in a mouse model of colitis.

Confirming mucosal healing is important in inflammatory bowel disease treatment. Complement C1q-mediated Wnt signaling activation has recently been suggested to mediate tissue repair and mucosal regeneration. We investigated the involvement of complement C1q and Wnt signaling in intestinal mucosal regeneration using a murine colitis model. The colitis model was established by providing C57BL/6J mice with 4% dextran sodium sulfate (DSS) for 1 week (inflammation phase) followed by regular water for 2 weeks (recovery phase). After 3 weeks, we investigated the relationship between C1q in serum and colonic tissue during the inflammation and recovery phases. We assessed Wnt signaling activity by evaluating ß-catenin expression in mouse intestinal tissue. Serum C1q levels were elevated during the recovery phase. C1q-specific staining indicated high C1q expression in pathological intestinal tissue during the inflammation and recovery phases. C1q mRNA and protein expression was increased during both phases. Interestingly, C1q-expressing cells were consistent with macrophages (F4/80-positive cells). Moreover, the expression of ß-catenin increased in the colonic tissues during the recovery phase of DSS-induced colitis but decreased during the inflammation phase of DSS-induced colitis. C1q expression may mediate Wnt signaling activity and intestinal epithelial regeneration.

Intestinal Behçet disease associated with myelodysplastic syndrome accompanying trisomy 8 successfully treated with abdominal surgery followed by hematopoietic stem cell transplantation: A case report.

RATIONALE: Intestinal Behçet disease (BD) with myelodysplastic syndrome (MDS) is a rare condition that is resistant to various immunosuppressive therapies. Several cases in which hematopoietic stem cell transplantation (HSCT) was effective for intestinal BD with MDS accompanying trisomy 8 have been reported. PATIENT CONCERNS: We report an 18-year-old female with a 7-year history of BD. Colonoscopy demonstrated a huge ulcer in the cecum. Chromosomal examination revealed a karyotype of trisomy 8 in 87% of cells. Bone marrow examination revealed dysplastic cells in multilineages. DIAGNOSES: A diagnosis of intestinal BD associated with MDS accompanying trisomy 8 was made. INTERVENTIONS: The patient underwent ileocecal resection due to microperforations of ileocecal ulcers; she then underwent allogeneic peripheral blood stem cell transplantation (PBSCT) with her mother as a donor. OUTCOMES: After the PBSCT, the patient's symptoms due to BD (fever, oral aphthae, abdominal pain, and genital ulcers) completely disappeared, with no severe adverse events. LESSONS: The present case demonstrates that HSCT including PBSCT might be an effective new therapeutic option for refractory intestinal BD with MDS when immunosuppressive therapy has achieved insufficient efficacy.

Anisakiasis in the Small Intestine with Excessive Bleeding That Was Difficult to Diagnose Endoscopically.

Anisakiasis involves the stomach in most cases and occurs rarely in the small intestine. Anisakiasis in the small intestine is associated with abdominal pain and obstruction and is rarely associated with intestinal bleeding. Unlike in the stomach, anisakiasis in the small intestine is difficult to diagnose anatomically. The patient in this case study developed hypovolemic shock due to excessive bleeding and underwent emergency surgery. With the recent increase in the consumption of raw fish around the world, this report provides an important finding of bleeding in the small intestine due to an unknown cause.

Delayed perforation after endoscopic submucosal dissection for mucosal colon cancer: A conservatively treated case.

A 66-year-old man was diagnosed from colonoscopy as having a 40-mm elevated tumor in the cecum. With a preoperative diagnosis of intramucosal carcinoma, endoscopic submucosal dissection (ESD) was performed. The tumor was resected en bloc, yielding a specimen with a 66-mm diameter. No perforation was detected during the operation.Although neither abdominal pain nor fever was observed immediately after ESD, abdominal pain developed on the following day. Two days after ESD, the abdominal pain ceased. The patient was managed conservatively with fasting and intravenous antibiotic treatment. Four days after ESD, abdominal X-ray revealed marked gas retention. Computed tomography revealed pneumoperitoneum and a pelvic abscess, leading to a diagnosis of delayed perforation after colonic ESD and paralytic intestinal obstruction. A decompression tube was then inserted transnasally into the small intestine. Because a gradual decrease occurred in intestinal gas, the decompression tube was removed. Oral ingestion was resumed 13 days post-ESD.Delayed perforation after colonic ESD often requires emergency surgery. The present case was managed conservatively, despite paralytic intestinal obstruction. This approach is rarely employed for this condition and is therefore worth reporting.

Evaluation of Brain Activity Using Near-infrared Spectroscopy in Inflammatory Bowel Disease Patients.

Depression is implicated as a risk factor for the recurrence of inflammatory bowel disease (IBD). Near-infrared spectroscopy (NIRS) and brain-derived neurotrophic factor (BDNF) are useful tools for evaluation of brain activity and a depressive state, respectively. The aim of this study was to clarify the association between brain activity or depressive symptoms and IBD using NIRS and BDNF. This study included 36 ulcerative colitis (UC) patients, 32 Crohn's disease (CD) patients, and 17 healthy controls (HC). Center for Epidemiologic Studies Depression Scale (CES-D) scores were determined, NIRS was performed, and serum BDNF levels were measured in all subjects. NIRS showed that the mean oxygenated hemoglobin concentration was significantly lower in the frontal lobe in the UC group than in the HC group (HC 167 ± 106 vs. UC 83.1 ± 85.3, p < 0.05). No significant difference was seen between the HC and CD groups. There were also no significant differences in CED-D scores and BDNF levels among the groups. Changes in the NIRS values of the UC group may indicate decreased brain activity and a fundamental difference between UC and CD, which are often lumped together as two types of IBD.

Imiquimod-induced CCR9 Ameliorates murine TNBS Colitis.

AIMS: To investigate whether Imiquimod (IMQ) as TLR7 ligand protects mice from colonic inflammation and the mechanisms underlying in such immunoregulatory conditions.　METHODS: Murine colitis was induced to Balb/c mice by administration of trinitrobenzene sulfonic acid (TNBS) with or without daily intraperitoneal administration of IMQ.　Colitis was evaluated by body weight decreases and by histological score.　Also colonic mRNA expression was measured by RT-PCR.　To confirm the induction of Regulatory T cells (Tregs) by type-1 IFN from pDCs, we generated mouse bone marrow-derived pDCs and co-cultured these with CD4+ T cells isolated from mouse spleen with or without IMQ stimulation.　Cytokine production in the culture supernatant was measured by ELISA and the number of Tregs were analyzed by flow cytometry.　Spleen and mesenteric lymph nodes (MLN) from IMQ-treated mice were collected, and mRNA expressions of cytokine were measured by RT-PCR and cytokine productions were measured by ELISA.　Tregs and chemokine expressions were analyzed in colon of TNBS-induced colitis mouse by immunohistochemistry.　RESULTS: Administration of IMQ significantly suppressed colonic inflammation of TNBS-induced colitis.　In the colons of IMQ-treated mice, mRNA expression of TNF-α was decreased, and strong expressions of IL-6, IFN-ß and TGF-ß were detected.　IL-10 and TGF-ß productions were increased in the supernatant of co-cultured cells stimulated with IMQ, although we were unable to detect Treg differentiaton in IMQ-stimulated co-cultured cells.　In MLN of IMQ-treated mice, strong expressions of TLR7, IFN-ß, TGF-ß and Foxp3 mRNA were detected.　IL-10 production from MLN cells was also increased in the IMQ-treated group.　Finally, Tregs in the inflamed colon and CCR9 in MLN of IMQ-treated mice were detected.　CONCLUSION: These results suggest that IMQ protects mice from TNBS colitis through induction of CCR9, which regulates accumulation of Tregs in the inflamed colon.

Primary rectal mucosa-associated lymphoid tissue lymphoma in a patient with previously identified primary biliary cirrhosis and secondary Sjögren's syndrome.

An 83-year-old female began treatment with prednisolone and ursodeoxycholic acid at 62 years of age, following a diagnosis of primary biliary cirrhosis (PBC) and secondary Sjögren's syndrome (SjS). With persisting bloody stools, the patient underwent colonoscopy at 83 years of age. Histopathological evaluation revealed mucosa-associated lymphoid tissue (MALT) lymphoma. The elevated rectal lesion resolved with rituximab treatment. We report this case because although patients with SjS are at increased risk of malignant lymphoma, primary rectal MALT lymphoma is very uncommon in association with PBC and secondary SjS.

Concurrent primary sclerosing cholangitis and eosinophilic colitis.

A 39-year-old man presented with diarrhea and abdominal pain. At 26 years of age, he was found to have eosinophilia and abnormal liver function parameters, for which prednisolone therapy was started. He subsequently underwent a liver biopsy and endoscopic retrograde cholangiopancreatography, and received a diagnosis of primary sclerosing cholangitis (PSC). On presentation to our hospital, he was further diagnosed with eosinophilic colitis based on aggravation of diarrhea and severe eosinophilic infiltration in the colonic mucosa. We herein report a rare case of concurrent PSC and eosinophilic colitis.