The most common CT finding in patients with SLE and acute abdominal pain is ischemic bowel disease. CT is useful for detecting the primary cause of gastrointestinal symptoms, planning treatment, and monitoring for infarction or perforation.

The study was undertaken to evaluate clinical and laboratory characteristics of patients with lupus enteritis and to investigate its association with anti-endothelial cell antibodies (AECAs). Systemic lupus erythematosus (SLE) patients who were admitted to Kangnam St. Mary's Hospital with complaints of acute abdominal pain from January 1990 to July 2006 were reviewed retrospectively. The clinical features, laboratory data and prognosis of these patients were analyzed. Among the 706 SLE patients admitted during the study period, 87 were found to admit for acute abdominal pain. Among them, 41 patients were identified with lupus enteritis. The SLE disease activity index score at admission and the mean prednisolone dose administered during the last three months prior to admission were significantly higher in patients with lupus enteritis than those with other causes (P < 0.001, P = 0.036). Serum anti-endothelial cell antibody (AECA-IgG) titer was also significantly higher in patients with lupus enteritis than those with other manifestations or healthy controls (P = 0.040, P < 0.001). Four out of 13 recurrent patients had pre-existing anti-phospholipid syndrome (APS), whereas only one out of 28 non-recurrent patients had pre-existing APS (P = 0.028). Most of the patients with lupus enteritis showed good response to high-dose intravenous steroids and there was no death directly associated with lupus enteritis.

The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.

Artificial intelligence is likely to perform several roles currently performed by humans, and the adoption of artificial intelligence-based medicine in gastroenterology practice is expected in the near future. Medical image-based diagnoses, such as pathology, radiology, and endoscopy, are expected to be the first in the medical field to be affected by artificial intelligence. A convolutional neural network, a kind of deep-learning method with multilayer perceptrons designed to use minimal preprocessing, was recently reported as being highly beneficial in the field of endoscopy, including esophagogastroduodenoscopy, colonoscopy, and capsule endoscopy. A convolutional neural network-based diagnostic program was challenged to recognize anatomical locations in esophagogastroduodenoscopy images, Helicobacter pylori infection, and gastric cancer for esophagogastroduodenoscopy; to detect and classify colorectal polyps; to recognize celiac disease and hookworm; and to perform small intestine motility characterization of capsule endoscopy images. Artificial intelligence is expected to help endoscopists provide a more accurate diagnosis by automatically detecting and classifying lesions; therefore, it is essential that endoscopists focus on this novel technology. In this review, we describe the effects of artificial intelligence on gastroenterology with a special focus on automatic diagnosis, based on endoscopic findings.

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Abbreviations: GSPE, grape seed proanthocyanidin extract; MIA, monosodium iodoacetate; MMP, matrix metalloproteinase; O2 -, superoxide anion; OA, osteoarthritis; OH, hydroxyl radicals; ONOO -, peroxynitrite; PWL, paw withdrawal latency; PWT, paw withdrawal threshold; ROS, reactive oxygen species; TRP, transient receptor potential; VIP, vasoactive intestinal peptide Abstract Osteoarthritis (OA) is an age-related joint disease that is characterized by degeneration of articular cartilage and chronic pain. Oxidative stress is considered one of the pathophysiological factors in the progression of OA. We investigated the effects of grape seed proanthocyanidin extract (GSPE), which is an antioxidant, on monosodium iodoacetate (MIA)-induced arthritis of the knee joint of rat, which is an animal model of human OA. GSPE (100 mg/kg or 300 mg/kg) or saline was given orally three times per week for 4 weeks after the MIA injection. Pain was measured using the paw withdrawal latency (PWL), the paw withdrawal threshold (PWT) and the hind limb weight bearing ability. Joint damage was assessed using histological and microscopic analysis and microcomputerized tomography. Matrix metalloproteinase-13 (MMP13) and nitrotyrosine were detected using immunohistochemistry. Administration of GSPE to the MIA-treated rats significantly increased the PWL and PWT and this resulted in recovery of hind paw weight distribution (P ＜ 0.05). GSPE reduced the loss of chondrocytes and proteoglycan, the production of MMP13, nitrotyrosine and IL-1β and the formation of osteophytes, and it reduced the number of subchondral bone fractures in the MIA-treated rats. These results indicate that GSPE is antinociceptive and it is protective against joint damage in the MIA-treated rat model of OA. GSPE could open up novel avenues for the treatment of OA.

The aim of this study was to investigate the role of IL‐12 in patients with RA. IL‐12 (p70) and its associated cytokines were measured in sera and synovial fluid (SF) using an enzyme‐linked immunosorbent method. Seven American College of Rheumatology (ACR) core set measures as well as IL‐12 levels were sequentially monitored at the commencement and 4 months after treatment with a low‐dose steroid and disease‐modifying anti‐rheumatic drugs (DMARDs). In sera, 64 (42.2%) of 152 RA patients had detectable concentrations of IL‐12 (p70), whereas one (1.4%) of 69 osteoarthritis (OA) patients and five (10%) of 50 healthy controls had detectable IL‐12 (P < 0.001). The median level of circulating IL‐12 was also higher in RA patients (P < 0.001). In SF, the number of patients with detectable IL‐12 and the median IL‐12 levels were significantly higher in RA patients (n = 53) than in OA patients (n = 22). In paired samples (n = 53) of sera and SF from RA patients, IL‐12 levels were higher in the SF than in sera (P < 0.001). Patients with detectable IL‐12 (n = 51) in sera had higher tender joint scores (P = 0.003), swollen joint scores (P < 0.001) and C‐reactive protein (CRP; P = 0.036), than those without (n = 55). Four months after treatment with DMARDs, the improved group showed a larger IL‐12 decrease than the non‐improved group (P = 0.017). The levels of IL‐12 correlated positively with those of IL‐2, interferon‐gamma, IL‐6, and tumour necrosis factor‐alpha, but were correlated inversely with those of IL‐10. Our results demonstrate that IL‐12 levels reflect RA disease activity and that IL‐12 is involved in the production of proinflammatory cytokines. An IL‐12 blockade could be useful for the treatment of RA.

Objective. Although oral tolerance is a well-known phenomenon, the role of dendritic cells (DCs) is not well characterized. This study was conducted to better understand the differential role played by each Peyer's patch DC subset in the induction of oral tolerance to type II collagen (CII) in murine collagen-induced arthritis (CIA).Methods. CII was fed 6 times to DBA/1 mice beginning 2 weeks before immunization, and the effect on arthritis was assessed. We compared the proportion of CD11c؉,CD11b؉ DCs and CD11c؉,CD8␣؉ DCs in the Peyer's patches of CII-fed tolerized and phosphate buffered saline-fed nontolerized mice after the induction of CIA. The immunosuppressive properties of each DC subset were determined using fluorescenceactivated cell sorter analysis for intracellular interleukin-10 (IL-10) and IL-12 and mixed lymphocyte culture. The ability of each DC subset to induce CD4؉,CD25؉ T regulatory cells was also examined. Mice were injected with CII-pulsed CD11c؉,CD11b؉ DCs isolated from Peyer's patches of tolerized mice, and the effect on CIA was examined.Results. The severity of arthritis was significantly lower in tolerized mice. The proportion of CD11c؉,CD11b؉ DCs was increased in the Peyer's patches of tolerized mice and those DCs exhibited immunosuppressive characteristics, such as increased IL-10 production, inhibition of T cell proliferative responses to CII, and CD4؉,CD25؉ regulatory T cell induction. Furthermore, the CD11c؉,CD11b؉ DCs suppressed the severity of arthritis upon adoptive transfer.Conclusion. Our observations demonstrate that CD11c؉,CD11b؉ DCs, which are abundant in Peyer's patches during the induction of oral tolerance to CII, are crucial for the suppression of CIA and could be exploited for immunotherapy of autoimmune diseases.Oral tolerance refers to the immunologic hyporesponsiveness provoked by repeated exposure of the mucosal immune system to ingested protein antigens. Oral administration of antigens or peptides that are structurally similar to the autoantigen leads to local and systemic priming and, usually, to systemic tolerance, making this a promising approach for the treatment of autoimmune diseases. In animal models, it has been shown that oral tolerance effectively ameliorates experimental autoimmune encephalitis and collagen-induced arthritis (CIA) (1-8). Repeated oral administration of type II collagen (CII) induces peripheral immune tolerance, resulting in the suppression of CIA, a representative experimental model of human rheumatoid arthritis