Background Although associations between various single nutrients and exacerbation of inflammatory bowel disease (IBD) have been reported, more recent attention has focused on overall dietary patterns and quality rather than a single nutrient. This study was to investigate the association of dietary inflammatory potential and dietary quality with disease severity in young adult Crohn’s disease (CD) patients. Methods Non-consecutive 3-day food records were investigated in 25 patients with CD aged 19-40 years. Patients with moderate or severe active disease were excluded to investigate their usual dietary habits. A survey on dietary behavior was conducted and clinical data including the disease progress were collected. To investigate potential pro-inflammatory dietary habits in a patient's usual diet, food-based index of dietary inflammatory potential score (FBDI), glycemic index (GI), and glycemic load (GL) were calculated. Diet quality was evaluated using a tool called Diet Quality Index-international (DQI). Results Although most patients showed adequate caloric intake, 72% of the enrolled patients had a potential pro-inflammatory pattern identified as FBDI. The FBDI was significantly associated with intake of mixed coffee and sweeten drinks, beef, and pork (P < 0.05). Patients who had a serious clinical course such as history of surgery or the use of biologics, tended to have a higher FBDI (6.45 vs 2.44, P = 0.08), and showed a higher proportion with a low DQI (53% vs 20%, P = 0.06). Only 30% of the high FBDI group showed deep remission after 12 to 18 months of follow-up endoscopic or image study, whereas 72.7% of the low FBDI group showed deep remission (P =0.05). A significantly positive correlation was derived between FBDI and GL (r =0.452, P = 0.02). Conclusion For the care of patients with CD, it is necessary to evaluate the dietary quality as well as the total nutrient intake, and we need to educate the patients that dietary habits can affect the disease prognosis.
Background It has been suggested that changes in gut microbiota have an important effect on the development of inflammatory bowel disease (IBD). In studies using germ-free mice, it has been reported that the absence of microbiota rarely causes dextran sulfate sodium (DSS)-colitis. This study was to investigate whether the changes in DSS-colonic inflammation in mice treated with antibiotics were comparable to the results in germ-free mice. Methods Ampicillin + enrofloxacin were treated in six 9-week-old C57BL/6 mice for initial 3 days and stools were sampled daily to measure the total amount of bacterial 16S rRNA. The time of loss and restoration of gut microbiota was investigated after repeated antibiotics. The severity of colitis and barrier damage were compared between the following groups: (i) control group, (ii) DSS group, and, and (iii) DSS + antibiotics group. The DSS group was allowed to drink 3% DSS from day 5 and maintained for 7 days, and colon tissues were obtained from all groups on day 12. The inflammatory markers (IL-1α, IL-6, IL-17, tumor necrosis factor (TNF)-α) and gut barrier markers (Zonular occludens (ZO)-1, occludin, claudin-1, claudin-4) in colon tissues were comparatively analyzed between groups. Results Bacterial 16S rRNA was not detected from day 4 after the antibiotics, and restoration started from day 11. After repeated antibiotics, microbial depletion was re-confirmed on day 14, but restoration appeared on day 18, confirming faster recovery. The expression levels of IL-1α, IL-17, and TNF-α in the DSS + antibiotics group did not differ from the control but were significantly lower than the DSS group (all p < 0.01). However, the expression of ZO-1 and claudin-4 was significantly lower in the DSS + antibiotics treatment group than in the control group (p < 0.05). Conclusion The antibiotic cocktail could dramatically reduce gut microbiota over a period, but the effect would decrease as it is repeated. Depletion of gut microbiota after antibiotics would dramatically reduce DSS-colonic inflammation but could damage the gut barrier or at least not prevent barrier dysfunction.
Introduction: Breast cancer is a heterogeneous diseases, which is based on expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Using these factors, molecular subtype can be determined as luminal A, luminal B, HER2+, and TNBC. This is considered as an important prognostic factor. In breast cancer, age is the one of the important prognostic factors and prognosis is varied according to patients’ age. We performed this study to analyze the impact of molecular subtypes on prognosis of breast cancer according to patients’ age. Patients and methods: We performed this study by using Korean Breast Cancer Society Registration Program data. Total 15,286 patients are included into this study, and they underwent surgery during the period Jan. 2001 to Dec. 2006. All patients were divided into two groups according to age (younger: age≤34, older: age≥35) and molecular subtypes were classified into four groups as follows: luminal A (ER+ and/or PR+, HER2-), luminal B (ER+ and/or PR+ HER2+), HER2+ (ER-, PR-, HER2+), and triple-negative (ER-, PR-, HER2-). We determined prognostic impact of molecular subtype on overall survivals (OS). Clinicopathologic results and OS were compared by chi-square test, Kaplan Meier test, and Cox's hazards model. Results: Younger group more frequently had tumors with negative hormone receptor (ER-/PR-), worse prognostic factors and diagnosed with more advanced stage compared to older group. In univariate analysis, molecular subtype was not related with OS in younger group (p = 0.069), but not in older group (p<0.001). In multivariate analysis, molecular subtype was an independent prognostic factor for OS only in older group (p = 0.690 vs p<0.001). Conclusion: In young breast cancer patients, less than 35 years, the impact of molecular subtypes on overall survival was not significant compared to other age group. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P6-06-42.
Backgrounds:18F-fluorodeoxyglucose positron emission tomography with computed tomography (18F-FDG PET/CT) is widely used for cancer evaluation and there are several studies which suggested maximum standard uptake value (SUVmax) may reflect the cancer patients' prognosis. Adenosine triphosphate-based chemotherapy response assay (ATP-CRA) is commonly used as a chemosensitivity assay modality for the treatment of various cancers in clinical settings and there have been several studies on its usefulness in breast cancer. We previously reported chemosensitivity (ATP-CRA) results might reflect patients' prognosis. So we supposed that SUVmax could reflect chemosenitivity (ATP-CRA) results of patients, so performed this study to analyze the relationship between PET/CT SUVmax and chemosenstivity (ATP-CRA) results of these drugs. Furthermore, we evaluated prognostic factors for breast cancer according to SUVmax. Materials and Methods: 102 breast cancer patients, who underwent PET/CT and chemosensitive (ATP-CRA) test between December 2010 and April 2012, were enrolled in this study. We analyzed, retrospectively, the correlation between SUVmax of PET/CT and chemosenitivity (ATP-CRA) results of doxorubicin/paclitaxel. SUVmax according to prognostic factors were also assessed. Results: Chemosensitivity (ATP-CRA) results of doxorubicin and paclitaxel have significant positive correlation with SUVmax. Their correlation coefficient were 0.236 (p = 0.020) and 0.216 (p = 0.030), respectively. Patients with larger tumor size, higher histologic and nuclear grade, estrogen receptor negative, progesterone receptor negative, HER2 positive, and Ki67 positive (≥14%) have higher mean SUVmax values (p < 0.05). In molecular subgroup analysis, triple negative group showed higher mean SUVmax values than luminal A group (p < 0.001). Conclusion: Higher SUVmax values of PET/CT is correlated with better chemosensitive (ATP-CRA) results of doxorubicin and paclitaxel, and poor prognostic factors of breast cancer. However, examination of additional cases might be needed. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P4-03-11.
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