Inflammatory bowel diseases(IBD) are chronic idiopathic inflammatory conditions characterized by relapsing and remitting episodes of inflammation which can affect several different regions of the gastrointestinal trac...Inflammatory bowel diseases(IBD) are chronic idiopathic inflammatory conditions characterized by relapsing and remitting episodes of inflammation which can affect several different regions of the gastrointestinal tract, but also shows extra-intestinal manifestations. IBD is most frequently diagnosed during peak female reproductive years, with 25% of women with IBD conceiving after their diagnosis. While IBD therapy has improved dramatically with enhanced surveillance and more abundant and powerful treatment options, IBD disease can have important effects on pregnancy and presents several challenges for maintaining optimal outcomes for mothers with IBD and the developing fetus/neonate. Women with IBD, the medical team treating them(both gastroenterologists and obstetricians/gynecologists) must often make highly complicated choices regarding conception, pregnancy, and post-natal care(particularly breastfeeding) related to their choice of treatment options at different phases of pregnancy as well as post-partum. This current review discusses current concerns and recommendations for pregnancy duringIBD and is intended for gastroenterologists, general practitioners and IBD patients intending to become,(or already) pregnant, and their families. We have addressed patterns of IBD inheritance, effects of IBD on fertility and conception(in both men and women), the effects of IBD disease activity on maintenance of pregnancy and outcomes, risks of diagnostic procedures during pregnancy and potential risks and complications associated with different classes of IBD therapeutics. We also have evaluated the clinical experience using "top-down" care with biologics, which is currently the standard care at our institution. Post-partum care and breastfeeding recommendations are also addressed.展开更多
Background: Helicobacter species are best known for their roles in the pathology of gastritis;however, several Helicobacter species also colonize the intestine, and less is known about effects of Helicobacter on the d...Background: Helicobacter species are best known for their roles in the pathology of gastritis;however, several Helicobacter species also colonize the intestine, and less is known about effects of Helicobacter on the development of intestinal inflammation. To evaluate contributions of Helicobacter in inflammatory bowel disease, we investigated whether and how pre-existing intestinal colonization would affect disease severity and biomarkers of inflammation in experimental IBD. Materials and Methods: Mice were infected with H. muridarum 2 weeks prior to induction of colitis mediated by 3% dextran sulfate (DSS). Disease activity index, stool blood and consistency, colon length, myeloperoxidase, histopathology, blood and lymphatic vessels, and numbers of dilated mucosal crypts were measured in control, DSS-only, H. muridarum-infected, and H. muridarum-infected + DSS mice. Results: Prior to DSS challenge, H. muridarum-infected mice showed little distal gut injury by several indices of colon inflammation with decreased blood vessel density in the submucosa, and lower lymphatic density in the mucosa and submucosa. However, after DSS colitis, H. muridarum-infected mice exhibited significantly greater disease. Weight change, stool bleeding, diarrhea, and angiogenesis were all increased in H. muridarum-infected mice in DSS colitis compared to DSS controls. Conclusions: Our data show that Helicobacter colonization of the intestine, unlike that of the stomach, lowers basal gut inflammatory scores, but increases disease activity and inflammation in an acute colitis model. Intestinal Helicobacter infection may therefore represent a significant sub-clinical factor which predisposes the gut to inflammatory injury.展开更多
AIM: To investigate whether regional geography influences ethnic and gender trends for the development of gastric cancer(GC).METHODS: This retrospective analysis of the INVISION patient database at Louisiana State Uni...AIM: To investigate whether regional geography influences ethnic and gender trends for the development of gastric cancer(GC).METHODS: This retrospective analysis of the INVISION patient database at Louisiana State University Health Sciences Center-Shreveport(LSUHSC-S), a southern United States regional hospital, was performed from 2005-2011. Using the international statistical classification of diseases 9(ICD-9), inpatient, day surgery outpatient, and emergency outpatient diagnosis codes entered into medical records were used to identify GC patients. For each study year, the patients were evaluated for age, ethnicity, and gender, and each patient was counted only once throughout the study. Subsequent patient encounters were counted as visits and separated by inpatient and clinic visits. Complex or severe disease may require more frequent and intensive clinical management; therefore, we evaluated annual clinic visits as "surrogate markers" of disease severity. Finally, we studied the primary diagnosis for Helicobacter pylori(H. pylori) infection(ICD-9 code 41.86) as an additional factor that might increase the risk of GC.RESULTS: A total of 285 patients were diagnosed with GC at LSUHSC-S between 2005 and 2011. African Americans(181 patients, 89 males and 92 females, 63.5% of total patients) had significantly higher frequencies of GC diagnosis compared with non-Hispanic whites(104 patients, 54 males and 50 females, 36.5% of total patients), at a ratio of 1.74(P = 0.002). Within each ethnic group, men and women were diagnosed at approximately equal annual rates. Our findings differed significantly from United States national trends, which found that African American females and white females had lower risks for GC than their corresponding male counterparts. The United States national trend between 2005 and 2011 showed that African Americans males had a higher incidence of GC, with an annual mean(per 100000) of 16.31 ± 0.76 compared with white males(9 ± 0.1, P < 0.001), African American females(8.7 ± 0.34, P < 0.001) and white females(4.05 ± 0.07, P < 0.001). Among the GC patients, the number of clinic visits was highest among African American males(195.1 ± 28.1), who had significantly more clinic visits than African Americans females(123 ± 13.02, P < 0.05), white males(41.57 ± 4.74, P < 0.001) and white females(35 ± 8.9, P < 0.001). Similar trends were found for inpatient visits, with an annual mean of 11.43 ± 1.5 forAfrican American males, followed by African American females(7.29 ± 1.36), white males(2.57 ± 0.69) and white females(1.57 ± 0.612). African American males had significantly more inpatient visits than white males(P < 0.001), and African American females had more inpatient visits than white females(P < 0.01). African American patients showed the highest frequency of H. pylori positive status, with approximately 72% vs 28% for the white patients. CONCLUSION: Increase in GC diagnoses among women at LSUHSC-S is significantly higher than United States national averages, suggesting local geographic and socioeconomic influences may alter GC disease course.展开更多
Inappropriate responses to normal commensal bacteria trigger immune activation in both inflammatory bowel disease and experimental colitis. How gut flora contribute to the pathogenesis of inflammatory bowel disease is...Inappropriate responses to normal commensal bacteria trigger immune activation in both inflammatory bowel disease and experimental colitis. How gut flora contribute to the pathogenesis of inflammatory bowel disease is unclear, but may involve entrapment of leukocytes and remodeling of the vascular system. Here we evaluated how the progression and tissue remodeling in experimental colitis differ in a germ- free model of mouse colitis. Four treatment groups were used: control, antibiotic-treated (ABX), dextran sulfate colitis (DSS) and DSS pre- and co-treated with antibiotics (DSS + ABX). In days 0 - 3 of the study, germ-free mice received antibiotics (vancomycin, neomycin, and metronidazole). During the next 11 days, antibiotics were continued and DSS (3%) added to “colitis” groups. Disease activity, weight, stool form and blood were monitored daily. Mice were sacrificed and tissue samples harvested. Histopathological scores in controls (0.00) and in ABX (1.0+/–0.81) were significantly (p –0). Extents of injury, inflammation and crypt damage were all improved in DSS + ABX. The Disease Activity Index score (day 11) was significantly worse in the DSS group compared to the DSS + ABX group. Stool blood and form scores were also significantly improved among these groups. Importantly, myeloper- oxidase was significantly reduced in DSS + ABX, indicating that neutrophil infiltration was blocked. Colitis was associated with an increase in blood and lymphatic vessels;both of these events were also significantly reduced by gut sterilization. Our experiment shows that clinical and histopathological severity of colitis was significantly worse in the DSS colitis group compared to the DSS + ABX group, supporting the hypothesis that development of IBD is likely to be less severe with appropriate antibiotic treatment. In particular, gut sterilization effectively reduces leuko- cyte-dependent (PMN) injury to improve outcomes and may be an important target for therapy.展开更多
文摘Inflammatory bowel diseases(IBD) are chronic idiopathic inflammatory conditions characterized by relapsing and remitting episodes of inflammation which can affect several different regions of the gastrointestinal tract, but also shows extra-intestinal manifestations. IBD is most frequently diagnosed during peak female reproductive years, with 25% of women with IBD conceiving after their diagnosis. While IBD therapy has improved dramatically with enhanced surveillance and more abundant and powerful treatment options, IBD disease can have important effects on pregnancy and presents several challenges for maintaining optimal outcomes for mothers with IBD and the developing fetus/neonate. Women with IBD, the medical team treating them(both gastroenterologists and obstetricians/gynecologists) must often make highly complicated choices regarding conception, pregnancy, and post-natal care(particularly breastfeeding) related to their choice of treatment options at different phases of pregnancy as well as post-partum. This current review discusses current concerns and recommendations for pregnancy duringIBD and is intended for gastroenterologists, general practitioners and IBD patients intending to become,(or already) pregnant, and their families. We have addressed patterns of IBD inheritance, effects of IBD on fertility and conception(in both men and women), the effects of IBD disease activity on maintenance of pregnancy and outcomes, risks of diagnostic procedures during pregnancy and potential risks and complications associated with different classes of IBD therapeutics. We also have evaluated the clinical experience using "top-down" care with biologics, which is currently the standard care at our institution. Post-partum care and breastfeeding recommendations are also addressed.
文摘Background: Helicobacter species are best known for their roles in the pathology of gastritis;however, several Helicobacter species also colonize the intestine, and less is known about effects of Helicobacter on the development of intestinal inflammation. To evaluate contributions of Helicobacter in inflammatory bowel disease, we investigated whether and how pre-existing intestinal colonization would affect disease severity and biomarkers of inflammation in experimental IBD. Materials and Methods: Mice were infected with H. muridarum 2 weeks prior to induction of colitis mediated by 3% dextran sulfate (DSS). Disease activity index, stool blood and consistency, colon length, myeloperoxidase, histopathology, blood and lymphatic vessels, and numbers of dilated mucosal crypts were measured in control, DSS-only, H. muridarum-infected, and H. muridarum-infected + DSS mice. Results: Prior to DSS challenge, H. muridarum-infected mice showed little distal gut injury by several indices of colon inflammation with decreased blood vessel density in the submucosa, and lower lymphatic density in the mucosa and submucosa. However, after DSS colitis, H. muridarum-infected mice exhibited significantly greater disease. Weight change, stool bleeding, diarrhea, and angiogenesis were all increased in H. muridarum-infected mice in DSS colitis compared to DSS controls. Conclusions: Our data show that Helicobacter colonization of the intestine, unlike that of the stomach, lowers basal gut inflammatory scores, but increases disease activity and inflammation in an acute colitis model. Intestinal Helicobacter infection may therefore represent a significant sub-clinical factor which predisposes the gut to inflammatory injury.
基金Supported by National Institute of General Medical Sciences of the National Institutes of Health under award,No.P30GM110703the Department of Defense,No.PR100451the German Research Foundation,No.DFG,F.B.BE 5619/1-1
文摘AIM: To investigate whether regional geography influences ethnic and gender trends for the development of gastric cancer(GC).METHODS: This retrospective analysis of the INVISION patient database at Louisiana State University Health Sciences Center-Shreveport(LSUHSC-S), a southern United States regional hospital, was performed from 2005-2011. Using the international statistical classification of diseases 9(ICD-9), inpatient, day surgery outpatient, and emergency outpatient diagnosis codes entered into medical records were used to identify GC patients. For each study year, the patients were evaluated for age, ethnicity, and gender, and each patient was counted only once throughout the study. Subsequent patient encounters were counted as visits and separated by inpatient and clinic visits. Complex or severe disease may require more frequent and intensive clinical management; therefore, we evaluated annual clinic visits as "surrogate markers" of disease severity. Finally, we studied the primary diagnosis for Helicobacter pylori(H. pylori) infection(ICD-9 code 41.86) as an additional factor that might increase the risk of GC.RESULTS: A total of 285 patients were diagnosed with GC at LSUHSC-S between 2005 and 2011. African Americans(181 patients, 89 males and 92 females, 63.5% of total patients) had significantly higher frequencies of GC diagnosis compared with non-Hispanic whites(104 patients, 54 males and 50 females, 36.5% of total patients), at a ratio of 1.74(P = 0.002). Within each ethnic group, men and women were diagnosed at approximately equal annual rates. Our findings differed significantly from United States national trends, which found that African American females and white females had lower risks for GC than their corresponding male counterparts. The United States national trend between 2005 and 2011 showed that African Americans males had a higher incidence of GC, with an annual mean(per 100000) of 16.31 ± 0.76 compared with white males(9 ± 0.1, P < 0.001), African American females(8.7 ± 0.34, P < 0.001) and white females(4.05 ± 0.07, P < 0.001). Among the GC patients, the number of clinic visits was highest among African American males(195.1 ± 28.1), who had significantly more clinic visits than African Americans females(123 ± 13.02, P < 0.05), white males(41.57 ± 4.74, P < 0.001) and white females(35 ± 8.9, P < 0.001). Similar trends were found for inpatient visits, with an annual mean of 11.43 ± 1.5 forAfrican American males, followed by African American females(7.29 ± 1.36), white males(2.57 ± 0.69) and white females(1.57 ± 0.612). African American males had significantly more inpatient visits than white males(P < 0.001), and African American females had more inpatient visits than white females(P < 0.01). African American patients showed the highest frequency of H. pylori positive status, with approximately 72% vs 28% for the white patients. CONCLUSION: Increase in GC diagnoses among women at LSUHSC-S is significantly higher than United States national averages, suggesting local geographic and socioeconomic influences may alter GC disease course.
文摘Inappropriate responses to normal commensal bacteria trigger immune activation in both inflammatory bowel disease and experimental colitis. How gut flora contribute to the pathogenesis of inflammatory bowel disease is unclear, but may involve entrapment of leukocytes and remodeling of the vascular system. Here we evaluated how the progression and tissue remodeling in experimental colitis differ in a germ- free model of mouse colitis. Four treatment groups were used: control, antibiotic-treated (ABX), dextran sulfate colitis (DSS) and DSS pre- and co-treated with antibiotics (DSS + ABX). In days 0 - 3 of the study, germ-free mice received antibiotics (vancomycin, neomycin, and metronidazole). During the next 11 days, antibiotics were continued and DSS (3%) added to “colitis” groups. Disease activity, weight, stool form and blood were monitored daily. Mice were sacrificed and tissue samples harvested. Histopathological scores in controls (0.00) and in ABX (1.0+/–0.81) were significantly (p –0). Extents of injury, inflammation and crypt damage were all improved in DSS + ABX. The Disease Activity Index score (day 11) was significantly worse in the DSS group compared to the DSS + ABX group. Stool blood and form scores were also significantly improved among these groups. Importantly, myeloper- oxidase was significantly reduced in DSS + ABX, indicating that neutrophil infiltration was blocked. Colitis was associated with an increase in blood and lymphatic vessels;both of these events were also significantly reduced by gut sterilization. Our experiment shows that clinical and histopathological severity of colitis was significantly worse in the DSS colitis group compared to the DSS + ABX group, supporting the hypothesis that development of IBD is likely to be less severe with appropriate antibiotic treatment. In particular, gut sterilization effectively reduces leuko- cyte-dependent (PMN) injury to improve outcomes and may be an important target for therapy.
