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Metabolic bone disease in patients diagnosed with inflammatory bowel disease from Spain.

ABSTRACT: Background:The objective of this study was to analyse the prevalence of metabolic bone disease (MBD) in a cohort of Southern European patients with inflammatory bowel disease (IBD) and to identify associated risk factors in this population. Methods:We conducted a retrospective, both cross-sectional and longitudinal study of MBD, assessed by dual energy X-ray absorptiometry (DXA), among patients diagnosed with IBD and previously recognized risk factors for this complication from two referral Spanish institutions. Results:A total of 612 patients (58.6% diagnosed with Crohn's disease) were included. Mean (SD) age was 44.9 (14.7) years; 71.7% of patients received at least one tapered dosage of corticosteroids before first DXA. MBD and osteoporosis were diagnosed in 66.4% and 21.4% of patients, respectively. At baseline, male gender, menopause and ulcerative colitis were found as independent risks factors for osteoporosis, whereas age, more than three IBD-related hospitalizations and previous steroid treatment were found as independent risks factors for MBD. A total of 261 patients had at least a second DXA and were included in the longitudinal study; median follow up was 56.4?months. Logistic regression model identified menopause, ulcerative colitis and baseline lumbar DXA T-score value, but not steroid treatment, as risk factors for worsening ?1 SD in follow-up DXA T-score. According to guidelines, all patients under treatment with corticosteroids received calcium and vitamin D supplements. Conclusion:MBD is a frequent complication in south-European IBD patients. Routine evaluation of bone density when risk factors are present, as well as calcium plus D vitamin prophylaxis in patients under corticosteroid treatment should be recommended.

SUBMITTER: Miranda-Bautista J

PROVIDER: S-EPMC6669853 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Metabolic bone disease in patients diagnosed with inflammatory bowel disease from Spain.

Miranda-Bautista José J Verdejo Cristina C Díaz-Redondo Alicia A Bretón Irene I Bellón José M JM Pérez-Valderas María Dolores MD Caballero-Marcos Aránzazu A de Dios-Lascuevas Marta M González-Río Elena E García-Sánchez Cristina C Marín-Jiménez Ignacio I Bañares Rafael R Menchén Luis L

Therapeutic advances in gastroenterology 20190731

<h4>Background</h4>The objective of this study was to analyse the prevalence of metabolic bone disease (MBD) in a cohort of Southern European patients with inflammatory bowel disease (IBD) and to identify associated risk factors in this population.<h4>Methods</h4>We conducted a retrospective, both cross-sectional and longitudinal study of MBD, assessed by dual energy X-ray absorptiometry (DXA), among patients diagnosed with IBD and previously recognized risk factors for this complication from tw ...[more]

PMID: 31391867

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Project description:ObjectivesTreatment targets in inflammatory bowel disease (IBD) move away from controlling symptoms towards complete recovery of the intestinal mucosa. Currently, the most frequently used noninvasive surrogate marker of mucosal healing is a faecal calprotectin concentration in the target range. This study tested if there was a relation between time-to-reach target calprotectin and first flare.MethodsWe prospectively included new-onset IBD patients ages 17 and younger in a cloud-based registry (FastForwardCare) and followed them for at least 52 weeks. They were treated according to Dutch national guidelines that advocate a step-up approach. Time-to-reach target was defined as the first calprotectin measurement below 250 μg/g after the start of induction therapy. Time-to-first flare was the time from the first calprotectin measurement below 250 μg/g until reappearance of symptoms with calprotectin values above 250 μg/g.ResultsWe included 76 patients (luminal Crohn disease [CD] 43); ulcerative colitis [UC] 33). Median age at diagnosis was, respectively 14.5 and 14.1 years. Median time-to-reach target calprotectin was 37 weeks in CD and 11 weeks in UC patients (Log-rank test, P = 0.001). Once the calprotectin target was reached, time-to-first flare was significantly longer in CD than in UC patients (Log-rank test, P = 0.001). CD patients with time-to-reach target calprotectin ≤12 weeks after conventional induction therapy (ie, exclusive enteral nutrition or steroids) had a more favorable disease course in the first year than those with time-to-reach target calprotectin >12 weeks (Log-rank test, P = 0.057). In UC patients, time-to-reach target calprotectin ≤12 weeks is not associated with a favorable disease course in the first year.ConclusionsThe findings of this prospective registry suggest that a quick response to conventional therapy predicts a favorable disease course in new-onset paediatric CD, but not in UC. The concept "time-to-reach target calprotectin level" rationalizes the indefinite term "response to treatment" and is well suited for studying treatment effectiveness in real-world practices.

Project description:OBJECTIVE:Primary Sclerosing Cholangitis (PSC) is a chronic cholestatic liver disease that is characterized by severe peri-biliary tract inflammation and fibrosis, elevated oxidative stress and hepatocellular injury. A hallmark of PSC patients is the concurrent diagnosis of Inflammatory Bowel Disease occurring in approximately 70%-80% of PSC patients (PSC/IBD). The objective of this study was to determine the impact of end stage PSC/IBD on cellular antioxidant responses and the formation of protein carbonylation. METHODS:Using hepatic tissue and whole cell extracts isolated from age-matched healthy humans and patients diagnosed with end stage PSC/IBD, overall inflammation, oxidative stress, and protein carbonylation were assessed by Western blotting, and immunohistochemistry. RESULTS:Increased immunohistochemical staining for CD3+ (lymphocyte), CD68 (Kupffer cell) and myeloperoxidase (neutrophil) colocalized with the extensive Picrosirius red stained fibrosis confirming the inflammatory aspect of PSC. Importantly, the increased inflammation also colocalized with elevated periportal post-translational modification by the reactive aldehydes 4-HNE, MDA and acrolein. 4-HNE, MDA and acrolein IHC all displayed a significant component in hepatocytes adjacent to fibrotic regions. Furthermore, acrolein was also elevated within the nuclei of periportal inflammatory cells whereas MDA staining was increased in hepatocytes across the lobule. Prussian Blue staining, when compared to the positive controls (ALD, NASH), did not display any evidence of iron accumulation in PSC/IBD livers. Western analysis of PSC/IBD anti-oxidant responses revealed elevated expression of SOD2, GST? as well as upregulation of Akt Ser473 phosphorylation. In contrast, expression of GST?, GSTA4, catalase, Gpx1 and Hsp70 were suppressed. These data were further supported by a significant decrease in measured GST activity. Dysregulation of anti-oxidant responses in the periportal region of the liver was supported by elevated SOD2 and GST? IHC signals in periportal hepatocytes and cholangiocytes. Expression of the Nrf2-regulated proteins HO-1, NAD(P)H quinone reductase (NQO1) and Gpx1 was primarily localized to macrophages. In contrast, catalase staining decreased within periportal hepatocytes and was not evident within cholangiocytes. CONCLUSIONS:Results herein provide additional evidence that cholestasis induces significant increases in periportal oxidative stress and suggest that there are significant differences in the cellular and subcellular generation of reactive aldehydes formed during cholestatic liver injury. Furthermore, these data suggest that anti-oxidant responses are dysregulated during end-stage PSC/IBD supporting pathological data. This work was funded by NIH5R37AA009300-22 D.R.P.

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Metabolic bone disease in patients diagnosed with inflammatory bowel disease from Spain.

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Metabolic bone disease in patients diagnosed with inflammatory bowel disease from Spain.

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