SUMMARY BackgroundSome of the most important questions relating to the use of biological therapy in inflammatory bowel diseases concern the duration of maintenance therapy.

BackgroundMicroscopic colitis presents with similar symptoms to classic inflammatory bowel diseases. Osteoporosis is a common complication of Crohn's disease but there are no data concerning bone metabolism in microscopic colitis.AimsThe aim of the present study was to evaluate bone density and metabolism in patients with microscopic colitis.MethodsFourteen patients microscopic colitis were included in the study, and 28 healthy persons and 28 age and gender matched Crohn's disease patients were enrolled as controls. Bone mineral density was measured using dual x-ray absorptiometry at the lumbar spine, femoral neck and the radius. Serum bone formation and bone resorption markers (osteocalcin and beta-crosslaps, respectively) were measured using immunoassays.ResultsLow bone mass was measured in 57.14% patients with microscopic colitis. Bone mineral density at the femoral neck in patients suffering from microscopic colitis and Crohn's disease was lower than in healthy controls (0.852 ± 0.165 and 0.807 ± 0.136 vs. 1.056 ± 0.126 g/cm2; p < 0.01). Bone mineral density at the non-dominant radius was decreased in microscopic colitis patients (0.565 ± 0.093 vs. 0.667 ± 0.072 g/cm2; p < 0.05) but unaffected in Crohn's disease patients (0.672 ± 0.056 g/cm2). Mean beta-crosslaps concentration was higher in microscopic colitis and Crohn's disease patients than controls (417.714 ± 250.37 and 466.071 ± 249.96 vs. 264.75 ± 138.65 pg/ml; p < 0.05). A negative correlation between beta-crosslaps concentration and the femoral and radius t-scores was evident in microscopic colitis patients.ConclusionsLow bone mass is frequent in microscopic colitis, and alterations to bone metabolism are similar to those present in Crohn's disease. Therefore, microscopic colitis-associated osteopenia could be a significant problem in such patients.

Monitoring drug levels and antibodies is expected to play an emerging role in the management of LOR (i.e., to confirm adherence, allow for dose adjustment, or provide a rationale for switching to another anti-TNF agent or to a different class of biological agent) in the coming years. The optimal method of detection is however not clear. In clinical practice, meticulous complex assessment of clinical symptoms, confirmation of active disease by endoscopic or radiological imaging, and exclusion of complications remains necessary.

ObjectiveThe efficacy of argon plasma coagulation (APC) on gastric antral vascular ectasia (GAVE) may be impaired over time and depends greatly on the application settings. Endoscopic band ligation (EBL) may be an alternative, but study on its efficacy is limited. This study aimed to evaluate and compare the clinical efficacy of APC and EBL in treating GAVE.MethodsChanges in the need for blood transfusion, number of treatment sessions and hospitalizations were retrospectively assessed in 63 transfusion‐dependent patients with GAVE (mean age: 67.1 y, 54.0% female) treated with either APC or EBL (45 and 18 patients, respectively) in four tertiary endoscopic centers.ResultsBoth methods substantially increased hemoglobin levels and decreased patients' need for a transfusion (22.0 ± 4.0 g/L and −5.62 ± 2.30 units of packed red blood cells [RBC] with APC, and 27.4 ± 6.1 g/L and −4.79 ± 2.46 units of packed RBC with EBL), without a significant statistical difference between the methods. However, fewer EBL sessions were required both for the cessation of need for a transfusion compared with those for the resolution of GAVE lesions (0.90 ± 0.10 vs 1.69 ± 0.31, P = 0.028).ConclusionsBoth APC and EBL are effective in GAVE treatment. EBL may be superior in terms of number of treatment sessions, but not in its influence on hemoglobin level and need for transfusion. Further prospective studies with large, homogeneous sample size and standardized APC settings are needed.

Low bone mineral density is an established, frequent, but often neglected complication in patients with inflammatory bowel disease (IBD). Data regarding the diagnosis, therapy and follow-up of low bone mass in IBD has been partially extrapolated from postmenopausal osteoporosis; however, the pathophysiology of bone loss is altered in young patients with IBD. Fracture, a disabling complication, is the most important clinical outcome of low bone mass. Estimation of fracture risk in IBD is difficult. Numerous risk factors have to be considered, and these factors should be weighed properly to help in the identification of the appropriate patients for screening. In this editorial, the authors aim to highlight the most important clinical aspects of the epidemiology, prevention, diagnosis and treatment of IBD-related bone loss.