OBJECTIVES Repeat colonoscopy in 10 years after a normal screening colonoscopy is recommended in an average-risk patient, and it has been proposed by American Gastroenterological Association (AGA), American College of Gastroenterology (ACG), and American Society for Gastrointestinal Endoscopy (ASGE) as a quality measure. However, there are little quantitative data about adherence to this recommendation or factors that may improve adherence. Our study quantifies adherence to this recommendation and the impact of suboptimal bowel preparation on adherence. METHODS In this retrospective database study, endoscopy reports of average-risk individuals ≥50 years old with a normal screening colonoscopy were reviewed. Quality of colon cleansing was recorded using the Aronchick scale as excellent, good, fair, or poor. Main outcome measurements were quality of bowel preparation and recommendation for timing of repeat colonoscopy. Recommendations were considered consistent with guidelines if 10-year follow-up was documented after excellent, good, or fair prep or if ≤1-year follow-up was recommended after poor prep. RESULTS Among 1,387 eligible patients, recommendations for follow-up colonoscopy inconsistent with guidelines were seen in 332 (23.9%) subjects. By bowel preparation quality, 15.3% of excellent/ good, 75% of fair, and 31.6% of poor bowel preparations were assigned recommendations inconsistent with guidelines (P < 0.001). Patients with fair (odds ratio = 18.0; 95% confidence interval 12.0–28.0) were more likely to have recommendations inconsistent with guidelines compared with patients with excellent/good preps. CONCLUSIONS Recommendations inconsistent with guidelines for 10-year intervals after a normal colonoscopy occurred in >20% of patients. Minimizing “fair” bowel preparations may be a helpful intervention to improve adherence to these recommendations.

Dystrophic calcifications often occur after injury, infection, or onset of certain rheumatic diseases. Treatment has been limited to surgical removal following failure of medical therapy. In an attempt to establish a reproducible animal model for dystrophic calcification that permitted the screening of potential interventions, we evaluated cardiotoxin (injury)-induced calcifications in three murine strains at both the cellular and ultrastructural levels. All osteopontin null mice and tumor necrosis factor receptor null mice on a C57B6 background had calcifications at days 3 and 7 after injury compared to 75% of wild-type C57B6 mice. There was no difference in mineral content among calcifications from the three mouse strains. Osteogenesis was suggested by the expression of osteocalcin, osterix, and alkaline phosphatase in calcified murine muscle tissue. Osteoclast-like cells facilitated the removal of transient dystrophic deposits (<28 days) in all models. However, none of the models showed an association of mineral crystals with collagen, suggesting that the deposits were not bone-like. The dystrophic mechanism was validated as cell death, and mitochondrial calcifications occurred soon after skeletal muscle injury in the three murine strains.

Objective. To determine the presence of small integrin-binding ligand N-linked glycoprotein (SIBLING) and bone components in juvenile dermatomyositis (DM) pathologic calcifications. Methods. Calcifications were removed from 4 girls with juvenile DM symptoms for mean ؎ SD 36.9 ؎ 48.3 months and were stained for SIBLING proteins: full-length osteopontin (OPN), bone sialoprotein (BSP), dentin matrix protein 1 (DMP1), dentin phosphoprotein (DPP), and matrix extracellular phosphoglycoprotein (MEPE); bone markers: osteocalcin (OC), core-binding factor ␣ 1 (CBF␣1), and alkaline phosphatase (AP) for osteoblasts; tartrate-resistant acid phosphatase (TRAP) for osteoclasts; and the mineral regulators osteonectin (ON) and matrix Gla protein (MGP). The deposit center, periphery, adjacent connective tissue, and vascular endothelial cells were examined. Results. Alizarin red stained calcified deposits that did not localize with collagen, like bone, under polarized light. Hematoxylin and eosin stain revealed a paucity of connective tissue and absence of bone-like structures. The deposits, connective tissue, and vascular endothelial cells were positive for BSP, DPP, DMP1, and AP; MEPE was not detected. OC, ON, and MGP were present in the deposits and vascular endothelial cells; OPN and CBF␣1 were present in deposits and connective tissue. TRAP-positive osteoclasts were localized to the calcification periphery. Conclusion. The disorganized juvenile DM calcifications differ in structure, composition, and protein content from bone, suggesting that they may not form through an osteogenic pathway. Osteoclasts at the deposit surface represent an attempt to initiate its resolution.

Diabetes, narcotics use and TCA use were identified as predictors of poor preparation in screening colonoscopies while Miralax-Gatorade preps were associated with better bowel preparation.

No abstract