Evaluating the practice of canceling colonoscopies for presumed inadequate bowel preparation.

BACKGROUND AND AIMS: Only scant data describe the practice of canceling colonoscopies before colonoscope insertion for presumed inadequate bowel preparation (PIBP). We sought to better understand the ramifications of such cancellations and to characterize the nationwide practice of cancellations for PIBP. METHODS: We determined the frequency of colonoscopies canceled for PIBP at our institution, assessing practice variation and whether patients who were canceled for PIBP completed colonoscopy or fecal immunohistochemical testing within 6 months. We also surveyed gastroenterology program directors to determine whether canceling colonoscopies for PIBP is commonly permitted and if such cancellations are included in calculations of bowel preparation adequacy rates. RESULTS: Three percent of patients were canceled because of PIBP at our institution, with significant provider practice variability in cancellation rates. Only 67% of patients whose cases were canceled for PIBP completed colonoscopy or fecal immunohistochemical testing within 6 months. The ability of an endoscopist to cancel a colonoscopy for PIBP was reported by 97% of survey respondents. Such cases are frequently not included in calculations of bowel preparation adequacy rates. CONCLUSIONS: The ability to cancel colonoscopies because of PIBP is near ubiquitous, but such cases are not uniformly included in calculations of bowel preparation adequacy rates. Variation in provider practice, and resulting impact on patient care, suggests a need for standardized protocols. Colonoscopies canceled for PIBP should be included in calculations of bowel preparation adequacy rates.

Neuronal CTGF/CCN2 negatively regulates myelination in a mouse model of tuberous sclerosis complex.

Disruption of myelination during development has been implicated in a range of neurodevelopmental disorders including tuberous sclerosis complex (TSC). TSC patients with autism display impairments in white matter integrity. Similarly, mice lacking neuronal Tsc1 have a hypomyelination phenotype. However, the mechanisms that underlie these phenotypes remain unknown. In this study, we demonstrate that neuronal TSC1/2 orchestrates a program of oligodendrocyte maturation through the regulated secretion of connective tissue growth factor (CTGF). We characterize oligodendrocyte maturation both in vitro and in vivo. We find that neuron-specific Tsc1 deletion results in an increase in CTGF secretion that non-cell autonomously stunts oligodendrocyte development and decreases the total number of oligodendrocytes. Genetic deletion of CTGF from neurons, in turn, mitigates the TSC-dependent hypomyelination phenotype. These results show that the mechanistic target of rapamycin (mTOR) pathway in neurons regulates CTGF production and secretion, revealing a paracrine mechanism by which neuronal signaling regulates oligodendrocyte maturation and myelination in TSC. This study highlights the role of mTOR-dependent signaling between neuronal and nonneuronal cells in the regulation of myelin and identifies an additional therapeutic avenue for this disease.