Self-reported cognitive impairments and quality of life in patients with gastrointestinal stromal tumor: Results of a multinational survey.

BACKGROUND: Cancer-related cognitive impairment (CRCI) has long-term effects on survivor quality of life, but CRCI research on patients with gastrointestinal stromal tumor (GIST) is lacking. The aims of this study were to investigate CRCI and concomitant quality of life among patients with GIST. METHODS: An online survey was used to assess CRCI in adult patients with GIST using the validated Functional Assessment of Cancer Therapy-Cognitive-v.3. Age, education, demographically indexed IQ, general health, and quality of life factors (e.g., fatigue, emotional distress) were also assessed. The online survey was administered through five international GIST and sarcoma support organizations. RESULTS: Over the 3-month recruitment period, the survey was completed by 485 participants: mean age, 57.80 (SD, 11.51), median 5 years after diagnosis. A majority (63.91%) reported experiencing cognitive symptoms with a significant negative quality of life impact. Controlling for age, patients with GIST ≥5 years after diagnosis reported worse cognitive function than those <5 years after diagnosis (p < .05) but did not differ in educational level or IQ. Whereas longer term survivors were more likely to have been treated with tyrosine kinase inhibitor (TKI) therapies, there was no observed association of TKI therapy with self-reported cognitive impairments. CONCLUSIONS: A majority of GIST patients report cognitive symptoms that have a negative impact on quality of life, with longer term survivors (≥5 years) tending to report more cognitive impairments. Given the success of TKI therapy to substantially increase overall survival of patients with GIST, addressing CRCI in clinical practice may improve long-term GIST survivor function and quality of life.

Glucagon-like peptide 2 enhances intestinal epithelial restitution.

BACKGROUND: Glucagon-like peptide 2 (GLP-2) is a potent intestinotrophic peptide that enhances recovery following intestinal injury. We tested the hypothesis that GLP-2 acutely enhances intestinal epithelial restitution. MATERIAL AND METHODS: Rat jejunal segments were mounted in Ussing chambers. HCl (10 mM) was applied to the mucosal surfaces for 10 min to induce injury. Tissues were then lavaged with modified Ringer's solution and maintained in the chambers for an additional 3 h. Tissues were treated with 10 microM GLP-2 or vehicle alone (control). Electrical parameters were recorded, and tissues were salvaged for morphometric analysis. RESULTS: GLP-2-treated tissues exhibited a significantly greater recovery of potential difference and resistance (P < 0.05) than did controls. Morphometric analysis revealed that columnar cells covered a greater percentage of the epithelial surface in GLP-2-treated tissues than in controls (P < 0.05). CONCLUSIONS: These results suggest that GLP-2 acutely enhances intestinal epithelial restitution following acid-induced injury. This novel biological action of GLP-2 may contribute to its therapeutic effect in models of intestinal disease.