Disease knowledge after an educational program in patients with GERD – a randomized controlled trial

<p>Abstract</p> <p>Background</p> <p>Patient education has proved beneficial in several but not all chronic disease. Inconsistent findings may rely on varying educational effects of various programs and differential effects on subgroups of patients. Patients' increase in disease knowledge may serve as a feedback to the educator on how well the education program works – but may not be associated to relevant clinical outcomes like quality of life (QoL). This study aimed to investigate the effects of a group based education program for patients with gastroesophageal reflux disease (GERD) on disease knowledge and the association between knowledge and QoL.</p> <p>Methods</p> <p>Patients with GERD were randomly allocated to education (102 patients) or control (109 patients). The education program was designed as a structured dialogue conveying information about pathophysiology, pharmacological and non-pharmacological treatment of GERD, patients' rights and use of healthcare. Outcomes were a 24 item knowledge test on GERD (score 0 – 24) 2 and 12 months after the educational program and disease specific and general QoL (Digestive symptoms and disease impact, DSIQ, and General Health Questionnaire, GHQ).</p> <p>Results</p> <p>Patients allocated to education achieved higher knowledge test scores than controls at 2 months (17.0 vs. 13.1, p < 0.001) and at 12 months (17.1 vs. 14.0, p < 0.001) follow-up. Knowledge test score was positively associated with having completed advanced school and inversely related to psychiatric illness and poor QoL as perceived by the patients at the time of inclusion. Overall, changes in knowledge test score were not associated with change in QoL.</p> <p>Conclusion</p> <p>A group based education program for patients with GERD designed as a structured dialogue increased patients' disease knowledge, which was retained after 1 year. Changes in GERD-knowledge were not associated with change in QoL.</p> <p>Trial registration</p> <p>ClinicalTrials.gov: NCT0061850</p

Lack of correlation between the vitamin D receptor Fokl start codon polymorphism and bone mineral density in patients with Crohn's disease

INTRODUCTION: We have examined the association of bone mineral density of patients with inflammatory bowel disease with a polymorphism in the gene encoding the vitamin D receptor. The thymine/cytosine (T/C) polymorphism in the first of two start codons can be defined by a restriction fragment length polymorphism using the restriction endonuclease FokI. Vitamin D receptor alleles containing the polymorphism have been denoted by f and alleles lacking the site by F. METHODS: We report on an association analysis of a basic population of 244 caucasian patients with Crohn's disease. We have genotyped the FokI polymorphism of the VDR in these patients and associated the genotype with the bone mineral density of the lumbar spine and the femoral neck. RESULTS: In the cohort 42% of the patients were scored FF homozygous, 43.7% Ff heterozygous, and 14.3% ff homozygous. 14.4% of the FF patients, 18.8% of the Ff patients, and 9.7% of the ff patients had osteoporosis of the lumbar spine and 21.25% of the FF patients, 25.3% of the Ff patients, and 18.5% of the ff patients had osteoporosis of the femoral neck. In this cohort no association between the genotype and the bone mineral density in the group as a whole nor when separated according to sex or age was found. CONCLUSIONS: In summary in our cohort no association of the FokI polymorphism and the BMD of the lumbar spine and femoral neck in patients with inflammatory bowel disease was found

Integrated cancer tissue engineering models for precision medicine.

Tumors are not merely cancerous cells that undergo mindless proliferation. Rather, they are highly organized and interconnected organ systems. Tumor cells reside in complex microenvironments in which they are subjected to a variety of physical and chemical stimuli that influence cell behavior and ultimately the progression and maintenance of the tumor. As cancer bioengineers, it is our responsibility to create physiologic models that enable accurate understanding of the multi-dimensional structure, organization, and complex relationships in diverse tumor microenvironments. Such models can greatly expedite clinical discovery and translation by closely replicating the physiological conditions while maintaining high tunability and control of extrinsic factors. In this review, we discuss the current models that target key aspects of the tumor microenvironment and their role in cancer progression. In order to address sources of experimental variation and model limitations, we also make recommendations for methods to improve overall physiologic reproducibility, experimental repeatability, and rigor within the field. Improvements can be made through an enhanced emphasis on mathematical modeling, standardized in vitro model characterization, transparent reporting of methodologies, and designing experiments with physiological metrics. Taken together these considerations will enhance the relevance of in vitro tumor models, biological understanding, and accelerate treatment exploration ultimately leading to improved clinical outcomes. Moreover, the development of robust, user-friendly models that integrate important stimuli will allow for the in-depth study of tumors as they undergo progression from non-transformed primary cells to metastatic disease and facilitate translation to a wide variety of biological and clinical studies