Modified Colson flap with subcutaneous liposuction for one-stage donor site removal: A case series.

OBJECTIVES: The aim of this study was to evaluate the functional and cosmetic results of an innovative procedure for modified Colson flap-graft consisting of immediate defatting of the flap by a liposuction cannula. METHODS: A cross-sectional study was performed among patients with deep hand burns requiring a modified Colson flap between 2018 and 2021. Outcomes included functional and cosmetic assessment of the hand through a quality-of-life questionnaire, a sensitivity scale and a scar assessment scale. RESULTS: During this period, 7 patients were operated on using our technique. One patient was lost to follow-up; 7 patients with a median age of 44 years were included, with a total of 10 burned hands. The burns were thermal in 5 out of 7 cases and the coverage concerned the whole hand in 50% of the cases. The flaps all received cannula defatting. The median time to flap weaning was 23 days (20 to 30 days). The median follow-up was 16 months. One case required remote flap weaning. The median POSAS (Patient and Observer Scar Assessment Scale) per patient was 4 and 2 per observer. The median BMRCSS (British Medical Research Council Sensory Scale) was 122. One case had recovered S2 sensitivity, the other cases had S3 or S4 sensitivity. CONCLUSION: Immediate defatting is one of the factors in tegumental quality allowing rapid functional recovery of the hand. The cannula defatting technique does not appear to require additional defatting time. The use of the liposuction cannula allows a one-step, homogeneous, and easier defatting, with a lower risk of devascularization.

Transepithelial leak in Barrett's esophagus patients: the role of proton pump inhibitors.

AIM: To determine if the observed paracellular sucrose leak in Barrett's esophagus patients is due to their proton pump inhibitor (PPI) use. METHODS: The in vivo sucrose permeability test was administered to healthy controls, to Barrett's patients and to non-Barrett's patients on continuous PPI therapy. Degree of leak was tested for correlation with presence of Barrett's, use of PPIs, and length of Barrett's segment and duration of PPI use. RESULTS: Barrett's patients manifested a near 3-fold greater, upper gastrointestinal sucrose leak than healthy controls. A decrease of sucrose leak was observed in Barrett's patients who ceased PPI use for 7 d. Although initial introduction of PPI use (in a PPI-naïve population) results in dramatic increase in sucrose leak, long-term, continuous PPI use manifested a slow spontaneous decline in leak. The sucrose leak observed in Barrett's patients showed no correlation to the amount of Barrett's tissue present in the esophagus. CONCLUSION: Although future research is needed to determine the degree of paracellular leak in actual Barrett's mucosa, the relatively high degree of leak observed with in vivo sucrose permeability measurement of Barrett's patients reflects their PPI use and not their Barrett's tissue per se.

Epithelial tight junctional changes in colorectal cancer tissues.

Colorectal cancer (CRC) is one of the most common cancers in the western world. Early screening and detection could be highly preventative and therefore reduce mortality. Tight junctions (TJ) are well known for their function in controlling paracellular traffic of ions and molecules. It has become increasingly evident that TJs play a crucial role in maintaining cell-cell integrity, and the loss of cell junctional sealing could involve itself in the processes of carcinoma and cancer metastasis. If correlations between altered TJ proteins and CRC presence or invasiveness could be established, they may serve as important markers and guidelines for prophylactic and prognostic purposes, along with other screening methods. This review will present recent data from clinical and animal studies showing how altered TJ protein expression is a feature of certain CRCs. The up-regulation of claudin-1 in many CRCs is especially noteworthy. The focus of this article is simply on the association - however imperfect - between CRC and the major TJ transmembrane barrier proteins, namely claudins and occludin. Any causal relationship between TJ protein change and neoplasia remains conclusively unproven at present.

Tumor necrosis factor blockade for treatment of inflammatory bowel disease: efficacy and safety.

Inflammatory bowel disease (IBD), including Crohn's Disease (CD) and Ulcerative Colitis (UC), is characterized by inflammation of the gastrointestinal tract. In UC, inflammation is confined to the mucosa, initially involving the rectum, and may extend proximally to involve the entire colon. In CD, transmural inflammation may affect any portion of the GI tract. The etiology of these disease processes has remained unclear. Therapies are aimed at reducing inflammation and thereby improving symptomatology and morbidity. Traditional medical therapies have included corticosteroids, aminosalicylates, and immunomodulators. Within the past decade, another class of medications has been utilized targeting Tumor Necrosis Factor (TNF), a key, early signaling molecule in the inflammatory cascade. Increased levels of TNF have been found in the blood, epithelial tissue, and stool of patients with active IBD. Anti-TNF medications can not only have direct effects on immune system components, but they also can ameliorate apoptotic cell death and tight junction compromise in the gastrointestinal epithelium. Several randomized, placebo controlled studies have demonstrated the efficacy of these medications in achieving induction and maintaining remission of disease. Their safety profile, however, remains a concern. There has been a reported association of biologic therapy and increased opportunistic infections. A link between biologic therapy and the development of certain malignancies has also been described. Despite these associations, TNF blockade remains an important therapeutic development in the modern therapy of IBD. The role of barrier breakdown at the tight junction level in IBD, and of TNF induction of barrier disruption, is also discussed.