Pancreaticoduodenectomy After Bariatric Surgery: Challenges and Available Techniques for Reconstruction

Introduction

Obesity is an epidemic in the USA, with approximately 7 % of the population considered morbidly obese (BMI?>?40 or >35 with significant comorbidities).

Discussion

Weight loss surgery is recognized as a durable solution to both obesity and obesity-associated morbidities. With an increasing number of pancreatic lesions being discovered on cross-sectional imaging, the pancreatic surgeon is increasingly likely to encounter patients with prior bariatric surgery who are in need of pancreaticoduodenectomy. As such, surgeons need to be familiar with the various bariatric operations, as well as the manner in which to handle prior bariatric reconstructions at the time of pancreatic surgery. Literature on this topic, however, is scarce with only a handful of small case series.

Conclusion

We herein review the different operations performed for weight loss, as well as provide an overview of the available operative approaches for reconstruction after pancreaticoduodenectomy in postbariatric surgical patients.     

Donor lymphocyte infusions mediate superior graft-versus-leukemia effects in mixed compared to fully allogeneic chimeras: a critical role for host antigen-presenting cells

In mice, donor leukocyte infusion (DLI) given to established mixed allogeneic chimeras can mediate powerful graft-versus-host (GVH) reactions confined to the lymphohematopoietic system without inducing graft-versus-host disease (GVHD). In a clinical trial attempting to capture this approach to achieve graft-versus-leukemia/lymphoma (GVL) effects without GVHD, we have observed surprisingly powerful antitumor effects of DLI in patients achieving mixed chimerism after nonmyeloablative bone marrow transplantation. This observation led us to hypothesize that host antigen-presenting cells in mixed chimeras might be required to optimally present recipient antigens to the donor lymphocytes, leading to maximal graft-versus-tumor effects. To test this hypothesis, we established mixed and fully allogeneic hematopoietic chimeras in B6 mice and evaluated the effect of DLI on EL4 T-cell lymphoma. DLI administration to mixed chimeras produced dramatically improved leukemia-free survival compared to administration of DLI to full donor chimeras. DLI also converted mixed chimeras to full chimeras without causing GVHD. The magnitude of the GVL effect was dependent on the level of major histocompatibility complex class I expression on recipient hematopoietic cells in mixed chimeras. Thus, the induction of mixed chimerism followed by delayed DLI provides an approach to inhibiting GVHD that optimizes GVL effects.     

Primary structural studies of an H-2L molecule confirm that it is a unique gene product with homology to H-2K and H-2D antigens.

Radiochemical methodology has been used in the isolation and preliminary biochemical characterization of the murine H-2Ld major histocompatibility complex gene product. The radiolabeled molecule was isolated by immunoprecipitation from the glycoprotein fraction of detergent-solubilized H-2d tumor cells. Six major CNBr fragments were isolated from a papain fragment of this molecule; three of the fragments are connected by disulfide bonds. Due to the high degree of homology between major transplantation antigens, it was possible to align the fragments by comparison of their amino acid sequences to that of the H-2Kb gene product. Of the positions available for comparison between H-2Ld and H-2Kb, H-2Dd, and H-2Kd gene products, 61 out of 80 (78%), 45 out of 55 (82%), and 12 out of 15 (80%), respectively, are identical. Differences between the Ld and Kb and Dd molecules are distributed throughout the amino acid sequence. These data indicate that the H-2Ld gene product is a molecular species distinct from, but homologous to, the H-2K and H-2D gene products.     

Receptor Mobility and the Mechanism of Cell-Cell Binding Induced by Concanavalin A

The cell-cell binding induced by concanavalin A between single cells has been analyzed by use of cells attached to nylon fibers. Binding of a concanavalin A-coated cell to an untreated cell was found to a high degree between two lymphoma tumor cells, less frequently between a lymphoma cell and a normal lymphocyte, and only rarely between two normal lymphocytes. The binding was inhibited by the presence of a saccharide inhibitor of concanavalin A, but could not be reversed by addition of the inhibitor after the cells had bound to each other. Although no binding was obtained when both cells were coated with lectin or fixed with glutaraldehyde, fixation of a cell before coating with concanavalin A enhanced its ability to bind an untreated cell. The results indicate that cell-cell binding induced by concanavalin A requires short-range lateral movement of cell receptors for the lectin, that only one cell has to have mobile receptors, and that some receptors must be unoccupied by lectin molecules before cell-cell contact. Clustering of the receptors is not necessary and seems to hinder cell-cell binding. It is suggested that the short-range movement is required for alignment of individual receptors so as to form multi-point bridges between two cells by lectin molecules. The bridging is then followed by the formation of irreversible bonds between the cells. The receptors on tumor cells appear to have a greater ability than receptors on normal cells to align themselves for cell-cell binding.