B-cell lymphoma presenting as acute pancreatitis.

BACKGROUND: Pancreatic lymphoma is uncommon, representing less than 0.5% of pancreatic tumors, with diffuse large B-cell lymphoma being the predominant histotype. Acute pancreatitis associated with pancreatic lymphoma is rare. CASE REPORT: We describe a case of synchronous pancreatic and pulmonary localizations of non-Hodgkin's lymphoma in a 42-year-old man who presented with acute pancreatitis. Acute pancreatitis resolved after standard treatment with a fasting regimen, gabexate mesilate and parenteral nutrition. However, ultrasound scan and abdominal computed tomography revealed two hypoechogenic areas within the pancreas, and chest X-ray film showed a pulmonary infiltrate in the right basal field. A percutaneous fine-needle aspiration biopsy of the pulmonary infiltrate under computed tomography guidance demonstrated a diffuse infiltration by atypical lymphoid cells positive for leukocyte common antigen, CD20 and CD30. Percutaneous fine-needle aspiration biopsy under ultrasound guidance of the pancreatic mass confirmed the diagnosis of diffuse large B-cell lymphoma. The patient was classified as stage IV-A, low-intermediate risk and received 6 cycles of chemotherapy. CONCLUSION: This is the first case of large B-cell lymphoma presenting with concomitant primary pancreatic and pulmonary involvement. Pancreatic lymphoma is uncommon and represents a rare cause of acute pancreatitis. The discovery of a pancreatic mass needs pathologic diagnosis to distinguish lymphoma from carcinoma or autoimmune pancreatitis. and IAP.

Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction.

BACKGROUND: It has been previously shown that hyperglycemia enhances free radical production, inducing oxidative damage, which in its turn activates the death pathways implicated in cell apoptosis and necrosis. But the possible involvement of this pathway in the hyperglycemia-induced apoptosis of endothelial cells has not yet been reported. METHODS: To verify a possible connection between mitochondrial ROS production and apoptosis induced by both stable and oscillating high glucose, SOD, MnTBAP and TTFA was added to HUVEC cell culture medium. We measured nitrotyrosine and 8OHdG as oxidative stress parameters and Bcl-2 expression and Caspase-3 expression and activity as apoptosis indicators. RESULTS: Our results show that hyperglycemia, both stable or oscillating, increases oxidative stress and endothelial cell apoptosis through ROS overproduction at the mitochondrial transport chain level. CONCLUSION: The prevention of mitochondrial oxidative damage seems to be a future important therapeutic strategy in diabetes.

Intermittent high glucose enhances ICAM-1, VCAM-1 and E-selectin expression in human umbilical vein endothelial cells in culture: the distinct role of protein kinase C and mitochondrial superoxide production.

In this study the effects of stable and intermittent high glucose concentrations on ICAM-1, VCAM-1 and E-selectin production, PKC activity and PKCbetaI, betaII and delta isoforms expression in cultured HUVEC have been examined. In stable high glucose ICAM-1, VCAM-1 and E-selectin concentration and mRNA expression increased, and this effect was even more evident in intermittent high glucose. PKC activity increased in fluctuating glucose compared to stable high glucose, due to an over-expression of betaI, betaII and delta isoforms. ICAM-1, VCAM-1 and E-selectin, after the adding of total PKC inhibitor bisindolylmaleimide-I (BIMI-I) and LY379196, a specific inhibitor of PKCbeta, were equally reduced. 8-Hydroxydeoxyguanosine (8-OHdG), a sensitive indicator of oxidative damage to DNA, increased in stable and even more in intermittent high glucose and was reduced by both BIMI-I and LY379196. However, when thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial complex II and the SOD mimetic Mn(III)tetrakis(4-benzoic acid) porphyrin chloride (MnTBAP) were added, all adhesion molecules, any PKC isoforms expression and 8-hydroxydeoxyguanosine were normalized in both constant and oscillating glucose. In conclusion intermittent high glucose induces a greater expression of the adhesion molecules than stable high glucose; this effect seems to be related to an activation of PKCbeta, but completely dependent from mitochondrial free radicals over-production.