Lipomatous Pseudohypertrophy of the Pancreas Taking the Form of Huge Massive Lesion of the Pancreatic Head

A 70-year-old woman presented with hypogastric pain. Computed tomography and magnetic resonance imaging revealed a retroperitoneal tumor 18.0 cm in diameter with fatty tissue density, ventrally compressing the pancreatic head. We suspected a well-differentiated liposarcoma compressing the pancreas. At laparotomy, the tumor mass was the size of an infant's head; its center was located in the area corresponding to the pancreatic uncus. It was continuous with the pancreatic parenchyma through a poorly demarcated border, and we resected as much of the tumor mass as possible while conserving the pancreatic capsule. Histopathological examination indicated lipomatous pseudohypertrophy of the pancreas with proliferation of mature fatty tissue as the main constituent. At the periphery, islands of acinar tissue were retained among the fatty infiltration, which also contained branches of the pancreatic duct and islets of Langerhans. Previous reports have stated that this disorder only causes fatty replacements throughout the pancreas or in the pancreatic body and tail; however, in this patient, imaging and macroscopic examination revealed no fatty replacements in the pancreatic body and tail. We report this case, which we consider extremely rare, along with a brief review of the literature

Tofu and fish oil independently modulate serum lipid profiles in rats: Analyses of 10 class lipoprotein profiles and the global hepatic transcriptome.

Soy protein and fish oil are food components that decrease the risk of cardiovascular disease. Previous studies demonstrated that these food components reduced serum cholesterol levels and suppressed hepatic lipogenesis. However, the underlying mechanisms of action of these food components remain unclear. Ten classes of serum lipoprotein profiles showed that dietary tofu, a soybean curd, suppressed cholesterol absorption, while fish oil reduced most of the lipoprotein classes in rats. Tofu and fish oil both halved the level of the lipoprotein class LAC1 (LDL-anti-protease complex), a 15-nm LDL-anti-protease complex, which is speculated to be a cause of atherosclerosis. Moreover, a global transcriptome analysis revealed that tofu inhibited the mRNA expression of genes involved in hepatic lipogenesis, while fish oil stimulated that of genes related to fatty acid degradation. Therefore, tofu and fish oil independently regulate lipid metabolism. The decrease observed in LAC1 may have been due to reduced cholesterol absorption in the tofu diet group and the interference of lipogenesis via the activation of polyunsaturated fatty acid detoxification in the fish oil group

Serum Granulocytic Elastase and Superoxide Dismutase Activity after Administration of Protease-Inhibitor to Postoperative Patients

Postroperative changes in the plasma levels of granulocytic elastase and superoxide dismutase were examined clinically. Seven patients who had undergone cholecystectomy and eight patients who had undergone subtotal esophageal resection were considered. The protease inhibitor ulinastatin was administered to four of the latter patients. The levels of granulocytic elastase were elevated, and those of superoxide dismutase, decreased, in the non-medicated patients who had undergone esophageal resection (p<0.05). Furthermore, in the patients given the daily medication of 3×105 units of urinastatin for more than 3 days postoperatively, the elevation of granulocytic elastase levels and the decline of the superoxide dismutase levels were markedly suppressed (p<0.05). On the other hand, granulocytic elastase levels of the plasma to which ulinastatin had been added in vitro did not decrease. It is considered that the medicament of ulinastatin may be useful in the prevention of tissue injury caused by granulocytic elastase in cases where a disproportion of proteases and endogenous protease inhibitors exists

Evaluation of hepatic integrin αvβ3 expression in non-alcoholic steatohepatitis (NASH) model mouse by 18F-FPP-RGD2 PET

Abstract Background Activated hepatic stellate cells (HSCs), which express integrin αvβ3, are a major fibrogenic factor in NASH pathophysiology. 18F-labeled cyclic arginine-glycine-aspartic acid penta-peptide (18F-FPP-RGD2) has been used as a PET probe for tumors expressing integrin αvβ3. The aim of this study was to assess the potential of PET with 18F-FPP-RGD2 to detect hepatic integrin αvβ3 expression in non-alcoholic steatohepatitis (NASH) model mice. Results Thirty-two male C57BL/6 mice aged 6 weeks were fed a choline-deficient, l-amino acid-defined, high-fat diet (CDAHFD) for 3 and 8 weeks. 18F-FPP-RGD2 PET imaging of the liver was performed at 3 and 8 weeks after CDAHFD feeding. After PET scanning, levels of hepatic integrin αvβ, 3α-smooth muscle actin (α-SMA), and collagen type 1 alpha 1(col1a1) were measured. Histopathological analysis of hepatic steatosis, inflammation, and fibrosis, as well as blood biochemistry analysis, was also performed. CDAHFD for 3 and 8 weeks produced a moderate-to-severe steatosis and inflammation of the liver in mice. NAFLD activity score (NAS) in mice fed the CDAHFD for 3 and 8 weeks were more than 4 indicating NASH or borderline NASH pathology. Fibrosis was observed only in mice fed the CDAHFD for 8 weeks. PET imaging showed that the hepatic standardized uptake value, SUV80–90 min, was increased with prolonged CDAHFD feeding compared with the respective controls (CDAHFD 3 weeks 0.32 ± 0.06 vs 0.48 ± 0.05, p < 0.01; CDAHFD 8 weeks 0.35 ± 0.04 vs 0.75 ± 0.07, p < 0.01, respectively). Prolonged CDAHFD feeding increased hepatic mRNA and protein levels of integrin αv and β3 at 3 and 8 weeks. Hepatic 18F-FPP-RGD2 uptake and amount of integrin αv and β3 protein were well correlated (r = 0.593, p < 0.05 and r = 0.835, p < 0.001, respectively). Hepatic 18F-FPP-RGD2 uptake also showed a positive correlation with Sirius red-positive area. Conclusions The hepatic uptake of 18F-FPP-RGD2 correlated well with integrin αv and β3 expression and histological fibrosis in a mouse model of NASH, suggesting the predictability of fibrosis in NASH pathology