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Background /Objectives: Severe acute pancreatitis (SAP) has a high mortality rate despite ongoing attempts to improve prognosis through a various therapeutic modalities. This study aimed to delineate etiology-based routes that may guide clinical decisions for the treatment of SAP. Methods Using data from a recent retrospective multicenter study in Japan, we analyzed the association between clinical outcomes, mainly in-hospital mortality and pancreatic infection, and various etiologies while considering confounding factors. We performed additional multivariate analyses and built decision tree models. Results The 1,097 participating patients were classified into the following groups by etiology: alcohol (n = 436, 39.7%); cholelithiasis (n = 230, 21.0%); idiopathic (n = 227, 20.7%); and others (n = 204, 18.6%). Mortality at hospital discharge was 8.4%, 12.2%, 16.7%, and 16.2% in the alcohol, cholelithiasis, idiopathic, and others groups, respectively. According to multivariable analysis, early enteral nutrition (EN) was significantly associated with reduced in-hospital mortality only in the cholelithiasis group. However, there was a consistent association between age and the need for mechanical ventilation and increased mortality, regardless of etiology. Our decision tree models presented different contributing factors depending on the etiology and patient background. Interaction analysis showed that EN and the use of prophylactic antibiotics may influence these results differently according to etiology. Conclusions No study has yet used comprehensive models to investigate etiology-related prognostic factors for SAP; our results can, therefore, be used as a reference for improving clinical decisions.

Apoptosis of alveolar epithelial type II (AEC-II) cells induced by reactive oxygen species (ROS) contributes to extensive alveolar damage during acute lung injury. Hypercapnic acidosis and hypocapnic alkalosis are known to modulate ROSmediated lung damage. This study assessed the effects of acid–base balance disturbances on hydrogen peroxide (H2O2)-induced apoptosis of the AEC-II-like human cell line A549, which was cultured under different conditions of pH and CO2 tension (normal pH and CO2, hypercapnic acidosis, metabolic acidosis, hypocapnic alkalosis and metabolic alkalosis). H2O2-induced apoptosis was assessed by a dye-uptake bioassay and induction of caspase activity, which were quantified using analytical digital photomicroscopy. Acidosis or alkalosis of the culture medium alone did not induce A549 cell apoptosis. Hypocapnic alkalosis significantly increased H2O2-induced apoptosis and caspase activation of A549 cells. Metabolic alkalosis non-significantly increased H2O2-induced A549 cell apoptosis and caspase activation. These data suggest that hypocapnic alkalosis intensifies oxidative-induced apoptosis of alveolar epithelial cells.

Intravascular lymphoma (IVL) is a rare form of B-cell lymphoma. We encountered a rare case of IVL diagnosed in an explanted liver. A 49-year-old man visited a clinic with high fever. Because of elevated liver function, he was diagnosed with acute liver failure. Deceased donor liver transplantation (LT) was performed 16 days after admission. The post-transplantation course was uneventful until IVL was reported in the explanted liver on postoperative day (POD) 21. Rituximab was administered on POD 27, and rituximab-cyclophosphamide, hydroxydaunorubicin, oncovin, prednisone (R-CHOP) treatment administered on POD 38. The R-CHOP treatment was repeated for eight cycles, and the patient remains free of recurrence 1 year post-transplantation. Although systemic lymphoma is a contraindication to transplantation, our experience indicates that IVL can be successfully treated by the administration of prompt chemotherapy after LT for fulminant hepatitis.

For continuous renal replacement therapy (CRRT), continuous administration of anticoagulant would be necessary to prevent the circuit clotting. Nafamostat mesilate (NM) is commonly used as its anticoagulant in Japan, although unfractionated heparin (UFH) is the most frequently used anticoagulant internationally. There is little study to compare the risk and benefit of NM with UFH as an anticoagulant during CRRT.

The alveolar epithelial cell type II (AEC-II) is itself able to amplify lung inflammation by producing inflammatory cytokines and chemokines, leading to the activation and recruitment of phagocytes. Sivelestat, a new neutrophil elastase inhibitor, has been shown to attenuate acute lung injury in animal experiments. In the current study, we assessed the effects of sivelestat on the production of chemokines from cultured A549 cells, a human AEC-II-like cell line.A549 cells were stimulated with endotoxin or tumor necrosis factor-alpha in the presence of sivelestat (1-100 microg x ml(-1)). Culture supernatant levels of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were determined by enzyme-linked immunosorbent assay. The expression of IL-8 and MCP-1 mRNAs in stimulated A549 cells in the presence of sivelestat (100 microg x ml(-1)) was quantified by real-time polymerase chain reaction.Sivelestat, at 100 microg x ml(-1) reduced the accumulation of IL-8 and MCP-1 in the culture medium. The high dose of sivelestat significantly inhibited the expression of IL-8 mRNA in A549 cells. The drug also decreased MCP-1 mRNA expression, although not significantly.These data suggest that a high dose of sivelestat regulates the production of IL-8 and MCP-1 in AEC-II.

Pulmonary thromboembolism (PTE) is a crucial complication characterized by rapid onset and a high mortality rate. There are few reports concerning perioperative incidence of PTE and deep vein thrombosis (DVT) among Japanese population. All surgical patients excluding young patients for minor surgery were equipped with calf- or thigh-length intermittent pneumatic compression (IPC) device as a DVT preventive method during the period of immobility. Incidence and clinical characteristics of perioperative PTE and DVT under the use of IPC device were analyzed at Kobe University Hospital. One patient developed DVT and four patients developed PTE among the 6500 surgical cases. All patients with DVT or PTE were 66 years or older, and all patients were diagnosed by computer tomography, venography and pulmonary angiography between 7 to 14 days after each operation. One patient was surgically treated by embolectomy and removal of intraarterial thrombus, and others were treated with thrombolysis, anticoagulants and placement of vena cava filters. For prevention of DVT and PTE, other preventive methods such as anticoagulants and prolonged application of IPC should be necessary.

could be accelerated, and have found that rolipram, a phosphodiesterase (PDE)-IV inhibitor, enhanced the growth of cultured AEC-II without infl uence on fi broblasts [2]. The enhancing effects of rolipram and KGF/ HGF were additive. Further studies are required to confi rm the clinical effi cacy of the drug in enhancing AECII proliferation. However, because pulmonary fi brosis is the main cause of death in the late phase of ALI, it is important to prevent fi brotic changes of the lung in response to various insults by inhibiting fi bloblast proliferation. Of interest is the observation that culture of lung fi broblasts in the presence of AEC-II can minimize fi broblasts growth through a mechanism mediated by prostaglandin E2. In the progress of ALI, the apoptosis of AEC-II contributes to extensive destruction of the alveolar epithelial architecture. Therefore, we assessed the effects of various drugs that are often used perioperatively on the endotoxin-induced apoptosis of cultured primary rat AEC-II. We observed that a clinically relevant concentration of propofol inhibited AEC-II apoptosis. Rolipram also had this action. The acid-base balance condition of the culture medium is thought to infl uence AEC-II apoptosis. In our experiment using cultured A549 cells, an AEC-II-like cell line, hypocapnic alkalosis potentiated the hydrogen peroxide-induced apoptosis of A549 cells and caspase activation, although an acidifi ed medium did not change the oxidativeinduced apoptosis of the A549 cells. Anesthetists have recently focused much attention on ventilatory management to prevent the exacerbation of lung damage in ALI. In several animal experiments, hypocapnic alkalosis has been recognized to worsen ALI induced by reactive oxygen species (ROS). Thus, the enhancement of AEC-II apoptosis by hypocapnic alkalosis may be responsible for hyperventilation-induced deterioration in ALI. Another plausible therapeutic strategy for ALI is to prevent the suicide of AEC-II. We must emphasize that AEC-II, as well as being victims in the pathogenesis of ALI, also act as attackers. In response to various Alveolar epithelial type II cells (AEC-II) play an important role in the repair of alveolar epithelium because of their differentiation into alveolar epithelial type I cells (AEC-I). In acute lung injury (ALI), various infl ammatory mediators produced in the lung attack AEC-II, leading to extensive loss of the alveolar epithelium. We discuss potential therapeutic approaches to ALI, targeting AEC-II. The basic concept of our strategy lies in the restoration of the quantity and function of AEC-II. Several growth factors (e.g., keratinocyte growth factor [KGF], and hepatocyte growth factor [HGF]) are known to potentiate AEC-II proliferation in both in vitro and in vivo systems. However, the clinical application of the growth factors does not seem feasible, because of their high cost. As an alternative to the administration of these agents, therefore, adenovirus-mediated KGF gene transfer into AEC-II has been attempted experimentally, with success [1]. For the same purpose, we have sought a simple pharmacological modality by which AEC-II proliferation

During mechanical ventilation, endotracheal tube cuff pressure should be maintained within proper range. We investigated the effect of frequent adjustment on cuff pressure in 27 mechanically ventilated patients. Cuff pressure was recorded every 2 h and was adjusted to 24 cmH2O each time. We found that cuff pressure was decreased by 4.9 ± 2.9 cmH2O from the target value. Cuff pressure decreased to less than 20 cmH2O in 45% of measurement occasions 2 h after adjusting it to 24 cmH2O.