Pancreatic Tail Cancer with Sole Manifestation of Left Flank Pain: A Very Rare Presentation

Pancreatic cancer is sometimes called a “silent disease” because it often causes no symptoms in the early stage. The symptoms can be quite vague and various depending on the location of cancer in the pancreas. The anatomic site distribution is 78% in the head of the pancreas, 11% in the body, and 11% in the tail. Pancreatic cancer is rarely detected in the early stage, and it is very uncommon to diagnose pancreatic tail cancer during an emergency department visit. The manifestation of pancreatic tail cancer as left flank pain is very rare and has seldom been identified in the literature. We present a case of pancreatic tail cancer with the sole manifestation of dull left flank pain. Having negative findings on an ultrasound study initially, this female patient was misdiagnosed as having possible acute gastritis, urolithiasis or muscle strain after she received gastroendoscopy and colonofiberscopy. Her symptoms persisted for several months and she visited our emergency department due to an acute exacerbation of a persistent dull pain in the left flank area. Radiographic evaluation with computed tomography was performed, and pancreatic tail tumor with multiple metastases was found unexpectedly. We review the literature and discuss this rare presentation of pancreatic tail cancer

Hesperetin-7,3'-O-dimethylether selectively inhibits phosphodiesterase 4 and effectively suppresses ovalbumin-induced airway hyperresponsiveness with a high therapeutic ratio

<p>Abstract</p> <p>Background</p> <p>Hesperetin was reported to selectively inhibit phosphodiesterase 4 (PDE4). While hesperetin-7,3'-<it>O</it>-dimethylether (HDME) is a synthetic liposoluble hesperetin. Therefore, we were interested in investigating its selectivity on PDE4 and binding ability on high-affinity rolipram-binding sites (HARBs) <it>in vitro</it>, and its effects on ovalbumin-induced airway hyperresponsiveness <it>in vivo</it>, and clarifying its potential for treating asthma and chronic obstructive pulmonary disease (COPD).</p> <p>Methods</p> <p>PDE1~5 activities were measured using a two-step procedure. The binding of HDME on high-affinity rolipram-binding sites was determined by replacing 2 nM [³<it>H</it>]-rolipram. AHR was assessed using the FlexiVent system and barometric plethysmography. Inflammatory cells were counted using a hemocytometer. Cytokines were determined using mouse T helper (Th)1/Th2 cytokine CBA kits, and total immunoglobulin (Ig)E or IgG_2alevels were done using ELISA method. Xylazine (10 mg/kg)/ketamine (70 mg/kg)-induced anesthesia was performed.</p> <p>Results</p> <p>HDME revealed selective phosphodiesterase 4 (PDE4) inhibition with a therapeutic (PDE4_H/PDE4_L) ratio of 35.5 <it>in vitro</it>. <it>In vivo</it>, HDME (3~30 μmol/kg, orally (p.o.)) dose-dependently and significantly attenuated the airway resistance (R_L) and increased lung dynamic compliance (C_dyn), and decreased enhanced pause (P_enh) values induced by methacholine in sensitized and challenged mice. It also significantly suppressed the increases in the numbers of total inflammatory cells, macrophages, lymphocytes, neutrophils, and eosinophils, and levels of cytokines, including interleukin (IL)-2, IL-4, IL-5, interferon-γ, and tumor necrosis factor-α in bronchoalveolar lavage fluid (BALF) of these mice. In addition, HDME (3~30 μmol/kg, p.o.) dose-dependently and significantly suppressed total and ovalbumin-specific immunoglobulin (Ig)E levels in the BALF and serum, and enhanced IgG_2alevel in the serum of these mice.</p> <p>Conclusions</p> <p>HDME exerted anti-inflammatory effects, including suppression of AHR, and reduced expressions of inflammatory cells and cytokines in this murine model, which appears to be suitable for studying the effects of drugs on atypical asthma and COPD, and for screening those on typical asthma. However, HDME did not influnce xylazine/ketamine-induced anesthesia. Thus HDME may have the potential for use in treating typical and atypical asthma, and COPD.</p

Predictors of intra-abdominal coagulopathic hemorrhage after living donor liver transplantation

AbstractBackgroundResults of preoperative conventional coagulation assays are a poor predictor of hemorrhage after liver transplantation. In this study, we evaluated the factors that are predictive of intra-abdominal coagulopathic hemorrhage after living donor liver transplantation surgery.MethodsDuring the period from January 2009 to December 2012, 118 adults underwent living donor liver transplantation (LDLT) in our institution. Of those patients, 18 (15.3%) developed intra-abdominal coagulopathic hemorrhage (n = 7) or hemorrhage due to non-coagulopathic causes (n = 11) that required emergency medical, radiological, or surgical intervention within the first month after LDLT. Possible predictors of postoperative coagulopathic hemorrhage included donor-related factors, age, body mass index, MELD score, INR value, intra-operative blood transfusion, graft/recipient weight ratio, anhepatic phase, cold ischemia time, operative time, APACHE II score, onset of re-bleeding, and hemoglobin levels during rebleeding episodes.ResultsThere were no differences in any of the variables between the two groups (coagulopathic and noncoagulopathic hemorrhage) except for cold ischemia time. We found that cold ischemia time was significantly longer in patients with postoperative coagulopathic hemorrhage (160.50 ± 45.02 min) than in patients with hemorrhage due to non-coagulopathic causes (113.55 ± 29.31 min; P = 0.027).ConclusionProlonged cold ischemia time is associated with postoperative intra-abdominal coagulopathic hemorrhage in patients after LDLT. It is, therefore, necessary to shorten the cold ischemia time in order to reduce the risk of postoperative intra-abdominal hemorrhage due to coagulopathic causes