The results revealed differential expression of a subset of lncRN

The results revealed differential expression of a subset of lncRNAs, notably a specific differentially expressed lncRNA associated with Wnt/β-catenin signaling during liver regeneration (an lncRNA associated with liver regeneration, termed lncRNA-LALR1). The functions of lncRNA-LALR1 were assessed by silencing and overexpressing this lncRNA in vitro and in vivo. We found that lncRNA-LALR1 enhanced hepatocyte proliferation by promoting progression of the cell cycle in vitro.

Furthermore, we showed that lncRNA-LALR1 accelerated mouse hepatocyte proliferation and cell cycle progression Daporinad research buy during liver regeneration in vivo. Mechanistically, we discovered that lncRNA-LALR1 facilitated cyclin D1 expression through see more activation of Wnt/β-catenin signaling by way of suppression of Axin1. In addition, lncRNA-LALR1 inhibited the expression of Axin1 mainly by recruiting CTCF to the AXIN1 promoter region. We also identified a human ortholog RNA of lncRNA-LALR1 (lncRNA-hLALR1) and found that it was expressed in human liver tissues. Conclusion: lncRNA-LALR1 promotes cell cycle progression and accelerates hepatocyte proliferation during liver regeneration by activating Wnt/β-catenin signaling. Pharmacological intervention targeting lncRNA-LALR1 may be therapeutically beneficial in liver failure

and liver transplantation by inducing liver regeneration. (Hepatology 2013;58:739–751) Liver regeneration is a series of physiopathological phenomena resulting in quantitative recovery from the loss of liver mass to compensate for decreased hepatic volume and impaired function.

Clinically, liver regeneration has important implications because many therapeutic strategies for the surgical treatment of liver diseases, such as removal of liver tumors and liver transplantation, depend on the ability of the liver to regenerate MCE physically and functionally. Insufficient liver regeneration may be potentially fatal for these patients.[1] Therefore, a better understanding of the mechanisms of liver regeneration could lead to clinical benefits. A complex network of cytokine and growth factor signaling involving molecules such as interleukin-6 (IL-6)[2] and hepatocyte growth factor (HGF)[3] regulates the hepatocyte cell cycle to ensure that liver regeneration occurs quickly.[4] Recent studies have shown the critical role of microRNAs (miRNAs), such as miR-221[5] and miR-21,[6] in liver regeneration. Although various cytokines, growth factors, and miRNAs have been shown to regulate genes that orchestrate proliferation during liver regeneration, new molecular therapeutic targets for liver failure and liver transplantation are still urgently needed. It is important to understand the overall molecular changes that occur during liver regeneration to enhance the effectiveness of current regenerative technology.

The screening tests that are routinely requested after noting a p

The screening tests that are routinely requested after noting a particular pattern of abnormal aminotransferases is described. An algorithm suggesting an approach to a child with abnormal transaminases is provided. “
“The availability of newer small-caliber videoendoscopes makes unsedated endoscopy an attractive option for the screening of Barrett’s esophagus, esophageal

varices and gastric cancers. Unsedated endoscopy, via a transnasal or peroral route, is well tolerated, has a diagnostic accuracy similar to standard upper Fostamatinib manufacturer endoscopy and leads to substantial cost savings. Preconceived notions on the part of physicians as well as patients continue to be an obstacle to the wide spread acceptance of this procedure “
“AASLD, American Association for the Study of Liver Diseases; CDC, Centers for Disease Control and Prevention; IOM, Institute of Medicine. Chronic viral hepatitis remains a major cause of preventable morbidity and mortality in the world. The landmark study from the prestigious Institute of Medicine (IOM)

summarized in this issue of HEPATOLOGY defines the issues that drive this problem and the need to tackle this aggressively,1 an issue advocated by the American Association for the Study of Liver Diseases (AASLD) for many years.2 The AASLD applauds this major effort that not only highlights the urgent need to address this public health problem but Rapamycin mw also provides direction for policy makers to begin to tackle the scourge of hepatitis B and C. The public health impact of a disease depends on its prevalence and its consequences for the affected individual. The IOM report notes that one of every 50 Americans is affected by hepatitis B or C

and that the majority of afflicted individuals are unaware of their disease. Many of these subjects thus go undetected and contribute to the burden of advanced liver disease and the rising tide of hepatocellular carcinoma. A principal cause for this is a lack of knowledge and awareness of chronic viral hepatitis on the part of health care and 上海皓元 social-service providers. This is, in turn, driven by a lack of resources allocated to the eradication of these conditions at a national and state level. A major consequence of the failure to detect the disease early is that the treatment options available for those who have progressed to cirrhosis are more limited and require more resources. The decreased ability to tolerate treatments and the impact of end-stage liver disease on the patient add a further social and economic burden on the affected individual and their family. These add to the cost of medical care nationally and negatively impact the ability of many small businesses to obtain affordable health care coverage. The implications of the IOM report for American, and indeed the world, are therefore highly significant. The AASLD is committed to working toward the ultimate eradication of hepatitis B and C.

The products of four genes (GPIBA, GPIBB, GP9 and GP5) assemble w

The products of four genes (GPIBA, GPIBB, GP9 and GP5) assemble within maturing MK in the marrow to form the GPIb-IX-V complex. Mutations within GPIBA, GPIBB and GP9 in BSS prevent formation or trafficking of the complex through endoplasmic reticulum (ER) and the Golgi apparatus [6]. In rare variant forms, platelets express nonfunctional GPIbα; in platelet-type von Willebrand selleck disease (VWD), specific GPIBA mutations lead to upregulated GPIbα function and a clinical condition resembling type 2B VWD where macrothrombocytopenia (and sometimes circulating platelet aggregates) due to activating mutations in exon 28 of the VWF gene may also affect

megakaryopoiesis [7]. The platelet-collagen interaction under flow is a multistep process involving α2β1 and GPVI which signals through the FcRγ-chain [2,6]. Like α2β1, GPVI density is under learn more the control of SNPs and epigenetic factors; however, a loss in the collagen response due to mutations in GP6 occurs in rare families. Members of the seven transmembrane domain family of G-protein-linked receptors mediate platelet responses to soluble agonists. Rare patients with a decreased and reversible platelet aggregation to ADP have mutant alleles at the P2YR12 locus while a defective platelet aggregation to TXA2 is caused by mutations in TA2R. Significantly, these patients mimic the

platelet function modifications achieved in anti-thrombotic

therapy by clopidogrel (and prasugrel) and aspirin respectively. Decreased platelet aggregation to adrenaline is often seen in routine screening although its contribution to excessive bleeding is unclear. Abnormalities of signal transduction pathways into which surface receptors are locked mostly concern patients with mild bleeding while congenital deficiencies of metabolic pathways also lead to platelet function abnormalities [2,6,8–10]. IPDs of secretion (storage pool disease, SPD) cause selective defects 上海皓元 in aggregation. SPD affecting dense granules, storage sites for serotonin, ADP and ATP, may be quite common and the granule deficiency severe or partial. When associated with abnormalities of other lysosome-related organelles they give clearly defined phenotypes [e.g. Hermansky–Pudlak (HPS) and Chediak–Higashi (CHS) syndromes] where melanosomal defects cause a lack of pigmentation of the skin and hair. Defects in at least 8 genes (HPS-1 through HPS-8) in HPS cause distinct subtypes with the encoded proteins interacting in complexes (BLOCS); the genetic defects disrupt these thereby affecting organelle biosynthesis and protein trafficking. In CHS, bleeding is associated with severe immunologic defects and progressive neurological dysfunction, a lymphoproliferative syndrome and an accelerated phase is seen in ∼90% of patients.

027) There was no significant difference in histologic different

027). There was no significant difference in histologic differentiation between K19-positive and -negative HCCs. mRNA expression levels of K19, three EMT-associated genes (Snail, Slug, and Twist), and four invasion-associated genes (uPAR, VIL2, MMP1, and MMP2) were investigated in 43 HCCs of cohort 2. The log-transformed K19 mRNA levels were significantly selleck screening library higher in K19 protein-positive HCCs than in K19 protein-negative HCCs (P = 0.048) (Fig. 3). Patients were classified into two groups (K19 mRNA high and K19 mRNA low), using the median of log-transformed K19 mRNA level as the cut-off value. The log-transformed mRNA expression levels of EMT-associated genes were positively correlated with

each other (P < 0.05), and positive correlations were observed between the log-transformed mRNA levels of invasion-associated genes (P < 0.05) (Supporting Table 4). Positive correlations were also observed between the mRNA levels of EMT-associated genes and invasion-associated genes (P < 0.05). The K19 mRNA high HCCs showed significantly higher mRNA levels of Snail (P = 0.012), Twist (P = 0.069), uPAR (P = 0.040), Pritelivir chemical structure and MMP2 (P = 0.040), whereas Slug, VIL2, and MMP1 mRNA

levels were not significantly different between the two groups. Significant positive correlations were observed between the log-transformed mRNA levels of K19 and Twist (P = 0.012), uPAR (P = 0.005), and MMP2 (P = 0.009). Univariable analysis revealed that AST >50 IU/mL, K19 expression, tumor size >5 cm, multiple tumors, major vascular invasion, microvascular invasion, and AFP >1,000 IU/mL were adverse prognostic factors for disease-free survival after resection (Table 3; Fig. 4). Multivariable analysis indicated that K19 expression, tumor size >5 cm, multiple tumors, major vascular invasion, and MCE公司 AST>50 IU/mL were independent prognostic factors for disease-free survival after resection (Table 4). When survival analysis was performed

separately for HBV-related (n = 190) and HBV-unrelated HCCs (n = 47), K19 expression was associated with decreased disease-free survival in both etiologic groups, but statistical significance was demonstrated only in the HBV-related HCCs (P = 0.011) (Supporting Fig. 3). No significant differences in overall survival were observed for both groups. HCC with stemness-related marker expression is a recently proposed subtype of HCC in which a fraction of tumor cells (>5%) expresses stem/progenitor cell markers, but is not otherwise recognizable by routine hematoxylin-eosin (H&E) stain.16 Because this subgroup of HCCs has been reported to show more aggressive behavior, compared to conventional HCCs without stemness-related marker expression, it is important that a suitable marker is developed to facilitate its diagnosis. This subtype is different from combined hepatocellular-cholangiocarcinomas—which include the recently described combined hepatocellular-cholangiocarcinoma with stem cell features (i.e.

Therefore, clinical suspicion of an inhibitor must be confirmed b

Therefore, clinical suspicion of an inhibitor must be confirmed by objective laboratory tests. Inhibitor investigation always starts with screening tests, followed, if needed, by specific tests to quantify and identify the exact nature of the inhibitor. A prolonged Doxorubicin datasheet activated partial thromboplastin time (APTT) clotting time

that is not corrected in a mixing study can indicate presence of an inhibitor, provided that the presence of heparin has been excluded. Special care with APTT mixing tests has to be taken when assessing acquired haemophilia with type 2 inhibitors that do not completely inactivate FVIII:C. Residual FVIII may cause normal or borderline abnormal mixing tests, leading to false-negative screening results. An abnormal mixing test is not specific for individual factor inhibitors as lupus anticoagulants show the same phenomenon. Quantitative FVIII inhibitor assays are based this website on a universal method of measuring decrease in FVIII activity in a mixture of an exogenous FVIII source (e.g. normal pooled plasma) and the putative inhibitor plasma in

a certain time period. A reference measurement is performed with the same method substituting patient plasma with control plasma lacking inhibitor. Residual factor activities in assay mixtures are measured by OS-based clotting assays (mostly APTT) or CS assays. The Nijmegen method medchemexpress [24], a modification of the Bethesda assay, has been recommended as the standard assay by the International Society on Thrombosis and Haemostasis Factor VIII/IX Scientific Subcommittee. The method has recently been reviewed [25]. Important features

of the assay are the use of buffered normal pool plasma as FVIII source and use of FVIII deficient plasma as control sample. In contrast with other coagulation inhibitors, FVIII inhibitors are time- and temperature-dependent because of the binding of FVIII to VWF. Therefore, it is extremely important to standardize both parameters; 2 h incubation at 37°C is optimal. Care must be taken with quantification of type 2 inhibitors as these do not show parallelism with the calibration curve. Therefore, patient plasma dilutions that give residual activity of ∼50% are used to obtain reliable results. Presence of heparin and lupus anticoagulant may interfere with the inhibitor assay. Heparin may be a problem in patients with catheters as their access seal is mostly heparin-filled to prevent occlusion. Heparin may contaminate the blood sample when puncturing this seal and thus it is advisable to screen these samples for heparin to exclude its presence. Presence of lupus anticoagulant may also give false-positive results. However, these effects can easily be bypassed using a CS to assay residual FVIII.

3) Expression of wildtype OCT1 induced quinine-sensitive TEA upt

3). Expression of wildtype OCT1 induced quinine-sensitive TEA uptake by HCC and CGC cells (Fig. 4A-C). This ability was also

observed in S14F, L160F, G401S, and P197S variants, whereas it was partly or completely lost in the rest of detected variants. To validate this transport assay, wildtype OCT1 was also expressed in frog oocytes. This maneuver markedly enhanced their ability to take up, in a quinine-sensitive manner, both TEA (Fig. 4D) and sorafenib (Fig. 4E). Moreover, the expression of the novel variants in this model also confirmed the lack of ability of R61S fs*10 and C88A fs*16 to transport sorafenib, which LDE225 was maintained in P197S (Fig. 4E). The effect of SNPs on the targeting to the plasma membrane was investigated by immunodetection of the V5-tag placed in the constructs. In this set of experiments, we also included C88R

and S189L, whose effects on protein targeting were not known, and G465R, whose functional consequences are controversial. Although G465R has been described as a loss-of-function variant,[24] our results indicate that when expressed in HCC and CGC cells this variant has a reduced, but not abolished, OCT1-mediated transport (Fig. 4A-C). When G465R was investigated in Alexander cells, similarly to wildtype OCT1, it was targeted to the plasma membrane (Fig. 5). In contrast, both C88R and S189L were mainly localized intracellularly selleck chemicals llc (Fig. 5). This was consistent with the abolished ability of the latter two variants to mediate TEA uptake (Fig. 4). Regarding the novel OCT1 variants, both R61S fs*10 and C88A fs*16, which encode truncated proteins (Fig. 2B), resulted in impaired targeting to the plasma membrane (Fig. 5) and lack of the MCE公司 ability to mediate sorafenib uptake by oocytes (Fig. 4E) and TEA uptake by transfected cells (Fig. 4A-C). In contrast, the functional variant P197S resulted in an entire OCT1 protein targeted to the plasma membrane (Fig. 5). Based on studies addressing the dose- (Fig. 3) and time- (Supporting Fig. 1) dependent sensitivity of Alexander cells to sorafenib, short-term (6 hours) exposure

of HCC and CGC cells to sorafenib was carried out (Fig. 6). Under these conditions only OCT1 variants with a relatively well-preserved ability to mediate TEA transport (Fig. 4) were able to induce sensitivity to sorafenib in all cells assayed (Fig. 6). Regarding the SNPs identified here, P197S, but not R61S fs*10 or C88A fs*16, enhanced the sensitivity to sorafenib in cells expressing these variants (Fig. 6). Interestingly, OCT1 inhibition with quinine reduced, in a dose-dependent manner, the sensitivity to sorafenib due to the expression of functional variants of this transporter. Selective identification of loss-of-function SNPs was performed by RT-QPCR in a larger series of HCC and CGC biopsies (Table 2). The abundance of each variant was normalized by the abundance of total OCT1 mRNA.

This distinguishes this signature with regard to long-term outcom

This distinguishes this signature with regard to long-term outcome, compared to the clinical situation early post-OLT. Acute cellular rejection (ACR) is difficult to distinguish from HCV recurrence, based on analysis of patient liver biopsies, as a result of common histological features. Previous studies comparing HCV

patients with and without ACR demonstrate that many of the learn more repressed genes are significantly up-regulated during ACR in HCV patients.3, 14 Additionally, repression of innate and inflammatory genes was characteristic of HCV recurrence, rather than ACR, in HCV transplant patients.15 This indicates that though short-term clinical factors, such as ACR, may confound long-term efforts to develop molecular signatures of liver disease pathogenesis, repression

of these innate immune genes is more widespread and of greater magnitude. Immune repression early in infection PS-341 mouse may contribute to increased hepatocyte infection during HCV recurrence and thus may create a more favorable environment for progression to severe disease. Although antigen presentation has been associated with HCV pathogenesis,16-18 these pathways are normally suppressed by allograft rejection drugs, causing impaired T-cell responses in HCV transplant patients. However, it is difficult to determine the effect of specific immunosuppressive regimens, because patients are routinely treated with different drugs and dosing regimens. Generally, the immunosuppressive regimens used are less likely to repress innate immune responses that could attenuate the severity of HCV recurrence. Innate immune

antagonism by HCV infection may result in the virus eliciting a transcriptional program that eventually results in fibrosis and disease progression, which is partially reflected by the increase in inflammatory genes over time caused by infiltrating leukocytes. HCV facilitates its replication by antagonizing the induction of antiviral interferons, ISGs, and antiviral cytokines through the action of the viral nonstructural protein (NS)3/4 protease and NS5A.19-22 Clinicians have not routinely treated HCV patients with post-OLT ribavirin and pegylated interferon, primarily because the high expense and harsh side effects of this treatment regimen do not justify its use in patients recovering from organ transplantation. However, MCE a recent study demonstrated that post-OLT treatment resulted in stable or improved fibrosis scores, even in some patients who did not demonstrate sustained virologic response.23 Our data indicating that repressed antiviral gene expression early in infection determines transition to severe disease suggests that patients may benefit from early therapeutic intervention during HCV recurrence to boost innate immune genes not effected by immunosuppressant drugs during the first 3 months post-OLT. Early repression of cell-division mediators in patients who progress also indicates that these transcriptional profiles are altered.

2 It is intriguing to think about outcomes, particularly for pati

2 It is intriguing to think about outcomes, particularly for patients with acute liver injury, in terms of a variation in the response to apoptotic signals. Usually, paradigms of acute liver injury address outcomes (including the possibility of fulminant hepatic failure) in terms of the toxin dosage, the amount of virus, and the variation of the immune response. The susceptibility to an agent such as acetaminophen is typically assessed on the basis of the ingested amount in selleck chemical combination

with variations in drug metabolism. Variations in outcomes for patients with acute hepatitis B virus have been postulated to be due to a combination of the viral load and an immune response. All these insults have been presumed to induce varying extents of hepatocyte apoptosis based on the injurious agent and not on variations in the cellular pathways controlling hepatocyte apoptosis. The possibility that outcomes can be determined not only by the heterogeneity of the inducing agent but also by a variation in the response

itself within the hepatocytes is intriguing. Hepatocytes are highly sensitive to stimuli of apoptosis, PF-01367338 molecular weight and this occurs via two pathways: an intrinsic mitochondria-mediated pathway and an extrinsic death receptor–mediated pathway.2 The extrinsic death receptor pathway comprises Fas (CD95), tumor necrosis factor receptor 1 (TNFR1), tumor necrosis factor–related apoptosis-inducing ligand 1 (TRAIL1), and TRAIL2. Select animal

models of acute liver injury target the extrinsic death receptor pathway.1, 3 The activation of extrinsic death receptors [Fas receptor (CD95 or APO-1), TNFR1, or both] rapidly induces hepatocyte apoptosis. Importantly, Fas and TNFR1 pathways have been regarded as independent triggers of apoptotic cell death. A number of factors, including the cell redox status and the activity of cell proliferation–associated pathways such as epidermal growth factor receptor (EGFR) signaling, are known to alter the susceptibility of hepatocytes to these apoptotic stimuli.4, 5 Furthermore, downstream signaling MCE公司 pathways, including c-Jun N-terminal kinase, nuclear factor kappa B (NF-κB), and extracellular signal-regulated kinase 1/2 (ERK1/2), have been shown to be activated in apoptosis and to alter hepatocyte apoptotic responses, but it is unclear how these apoptotic signaling responses are coordinated.6, 7 These pathways converge as tumor necrosis factor (TNF), TNFR, and EGFR ligands undergo activation by cleavage at the cell membrane; this process is known as ectodomain shedding. This process of protein cleavage is mediated by a disintegrin and metallopeptidase 17 (ADAM17).8 Furthermore, ADAM17 enzyme activity, which results in ectodomain shedding (protein cleavage), is mediated by tissue inhibitor of matrix metalloproteinase 3 (TIMP3).

Pre-examination survey showed that 246 women (895%) had some typ

Pre-examination survey showed that 246 women (89.5%) had some type of negative images to colonoscopy, 166 women (60.4%) answered “scary”, 119 women (43.2%) answered “embarrassed”, 105 women (38.2%) answered “painful”, and 19 women (7.0%) answered “others”. The main reason for women who preferred female colonoscopist was “embarrassed”. Among the 98 women who preferred female colonoscopists, none of them preferred male INCB018424 price colonoscopists for the next exam, 31 people (31.6%) had “no preference” and 67 people (68.4%) preferred female colonoscopists. The reasons for having no preference was that 4 people said “sex does not matter as long as they are experts”, and 1 person said “because

of the anesthetics, sex of the examiner was not a bother”. Conclusion: Majority of the women who have colonoscopy for the first time have negative images for colonoscopy and younger and employed women tend to prefer female endoscopists. About 30% of the women PI3K inhibitor who

desired female endoscopists did not have preference for the next examination. It was suggested that female doctors should be actively assigned for younger and employed women so they will not lose the opportunity for having an exam because of embarrassment and anxiety and contribute to the improvement of colonoscopy examination rate. Key Word(s): 1. sex preference; 2. women subjects; 3. colonoscopy Presenting Author: MICHAL TICHY Additional Authors: MARTIN CEGAN, JIRI LASTUVKA, JIRI STEHLIK Corresponding Author: TICHY MICHAL Affiliations: Krajska Zdravotni, A.S. – Masaryk Hospital, Krajska Zdravotni, A.S. – Masaryk Hospital, Krajska Zdravotni, A.S. – Masaryk Hospital Objective: Introduction: Lymphocytic colitis is characterized by chronic diarrhea with microscopic changes (presence of more than 20 intraepithelial lymphocytes/100 enterocytes) and normal appearence of the mucosa. Possibile pathological endoscopic findings are non-specific and discreet. The etiology is unknown, occurence is higher after 40 years

of age. Association with autoimmune diseases (e.g. celic desease, diabetes, thyroiditis) or drugs (carbamezepine, sertraline, ticlopidine) has been reported. More smokers than non-smokers are affected. No treatment is accepted as the standard (loperamine, medchemexpress cholestyramine, metronidazole, mesalazine, corticosteroids are used). More authors report good effect of the corticosteroids. The prognosis of the condition is usually good. Methods: Case descripcion: Colonoscopy was peformed in a 70-year-old Caucasian male. Large ulcers in the right colon were found (Figure 1). The patient had smoked for many years, he used antiarrhythmic drugs, clopidogrel and PPI. NSAID-induced colitis was thus excluded. Endoscopy apperance suggested the possibility of Crohn′s disease. MRI enteroclysis was in accordance with this hypothesis; it indicated terminal ileum involvement, too.

Results: This is a case of a 64 year old, female who was admitted

Results: This is a case of a 64 year old, female who was admitted in our institution due to hematochezia. One day prior to admission, patient had 4 episodes of hematochezia not associated

with abdominal pain nor vomiting. Persistence of hematochezia resulted in consultation at the emergency room. Physical examination was unremarkable. At the emergency room, vital signs were stable. Complete blood count showed mild anemia with hemoglobin of 110 g/L find more and platelet of 325,000. She underwent colonoscopy and showed a smooth tubular structure originating from the appendiceal lumen and projecting into the cecum. The tip of the tubular structure ends in a necrotic fungating polypoid mass occupying about 60% of the cecal lumen. Colonoscopy also showed a solitary cecal diverticulum and internal hemorrhoids. CT scan of the whole abdomen with IV contrast was also done,

and this revealed a tubular structure within the cecal area measuring about 7.1 cm × 0.4 cm ending in an ovoid soft tissue density about 2.6 cm × 1.8 cm in size. She eventually underwent exploratory laparotomy and right CHIR99021 hemicolectomy with side to end anastomosis and lymph node dissection because malignancy cannot be ruled out. Intraoperative findings showed appendix inverted into the cecal lumen with tip exhibiting polypoid mass. The appendix measured 6.0 cm × 1.1–1.5 cm and the mass measured 4.0 × 3.0 × 2.0 cm. The postoperative course was uneventful and the patient was eventually discharged. Histopathological finding of the mass showed hamartomatous polyp. Conclusion: Our case was definitely diagnosed on colonoscopy by following the appendiceal orifice. Recognition of appendiceal intussusception is important in avoiding misdiagnosis and misguided attempts at endoscopic removal or inappropriate surgery. Failure MCE公司 to recognize this condition has resulted in patients undergoing colonoscopic polypectomy with resultant perforation and peritonitis. Key Word(s): 1. appendix; 2. intussusception; 3. hamartomatous polyp Presenting Author: ERIKO YASUTOMI Additional Authors: YUKI BABA, SHOTARO OKANOUE, MAYU MURAKAMI, CHIHIRO SAKAGUCHI, TOMOKO SUNAMI,

SHOHEI OKA, NORIKO OKAZAKI, DAISUKE KAWAI, KOJI TAKEMOTO, RYUTA TAKENAKA, HIROFUMI TSUGENO, SHIGEATSU FUJIKI Corresponding Author: ERIKO YASUTOMI Affiliations: Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital, Tsuyama Central Hospital Objective: Schönlein-Henoch purpura (SHP) is a small vessel vasculitis associated with immunoglobulin A (IgA) complex deposition. Though it primarily affects children (over 90% of cases), the occurence on adults has been rarely reported (about 5% of cases). It is characterized by the clinical tetrad of non-thrombocytopenic palpable purpura, abdominal pain, arthritis and renal involvement.