Sarin.) Dr Roger Butterworth, Dr Subrat K. Acharya, Dr Abraham Koshy, Dr Sri Prakash Mishra and Dr Jang

B. Dilawari were special invitees and actively participated in the entire discussion. The Working Party adopted the use of the Oxford Pexidartinib supplier system for developing an evidence-based approach. The group assessed the level of existing evidence and accordingly ranked the recommendations, i.e. level of evidence from 1 (highest) to 5 (lowest); grade of recommendation from A (strongest) to D (weakest).5 The Working Party on Hepatic Encephalopathy convened by the Organisation Mondiale de Gastroenterologie presented its deliberations at the 11th World Congress of Gastroenterology, Vienna (1998). It defined HE as a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction, after exclusion of other known brain diseases, and proposed

new nomenclature with respect to: (i) the nature of the hepatic abnormality; and (ii) the duration and characteristics of the neurological manifestations, broadly categorizing HE into three types (Table 1).2,6 MHE was included as the third and final category of type B and C HE. Although implicit in the Vienna definition, the increasing recognition of MHE in non-cirrhotic selleck compound library liver diseases such as non-cirrhotic portal fibrosis,7 extrahepatic portal venous obstruction (EHPVO)8–10 and acute viral hepatitis11 warrants their explicit inclusion in the definition of MHE. The INASL Working Party recommended broadening the definition of MHE to include liver diseases and causes of portal hypertension other than cirrhosis and also to include mention of neuropsychometric

or neurophysiological tests, which can be performed in the outpatient 上海皓元 setting, for diagnosis of MHE. 1 MHE may be defined as the presence of measurable cognitive defects in patients with liver disease and/ or portal-systemic shunting, that are not identified by detailed clinical history and complete neurological examination, including interview of close family members, but are detected by abnormalities in neuropsychometric or neurophysiological tests that can be performed at the bedside and in the out-patient setting, in the absence of other known causes of abnormal cognitive tests. (5, D) The true prevalence of MHE in patients with portal hypertension is unknown. Though MHE has traditionally been diagnosed in patients with cirrhosis of the liver, impairment of cognitive function has also been demonstrated in patients with noncirrhotic portal hypertension.7–10 Prevalence of MHE has been reported to vary between 22% and 74% in patients with cirrhosis of the liver,3,4,12–22 depending on both the examinable dimensions of the disease and fixed diagnostic cut-offs.

Our previous study indicated that postoperative adjuvant transcatheter arterial chemoembolization (TACE) could improve the survival of patients with risk factors for residual tumor.34 In our study, patients with a high risk of recurrence, evidenced by clinical features such as vascular invasion and microsatellite lesions, were given one to three courses of prophylactic TACE

(doxorubicin, cisplatin, 5-fluorouracil, and iodized oil) 1 month after surgery.35 Fulvestrant We retrospectively collected the data of HCC patients with ≥2 CTCs who performed the prophylactic TACE and compared the antirecurrence results with those who did not perform TACE, and found that prophylactic TACE was RO4929097 beneficial in preventing recurrence in patients with ≥2 CTCs (P = 0.006) (Supporting Fig. 4). However, randomized controlled trials are needed for further validation. The limitations of this study are its relatively small cohort size, short follow-up time, and data from a single study center. A prospective, multicenter, randomized clinical trial should be designed to further validate the prognostic significance of CTCs in HCC. To our knowledge, this is the first report to identify the stem cell–like characteristics of EpCAM+ CTCs and their prognostic significance using the standardized CellSearch system in HCC patients. A preoperative EpCAM+ CTC7.5 level of ≥2 is an independent prognostic

indicator for recurrence in

HCC patients undergoing curative resection. Monitoring dynamic changes of perioperative CTCs may be a promising predictor of the response of the therapeutic regimen. Eradicating these cells might open a therapeutic avenue toward preventing HCC recurrence. Additional Supporting Information may be found in the online version of this article. “
“The differentiation of embryonic or determined stem cell populations into adult liver fates under known conditions yields cells with some adult-specific genes but not others, aberrant regulation of one or more genes, and variations in the results from experiment to experiment. We tested the hypothesis that sets of signals produced by freshly isolated, lineage-dependent mesenchymal cell populations would yield greater efficiency and reproducibility in driving 上海皓元 the differentiation of human hepatic stem cells (hHpSCs) into adult liver fates. The subpopulations of liver-derived mesenchymal cells, purified by immunoselection technologies, included (1) angioblasts, (2) mature endothelia, (3) hepatic stellate cell precursors, (4) mature stellate cells (pericytes), and (5) myofibroblasts. Freshly immunoselected cells of each of these subpopulations were established in primary cultures under wholly defined (serum-free) conditions that we developed for short-term cultures and were used as feeders with hHpSCs.

12 SAMe also donates propylamine moiety for polyamine biosynthesis and in the process generates methylthioadenosine (MTA), which is an inhibitor of methylation.13 Transmethylation reactions of SAMe result in its conversion to another potent methylation inhibitor, S-adenosylhomocysteine (SAH).14 Mammalian cells express two genes, MAT1A and MAT2A, that encode the two MAT catalytic subunits, α1 and α2, and a third gene MAT2β, which encodes the regulatory subunit β that regulates the activity of MAT2A-encoded

isoenzyme MAT II by lowering the inhibition constant (Ki) for SAMe and Michaeli’s constant (Km) for methionine.15, 16 MAT1A is expressed mainly in hepatocytes and maintains the differentiated state of these cells.12 MAT2A is expressed in all extrahepatic tissues and is induced in liver during active growth and dedifferentiation.12, 17, 18 The MAT2β gene is induced during this website liver cirrhosis and hepatocellular carcinoma (HCC).19 Hepatic stellate cells do not express MAT1A.20 MAT2A is the only enzyme responsible for SAMe biosynthesis in these LY2109761 in vitro cells. Our recent work in liver cancer cells showed that induction of MAT2A and MAT2β genes is required for cell

growth that is induced by leptin,21 an adipokine that plays a pivotal role in liver fibrogenesis and carcinogenesis.4, 22 Furthermore, leptin signaling in the liver cancer cell line HepG2 requires the expression of the MAT2β gene but not that of MAT2A. MCE Knockdown of MAT2β inhibits upstream events like leptin-mediated signal transducers and activators of transcription 3 (STAT3) activation as well as downstream events like extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3-kinase (PI3-K) activation.21 Because leptin is a potent profibrogenic growth factor regulated by MAT gene expression and MAT genes are associated with cellular proliferation,

we investigated the hypothesis that MAT2A and MAT2β genes may play important roles in the activation of HSCs. Our results indicate dramatic changes in MAT genes and SAMe homeostasis during activation of HSCs and provide evidence that activation of the MAT genes is an essential event during fibrogenesis. α-SMA, alpha-smooth muscle actin; AKT, AK strain transforming; BDL, bile duct ligation; BrDU, bromodeoxyuridine; Col1A2, alpha2(1) collagen mRNA; ECM, extracellular matrix; ERK, extracellular signal-regulated kinase; FBS, fetal bovine serum; HPLC, high-performance liquid chromatography; HPRT1, hypoxanthine phosphoribosyl-transferase 1; HSC, hepatic stellate cell; MAT, methionine adenosyltransferase; MTA, methylthioadenosine; RT, reverse transcription; SAH, S-adenosylhomocysteine; SAMe, S-adenosylmethionine; siRNA, short interfering RNA; RNAi, RNA interference, STAT, signal transducers and activators of transcription. All reagents used in this study were of analytical grade and obtained from commercial sources.

Conclusion: ESP for ampullary tumors is effective and safe. It can be curative for most ampullary adenomas. ESP for localized adenocarcinoma may be potentially curative in >50% patients.

Key Word(s): 1. ampullary tumours; 2. endoscopic papillectomy Presenting Author: YOUNG OOK EUM Additional Authors: SANG EON JANG, BYEONG SEONG KO Corresponding Author: YOUNG OOK EUM Affiliations: Cheongju Saint Mary’s Hospital, Cheongju Saint Mary’s Hospital Objective: Cholecystocolonic fistulas are rare complications of gallstones with a variable clinical presentation. Cholecystocolonic fistulas are often asymptomatic and it is difficult to diagnose them preoperatively. Methods: A patient who complaint diarrehea for one month visited local clinic and underwent colonoscopy. During colonoscopy, an 1 cm sized polypoid lesion was noted on ascending colon. During suction the air to observe the lesion closely, the polypoid lesion was sucked up and a hole like perforation was appeared. OTX015 manufacturer The patient was transferred to our hospital suspected bowel perforation. Results: On the physical exam, there was no specific findings such as abdominal tenderness. On abdominal computed tomography, small air was noted in the gallbladder and several common bile duct stones and gallbladder stones. We did ERCP (endoscopic

retrograde cholangiopancreatography) and removed CBD stones. Then cholecystectomy with segmental colonic resection was done. Conclusion: On operation field, a cholecystocolonic fistula was noted. After the operation, MK0683 datasheet the diarrhea was stopped and the patient recovered completely. Key Word(s): 1. cholecystocolonic fistula Presenting Author: HISASHI HATANAKA Additional Authors: TOMONORI YANO, NORIKATSU NUMAO, KENSUKE YOKOYAMA, JUN USHIO, TAKESHI TOMIYAMA, KIICHI TAMADA, HIRONORI YAMAMOTO Corresponding Author: HISASHI HATANAKA Affiliations: Jichi Medical University,

Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University Objective: This study was undertaken 上海皓元医药股份有限公司 to evaluate the efficacy of indigo carmine (IC) method in identifying the afferent limb with Roux-en Y (RY) reconstruction during double-balloon ERCP (DBERCP). Methods: DBERCP was performed in 94 patients with RY reconstruction from February 2009 to October 2013 at Jichi Medical University Hospital. We investigated accuracy rate of IC method in total gastrectomy (TG) group and in non TG group. In the second portion of the duodenum or at the distal site of esophagojejunostomy, after inflation of a balloon at the tip of the endoscope, 50 ml of IC was injected into the lumen. At the RY site, we evaluated the inflow of IC into both limbs and identified the limb with less inflow as the afferent limb. When the limb with less inflow was confirmed as afferent limb, the case was classified as “correct group”. Insertion time in correct group was compared to that in incorrect group.

We systematically examined both pathways and found that HGF increased earlier in CO-treated animals, whereas TGF-β and IL-6 did not show any difference among the treatment groups. Met is an HGF receptor

tyrosine kinase, and upon binding with HGF triggers transphosphorylation of the tyrosines Tyr1234 and Tyr 1235 that leads to activation of PI3K and MAP kinases. To corroborate this hypothesis, we evaluated the expression level of downstream targets including Akt and STAT-3 as well as cell proliferation genes involved in HGF signaling. Phosphorylation Selleckchem GW-572016 of Akt, Met, cyclin D1, cyclin E, and Rb showed earlier activation, whereas p21 and STAT-3 showed decreased expression in the liver of CO-treated mice when compared to air controls. Given that our cumulative immunocytochemical and coculture studies demonstrate the requirement of CO to enhance hepatocyte proliferation after PHTx, we conclude that CO in part increases HGF expression primarily by the HSC, which

in turn acts on Met to trigger downstream signaling through Akt in the HC, which sets in motion the proliferation apparatus of the hepatocyte and perhaps the endothelial cell (Fig. 8). Importantly, there are potentially other factors that may contribute to the CO effects in this model including Selleck PLX4032 increased sensitivity of the hepatocyte to HGF, which was observed with adenosine receptor expression in 上海皓元医药股份有限公司 macrophages exposed to CO.50 The effects on cell cycle genes may then be influenced indirectly through differential effects on the expression of additional growth factors, cytokines, and mediators. Although numerous numbers of experimental models have proposed means by which to accelerate liver regeneration focusing on circulating factors,45 cytokines,46 and growth factors,47 there remain no therapeutic options in the

clinic to enhance liver regeneration after resection. Because CO is currently in phase II clinical trials for organ transplantation,48 our fundamental analysis delineating the effects of CO in the process of liver regeneration after PHTx offers a potential benefit to patients with cirrhosis and hepatocellular carcinoma where PHTx may be the best or only treatment option. Furthermore, recipients of LDLT, particularly those recipients who are at risk for small for size syndrome, as well as recipients of extended criteria donors could potentially benefit by therapies such as CO that could increase earlier liver recovery, leading to improved graft function and survival and shorter hospital stay. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Locoregional therapies for hepatocellular carcinoma (HCC) are considered to confer a survival advantage, however, the patient group that should be targeted is not clearly defined.

Anti-inflammatory and especially antifibrotic therapies for NASH are urgently needed.Glucagon-like peptide-1 (GLP-1) enhances Epacadostat glucose-dependent insulin secretion, delays gastric emptying and exhibits other antihyperglycemic actions following its release into the circulation from the gut. We examined the effect of a long-acting GLP-1 agonist exenatide (BYDUREON, BY) on inflammation and fibrosis in models of fibrotic NASH and biliary fibrosis. Methods: BY was administered twice weekly by subcutaneous injection at 0.4or 2 mg per kg BW to Mdr2KO mice from week 7-1 1 of age, and to 8 week old C57BL/6 mice fed a methionine

and choline deficient diet (MCD) for 4 weeks. Hepatic fibrosis was assessed by morphometric analysis of sirius redstained collagen and measurement of hydrox-yproline content. Serum biochemistries were determined by an autoanalyzer, and hepatic inflammation was assessed by semi-quantitative immunohistochemistry. Fibrosis and inflammation related transcript levels were quantified by quantitative realtime polymerase chain reaction (qPCR). Results: In mice on the MCD diet, 0.4 more than 2.0 mg/kg BY causeda significant reduction of hepatic steatosis, inflammation and a 30%reduc-tion in total collagen content compared to untreated

controls.BYsignificantly decreased fibrosis related transcripts such as αSMA, procollagenα1 (I),TGFβ1, TIMP-1, but also of putatively fibrolyticMMP-8,MMP-9 and -13. BY also suppressed inflammation related transcripts such

as learn more CD68, CCL3, and TNFα, and increased (anti-inflammatory) Arg1 transcripts. In Mdr2 -/- mice, 0.4 mg/kg BYsignificantly lowered liver collagen content, decreased MMP-13 but increased Arg1 transcripts. Conclusions: A long-acting GLP-1 agonist which is already in clinical use for treatment of type 2 diabetesreduced parameters of hepatic MCE steatosis, inflammation and fibrosis, without negative effects on weight gain, supporting its usefulness to treat human NASH and liver fibrosis. Disclosures: Detlef Schuppan – Advisory Committees or Review Panels: Aegerion, Eli Lilly, Gilead; Consulting: Boehringer-Ingelheim, Isis, Takeda; Grant/Research Support: Boehringer-Ingelheim The following people have nothing to disclose: Xiao-Yu Wang, Shih-yen Weng, Thomas Klein, Yong Ook Kim Placenta-derived stem cells (PDSCs) have been focused as a cell source for liver regeneration. Emerging evidence provides the anti-fibrotic effect of PDSCs on liver fibrosis. However, underlying mechanisms on the effect of PDSCs on liver fibrogenesis remain unclear. The hedgehog (Hh) signaling pathway orchestrates tissue reconstruction in the damaged liver. Recently, micro (mi) RNA-125b is reported to regulate smoothened (smo), Hh signaling activator. Hence, we hypothesized that miRNA-125b mediated Hh signaling pathway might regulate liver regeneration by PDSCs.

Samples were normalized using Significance Analysis of Microarrays (SAM), and differentially expressed genes were identified at a nominal P ≤ 0.05. Unsupervised cluster analysis was performed using Cluster and TreeView programs.2. Only genes with a fold change ≥2 were included in the analyses. Functional classification and network analysis were performed using Ingenuity Pathway Analysis tool (Ingenuity Systems Inc.) and the GeneGo microarray tool. Microarray data from 139 HCC samples[21] were used for the survival

analysis according to the SIRT6 signatures. SIRT6 expression was MK-8669 solubility dmso investigated in a subcontingent of 53 HCC tumor specimens.[22] The Oncomine Cancer Microarray database (http://www.oncomine.org) was used to study gene expression of the SIRT6 signature in human HCC and conduct a meta-analysis for the predictive value of the SIRT6 signature in more than 40 different cancer types. Expression values of tumor samples were log-transformed and median-centered and standard deviation was normalized to one per array before comparison to their normal tissue counterparts as described

recently.[23] Statistical analysis was performed using Student t test or analysis of variance as indicated. P ≤ 0.05 was considered statistically significant. Results are presented as the mean ± SD or mean ± SEM as indicated. Univariate and multivariate analysis were performed using a chi-squared test and PD98059 mouse Cox proportional hazard regression, respectively. For the multivariate analyses, only significant variables with sufficient data points were included. To investigate the relevance of SIRT6 for primary human HCC, we first used publically available gene expression data of liver cancer patients from the Oncomine Cancer Microarray database.[23] A significant reduction of SIRT6 expression was revealed in cirrhotic livers and HCC specimens (P < 0.001) compared with levels observed in noncirrhotic

livers (Fig. 1A). In confirmation of these findings, a down-regulation of SIRT6 in HCC tissues compared with nondiseased normal livers was also observed in around 45% (24/53) using independent gene expression data from our recently published cohort of 53 human 上海皓元医药股份有限公司 HCCs (Fig. 1B, upper panel).[22] Consistently, around 42% (16/38) of the tumor samples showed SIRT6 levels below the median center of the expression data of all samples (normalized expression units < 0) of patient samples analyzed in Fig. 1A (Fig. 1B, lower panel). These data indicate a stepwise reduction of SIRT6 in both premalignant and malignant stages of hepatocarcinogenesis. To investigate the gene expression pattern deregulated by SIRT6 loss, we established a SIRT6 KO gene expression signature. To obtain a hepatocyte-specific transcriptome analysis, we isolated primary mouse hepatocytes from wild-type (WT) and Sirt6-deficient livers at 3 weeks of age.

Skulls from the University of Canterbury (UC) collection (n = 9) were used without additional preparation.

Cranial volume of clean, dry skulls (n = 21) was determined in triplicate using spherical plastic beads with a mean diameter of 5.6 ± 0.03 mm. The density of packed beads was first determined from the mass of beads that could be packed into the spherical (i.e., cranium-like) portion of volumetric flasks (100, 250, 500, mTOR inhibitor and 1,000 mL capacity); the volume of the spherical portion was measured by weighing distilled water at 20°C and dividing the resulting mass by the density of water at this temperature (0.998203 g/cm3). The relationship of bead bulk volume (y, cm3) to bead mass (x, g) was (1) Skulls sectioned for brain mass (Fig. 1) were reassembled using masking tape, and in all skulls foramina were plugged with foam ear plugs and/or masking tape to prevent loss of beads. Prepared skulls were

weighed empty to determine the tare mass before filling the cranial CHIR-99021 chemical structure cavity with beads through the foramen magnum. Care was taken to shake skulls during filling to ensure close packing of beads (Donev et al. 2004) and reduce interference by the bony tentorium (tentorium cerebelli osseum) present in Weddell seals. The net mass of the beads was determined as the difference between the mass of empty (tare) and filled skulls (tare + beads), and cranial capacity was calculated from net bead mass according to the relationship between bead mass and bead volume derived previously in vitro (Eq. (1) above).

The relationship between measured brM (x, g) and measured CC (y, cm3) was used to estimate brM from CC for adult (n = 9; UC collection) and neonatal (n = 3) skulls for which brM could not be directly determined (Fig. 2, Table 1). Unless otherwise indicated, results are expressed as mean ± SEM. BL, body length; BM, body mass; brM, brain mass; CC, cranial capacity (intracranial volume); CMR, cerebral metabolic rate; DGB, daily glucose demand of the brain; f. dom., forma domestica; MF, multiplication factor; RCMR, relative cerebral metabolic rate; medchemexpress UC, University of Canterbury, New Zealand. The relationship of measured brain mass (brM: x, g) and cranial capacity measured using plastic beads (CC: y, cm3) for pups and adults is shown in Fig. 2. Mean CC and brM of the two adult females measured directly (181, 5028; Table 1) were 574.7 cm3 and 563.4 g, respectively. Mean CC of skulls from the UC collection (n = 9) was 624.4 ± 16 cm3 (range 539–709 cm3), corresponding to a mean estimated brM of 626.9 ± 21 g. There was no significant difference in CC between the two sets of adult seals (t-test, P = 0.21). One stillborn pup (7547; Table 1) appeared to be premature on the basis of low body mass and small size, and was therefore omitted from analysis of brain size (but not from the comparison of brM and CC shown in Fig. 2, n = 7). Only skulls were available for pups 7639 and 7949, and brM for pup 7524 was not determined due to a taring error.

low-risk patients: optimization using statistical models. Liver Transpl. 2006; 12(2): 231-9. 2. Kaido T, Egawa H, Tsuji H, Ashihara E, Maekawa T, Uemoto S. In-hospital mortality in adult recipients of living donor liver transplantation: experience of 576 consecutive

cases at a single center. Liver Transpl. 2009; 15(11): 1420-5. Clinical features of 450 adult LDLT recipients GRWR, graft-to-recipient weight ratio Disclosures: The following people have nothing to disclose: Murat Dayangac, Murat Akyildiz, Yalcin Erdogan, Gokhan Gungor, Yaman Tokat Introduction: Priming is essential for hepatocytes to proceed and AZD1208 datasheet complete the cell cycle culminating in mitosis and replication. It remains poorly understood how hepatocytes fail to regenerate promptly in elderly animals following a two-third partial hepatectomy (PH). Since γ-aminobutyric acid (GABA) promotes hepatocytes click here into G2 phase of cell cycle, we hypothesized that by priming old hepatocytes

to G2 phase, the liver remnants of old mice regain their regenerative capacity. Methods: We used 24-month (old) and 4-month (young) C57BL/6 mice and evaluated cell cycle distribution by immunohistochemistry for cyclin D1 (G1 phase), cyclin A (S phase), cyclin B1 (G2 phase), Ki67 and pHH3 (M phase). Results: Marked increase of Cyclin B1 positive hepatocytes was seen in aged mice following 7 days of GABA pretreatment, while control mice had mostly quiescent and Cyclin D1 positive cells (Figure 1A). The GABA treated livers regained similar mitotic activity to young controls as seen by pHH3 and Ki67 staining at 36 h after PH. The results were confirmed with western and further explored through gene expression analyses (data not shown). In a separate experiment, mice with and without GABA pre-treatment were followed daily through day 7 post PH to establish cell cycle profile by IHC. We found that Old-GABA mice had proliferative Ki-67 and MCE mitotic pHH3 profiles that were similar to those of young

mice (Figure 1B). Conclusion: Our results indicate that hepatic regenerative capacity after PH in elderly mice can be restored by priming hepatocytes to G2 state prior to PH. Improvement in liver regeneration in elderly will impact quality of liver grafts from elderly donors. Disclosures: The following people have nothing to disclose: Fatima K. Rehman, Toshiyuki Hata, Zhaoyu Li, Guojun Bu, Justin H. Nguyen Introduction: MELD score (Model for End Stage Liver Disease) is universally used to priorities patients on the liver transplant waiting list. It is potentially used to predict survival as well. There has been conflicting evidence on using living donor liver transplantation (LDLT) in patients with high MELD score. We herein showing a retrospective analysis of survival data in these two categories of patients and comparing survival between LDLT and Deceased Donor liver Transplantation (DDLT) in a single center experience.

Also, among the 59 patients with GT of the international survey, two patients who received a high dose of rFVIIa given as a continuous infusion supplemented by an antifibrinolytic agent, developed pulmonary embolism and a ureteric clot, respectively [16]. Consequently, the use of rFVIIa should be carefully considered particularly in patients

with cardiovascular disease. The use of rFVIIa was approved by the European Medicines Agency in 2004 for the use in patients with GT who became refractory to platelet transfusions or have developed antiplatelet antibodies. Transfusion of platelets has been the most efficient mode of therapy for bleeding episodes and prophylaxis during surgery in patients with GT or BSS. For patients with the milder inherited platelet dysfunctions, platelet transfusions are rarely needed. The major concerns regarding the use of blood components in patients with selleck chemical the severe types of platelet dysfunction are the potential development of allo-immune antibodies against

HLA antigens and/or against the missing platelet glycoproteins (GP), αIIb, β3 or αIIbβ3 in GT and GPI-IX-V in BSS. In one study of GT patients who were exposed to blood components, the frequencies of HLA antibodies were 8/54 (14.8%), for αIIbβ3 antibodies, the frequency was 16/54 (29.6%), and for antibodies against both HLA and αIIbβ3, 5/54 (9.3%) [16]. In C646 in vivo a smaller study of 16 patients with GT, the frequency of HLA-alloantibodies MCE was quite similar. However, for anti-αIIbβ3 antibodies, the frequency was substantially lower than in the larger study (12.5% vs. 39%) [24]. Additional risks of blood component therapy include allergic reactions, transmission of infectious agents, Rh immunization in Rh-negative patients, and on rare occasions – haemolytic transfusion reactions when the donor is type O and recipient is type A [25]. For partial circumvention of the problems related to platelet transfusion, HLA and ABO-matched donors should be sought. If such donors are unavailable, leucocyte-depleted blood components should be used

because it was shown to be effective in reducing the rate of HLA allo-immunization. Use of platelet pheresis from single donors reduces the risk of allo-immunization against αIIbβ3, thereby diminishing the risk of refractoriness to platelet transfusions. Rh negative patients in the child-bearing age, in whom transfusion of Rh positive blood components is unavoidable, should receive anti-D therapy to neutralize the D-antigen. Using family members for donation of platelets is usually convenient, but should not be done if stem-cell transplantation in the affected patient(s) is considered. Blood from family members should be irradiated to prevent transfusion-related graft-versus-host disease. Platelet transfusions after surgery should be continued until wound healing has been achieved [26] and for at least 2 days after severe bleeding episodes have abated.