Reports describing transplantation of in vitro transduced fetal hepatoblasts21 or injection of oncogene-expressing transposon plasmids22 into mouse liver demonstrated feasibility of restricting oncogene expression to clones of hepatocytes, from which neoplasms arose, but were not quantitative. The comparative hepatocyte growth assay (CHeGA) represents a complement to other experimental in vivo models of liver carcinogenesis. Unlike previous systems, which assess oncogene carcinogenicity, CHeGA allows us to separate and quantify the effects of gene alterations on cellular growth in growth stimulatory and quiescent environments. Furthermore, we can determine whether there is posttransplantation

development Selleck STI571 of hepatocyte focus growth outliers. The presence of outliers implies that some transplanted cells possessed stable changes (genetic or epigenetic) in addition to oncogene expression at the time of transplantation, or developed these Selleckchem CH5424802 changes shortly after transplantation. Because outlier growth continues in quiescent liver, these underlying changes must create the potential in affected cells for cell-autonomous

(environment-independent) growth, and in this way progenitors of outliers meet one criterion for preneoplastic cells. Using our growth assay, we can quantify, for any potential oncogene or oncogene combination, the associated risk of developing extreme outliers (EOs) with preneoplastic behavior. In fact, EO frequency is the best predictor of oncogene carcinogenicity in transgenic mice (see below), as expected if outliers are medchemexpress preneoplastic. This finding and our observation that EO microscopic anatomy is abnormal are consistent with suggestions by Laconi and colleagues20 that altered growth pattern is a principal marker of altered/nodular hepatocytes, although, in our system, these foci were identified by their ability to continue growth in a quiescent liver. Our findings, together with published data regarding oncogene effects in transgenic

mice, provide insight into the role of each oncogene in hepatocarcinogenesis. The principal effects of TGFα in transgenic mice are to stably increase hepatocyte number (liver mass increases up to twofold in transgenic mice),5, 8 and to increase the rate of hepatocyte replication after two-thirds partial hepatectomy and in 4-week-old but not 7-week-old mouse liver.7, 8 Consistent with these findings, TGFα quantifiably increases the rate at which hepatocytes can replicate under growth permissive conditions in CHeGA, but it does not uncouple replication from environmental controls in quiescent liver nor does it increase posttransplantation EOs. This liver phenotype is associated with a low risk for neoplastic progression on a per hepatocyte basis, because MT-TGFα transgenic mice develop a low tumor multiplicity with 10-month to 12-month latency.

Similar to the observation among males, there was a marked decrease (46%) in the incidence of colorectal cancer in the 30–34 years group in last two decades (Table 1). The present study shows that the ASR of colorectal cancer in Hong Kong increased in the period from 1983 to 2006.

GSK2118436 However, the increase was mainly among the male population. The ASR of colorectal cancer in females peaked in 1994 and declined in the past decade. The trends of colorectal cancer differ in different countries. However, the risk of colorectal cancer was higher and increasing among males, but stable or decreasing among females in most countries. In more detailed analysis of our local data, the increase was noted only in those above 60 years of age in males and those above 70 years of age in females. The rise was much higher among males than females. A gender difference and rising risk in the older, but not young population were noted also in other developed and Asian countries.6,7 The distribution of colorectal cancer was not examined in the present Palbociclib ic50 study, but it was found that the decrease in colorectal cancer in women and the young population is mainly due to a decrease in colon cancer rather than rectal cancer when the data were examined again in the reviewing process. As there was a tendency towards right-sided lesions in the older population,13 and there

was an increasing proportion of colorectal cancer in the older population recently, this may explain the right-shift of colorectal neoplasm observed in a local study.14 The westernized diet, which is high in fat and low in fiber, is found to be associated with colorectal cancer in many epidemiological studies.15–19 This was further confirmed in a cohort study using cluster analysis. In the present study, a micronutrient-rich, low fat, and high-fiber food pattern was found to be associated with

lower risk of colorectal cancer.20 The Hong Kong population medchemexpress adopted a westernized lifestyle early in the past century with decreased intake in vegetables and fruits, but increased consumption of processed meat, fat, beer and liquor. In a local telephone study, only 15% to 21% of respondents consumed fruit at least twice a day, about 50% consumed vegetable at least twice a day and about 40% ate high fat food more than once a week.21 This may explain the overall increase in ASR locally. However, it cannot explain the decreasing risk of colorectal cancer in the younger age groups, nor the discrepancy in the ASR of men and women. Instead greater screening use in women, who are in general more health conscious, leading to greater detection and removal of neoplastic polyps may be a possible reason of the latter observation. However, concrete data are not available to support this hypothesis. Waist circumference and body mass index are associated with increased risk of colorectal cancer.

To interpret HRQoL data precisely, knowledge of the content, scoring, reliability, and validity of a questionnaire is important. Recently, there is a growing interest in the assessment of HRQoL in the field of hemophilia; results are presented for pediatric and adult hemophilia patients. “
“Summary.  Pregnancy, labour and delivery present intrinsic haemostatic challenges to women with and carriers of bleeding disorders

and their offspring. Deficiency of fibrinogen and factor XIII are associated with miscarriage, placental abruption and foetal loss. The risk of antenatal complications including antepartum haemorrhage DAPT mouse is unknown in women with other bleeding disorders. There is a significant risk of postpartum haemorrhage (primary and secondary) in women with all types of bleeding disorders. This can be serious and life threatening in those with severe defects such as Bernard Soulier syndrome and Glanzmann’s thrombasthenia. Three to four percent of infants with haemophilia experience cranial bleeding that occurs during labour and delivery.

The safest method of delivery for affected babies remains controversial. However, the rate of planned Caesarean section is increasing among known carriers of haemophilia. If vaginal delivery is planned, prolonged labour and difficult delivery especially vacuum extraction are associated with the highest risk of cranial bleeding and should be avoided. The optimal management medchemexpress of pregnancy in women with inherited bleeding disorders requires a multidisciplinary approach and advanced individualized management plan taking check details into consideration obstetric and bleeding risk factors. Women with mild or moderate bleeding disorders can be managed at their local maternity unit in close collaboration

with a tertiary centre. However, those with severe or rare disorders or carrying an affected infant should be managed in a tertiary centre with an onsite Haemophilia centre. “
“Summary.  Factor replacement with BIOSTATE®, a factor VIII (FVIII)/von Willebrand factor concentrate, forms the mainstay of treatment for children with von Willebrand disorder (VWD) in Australia and New Zealand. However, published data on the clinical efficacy and safety of BIOSTATE in the VWD paediatric population are limited. We retrospectively assessed the efficacy and safety of BIOSTATE in 43 children with VWD who received treatment for surgery, non-surgical bleeds or continuous prophylaxis at eight paediatric haemophilia centres in Australia and New Zealand. Data were collected on patient demographics, disease history, treatment history, dosage, administration, adverse reactions, concomitant medications and excessive bleeding events. BIOSTATE provided excellent/good haemostatic efficacy in 90% of surgical procedures (n = 42) with a mean daily FVIII dose of 47 IU FVIII:C kg−1 and a median treatment duration of 3 days.

As the BDD long-acting products come into the mainstream

of haemophilia care, however, it is likely that laboratories will need to offer a range of FVIII activity assays with the real possibility of requiring a different assay for each long-acting FVIII product. While this editorial dealt with FVIII products, the new generation FIX concentrates have similar issues. MM has acted as consultant to CSL Behring and NovoNordisk. He took part in an Advisory Panel organized by BPL and gave lectures and his institution has received honoraria for Baxter, Bayer, Biogen Idec, Biotest, Octapharma, Pfizer and SOBI. He has received travel support from Baxter and Bayer. FP has received honoraria selleckchem for participating as speaker at educational meetings organized by Novo Nordisk, CSL Behring, Bayer and Baxter. Research Grant: Novo Nordisk (for FXIII deficiency). “
“Prophylaxis, i.e. regular buy Saracatinib preventive infusions of factor replacement therapy [Factor VIII (FVIII) or Factor IX (FIX)] [1,2], is widely accepted as the gold-standard treatment in children with severe haemophilia [3,4]. Long-term prophylaxis has proven effective in reducing bleeds and thus preventing haemophilic arthropathy [5–7]. Given the acceptance of prophylaxis as a mainstay of bleeding control and prevention in patients with haemophilia, it is surprising that unresolved differences remain concerning

regimen implementation and dosing schedules. Treatment of patients who develop inhibitors (antibodies) to factor replacement may include prophylaxis with bypass agents, 上海皓元 but few results are available in this field and evidence for efficacy are of the lowest level. Prevention

in patients with haemophilia’ was an international meeting held in Marseille, France, on 2 July 2009, that involved world-renowned experts based in Europe and North America who met to review country-specific variations in current prophylaxis practice, and discuss future directions in haemophilia management for patients with and without inhibitor. This supplement is a compilation of the presentations and discussions held at the meeting that highlight experience with haemophilia prophylaxis in a global context, while also reviewing current data and areas for ongoing research. Frequency of prophylaxis use in boys without inhibitor varies between countries, which may be a reflection of differences in timing of treatment initiation or intensity of treatment in the regimens used. In the first article of this supplement, Professors Rolf Ljung, Manuel Carcao and I discuss current prophylaxis treatment strategies employed in Swedish, Canadian and French centres. Using these examples, the authors outline areas of agreement (e.g. early prophylaxis) or debate (e.g. when to intensify treatment) that, with further refinement, could be used to optimize practice approach.

5A]). Hepatic expression of SREBP-1c, ACC1, and FAS was higher in IL-6−/− mice but lower in IL-10−/− mice compared with those in

WT mice (Fig. 5A,B). Reduced expression of these genes in IL-10−/− mice was partially reversed in IL-10−/−IL-6−/− dKO mice (Fig. 5A,B). Activation of adenosine monophosphate-activated protein kinase (AMPK) plays a key role in controlling lipid metabolism by phosphorylating and subsequently inhibiting ACC and suppressing the expression of ACC and FAS through down-regulation of SREBP-1c.32 ACC is an important enzyme for fatty acid synthesis, which catalyzes the first step in de novo fatty acid biosynthesis by converting acetyl coenzyme A to malonyl coenzyme A. Malonyl coenzyme A acts as a potent inhibitor of fatty acid oxidation by inhibiting carnitine palmitoyltransferase 1 (CPT-1), Dabrafenib in vitro which transports fatty acids into the mitochondria for oxidation.33, 34 As shown in Fig. 5, expression of activated (i.e., phosphorylated) AMPK (pAMPK) was significantly higher in IL-10−/− mice than that in WT mice in both the selleckchem STD and

HFD groups, whereas such up-regulation was diminished in IL-10−/−IL-6−/− mice. Expression of pAMPK was comparable between IL-6−/− mice and WT mice. Consistent with the elevated levels of pAMPK, IL-10−/− mice had higher levels of inhibited (i.e., phosphorylated) ACC1 (pACC1) compared with WT mice. Such elevated phosphorylated ACC1 was reduced in IL-10−/−IL-6−/− mice versus IL-10−/− mice. In addition, hepatic expression of CPT1 was higher in HFD-fed IL-10−/− mice compared with WT mice. An additional deletion of IL-6 reduced hepatic CPT1 expression in IL-10−/−IL-6−/− mice versus IL-10−/− mice. Expression of these lipid metabolism-associated genes were also examined in WT, IL-10−/−, and IL-10−/− STAT3Hep−/− mice (Fig. 6). Compared with WT mice, IL-10−/− mice had reduced expression of SREBP-1c, ACC1, and MCE公司 FAS but enhanced expression of pAMPK, pACC1, and CPT-1 in the liver. These

dysregulations were partially corrected in IL-10−/− STAT3Hep−/− mice. In this article, we have demonstrated that IL-10−/− mice have greater liver inflammatory response but less steatosis and liver injury compared with WT mice after feeding with an ETOH or HFD diet. Our data suggest that in our models, inflammatory response reduces rather than promotes steatosis through activation of hepatic IL-6/STAT3, which subsequently inhibits the expression of lipogenic genes (SREBP-1c, ACC1, and FAS). In concert, IL-6 up-regulates the expression of CPT-1 and activates AMPK, which in turn further attenuates the expression of SREBP-1c and its target genes and inhibits ACC1. We have integrated our findings in a model depicting the effects of inflammation on steatosis in IL-10−/− mice (Fig. 7).

“
“The interferon-stimulated gene, viperin, has been shown to have antiviral activity against hepatitis C virus (HCV) in the context of the HCV replicon, although the molecular mechanisms responsible are not well understood. Here, we demonstrate that viperin plays an integral part in the ability of interferon to limit the replication of cell-culture–derived HCV (JFH-1) that accurately reflects the complete viral life cycle. Using confocal microscopy and fluorescence resonance energy transfer (FRET) analysis, we demonstrate that viperin localizes and interacts with HCV nonstructural Decitabine concentration protein 5A (NS5A)

at the lipid-droplet (LD) interface. In addition, viperin also associates with NS5A and the proviral cellular factor, human vesicle-associated membrane protein-associated protein check details subtype A (VAP-A), at the HCV replication complex. The ability of viperin to limit

HCV replication was dependent on residues within the C-terminus, as well as an N-terminal amphipathic helix. Removal of the amphipathic helix-redirected viperin from the cytosolic face of the endoplasmic reticulum and the LD to a homogenous cytoplasmic distribution, coinciding with a loss of antiviral effect. C-terminal viperin mutants still localized to the LD interface and replication complexes, but did not interact with NS5A proteins, as determined by FRET analysis. Conclusion: In conclusion, we propose that viperin interacts with NS5A and the host factor, VAP-A, to limit HCV replication at the replication complex. This highlights the complexity of the host control of viral replication by

interferon-stimulated gene expression. (HEPATOLOGY 2011;) Hepatitis C virus (HCV) is a leading cause of chronic hepatitis and liver-related morbidity worldwide. A significant proportion MCE of infected individuals fail to develop an effective host antiviral response and develop a chronic infection, often resulting in a progressive liver disease, including cirrhosis and hepatocellular carcinoma.1 The current standard-of-care therapy for chronic hepatitis C (CHC) is a combination of pegylated interferon alpha (IFN-α) and ribavirin that results in sustained viral clearance in, at best, 50% of patients. Viral infection of mammalian cells results in the activation of a number of viral recognition pathways triggered by replication intermediates and/or viral proteins that ultimately induce innate defenses to limit viral replication.2-4 Pivotal to this antiviral response is the induction of IFN. The type I IFNs (IFN-α and β) are essential for immune defenses against viruses and, after binding to the type I IFN receptor, induce the expression of hundreds of interferon-stimulated genes (ISGs), many of which act to limit viral replication. Although a number of these ISGs have well-characterized antiviral activity (i.e.

S7). Our data suggest that SH-J1 cells infected with Lcn2-expression adenovirus expressed Lcn2 as a 25 kDa protein, after which it was secreted into the

medium where it formed homo- and heterodimeric complexes (Supporting Fig. S8). Immunohistochemical staining in our cohort of patients demonstrated that Lcn2 immunoreactivity was localized at the front of tumor tissue adjacent to the connective matrix (Fig. 1E, upper panels). Lcn2 expression increased in various tumor stages (Fig. 1E, middle panels). However, analysis of tissue microarray (TMA) data from an independent cohort of patients revealed various staining intensities according to the grade of differentiation of HCCs; very little staining was observed in dedifferentiated HCCs (GIII/IV) (Fig. 1E, lower panels). In addition, cells that had undergone Epigenetics Compound Library EMT (SH-J1 and SCK) and EMT-relevant HCCs (GIV) appeared to express less Lcn2 than cells and tissues with an epithelial selleck inhibitor phenotype. Thus, we investigated the correlation between Lcn2 expression and EMT marker expression in HCC samples using TMA analysis (Supporting Fig. S9). The staining intensity of Lcn2 was positively correlated with the expression of epithelial markers such as E-cadherin (P < 0.001), desmoplakin I/II (P < 0.001), and CK18 (P = 0.03), and inversely correlated

with the expression of fibronectin (P = 0.016) and vimentin (P = 0.002), implying that Lcn2 上海皓元医药股份有限公司 expression

is positively correlated with epithelial marker expression and inversely related to EMT marker expression (Supporting Table S6). In our cohort of patients, statistical analysis revealed that Lcn2 immunoreactivity was positively correlated with stage, but not Edmondson differentiation grade or recurrence, in patients without a distant metastasis who underwent surgical resection (Table 1). Immunofluorescence assays revealed that GFP-tagged Lcn2 overlapped with Lcn2 immunoreactivity and that GFP-tagged Lcn2 was localized in both the nucleus and cytoplasm of Hep3B and THLE2 cells (Supporting Fig. S10), whereas endogenous Lcn2 was localized mainly in the cytoplasm. To determine whether human Lcn2 is involved in tumor cell proliferation or tumorigenicity in HCC cells with an EMT phenotype, we established SH-J1 cells stably expressing Lcn2. The transfectants showed a more adherent morphology than vector control cells (Fig. 2A). Furthermore, the tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)−2,5-diphenyl tetrazoliumbromide (MTT) assay revealed that the proliferation rate of SH-J1 cells stably expressing Lcn2 was lower than that of vector control cells (Fig. 2B). Next, Lcn2-expressing SH-J1 cells were inoculated subcutaneously into nude mice to determine whether Lcn2 affects tumorigenicity.

We conducted a systematic review and Meta analysis of all randomized controlled trials (RCT) to study if use of everolimus along AZD1152-HQPA with CNI minimization or withdrawal improves the renal function in LT recipients. Methods: We performed search of all major databases through May 2014. We included studies of primary adult LT recipients with GFR> 30ml/min with use of everolimus either with reduced dose or complete withdrawal of CNI. A random effect model was used to determine the pooled estimate of the change in renal function at 1 year and pooled estimate relative risk (RR) of adverse reactions associated with everolimus

based therapy. Results: Six RCT and 6 observational studies reported the results of everolimus use in LT recipients. Four randomized controlled trials met the inclusion criteria. There were total 883 patients (Everolimus n= 465, control n= 428) with baseline GFR > 50 ml/min in all patients. In 3 RCT everolimus was initiated early at 4 weeks after LT (2 CNI withdrawal and one CNI minimization), whereas in one study

mean time since transplantation was 3 years (CNI withdrawal). At 12 months everolimus use was associated with significant improvement in GFR 7.4 ml/min (095 % CI= 0.28-14.85). In subgroup analysis of three studies Selleck EGFR inhibitor with everolimus initiation at 4 weeks after LT improvement in GFR was 10.2 ml/min (95 % CI= 2.75-17.8). Everolimus use was not associated with increased risk of biopsy proven acute rejection relative risk (RR) =0.70 (95% CI 0.34-1.44)} or wound dehiscence (RR=1.22 T95% CI=0.93-1.61) or increased mortality (RR=1.54 95%CI-0.82-2.88). There was no increased risk of hepatic artery thrombosis (HAT). However, everolimus use was associated with increased risk of infections (RR 1.18, 95% CI 1.04-1.34). In conclusion in LT recipients’ everolimus use without CNI or with reduced dose CNI results in improved renal function at 12 months. Everolimus was not associated with increased risk of death or graft failure or wound dehiscence or hepatic artery thrombosis. Disclosures: The following people have nothing to disclose: Frahad Sahebjam, Sahil

Mittal, Gagan K. Sood Background: Portal vein thrombosis (PVT) medchemexpress is present in an estimated 7.8% of patients undergoing liver transplantation (LT). The decision to anti-coagulate a LT candidate for PVT requires an understanding of the risk of LT with PVT. Aim: To analyze LT outcomes in patients with PVT. Methods: UNOS data (20022013) was used to identify 50,393 adult recipients undergoing first LT (excluding patients with split grafts, donation after cardiac death, live donor and multi-organ transplants). PVT was reported as present at LT in 3321 (6.6%), absent in 45,249 (89.8%) and data missing in 1823 (3.6%) patients. Demographic and clinical characteristics (% or mean± standard deviation) were compared in patients with and without PVT. Patient and graft survival were analyzed by the Kaplan-Meier method (log rank test).

5B). The number of fenestrae in Cas ΔSH3–expressing cells was 0.58 ± 0.16, which was statistically Everolimus supplier significantly low in comparison with those in parental and Cas FL–expressing NP31 cells (P < 0.001; left right bars and middle right bars in Fig. 5C). These results strongly indicate that Cas plays pivotal roles in the regulation of the actin cytoskeleton and in the formation of fenestrae in SECs. Cas is an adaptor/scaffold protein that contributes to various biological

processes through the regulation of actin stress fiber formation.9, 10 Upon physiological and pathological stimuli, Cas becomes tyrosine-phosphorylated mainly in the SD, which offers binding sites for the SH2 domain of downstream target molecules, including CrkII.9, 10 The Cas/CrkII complex sequentially activates downstream effectors, such as Rac and C3G, which consequently reorganize the actin cytoskeleton and finally define cellular dynamics.9, 10 We previously generated mice lacking Cas (Cas−/−) and demonstrated that they died in utero and exhibited cardiovascular anomalies.22 In the present study, we generated mice carrying a hypomorphic Cas allele lacking the exon 2–derived region. Exon 2 was targeted

in this study for several reasons. First, it is the only exon that encodes the whole region of a functional domain of Cas.8 Second, it encodes GSK1120212 SH3, which binds to the proline-rich region of focal adhesion kinase11 and mediates the initial signaling event from the extracellular matrix to intracellular molecules.32, 33

Third, our previous compensation study revealed the importance of SD and SB for cell migration and cell transformation, respectively, but the role of SH3 is less understood.28 Mice harboring Cas with an exon 2 deletion (CasΔex2/Δex2) died as embryos (Table 1) but differed in phenotype from Cas−/− mice; CasΔex2/Δex2 mice exhibited impaired liver development with massive hepatocyte apoptosis (Fig. 2), and in contrast to Cas−/− mice, their cardiovascular system was preserved, presumably because of the conserved ability of Cas Δex2 to partially become tyrosine-phosphorylated and retain CrkII binding32 上海皓元 (Fig. 4). In the former work,22 we noted that Cas−/− mice also showed retarded liver growth. We previously hypothesized it to be secondary to circulatory failure because the Cas protein was barely detectable in hepatocytes, as in this study22 (Fig. 3). However, the current observation that CasΔex2/Δex2 mice exhibit liver degeneration without suffering from cardiovascular anomalies strongly implies that dysfunction of Cas directly impairs liver development. The findings that Cas is preferentially expressed in SECs in the liver (Fig. 3) and that the expression patterns of Cas well correlate with the maturation of sinusoids (Supporting Fig. 1) indicate that Cas is functionally and developmentally involved in SECs and strongly suggest that Cas Δex2 impairs SEC function and leads to hepatocyte apoptosis.

“
“Summary.  Persistence of inhibitors against factor VIII (FVIII) may be a risk factor that increases physical disability in haemophilia A (HA) patients. This study aimed to evaluate prevalence of FVIII inhibitors in previously treated children with severe HA and the impact of persistent inhibitors

on knee joint status and lumbar bone mineral density (BMD). Fifty children with severe HA, FVIII <1%; aged 5–16 years were enrolled in this study; they received plasma-derived FVIII on-demand treatment for 50–250 exposure days (EDs). Inhibitors were checked at Acalabrutinib mouse basal visit and were followed up for 1 year, using Bethesda assay. Cross-sectional clinical scoring and radiological evaluation of the knee joint (by Arnold-Hilgartner staging and Pettersson score), along with lumbar BMD by Dual Energy X-ray Absorptiometry (DEXA) were performed. Patients with persistent inhibitors for 1 to 5 years, median 2.5 years, were 10 (20%). Six had high titre and none of them had completely normal knees, seven had advanced knee arthropathy and six had low lumbar BMD in comparison to 2 and 8 of the 40 patients without inhibitors respectively (P < 0.05). Persistence of inhibitors for more than 2 years without immuno-prophylaxis was a risk factor for joint damage. Low lumbar BMD was found in

88.9% of patients with stages four and five knee arthropathy and in 66.7% of patients with positive hepatitis C. Severe HA children in this Egyptian study had a relatively low prevalence of persistent FVIII inhibitors, which, if not ALK mutation treated, may increase the risk of knee arthropathy and lumbar osteopenia. “
“The increasing emphasis on home-based treatment for the management of children with haemophilia has meant that many of these children no longer regularly report to a medical facility. Consequently, it is difficult to monitor incidence of bleeding episodes. The aim of this study was to assess the feasibility of using a short message service (SMS) to monitor incidence of bleeding episodes in children with haemophilia. One hundred

and four children with moderate and severe MCE haemophilia A or B took part in a 1-year prospective study between 2008 and 2010. Children or their parents were asked to maintain a bleeds diary. They received a weekly SMS asking whether there had been a bleeding episode in the preceding week. Response rates were calculated. Children were followed for a total of 4839 person-weeks. SMS replies were received for 4201 weeks. Thus, the rate of follow-up was 86.8%. Median responses rates were 94.2% (IQR: 86.1–100%). Weekly SMS is a feasible reporting tool for documenting bleeding episodes in children with haemophilia. It is associated with high response rates and minimal expense and intrusion. The use of SMS could be extended to encourage compliance to prophylactic treatment, particularly in adolescents with haemophilia. “
“Summary.