pylori associated to Irritable Bowel Syndrome (IBS) selleck chemical Barrios F. A., Barrios A., Álvarez A., Mendez E., Digestive Endoscopy Unit, Las Torres Clinic, Quetzaltenango, Guatemala. AIMS. Objective: To determine the role of H. Pylori in the pathogenesis of Irritable Bowel Syndrome (IBS). We previously demonstrated that the presence of biliary acids in the stomach (Duodeno-gastric Reflux Disease, DGRD) changes the gastric pH, favoring the growth of H. Pylori, as this bacterium is sensitive to pH values bellow 4.5. We investigated that the presence of H. Pylori in the colonic

mucosa in patients with IBD. Methods: Colonoscopy, Biopsy and Rapid Urease Test (CLO-Test). All patients have been diagnosed and treated for IBS, without any improvement. Results: Universe: 47 patients were studied. MALE: 21 (45%), FEMALE: 26 (55%). H. Pylori Positives 25 (53%). H. Pylori Negatives 22 (47%). One patient in this study, previously presented

Colonic Carcinoma. Conclusion: All patients showed improvement, including the patient with Colonic Carcinoma, which in the beginning presented 99% of stricture and after one month of treatment, the stricture decreased to 50%. Accordingly, we consider that the presence of H. Pylori in the colonic mucosa is just another important co-factor in the pathogenesis of IBS and probably in the development of Colonic Carcinoma. Subjects were administered H. Pylori treatment. Key Word(s): 1. IBD; 2. H. pylori; 3. Colonic Cancer; 4. Clotest; Presenting Author: YAN PAN Additional Authors: QIN OUYANG Corresponding Author: find more QIN OUYANG Affiliations: Department of Gastroenterology, West China Hospital Objective: Ulcerative colitis (UC) is thought to result from inappropriate and ongoing activation of the mucosal immune system. In China, UC mostly affect

left sided colon and topical therapy play a vital role in UC treatment. The trial was carried out to investigate the efficacy and safety of Baweixileisan (BWXLS) enema, a compound of traditional Chinese herbal medicine and to explore the therapeutical MCE公司 mechanisms. Methods: A prospective randomized controlled trial was carried out. Patients with active left-sided mild to moderate UC from the outpatient clinic of West China Hospital from June, 2009 to October, 2010 were allocated alternatively into treatment group with BWXLS enama 1 g/60 ml and the control group with hydrocortisone enema 50 mg/60 ml for 4 weeks. The clinical, endoscopic and histologic manifestations were evaluated according to the protocols in the end of trial. The expression of TLR4, NF-κB and Occludin were investigated immunohistochemically before and after the treatment. Results: 103 patients were included. The clinical remission rate and response rate in the treatment group were 78.2% and 89.1% respectively and 58.3% and 72.9% in the control (p < 0.05). Endoscopically, mucosal healing rate was 50.9% in the treatment group and 31.3% in the control (p < 0.05).

Podarcis muralis were able to return home as 56.7% of translocated individuals in the first site and 35.1% of translocated individuals in the second site successfully returned to their home range. The homing ability decreased with increasing distances, whereas body size positively affected homing behaviour, probably depending on the territoriality of adult lizards. More interestingly, homing performance differed among colour morphs, as yellow lizards of both

sexes had significantly better homing skill than other morphs. “
“Locomotor capacity is often Cell Cycle inhibitor considered an excellent measure of whole animal performance because it requires the integrated functioning of many morphological, physiological (and biochemical) traits.

However, because studies tend to focus on either structural or functional suits of traits, we know little on whether and how morphological and physiological traits coevolve to produce adequate locomotor capacities. Hence, we investigate the evolutionary relationships between morphological and physiological parameters related to exercise physiology, using tropidurine lizards as a model. We employ a phylogenetic principal component analysis (PCA) to identify variable clusters (factors) related to morphology, energetic metabolism and muscle metabolism, and then analyze the relationships between these clusters and measures of locomotor performance, using two models (star and hierarchical phylogenies). Our data indicate that sprint performance is enhanced by simultaneous evolutionary tendencies affecting

relative limb and tail size and physiological traits. Selleckchem CHIR99021 Specifically, the high absolute sprint speeds exhibited by tropidurines from the sand dunes are explained by longer limbs, feet and tails and an increased proportion of glycolytic fibers in the leg muscle, contrasting with their lower capacity for overall oxidative metabolism [principal component (PC1)]. However, when sprint speeds are corrected for body size, performance correlates with a cluster (PC3) composed by moderate loads for activity metabolic rate and body size. The simultaneous measurement of morphological and physiological parameters is a powerful medchemexpress tool for exploring patterns of coadaptation and proposing morphophysiological associations that are not directly predictable from theory. This approach may trigger novel directions for investigating the evolution of form and function, particularly in the context of organismal performance. “
“As birds have a diversity of locomotor behaviors, their skeleton is subjected to a variety of mechanical constraints (gravitational, aerodynamic and sometimes hydrodynamic forces). Yet, only minor modifications in post-cranial skeleton shape are observed across the diversity of avian species in comparison with other vertebrates. The goal of this study was to explore potential morphological adjustments that allow locomotion in different habitats in Anatidae.

The entire NS5A coding region of a GT-1b Con1 replicon was replaced with cDNA of NS5A derived from six BL specimens of GT-1b-infected subjects14, 16 (Table 1A). HCV NS5A sequences derived from clinical specimens of GT-1b share a high degree of amino-acid identity with the GT-1b Con1 replicon (≥95.2%). As expected, even greater identity (≥98.9%) was observed between multiple clones derived from the same specimen (Table 1A). Special attention was given to the signature Temsirolimus supplier polymorphisms of each specimen to ensure

no cross-contamination among different specimens and/or replicons (data not shown). The replication-enhancing adaptive mutation, S2204I, in NS5A was introduced into all clones to enhance the ability for replicon replication. check details To obtain reliable EC50 values, hybrid replicons with a replication window (i.e., signal-to-noise ratio) ≥3 were used in transient replication assays (Table 1A). The Con1 replicon was used as a wild-type (WT) control for EC50 determination and also as a comparator for replication ability. Averaged EC50 and standard deviation (SD) values for multiple clones derived from each specimen are shown in Table 1B. NS3 protease and NS5B polymerase inhibitors were used as assay

controls. Previously characterized resistant substitutions were not identified by population sequencing in the BL specimens, except for subject T.14, 16 The EC50 values for BMS-790052 with clones derived from BL ranged from 0.001 to 0.003 nM, which is similar to WT (Con1) replicon (0.003 nM for BMS-790052; Table medchemexpress 1B). The specimen derived from subject T had ∼100% NS5A Q54H-Y93H substitutions at BL.16 The EC50 value for BMS-790052 on this variant was 0.050 nM, or ∼23-fold resistance to BMS-790052 (Table 1B).15, 16 The entire NS5A coding region of a GT-1a (H77c) replicon was replaced with cDNA of NS5A derived from 12 clinical specimens of 11 GT-1a-infected subjects.14, 16 Ten cDNAs were derived from BL specimens, one from a T4 specimen (4 hours after the first dosing), and one from a day 14 specimen (T312) (Table 2A) of subject P who received 60 mg of BMS-790052 once-daily as

monotherapy for 14 days.16 The replication-enhancing adaptive mutation, S2204I, in NS5A was introduced into all clones to enhance replicon replication. A total of 12 clones derived from subject E with a replication window (i.e., signal-to-noise ratio) less than 2 were not used for EC50 determinations. The amino-acid sequence identity between the NS5A consensus of each specimen and the GT-1a replicon, H77c, is ≥92.6%, and the identity between each clone and the consensus of the individual specimen is ≥93.3% (Table 2A). The EC50 values of BMS-790052 were determined with these GT-1a hybrid replicons (Table 2B). No previously characterized resistance substitutions were identified by population sequencing in the BL specimens. The averaged EC50 values ranged from 0.003 to 0.

Western blot analysis showed that treatment with the Gli inhibitor GANT61 induced the accumulation of BVD-523 clinical trial LC3II in all three HCC cell lines (Fig. 2A). Treatment with the Smo inhibitor GDC-0449 also increased the LC3II level, albeit the effect was less prominent compared to GANT61. In contrast, activation of Hh signaling by its ligand (Shh) and agonists (SAG or Pur) decreased the level of LC3II. In addition to LC3II western blot, we further used fluorescence microscopy to determine the redistribution of GFP-LC3 (LC3 is a mammalian homolog of yeast Atg8 and is

normally expressed in a diffuse pattern in resting cells; during autophagy, autophagosomes engulf bulk cytoplasmic constituents including proteins and organelles, and along this process, the cytosolic form of LC3 [LC3I] is conjugated to phosphatidylethanolamine to form LC3II, which is recruited to autophagosomal membranes resulting in a more punctate distribution pattern). As shown in Fig. 2B, GANT61 treatment induced GFP-LC3

dot redistribution from a diffuse pattern to a punctate cytoplasmic pattern (GFP-LC3 puncta) in all three HCC cell lines. The Smo inhibitor GDC-0449 also induced GFP-LC3 puncta formation, although the effect was slightly less prominent compared to GANT61. These findings indicate that inhibition of Hh signaling induces autophagy and that the Gli inhibitor GANT61 is a potent agent that induces autophagy. Although GANT61-induced autophagy is observed in all three HCC cell lines, the effect is most prominent Epigenetics Compound Library purchase in Huh7 cells (Fig. 2A). To further document the effect of GANT61 on autophagy, we performed dose-dependent experiments in Huh7 cells (the cells were treated with GANT61 at 5 μM, 10 μM, or 20 μM concentration for 24 and 48 hours; quantitative assessment for the ratio of LC3II to LC3I was used as the primary indicator of autophagy induction). As shown in Fig. 2C, GANT61-induced LC3II accumulation in a dose-dependent manner. Increased detection of autophagic markers, such as LC3II accumulation and GFP-LC3 redistribution,

can result from either increased autophagosome formation or inhibition of ongoing autophagosomal maturation.[10] To delineate these possibilities, the cells were pretreated with 3-methyladenine (3-MA, a classical inhibitor of autophagy at the sequestration stage) or E-64d/pepstatin A (lysosomal protease inhibitors that block autophagolysosomal MCE degradation) prior to GANT61 treatment. As shown in Fig. 2D, 3-MA treatment abolished GANT61-induced LC3-II formation, whereas E-64d/pepstatin A treatment augmented GANT61-induced LC3-II accumulation. The protein, p62/SQSTM1, binds directly to LC3, incorporates into the completed autophagosomes, and becomes degraded in autolysosomes. In our system we observed that GANT61 treatment decreased the level of p62 in Huh7 cells and the effect was reversed by 3-MA and E-64d/pepstatin A. Taken together, these findings suggest that the Gli inhibitor GANT61 enhanced autophagic flux.

Generally, 15–25% of cases have colorectal liver metastasis (CRLM) at diagnosis.[1, 2] Furthermore, CRLM occurs in 25–50% of cases with the resection of primary colorectal tumor over 3 years.[3-5] Hepatic resection is accepted as the only treatment contributing to the long-term survival and cure of patients with CRLM.[6] However, only 15–20% of patients with CRLM are considered candidates for hepatic resection at the time of presentation.[7-10] The significance of other tumor destruction modalities, such as radiofrequency ablation, remains controversial.[11] Of those patients who

undergo hepatic resection, there are at least two categories of patients with CRLM. The first category is clearly or potentially resectable at the time

of presentation. Smoothened Agonist purchase The second category is initially unresectable, but convertible to be resectable after treatment with anticancer agents including molecular targeted agents, which we refer to as “conversion surgery”. The purpose of neoadjuvant chemotherapy for resectable CRLM is to downsize CRLM lesions and maximize the remnant liver as well as to reduce the residual micrometastasis, while less extensive resections can be carried out in keeping with the curative intent. However, until now, the role of neoadjuvant therapy prior to the resection of CRLM is not yet proven and remains controversial. selleck screening library The largest prospective trial consisted of 364 patients with less than five initially resectable CRLM (European Organization for Research and Treatment of Cancer Intergroup 40983 trial) randomized with perioperative chemotherapy (four to six preoperative and six postoperative cycles of FOLFOX4) or surgery alone, and showed a clinical benefit in 3-year progression-free survival (36.2% vs 28.1%) but not in 5-year overall survival.[12] The FOLFOX regimen may reduce the risk of events in terms of progression-free survival but not necessarily improve long-term survival compared with surgery alone in eligible and initially resectable patients. On the other hand, regarding initially unresectable CRLM, the “conversion surgery” strategy

has been widely used and accepted. Actually, 5-fluorouracil (5-FU)/leucovorin (LV) plus oxaliplatin (L-OHP); FOLFOX or irinotecan (Iri); FOLFIRI or combination 上海皓元 of both; FOLFOXIRI with or without molecular-targeted agents as preoperative strategy have recently achieved higher conversion rates and better clinical outcomes.[13-20] Particularly in L-OHP-based chemotherapy, the conversion rate ranged 7–51% in patients with unresectable CRLM. The effectiveness of triple combination chemotherapy, FOLFOXIRI, for patients with initially unresectable CRLM has been reported to have an improved response rate (60% vs 34%) and higher R0 resection rate among patients with CRLM only compared with the FOLFIRI regimen (36% vs 12%).

7 Taking all of these observations together, it is likely that serotonin decreases hepatocyte proliferation by binding

to the 5-HT2B receptor on activated HSCs, whereas serotonin promotes hepatocyte proliferation through the 5-HT2A receptor on hepatocytes in healthy livers (Fig. 1). The authors AZD3965 further determined the mechanism as to how serotonin, through the 5-HT2B receptor, induces TGFB1 gene expression. Binding of serotonin to the 5-HT2B receptor induces an activation of mitogen-activated protein kinase 1 and 2, which then phosphorylates JunD, a transcription factor that binds to the promoter region of the TGFB1 gene, thereby increasing TGF-β1 expression in activated HSCs. Moreover, expression of the 5-HT2B receptor is context-dependent. Its expression is relatively low in healthy livers,8 but increases significantly in activated HSCs. These differences in the expression pattern of serotonin receptors may reflect the varying stages of hepatocyte proliferation mediated by serotonin in healthy versus diseased livers. Furthermore, apoptotic clearance of activated HSCs that occurs during the resolving stage of wound repair may switch serotonin signaling in favor of liver regeneration via 5-HT2A receptors on hepatocytes. The authors also showed a significant increase in expression

of the 5-HT2B receptor in HSCs isolated from mice undergoing PHx. This finding raises an interesting question about the Staurosporine price activation status of HSCs in the regenerating liver. If 5-HT2B receptors are specifically expressed in activated HSCs, those HSCs found in the regenerating liver after PHx could also be activated and similar to those found 上海皓元 in fibrotic livers. Given that TGF-β1 is known to inhibit hepatocyte proliferation in the regenerating liver,11 those HSCs, through the 5-HT2B–mediated

TGF-β1 synthesis, may also help the liver to end regeneration. This aspect of HSC biology warrants further investigation. From a pathophysiological perspective, Wanless and colleagues many years ago showed that extensive intrahepatic thrombosis was found in 70% of cirrhotic explants.12 Because platelets, the major source of serotonin, initiate the thrombotic cascade, it can be presumed that the areas of thrombosis would also be associated with the greatest degree of serotonin signaling and fibrosis. In fact, thrombosis was associated with the most confluent areas of fibrosis and parenchymal extinction,12 thereby providing an anatomical correlation with the findings presented in the current study. The current findings, moreover, may extend to other vascular-related liver disorders where thrombosis is a hallmark. The findings of this study also have potential therapeutic implications.

For the experiments, GES-1 cells were seeded at a density of 5 × 105 cells/mL of medium MG-132 supplier in six-well plates and grown to 80% confluence prior to the

experiments. Helicobacter pylori strain SS1 (both VacA+ and CagA+) was obtained from the National Institute for Communicable Disease Control and Prevention (NICDC), Beijing, China. The strains were grown in a microaerobic humidified atmosphere (5% O2, 10% CO2, 85% N2) on 10% lysed sheep blood Columbia agar at 37 °C. After 48–72 h, bacteria were harvested in phosphate-buffered saline (PBS) (pH 7.4) or in RPMI-1640 medium without antibiotics, resuspended to a concentration of 6 × 108 CFU/mL and used immediately. Subconfluent GES-1 cells were cultured alone or with various doses of freshly harvested H. pylori (1 × 104–6 × 108 CFU/mL) for various periods of time. At the end of the treatment, GES-1 cells were harvested and processed for the preparation of whole-cell extracts and western blotting. Total RNA was isolated from GES-1 cells

or gastric mucosa tissues using the Trizol reagent (BBI) according to the manufacturer’s instructions. The first-strand cDNAs were synthesized from total RNA using reverse transcriptase (Takara, Dalian, China) according to the manufacturer’s instructions. All PCR primers were synthesized by Bio Basic Inc. (Shanghai, China) (Table 1). cDNA samples in each treatment group were pooled in subsequent experiments and reactions d Selleck PKC412 set in a 15-μL reaction mixture in 96-well plates. Real-time RT-PCR quantitation for individual target mRNA was performed on an ABI Model 7500 Sequence Detector (Applied Biosystems, Foster City, CA) using a TaKaRa real-time PCR kit. RT-PCRs were performed using the following parameters: 95 °C for 2 min followed by 40 cycles of 95 °C for 15 s, 60 °C for 34 s and

72 °C for 15 s. For each sample, a melting curve was generated at the end of the reaction to ensure specificity. Gene expression levels were normalized to those of GAPDH, and the data were analyzed using comparative cycle medchemexpress threshold calculations. Data were expressed as fold changes relative to the control group. Each real-time PCR experiment was run three times. The comparative 2− ΔΔCT method was used for quantification and statistical analysis (the results were expressed as fold changes relative to normal controls). GES-1 cells were transfected with either nonspecific siRNA oligomers or siRNAs targeting the VDR mRNA (Invitrogen, Shanghai, China) by using the Lipofectamine 2000 reagent (Invitrogen) according to the manufacturer’s instructions. The cells were seeded into 24-well plates and grown in phenol red-free RPMI1640 supplemented with 5% FBS.

For the experiments, GES-1 cells were seeded at a density of 5 × 105 cells/mL of medium Palbociclib purchase in six-well plates and grown to 80% confluence prior to the

experiments. Helicobacter pylori strain SS1 (both VacA+ and CagA+) was obtained from the National Institute for Communicable Disease Control and Prevention (NICDC), Beijing, China. The strains were grown in a microaerobic humidified atmosphere (5% O2, 10% CO2, 85% N2) on 10% lysed sheep blood Columbia agar at 37 °C. After 48–72 h, bacteria were harvested in phosphate-buffered saline (PBS) (pH 7.4) or in RPMI-1640 medium without antibiotics, resuspended to a concentration of 6 × 108 CFU/mL and used immediately. Subconfluent GES-1 cells were cultured alone or with various doses of freshly harvested H. pylori (1 × 104–6 × 108 CFU/mL) for various periods of time. At the end of the treatment, GES-1 cells were harvested and processed for the preparation of whole-cell extracts and western blotting. Total RNA was isolated from GES-1 cells

or gastric mucosa tissues using the Trizol reagent (BBI) according to the manufacturer’s instructions. The first-strand cDNAs were synthesized from total RNA using reverse transcriptase (Takara, Dalian, China) according to the manufacturer’s instructions. All PCR primers were synthesized by Bio Basic Inc. (Shanghai, China) (Table 1). cDNA samples in each treatment group were pooled in subsequent experiments and reactions d see more set in a 15-μL reaction mixture in 96-well plates. Real-time RT-PCR quantitation for individual target mRNA was performed on an ABI Model 7500 Sequence Detector (Applied Biosystems, Foster City, CA) using a TaKaRa real-time PCR kit. RT-PCRs were performed using the following parameters: 95 °C for 2 min followed by 40 cycles of 95 °C for 15 s, 60 °C for 34 s and

72 °C for 15 s. For each sample, a melting curve was generated at the end of the reaction to ensure specificity. Gene expression levels were normalized to those of GAPDH, and the data were analyzed using comparative cycle MCE公司 threshold calculations. Data were expressed as fold changes relative to the control group. Each real-time PCR experiment was run three times. The comparative 2− ΔΔCT method was used for quantification and statistical analysis (the results were expressed as fold changes relative to normal controls). GES-1 cells were transfected with either nonspecific siRNA oligomers or siRNAs targeting the VDR mRNA (Invitrogen, Shanghai, China) by using the Lipofectamine 2000 reagent (Invitrogen) according to the manufacturer’s instructions. The cells were seeded into 24-well plates and grown in phenol red-free RPMI1640 supplemented with 5% FBS.

4% (5/7) in partial responders with genotype 1b treated with response-guided therapy, namely, patients who achieved and did not achieve www.selleckchem.com/products/PLX-4032.html eRVR were treated with T12PR24 and T12PR48, respectively.[15]

These results suggest that approximately 70% of partial responders may achieve SVR using response-guided therapy, but the SVR rate was extremely low in null responders treated with T12PR24. Although the study of Muir et al. was not a randomized controlled trial study, their results indicated that T12PR48 may improve the SVR rate in null responders to a greater extent than T12PR24.[15] The present study revealed the SVR rates of partial and null responders treated with T12PR24 were 70.0% and 22.6%, respectively. The lower SVR rate in null responders than partial responders is concordant with the results of the previous study on T12PR24.[15] To our knowledge, besides our previous reports,[22-24] only two studies performed in Japan have analyzed non-responders to PR classified as partial and null responders.[16, 25] Akuta et al. reported that the SVR rates in partial and null responders treated with T12PR24 in clinical trials were 50% (4/8) and 0% (0/7), respectively.[16] Meanwhile, Ogawa Selleck ZVADFMK et al. recently reported that the SVR rates in partial and null responders for CHC patients with advanced fibrosis (METAVIR score F3–4) treated with T12PR24 in clinical practice were 50% (9/18) and 16.7% (2/12), respectively.[25]

Similarly, the SVR rate was medchemexpress lower in null responders than partial responders in the present study, when treated with T12PR24. Genetic variations near the IL28B gene (rs8099917 and rs12979860) are strongly associated with treatment outcome of PR.[32-34] In addition, these genetic variations are also strong predictors of SVR with the T12PR24 regimen when including both treatment-naïve and treatment-experienced patients.[14, 20-25, 35] However, Pol et al. reported the IL28B genotype (rs12979860) has a limited and non-significant impact on SVR in treatment-experienced patients treated with T12PR48 regardless of relapsers, partial responders or null responders to previous PR.[19] In the present study, the SVR rate of partial

responders with the TT genotype treated with T12PR24 was very high at approximately 90%, whereas that in patients with the non-TT genotype was significantly lower. Similarly, among null responders, the SVR rate was significantly lower in those with the non-TT genotype than those with the TT genotype. Ogawa et al. reported a similar trend that among previous partial and null responders treated with T12PR24, the SVR rate was lower in patients with the non-TT genotype than those with the TT genotype.[25] In contrast, the SVR rate did not differ significantly between either partial or null responders with the IL28B TT or non-TT genotype treated with T12PR48 in our study, although there were too few patients to make a meaningful comparison.

Other DAA combinations under evaluation for G1-HCV include SOF/simeprevir, SOF/daclatasvir, SOF/GS9669, ABT450/r/ABT267/ABT-333+/− ribavirin, daclatasvir/asunaprevir and faldaprevir/BI207127+/−

RBV. These regimens have not yet been evaluated in patients with bleeding disorders, but would be expected to be effective. G3-HCV is emerging as more difficult to treat in the interferon-free era, with a longer duration of treatment with SOF/RBV appearing beneficial [6]. Studies of SOF combined with NS5A inhibitors for treatment of G3-HCV are ongoing. All-oral, interferon-free treatment of HCV is now a reality, although the optimal regimens are still being evaluated. Elderly patients with haemophilia (PWH) have different problems to patients of younger generations. With ageing, patients GSK-3 inhibition suffer from haemophilia-related co-morbidities like chronic arthritis and viral infection. Age-related co-morbidities, internal and cardiovascular disease (CVD), urological problems and cancer are becoming more common. It is important to look for ways

to prevent or reduce co-morbidity and improve the quality of life of ageing PWH. Haemophilia care givers should play a role in this and during annual check-ups not only pay attention to haematological and orthopaedic aspects of haemophilia, but also to age-related co-morbidities. Co-morbidities in PWH may lead to complex treatment. Lack of coordination between various healthcare workers BYL719 nmr may result in slow and ponderous healthcare delivery, uncontrolled polypharmacy, and further loss of wellbeing and quality of life. Therefore,

haemophilia centres should play an important part in coordinating care for these patients. Except for hepatocellular carcinoma, due to chronic hepatitis C virus (HCV) infection, the risk of developing malignancy is not increased in PWH not infected with HIV. In general treatment for PWH is the same as for other patients. When chemotherapy is required, blood counts may drop and it is recommended to perform blood counts regularly. In case of thrombocytopenia, intensive prophylaxis with clotting factor may be indicated [14]. Haemophilia patients have a higher mean blood pressure and use more MCE antihypertensive medication than the general population [15]. The cause of this increased prevalence is not completely understood. A recent Dutch study showed that the prevalence of hypertension was significantly higher in PWH than in the general population in the age categories 40–49 years [41% (95% CI, 34–48) vs. 29% (95% CI, 26–32)] and 60 years or older [82% (95% CI, 75–88) vs. 71% (95% CI, 68–74)]. In this study, hypertension was not significantly associated with severity of haemophilia, renal function, a history of renal bleeding or infection with HCV or HIV, but it was associated with being overweight/obesity and age [16]. As hypertension is a risk factor for CVD and intracranial bleeding, blood pressure in PWH should be regularly checked and hypertension adequately treated.