“
“Neurologists must entertain a broad differential diagnosis when considering a patient with cavernous sinus syndrome, including neoplasm, trauma, vascular causes, inflammatory processes, and infections. We report the case of a 37-year-old woman initially diagnosed with cavernous sinus syndrome, where subsequent investigations revealed findings of Takayasu’s arteritis, a large vessel vasculitis. The patient also tested positive for perinuclear antineutrophil cytoplasmic antibodies, suggesting the possibility of a vasculitic spectrum disorder although no clinical features of Wegener’s granulomatosis

were present. Criteria for Takayasu’s arteritis and its protean neurologic manifestations are reviewed. This case highlights the spectrum of

vasculitic conditions that may be associated anti-PD-1 antibody inhibitor with cavernous sinus inflammation. “
“(Headache 2011;51:287-291) Background.— LY2157299 cost Zonisamide, a sulfonamide analog, is an antiepileptic drug with mechanisms of action similar to topiramate. Because of its pharmacodynamic and pharmacokinetics profiles, zonisamide is also potentially suitable for migraine prevention. Methods.— Tolerability and effectiveness of zonisamide for migraine prophylaxis in patients with a good response to topiramate, but interrupting it for intolerable side effects, were evaluated in 34 patients. After a 1-month period of wash-out, patients were treated with zonisamide (up to a 100 mg/day dosage) for 6 consecutive months. Results.— Zonisamide was well tolerated, only 4 (12%) patients reported transient and tolerable side Evodiamine effects. Mean number of days with headache per month was reduced from 14.9 ± 5.3 during the wash-out period to 2.5 ± 0.6 after 6 months of zonisamide (P < .001). We observed a significant reduction in headache severity and disability, as assessed by visual analog scale and migraine disability assessment scale. Finally, when compared with the 1-month period prior to starting zonisamide, a reduced use of analgesics was recorded

at the end of the follow-up. Conclusion.— Our findings support the use of zonisamide as an alternative therapy for migraine prevention in patients with good response, but poor tolerance to topiramate. “
“(Headache 2011;51:923-931) Sex and gender differences in humans are being increasingly recognized not only in experimental pain paradigms but also clinically. Women experience various chronic pain conditions such as headache more than men and evidence differences in pain threshold and pain tolerance experimentally. In addition to biological underpinnings, psychosocial factors such as gender and social role expectations, coping strategies, and affective variables likely contribute to observed sex- and gender-related differences in headache. The present narrative reviews and summarizes extant literature pertaining to these psychosocial factors.

A major contributor to this failure is likely to be the adipose tissue. An insufficient response could initiate a cascade of events Decitabine including rapid hypertrophy of adipocytes without compensatory proliferation, leading to ectopic lipid deposition in muscle and liver. This worsens insulin resistance, further impairing adipocyte proliferation and reinforcing the cycle of impaired metabolic regulation (Fig. 6). In this autopropagative scenario, key adipocyte proteins are likely to play a role, including CD36 which also governs fatty

acid uptake in fat tissue and muscle,133,159 phospholipases, such as members of the adiponutrin family mentioned earlier,84–86 and HSL. Adipokines are important players in this process:160 increased expression and secretion of pro-inflammatory adipokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6,161 worsens insulin resistance, while anti-inflammatory and anti-lipotoxic adipokines, including adiponectin and leptin, are dysregulated. Thus, leptin levels rise but tissue leptin resistance develops,48,54

thereby impairing INK 128 the ability of leptin to decrease food intake, increase energy expenditure and prevent partitioning of lipid into ectopic stores such as muscle and liver (where leptin physiologically activates AMPK and suppresses stearoyl Co-A desaturase-1 [SCD1]). In contrast, adiponectin levels fall in both metabolic syndrome and NASH (reviewed in 7,138,160), attenuating the anti-inflammatory and pro-proliferative effects of this adipokine on adipose.162 Low serum adiponectin levels also alter lipid partitioning in hepatocytes, where adiponectin switches the metabolic profile by inhibiting lipogenesis and

activating fatty acid oxidation through effects on AMPK and PPAR-α.163,164 As evidenced by the adiponectin transgenic ob/ob mouse,135 enhancing subcutaneous fat stores can www.selleck.co.jp/products/erastin.html reverse steatosis and insulin resistance by restoring ‘metabolically healthy’ whole-body lipid distribution. Likewise, treating NASH patients with thiazolidinedione PPAR-γ agonists decreases hepatic lipid content while body weight increases because more fat is stored subcutaneously.14,165 Thus, Harrison and colleagues noted that the most impressive pathophysiological change after institution of pioglitazone therapy in NASH was reversal of adipose insulin resistance,166 thereby restituting HSL-mediated suppression of fasting lipolysis so as to interrupt the unmitigated flow of FFA from adipose to liver. An important ‘missing link’ in the chain from over-nutrition to NAFLD/NASH and other metabolic disorders, is why some individuals expand VAT at the expense of (or in addition to) SAT expansion. One possibility is innate differences in adipose tissue depots.167 In some individuals, these differences may be genetically exacerbated or compromised.

Allo-antibodies are mainly of the IgG class and contain both types of chains, indicating that most of the known

allo-antibodies against VWF are of polyclonal origin. They can not only inhibit the activities Napabucasin clinical trial of VWF (neutralizing antibody) but they are also able to precipitate VWF once the immuno-complexes are formed (precipitating antibody). These inhibitors tested in vitro in VWD3 cases did not inactivate FVIII: the reduced FVIII:C after VWF concentrates is probably due to steric hindrance of the FVIII molecule bound to VWF. In most reported cases, antibody development was heralded by poor clinical response to replacement therapy accompanied by lower than expected recovery of VWF with absence of delayed and sustained rise of FVIII (secondary response of FVIII). When inhibitor titre is relatively low therefore, it is not difficult to treat soft-tissue bleeds and to prevent bleeding in surgery. In patients with high titres, replacement VX-809 chemical structure therapy is not only ineffective but it may also trigger life-threatening anaphylactic reactions, associated with activation of the complement system. A rise in antibody levels is usually seen 5–10 days after replacement therapy with VWF concentrates, with features typical of a secondary response to a foreign antigen. A VWD3

patient undergoing emergency abdominal surgery was treated with recombinant FVIII (no VWF), because this product could not cause anaphylactic

reactions. Because of the short half-life of FVIII without its VWF carrier, recombinant FVIII had to be administered by continuous intravenous infusion, at very large doses, to keep FVIII levels above 50 IU dL−1 for 10 days after surgery [84]. Another possible therapeutic approach is recombinant activated factor VII (rFVIIa) that can be used in VWD with allo-antibodies according to the same dosage and regimens as for haemophilia A with inhibitors. Type 3 VWD INTErnational RegistrieS and Inhibitor Prospective Study (3WINTERS–IPS, 2011–2016) has been set up to record clinical and laboratory MycoClean Mycoplasma Removal Kit data on a large cohort (at least 250 VWD3) collected locally from a network of European and Iranian Centres [85]. Plasma and DNA of VWD3 patients enrolled will be sent for centralized laboratory investigations. There will also be centralized evaluation of clinical and laboratory parameters (FVIII and VWF). Standardized methods for gene screening and for inhibitors against VWF in plasma will be used. In those patients with confirmed diagnosis of VWD3, there will be a 2-year clinical follow-up to evaluate frequency and risk of bleeding. The study is a prospective, multicentre, international, non-interventional 5-year clinical study. It is promoted by the AB BONOMI Foundation, a non-profit organization with funds obtained from unrestricted grants of five companies.

Results: During the course of chemotherapy, the most common adverse reactions were nausea, vomiting, neurotoxicity and phlebitis. Bone marrow suppression occurred relatively less. There were no significant statistical differences between male and female. Conclusion: The toxicity and side effects of Oxaliplatin based chemotherapy Idasanutlin purchase are mainly nausea and vomiting, followed by neuron toxicity and phlebitis, and relatively less for bone marrow suppression. Proper nursing intervention can decrease the frequency and severity of these side effects. Key Word(s): 1. adverse reactions;

2. nursing care; 3. Oxaliplatin; 4. observation; Presenting Author: LIAOLIAO XIN Additional Authors: MEIXIA WANG, LI HE, FENXIA LIU, MEIXIU LIU, JING ZHANG, ZHIJUAN YANG Corresponding Author: LIAOLIAO XIN Affiliations:

Xijing Hospital of Digestive Diseases Objective: To compare the effects of central venous catheter with superficial vein indwelling needle for tumor patients with long-term chemotherapy. Methods: we recruited 31 patients with central venous catheters and 208 patients with superficial vein indwelling needles in our department between January and March of 2013 into 2 groups based on their admission time. Comparison was made by observing the leakage, redness, induration, pain, phlebitis, pigmentation, and their chief complaints. Results: Patients with PICC felt that they benefited from it in their daily life, such as avoiding inconvenience during taking meals and using the toilet. More importantly, PICC reduced the pain brought by avoiding multiple puncture, and damaging blood vessels in the infusion process no pigmentations selleck was reported on the skin by chemo drugs. On the other hand, patients Farnesyltransferase with superficial vein indwelling needles had to be observed regularly in the puncture area, which increased the burdens of nurses. As Long-term chemotherapy damaged blood vessels, it made more difficult for nurses to do the puncture. Some patients suffered from the pigmentations on the skin along the puncture area after infusion. In comparison, the effective rate of using PICC is 90.3%, while the superficial vein-indwelling needle

is 48%. Conclusion: For Patients with Long-term chemotherapy, using PICC is safer, more effective, reduces pain, and protects blood vessels well with fewer complications. Therefore, PICC is significantly better than the superficial vein-indwelling needle. Key Word(s): 1. PICC; 2. indwelling needle,; 3. safety; Presenting Author: MEIXIU LIU Additional Authors: MEIXIA WANG, LIAOLIAO XIN, FENXIA LIU, PEI QIN, JING ZHANG, LI HE Corresponding Author: MEIXIU LIU Affiliations: XiJing Hospital of Digestive Diseases Objective: To explore the value of Pain Intervention by nursing For Gastric Cancer Patients with Peritoneal Metastasis. Methods: Nursing guidance was offered to 58 gastric cancer patients with peritoneal metastasis suffering from pain in the course of treatment.

To assess HBV uptake by the cells studied, and cellular ability to synthesize viral proteins, PHHs, UD- and D-UCMSCs were inoculated at an MOI of 105 for 4 hours at 37°C. After extensive washing they were cultured in standard conditions for 24 hours. After fixation, permeabilization, and preblocking, a mouse monoclonal antibody against HBcAg (NCL-HBcAg-506, Leica) was used (1:100). Staining for ASGPR was obtained on noninfected cells with a rabbit polyclonal antibody (1:400; HPA011954, Sigma).

Alexa Fluor 594-labeled antibodies (A11012, A21203, Invitrogen) were used for secondary staining (1:200). DAPI was used to Saracatinib concentration stain the nuclei. Results were analyzed with the Cell Observer SD laser confocal microscope (Carl Zeiss). Conditioned media from a culture of 150,000 cells were concentrated 10 times by centrifugation at 4,000g for 15 minutes in 10 kDa Amicon Ultra centrifugal filter tubes (Millipore). The resulting samples were analyzed for HBeAg and HBsAg (Monolisa HBeAg/Ab Plus and HBsAg Ultra, Bio-Rad) according to the manufacturer’s instructions. Reading of the optical densities at 450/620 nm was carried out with an absorbance reader (Reader 250, BioMérieux). For ASGPR detection, 20 μg of total cellular proteins was separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to PVDF membranes through semidry transfer. After blocking,

a rabbit polyclonal antibody against ASGPR (HPA011954, Sigma) was used for overnight incubation at 4°C (1:5,000). A goat polyclonal

anti-α-actin antibody (1:2,000; sc-1616, Santa Cruz CP-690550 price Biotechnology) served as internal control. Fluorescent secondary antibodies (Biotium) were used (1:10,000) and the results were read with the Odyssey infrared imaging system (Li-Cor Biosciences). For HBcAg detection, an immunoprecipitation was performed on lysate from 106 cells (10 days postinfection) using protein A Sepharose beads (GE Healthcare) bound to a rabbit polyclonal anti-HBc antibody (B0586, Dako). After SDS-PAGE BCKDHA separation and transfer, staining was obtained incubating the membrane with a mouse monoclonal antibody against HBcAg (1:2,000; NCL-HBcAg-506, Leica). Conditioned medium was collected from D-UCMSCs culture 14 days postinfection. After centrifugation to remove cellular debris, HBV was concentrated by PEG precipitation. Pellets were resuspended in PBS and used to infect PHHs by overnight incubation at 37°C. After extensive washing, PHHs were cultured as described above. DNA was extracted after 24 hours and 7 days to test for viral replication. Statistical analysis was performed with PRISM 4 (GraphPad Software). Mann-Whitney U test, Wilcoxon signed-rank test, and one-sample two-tailed t test were used as appropriate. P ≤ 0.05 was considered significant. Values are expressed as mean ± standard deviation or standard error of the mean. UCMSCs were isolated from Wharton’s jelly of six healthy donors.

32 These observations suggest that the proinflammatory responses in peritumoral stroma may not represent the host reaction to the malignancy, but that they instead constitute effects that are rerouted in a tumor-promoting direction to induce selleck screening library tissue remodeling and angiogenesis. This notion is supported by our recent investigations in which we found that the frequency of tissue Th17 cells was positively correlated with microvessel density in tumors, and high numbers of monocytes in peritumoral stroma were selectively

associated with vascular invasion and poor prognosis in HCC patients.10, 21 Consistent with our observations, recent studies have shown that IL-17 could recruit neutrophils, which in turn stimulate angiogenesis and tissue remodeling.33–34 Despite recent advances in understanding the differentiation of Th17 cells in humans,15–19 little is known about the mechanisms underlying the regulation

of Th17 cells in tumors. The present investigation provides evidence that proinflammatory cytokines released by tumor-activated monocytes/Mψ play a dominant role in the development of Th17 cells in HCCs, as indicated by the results of four sets of experiments. First, we observed that the level of Th17 cells was about 4 times higher in peritumoral stroma than in cancer nests, and there were significant correlations between the densities of Th17 and HLA-DRhighCD68+ cells in learn more peritumoral stroma, which was not the case in cancer nests, where most of the CD68+ cells were negative for HLA-DR. Second, tumor-activated monocytes were significantly superior to the suppressive TAMs in inducing expansion of Th17 cells exhibiting phenotypic features more similar to those of tumor-infiltrating Th17 cells (e.g., a remarkable proportion of Th17/Th1). Third, blocking a set of cytokines released

from tumor-activated monocytes clearly inhibited the generation of Th17 cells, and relatively low concentrations of the recombinant cytokines could mimic the stimulatory effect of TCM culturing in this regard. Fourth, inhibition of monocytes/Mψ inflammation Pembrolizumab purchase in hepatoma-bearing mice markedly reduced the number of tumor Th17 cells and tumor growth. Therefore, activation of monocytes in tumors may represent a novel route to promote Th17 expansion in human cancer. This concept is supported by studies showing that activated APCs are involved in the differentiation and expansion of Th17 cells and thereby also in Th17-mediated chronic inflammation.16, 35, 36 It should be noted that, in addition to the local expansion of Th17 cells, migration from blood is also a potential source for the increased Th17 cells in tumors. In this context, we have recently found that CCR6 is expressed in the majority of Th17 cells and that CCL20, the ligand for CCR6, is significantly increased in HCCs.21 In one of our latest studies21 we observed that most of the Th17 isolated from HCCs exhibited a CD45RO+CD62L−CCR7− effector memory phenotype.

Importantly, check details our results also indicate that pdVWF/FVIII and rFVIII/VWF may behave differently towards anti-FVIII antibodies. It can be speculated that rFVIII complex formation with VWF would be incomplete and residual free rFVIII would still be able to interact

with inhibitors, preserving some degree of antigenicity. S Grancha is an employee of Instituto Grifols. The other authors received an honorarium from Grifols S.A. for their participation in the symposium and production of the article. The authors thank Content Ed Net for providing valuable editorial assistance in the preparation of the article; funding for this assistance was provided by Grifols S.A. “
“Desmopressin is a synthetic analog of the antidiuretic hormone vasopressin that, when given intravenously or intranasally, induces a consistent albeit transient increase of plasma factor VIII (FVIII) and von Willebrand factor (VWF). This property has been exploited since 1977 to treat patients with FVIII and/or VWF deficiency, i.e. mild hemophilia and von Willebrand disease (VWD). The VWD subtype that responds better to desmopressin is type 1, whereas patients with type 2 and 3 VWD are usually unresponsive. The advantages of this compound over other forms of replacement therapy (e.g. VWF-FVIII concentrates from plasma) are the lower cost and the lack of risk

of the transmission of bloodborne pathogens. “
“Summary.  In older men with haemophilia, arthropathy resulting from a lifetime of intra-articular bleeding contributes to the loss of independence and increased morbidity that occurs Pazopanib order click here with age. A regular exercise programme that incorporates aerobics, strength training and balance and

flexibility activities is a key component of successful ageing, helping to improve functional mobility and reduce the risk of falls, osteoporosis and osteoporotic fractures. Because of the special challenges associated with haemophilia, which include both the underlying coagulopathy and, in many cases, extensive joint damage, patients beginning an exercise regimen should be referred to appropriately trained physiotherapists (preferably someone associated with a haemophilia treatment centre) for evaluation, education and instruction and follow-up. Various assistive devices may make exercise easier to perform and more comfortable. “
“Patients with congenital haemophilia with inhibitors or acquired haemophilia are at risk of bleeding complications during surgery. In these patients, replacement therapy for the missing coagulation factor is ineffective, and a bypassing agent such as recombinant activated factor VII (rFVIIa) is required to manage bleeding. To evaluate the safety and haemostatic efficacy of rFVIIa treatment in Japanese patients with congenital haemophilia with inhibitors to FVIII/FIX or acquired haemophilia undergoing surgery.

c-Src, the

cellular prototype Proteasome assay of this kinase family, has been originally discovered as the mammalian homologue of viral Src kinase encoded by the Rous sarcoma virus.18, 19 c-Src is ubiquitously expressed and is of particular importance for governing cellular processes associated with cellular proliferation, differentiation, and cell survival such as cell cycle control, protein synthesis, organization of the cytoskeleton, and the cell adhesion network.6, 7 The present study provides evidence that c-Src contributes toward maintenance of HCV replication, as suppression of c-Src expression by specific siRNAs resulted in an effective down-regulation of HCV replication (Fig. 2). Neither Fyn nor Yes was able to annihilate this inhibitory effect of c-Src knockdown on HCV replication.

This suggests that c-Src plays a specific role for HCV replication and cannot be substituted by the two other ubiquitously expressed SFK members Yes and Fyn, a notion that is further supported by the fact that siRNA directed against these two kinases has no influence on HCV replication. In line with this, HCV replication is also highly sensitive toward the protein tyrosine kinase inhibitor herbimycin A (Fig. 1), which has been originally described as an inhibitor of viral Src activity14 and Tyrosine Kinase Inhibitor Library ic50 subsequently demonstrated to likewise inhibit c-Src activity.13, 15 Our notion that this effect of herbimycin A on HCV replication is indeed mainly due to the inhibition of c-Src function is further supported by the observation that Tolmetin down-regulation of c-Src expression by siRNA is accompanied by a reduction of the IC50 of herbimycin A, which is commensurate to the reduction of c-Src protein levels (Fig. 2D). It has been demonstrated in previous reports that HCV-encoded proteins interact with members of the Src family kinases. Notably, NS5A has been suggested to interact with the SH3 domain of Hck,

Lck, Lyn, and Fyn, but interestingly not with that of c-Src.8, 20 The interaction of NS5A with the respective member of the SFK family was suggested to inhibit the activity of Hck, Lck, and Lyn and enhances activation of Fyn, which in turn resulted in an increased activation of STAT3.8 In contrast to this, a recent report used an siRNA-based screening approach and identified the C-terminal Src kinase, which mediates phosphorylation of the C-terminal inhibitory tyrosine residue of SFKs, to be required for replication. This effect of C-terminal Src kinase was suggested to be due to negative regulation of Fyn,9 because siRNA-mediated suppression of Fyn expression was reported to enhance replication, whereas siRNAs directed against the other ubiquitously expressed SFKs c-Src and Yes were reported to have no effect on replication. In the present study, we were unable to confirm the proposed inhibitory effect of Fyn on HCV replication.

049). Within the total IBD cohort, diarrhoea sub-score correlated with symptoms (r = 0.75, p = <0.001) and CLS (r = 0.43, p = 0.005) but abdominal pain as a symptom did not correlate to either (p > 0.05). On linear regression correcting for medication use, each increase of one diarrheal motion per day correlated with an increase in CLS of 2.14. (B coefficient = 2.14, selleck chemicals llc p = 0.005). Similarly a 1 point increase of CLS correlated to a 0.09 increase of diarrheal motions/day (B coefficient = 0.089, p = 0.004). Conclusion: Increased permeability may be responsible for ongoing symptoms

in patients who have achieved mucosal healing in both CD and UC. Increased permeability in symptomatic patients was best explained by diarrhea as a symptom. Reversal of impaired mucosal permeability may be a potential target

of treatment in these patients and should be evaluated in further studies. C KIELY,1 K SUBRAMANIAM,1 P PAVLI1 1Gastroenterology and Hepatology Unit, The Canberra Hospital, Garran, ACT, Australia Background: Biological therapy, particularly the anti-tumor necrosis factor antibodies, infliximab and adalimumab, are used for the maintenance of remission for patients selleck inhibitor with inflammatory bowel diseases (IBD; Crohn’s disease (CD) and ulcerative colitis (UC)). International guidelines recommend maintaining these agents throughout pregnancy and in the immediate post partum period1,2. Aim and Methods: To analyse maternal and Ureohydrolase fetal outcomes of pregnant patients with IBD treated with anti-TNF agents. Data for patients treated in a tertiary hospital was recorded prospectively and analyzed. Results: Nineteen pregnancies were recorded in 16 patients receiving anti-TNF therapy for IBD between 2007–2014 (Table 1). One patient with acute severe UC requiring colectomy during pregnancy had a stillbirth after attempted salvage therapy using adalimumab. Another patient admitted to

hospital during the third trimester with acute severe UC was treated successfully with infliximab rescue therapy. All other patients were in remission prior to pregnancy. One patient is currently pregnant and receiving anti-TNF therapy. Conclusion: Anti-TNF therapy can be used safely in pregnancy. Table 1   Crohn’s Disease (n = 14) Ulcerative Colitis (n = 5) All IBD (n = 19) Mean age at delivery (years) 34.3 32.6 33.8 Perianal disease 8 (57%) N/A 8 Concomitant medications azathioprine 3 (21%) 2 (40%) 5 (26%) prednisolone 5 (36%) 3 (60%) 8 (42%) Flare 3 (21%) 2 (40%) 5 (26%) Anti-TNF use adalimumab 8 (57%) 1 (20%) 9 (47%) infliximab 6 (43%) 4 (80%) 10 (53%) Continued use 3 (21%) 0 3 (16%) Cessation in 1st trimester 1 (7%) 0 1 (5%) Cessation in 3rd trimester 10 (71%) 4 (80%) 14 (74%) Commencement in 3rd trimester 0 1 (20%) 1 (5%) Gestational diabetes 2 (14%) 1 (20%) 3 (16%) Preterm delivery (<37 weeks) 1 (7%) 1 (20%) 2 (11%) Low birth weight (<3200 g) 7 (50%) 2 (40%) 9 (47%) Caesarian section 10 (71%) 2 (40%) 12 (63%) Congenital defects 0 0 0 1 Janneke van der Woude, C.

172, -0.453-0.110) (SMD in spine BMD: -0.169, -0.476-0.138). Selleck SCH772984 Sensitivity analyses showed consistent results. Publication bias was detected in the analysis of bone fractures and osteoporosis. Conclusion: Current publications

indicate significant association between bone fractures and ALD, independent of osteoporosis or BMD. Due to the qualitative and quantitative heterogeneity among studies, further research using homogeneous populations and control of confounding risk factors for fractures are needed to elucidate the mechanism of bone fractures in ALD. Association between alcoholic liver disease and bone fractures. The size of each square is proportional to the study’s weight. Diamond is the summary estimate from the pooled studies with 95% CI. CI: confidence interval. (Random effect

model) Disclosures: The following people have nothing to disclose: Chang Seok Bang, Hyo Sun Kim, Sang Hyun Park, Eun Jin Kim, Ki Tae Suk, Dong Joon Kim Somatostatin analogues (SA) reduce liver volumes (LVs) in patients with polycystic liver disease (PLD). However, these patients show a considerable variability in treatment responses, making it difficult to predict response to SA therapy. Our aim was to BMN 673 identify specific patient, disease or treatment characteristics that predict response in PLD during SA therapy. We pooled the individual patient data of 4 trials (NCT00771888,NCT00426153, NCT01157858, NCT01354405) of long-acting SAs (120 mg lanreotide or 40 mg octreotide) for 6 or 12 months in PLD that included liver volume as the primary outcome. We performed uni- and multivariate linear regression analysis with 9 preselected patient, disease and drug variables to identify independent predictors of response, defined as percent change in LV. Secondary outcome was percent

change in kidney volume in the ADPKD subgroup. All analyses were Bcl-w adjusted for baseline LV and center effect (random). We included 153 PLD patients (86% female, mean age 50 years, median LV 4974 ml, 69% ADPKD) from 3 international centers, all treated with octreotide (n=70) or lanreotide (n=83). Mean reduction in LV was 4.2% (range −31.7% to +9.7%). Uni- and multivariate linear regression revealed that elevated baseline alkaline phosphatase (ALP) was associated with increased response during SA therapy (−2.7%, 95% CI −5.1% to −0.2%, p = 0.037), independently of baseline LV. Duration of therapy (6 vs 12 months), SA type and eGFR did not affect response. Elevated ALP remained associated with LV response (−3.2%, 95% CI −6.0 to −0.3%, p=0.029) in ADPKD patients (n=100), but did not predict response in kidney volumes (0.1%, 95% CI −3.1 to 3.3%, p = 0.97). Elevated ALP is associated with response in polycystic liver disease during SA therapy, and could possibly serve as a prognostic marker in this disease.