Age and sex matched control group (18 volunteers) was also included into the study. PCBs were determined in blood samples by capillary gas chromatography with the electron capture detector (column SE-54, internal standard PCB119). Identification of individual congeners was carried out by a relative retention times, quantitative calculations were performed using relative response factors. Results: Mean serum total PCBs concentration was significantly higher in NASH patients Dorsomorphin cell line in compare to healthy controls (1,46 ± 1,39 vs 0,66 ± 0,29 ng/g, p=0,02). There were no differences between groups in serum concentrations of congener 118 (0,22 ±0,14 vs 0,20 ±0,16 ng/g p=0,2). Congeners

183 and 185 were found only in 41% of controls, but not in patients with NASH. Mean serum concentration of congeners 99, 101, 138 and 153 were lower in control in compare to patients with NASH (0,12 ± 0.05 vs 0.06 ± 0.04, p=0.007; 0.72 ± 0.57 vs 0.05 ± 0.07, p=0.0002; 0.48 ± 0.78 vs 0.08 ± 0.06, p=0.04; 0.33 ± 0.33 vs 0.06 ± 0.07, p=0.007). In conclusion, total serum PCBs concentration and concentration of congeners 99, 101, 138 and 153 were lower in healthy control than in patients with NASH. Congeners 183 and 185 were found only in healthy controls. It means that NASH patients in compare to healthy controls

experienced long-term exposure for toxic lipophilic environmental pollutants, which can be additional factors facilitating development and progression of NAFLD. Further studies are needed to clarify Cobimetinib price the role of different congeners and its transporters 上海皓元 in liver for development of the disease. Disclosures: Vasily Isakov – Advisory Committees or Review Panels: Abbvie, Bristol-Myers Squibb, Gilead, Janssen, Merck,

Vertex; Consulting: Bristol-Myers Squibb, Merck; Speaking and Teaching: Bristol-Myers Squibb, Janssen, Merck The following people have nothing to disclose: Vladimir Bessonov, Elena Khromchenkova, Natalia Topilskaya, Ksenia Selezneva, Victor Tutelyan Background: AgRP is an orexigenic peptide directly regulated by fatty acid uptake; FASN is involved in fatty acid synthesis and its expression is sensitive to glucose concentration. Aim: The aim of this pilot study is to measure the expression of AgRP and FASN in vitro under elevated glucose and lipid concentrations and compare findings to a set of NAFLD patients. Methods: HepG2 cells were challenged with 10mM of oleic acid (OA), 50mM glucose (GLU), or both and expression of AgRP and FASN was measured by qPCR and compared to untreated controls. Visceral adipose tissue was collected and flash frozen for preconcented patients with biopsy-proven NAFLD and AgRP and FASN gene expression was measured by qPCR. Additionally, expression of both genes was measured in formalin fixed paraffin embedded hepatic tissue from a subset of patients.

29–31 For instance, Theise et al.31 demonstrated that cells morphologically and immunohistochemically resembling hepatic progenitor cells merged with the HCC and CC components and with mature-appearing hepatocytes within some combined HCC-CC, supporting the notions that carcinogenesis of this unique neoplasm may be explained by the malignant transformation of the hepatic progenitor cells. Furthermore, a recent study32 demonstrated the cell of origin of cholangiolocellular carcinoma (Fig. 6), a very rare neoplasm accounting for less than 1% of primary liver cancer,33,34

may also be the hepatic progenitor cells. Because the HCC (Fig. 6a) and CC (Fig. 6b) components altogether comprised less Pexidartinib ic50 than

10% of the neoplasm and the cholangiolocellular carcinoma area (mixture of small monotonous glands, antler-like anastomosing pattern, selleckchem Fig 6c) occupied more than 90% of the neoplasm in this study, although these three histological components showed transitions between each other, the exact relationship between this unique neoplasm and the typical combined HCC-CC remains to be clarified. It is possible they may overlap to some degree and belong to a spectrum of the primary liver neoplasm arising from the hepatic progenitor cells. For the purpose of diagnosis, combined HCC-CC needs to be distinguished from conventional

HCC or CC. Pseudoglands (Fig. 7) reflecting rapid and active neoplastic replication are very common in HCC and they should not be confused with the true glandular formation in CC. In fact, Popper and Schaffner in 1957 stated that with careful examination most primary hepatic carcinomas could be found to have both hepatocellular and ductal elements,7 medchemexpress but Edmondson in the following year pointed out that in the majority of cases these ductal elements were from hepatocyte-like tumor cells and that such tumors are in fact a variant of HCC.3 Retrospectively, most of these ductal elements likely represent pseudoglands in HCC. In this regard, detection of mucin by a mucin stain in the CC component or identification of bile in the HCC component can be very helpful. As mentioned previously, it has been recognized that the expression of CK7 and CK19 in HCC is not uncommon from several series and therefore a diagnosis solely based on immunohistochemistry may not be fully reliable.23–25 In fact, a recent study using a comparative functional genomics approach has demonstrated that the CK19-associated gene expression signature may predict poor patient survival.35 Whether this poorer outcome can be largely attributed to the progenitor cell lineage of the carcinoma awaits further investigation.

The clinical phenotype of H. pylori

infection depends on several determinants that include virulence factors, the host susceptibility to infection and other environmental co-factors [4-7]. It was previously believed that CagPAI was the chief virulence factor that strongly associates with severe gastric inflammation while encoding proteins that induce IL-8 secretion by epithelial cells [8]. However, subsequent studies could not identify a strong association between IL-8 induction and the presence or the functionality of the cagPAI; they found that several other genes unrelated to CagA status, such as oipA, flagellar proteins, heat shock proteins, and several other H. pylori products could also induce IL-8 secretion [9, 10]. Chronic active inflammatory response is the hallmark see more of H. pylori infection and the main underlying molecule seems to be IL-8 [11]. Many putative virulence genes have been described to determine the clinical outcome; among these are the genes present in the plasticity region cluster (that is located outside the CagPAI) that correspond to nearly half of the strain-specific genes [12]. Plasticity region is recently being considered to be a novel transposable element and the genes present in this cluster possibly affect bacterial fitness and phenotypes [13]. Similar to CagPAI, plasticity region displays some characteristics of a genomic island such as its large size and selleck kinase inhibitor a different percentage of

G+C content than

in the rest of the bacterial genome [14]. Most MCE公司 of the genes in the plasticity region of H. pylori are functionally unknown although they may epidemiologically associate with the strains from different disease conditions in certain human populations [15, 16]. Previous studies have shown that there are regional and ethnic differences in the distribution of H. pylori subtypes with respect to strain variable genes; this in turn suggests that, in a given geographic area, the H. pylori genotypes may play a significant role in infection or progression of infection [17, 18]. Moreover, plasticity region encoded proteins such as JHP0940 and HP0986 have already been reported to stimulate pro-inflammatory cytokines and activate NFκB mediated pathway in cultured mammalian cells [19-21]. In this regard, it is prudent to functionally characterize these genes/proteins with respect to their putative roles in persistence and virulence of H. pylori. Our group previously reported that HP0986 was a pro-inflammatory protein that upregulates tumor necrosis factor alpha (TNF-α) and triggered IL-8 secretion and at the same time induced apoptosis through Fas-mediated pathway [21]. Although this pioneering study focused on the function of HP0986 outside the bacterial environment (as it was based on the effects of recombinant HP0986 on cultured human macrophages and peripheral blood mononuclear cells), the interaction of HP0986 with human gastric epithelial cells was not analyzed.

01). Although the study was not double-blinded or placebo-controlled, both the researchers and subjects were blinded to the IMg2+ levels. A subsequent study21 showed that 1 g of magnesium sulfate resulted in rapid headache relief in patients with low serum IMg2+ levels. In a single-blind RCT involving 30 patients with moderate to severe migraine attacks41 treatment with 1 g intravenous magnesium sulfate was superior to placebo in terms of both response rate (100% for magnesium sulfate vs 7%

for placebo) and pain-free rate (87% for magnesium sulfate and 0% for placebo). Mild side effects including flushing and a check details burning sensation in the face and neck were common during the infusion, but subjects were able to continue treatment. Of note, none of the subjects reported headache recurrence during the 24 hours after treatment. Bigal et al42 in a double-blind RCT, showed that 1 g of magnesium sulfate resulted in a statistically SB525334 ic50 significant improvement in pain and associated symptoms in subjects with migraine with aura, as compared to controls. Although migraine without aura patients did not show a significant

difference in pain relief compared to those receiving placebo, they did have a significantly lower intensity of photophobia and phonophobia. Two RCTs have been conducted in emergency room settings, neither of which showed that magnesium was more effective than placebo in aborting attacks.43,44 Supplements and Mitochondrial Dysfunction Mitochondrial dysfunction, which leads to impaired oxygen metabolism, has been speculated to play a role in migraine pathophysiology45,46 as migraineurs have been shown to have reduced mitochondrial phosphorylation potential in between headaches.47,48 An impairment

of mitochondrial oxidative metabolism might influence neuronal information processing, therefore reducing the threshold for migraine attacks.49 This is the rationale for the use of supplements that enhance mitochondrial function MCE公司 in the treatment of migraine, such as riboflavin, CoQ10, and alpha lipoic acid. Riboflavin Riboflavin, also known as vitamin B2, is a component of 2 coenzymes (flavin adenine dinucleotide and flavin mononucleotide) that are cofactors in the electron transport chain of the Krebs cycle. It plays a vital role in membrane stability and the maintenance of energy-related cellular functions. One well-designed RCT found that it is beneficial in migraine prophylaxis, showing that daily use of 400 mg riboflavin for 3 months resulted in a 50% reduction in attacks in 59% of patients, compared to 15% for placebo. Two minor adverse reactions, diarrhea and polyuria, were reported in the treatment group.50 In a small study51 investigating the effects of different treatments on auditory evoked cortical potentials in migrainers, riboflavin and beta-blockers were shown to act on 2 distinct aspects of migraine pathophysiology.

Several inflammatory genes including chemokines and Selleck Autophagy inhibitor chemokine receptors were previously described to be regulated by NF-κB pathway and might be responsible for the observed phenotype. For example,

the chemokine CCL2 and the chemokine receptors CCR1 and CCR2 were implicated in monocyte recruitment during experimental liver fibrosis.5, 30-33 In our study, macrophage depletion attenuated experimental liver fibrosis development without affecting the extent of liver injury or the extent of overall inflammation. This suggests that not only the magnitude, but also the type of liver injury/inflammation influences liver fibrogenesis. Although macrophages were crucial for fibrosis development, the contribution of liver injury to this process needs to be investigated further. Several other findings provide a support for the important http://www.selleckchem.com/products/Metformin-hydrochloride(Glucophage).html role of macrophages in liver fibrosis development. For example, macrophage depletion can reduce carbon tetrachloride-induced liver fibrosis.34 Macrophages and also infiltrating monocytes are considered the main producers of transforming

growth factor beta (TGF-β), one of the most powerful mediators of HSC activation in vitro and in vivo.35 Furthermore, macrophage-produced chemokines contribute to additional recruitment of inflammatory cells.36 In summary, our study provides an important link between hepatocellular NF-κB activation, induction of chronic inflammation, and liver fibrosis development, which might be of relevance for liver disease development in multiple chronic liver disorders. We thank Olena Sakk and Vadim MCE Sakk for help with establishing the transgenic model and in characterization of the fibrosis phenotype. We also thank Melanie Gerstenlauer, Kristina Diepold, Birgit Rettenmeier, and Julia Melzner for histological experiments, and Susanne Schatz for help with the mouse studies. We thank Sibille Sauer-Lehnen and Carmen G. Tag for technical assistance, and Karina

Kreggenwinkel for helpful discussion. We thank Prof. Hermann Bujard for providing the LAP-tTA mice, Dr. André Lechel, and Prof. Karl Lenhard Rudolph for partial-hepatectomized mouse livers. Author contributions: Study concept and design: Y.S., P.S., T.W.; Acquisition of data: Y.S., F.L., S.G., K.F., N.G., S.E., K.H.H., N.H., A.S., S.W.; Analysis and interpretation of data: Y.S., F.L., S.G., K.F., K.H.H., N.H., A.S., P.S., T.W.; Drafting the article: Y.S., F.L., K.H.H., P.S., T.W.; Statistical analysis: Y.S., K.H.H.; Obtained funding: Y.S., P.S., T.W.; Discussion: F.K. M.S. K.S.K. S.K.; Technical or material support: S.E. T.L. B.B. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Docetaxel has been chosen as one of the most popular anticancer drugs in the treatment of breast cancer for more than a decade.

Subsequently, at UT Southwestern, he analyzed mammalian responses to bacterial lipopolysaccharide. This work culminated in the identification of Toll-like receptors as key sensors of the innate immune system, used to detect infection. In further studies, Beutler employed a forward genetic strategy to elucidate many aspects of mammalian immunity. In addition to the Nobel Prize, he has received many other awards for his work, a partial list of which includes the Balzan Prize

(2007), the Albany Medical Center Prize (2009), the Shaw Prize (2011), the Korsmeyer Barasertib Award (2013), and election to both the US National Academy of Sciences and the Institute of Medicine (2008). Beutler is also a member of the German Academy of Sciences (Leopoldina) and of the French Legion d’Honneur.

Learning Objectives: Discuss how the immune system operates, particularly with respect to the production of antibodies against and infectious agent Create and solve immune diseases using a germline mutagen Identify parallels between the mouse and human where immune function is concerned Exhibit Hall D 1:30 – 2:00 PM Snack Break AASLD Distinguished Awards Sunday, November 3 2:45 – 3:00 PM Hall E/General Session AASLD Distinguished Clinician Educator/Mentor Award Presented to: Arthur J. McCullough, MD Presented by: Anthony S. Tavill, MD General Hepatology Update Sunday, November 3 3:00 – 4:30 PM Ballroom AB General CAL 101 Hepatology Update MODERATORS: Ester C. Little, MD Paul Angulo, MD 1.5 CME Credits This annual forum is intended to provide hepatologists an update on the diagnosis and management of three clinically relevant topics that are commonly encountered in routine clinical practice. Issues including diagnostic strategies and approaches to management are reviewed

to provide state-of-the-art guidelines particularly for diagnostic dilemmas. Learning Objectives: Describe the current guidelines for the diagnosis and management of hepatocellular carcinoma Identify the most common drugs that can cause liver damage and understand the mechanisms of liver toxicity Discuss the current guidelines for the diagnosis and management of 上海皓元 Primary Biliary Cirrhosis 3:00 – 3:25 PM Update on Management of Hepatocellular Carcinoma Jorge A. Marrero, MD 3:25 – 3:50 PM Drug-induced Liver Injury Update Paul B. Watkins, MD 3:50 – 4:15 PM PBC Keith D. Lindor, MD 4:15 – 4:30 PM Discussion Parallel Session Parallel 1:Biliary Atresia and Neonatal Cholestasis Sunday, November 3 3:00 – 4:30 PM Room 146A MODERATORS: Regino P. Gonzalez-Peralta, MD Ronald J. Sokol, MD 3:00 PM 13: ARF6 gene dysregulation may contribute to biliary dysgenesis in biliary atresia (BA) Mylarappa Ningappa, Joseph Glessner, Johoon So, Donghun Shin, Chethan Ashokkumar, Hakon Hakonarson, Rakesh Sindhi 3:15 PM 14: Diagnostic and Predictive Value of Serum Biomarkers in Biliary Atresia James E.

Another important epigenetic mechanism underlying the suppression of Wnt antagonists in human HCCs is mediated by enhancer of zeste homolog 2 (EZH2),[6] the catalytic subunit of the polycomb repressor complex 2 that represses gene transcription through histone H3 lysine 27 trimethylation (H3K27me3).[12] Numerous Wnt inhibitors operating at different subcellular compartments, including AXIN2, NKD1, PPP2R2B, PRICKLE1, and sFRP5 were uncovered to be concordantly silenced by EZH2-catalyzed H3K27me3 (Fig. 1), which in

turn drive Wnt/β-catenin screening assay signaling and HCC cell proliferation.[6] This is particularly intriguing because the majority of EZH2- and β-catenin-coexpressing HCCs, which constitutes more than one third of the examined cases (61/179), do not harbor CTNNB1/AXIN1/AXIN2

mutation,[6] thus highlighting the significance and independence of Wnt activation by EZH2-mediated epigenetic mechanism in HCC. Accumulating evidence support the importance of miRNAs in the epigenetic deregulation of oncogenic signaling pathways in HCC.[13] In this connection, miR-155 has been recently shown to promote hepatic oncogenesis by activating Wnt signaling.[14] Activated by nuclear factor kappa B, miR-155 directly represses adenomatous polyposis coli, a negative regulator of Wnt signaling (Fig. 1) and stimulates Wnt/β-catenin-dependent hepatocarcinogenesis.[14] In contrast with the aforementioned gene silencing mechanisms, emerging evidence suggest that promoter DNA hypomethylation

may also participate in cancer initiation and progression via buy 5-Fluoracil reactivation of potential tumor-causing genes.[13] Recent genome-wide methylation studies in HCC tissues have revealed that ∼50–75% MCE of the interrogated gene promoters in tumors are indeed hypomethylated, that is, showing less methylation compared with nontumor tissues.[15, 16] Whether these epigenetic alterations contribute to expression of activators in Wnt or other pathways warrants further investigation. Knowledge of the molecular pathway from the etiological factors to the oncogenic signaling in HCC can be translated into therapeutic potential.[17] For instance, a direct transcriptional target of androgen receptor has been shown to promote hepatocarcinogenesis through the upregulation of β-catenin/TCF signaling,[18] providing a novel therapeutic target in HCC that exhibits gender disparity toward male.[19] Would other risk factors like viral hepatitis or metabolic syndrome induce HCC development via epigenetic mechanisms? Would Wnt/β-catenin or other frequently deregulated signaling be met at the crossroads? Genome-wide high-resolution technologies such as chromatin immunoprecipitation coupled with next-generation sequencing or RNA sequencing will greatly facilitate the identification of target genes of specific chromatin regulators and the signaling interactions relevant to a malignant phenotype.

Conclusion: LdT therapy in CHB patients could significantly increase eGFR during antiviral therapy when compared with ETV and TDF and was a predicting factor associated with upstage of eGFR. ETV and TDF had comparable effect on eGFR during 2-year treatment. The long-term eGFR changes among different Nucs deserves further study. Disclosures: Yun -Fan Liaw – Advisory Committees

or Review Panels: Roche; Grant/Research Support: Roche The following people have nothing to disclose: Yi-Cheng Chen, ERK inhibitor Rachel Wen-Juei Jeng, Wei Teng, Chao-Wei Hsu, Chun-Yen Lin, I-Shyan Sheen, Rong-Nan Chien Purpose: To investigate the efficacy and safety of telbivudine treatment for 52 weeks of HBeAg-positive chronic hepatitis Sorafenib B (CHB) children and adolescents. Methods: A total of 41 HBeAg-positive CHB children and adolescents aged from 3 to 16 years were treated with telbivudine for 52 weeks. Eligible subjects were assigned to receive telbivudine 15 mg/kg/d, and those with weight more than 30 kg were treated with telbivudine 600 mg/d . Biochemical responses, HBVM and HBV DNA quantitation were detected every three

months since baseline, adverse events were also recorded. Results: After 52 weeks of telbivudine treatment, the rates of ALT normalization, HBeAg loss and HBeAg seroconversion were 85.4% (35), 43.9% (18) and 24.4% (10), respectively. Mean HBV DNA load declined by (6.97 ± 0.96) log IU/ml (median, 7.3 log IU/ml), and 31 (75.6%) cases had HBV DNA undetectable. 2 cases had a decline of

quantitative HBsAg<10 IU/ml. Patients who achieved HBV DNA undetectable at week 24 had higher rates of ALT normalization, HBV DNA undetectable, HBeAg loss and HBeAg seroconversion than those with HBV DNA detectable. Decline 上海皓元医药股份有限公司 in HBV DNA levels correlated with prior treatment with interferon (IFN) (P=0.004), but did not correlate with a family history of hepatitis B (P=0.122). Mild and transient adverse events were observed, 7.3% of subjects developed elevated levels of CK. No gene mutations were observed. Conclusion: Telbivudine treatment for HBeAg-positive CHB children and adolescents shows good efficacy and safety. Baseline characteristics *ULN was 40 IU/L Disclosures: The following people have nothing to disclose: Hongfei Zhang, Shishu Zhu, Yi Dong, Limin Wang, Zhiqiang Xu, Dawei Chen, Yu Gan, Fuchuan Wang Introduction: TDF- associated renal dysfunction has been described in HIV-infected patients. However, data in HBV infected patients treated with TDF is lacking. Our goal is to examine renal profile of TDF-treated HBV patients. Methods: We performed a multicenter mathched case cohort study of 103 consecutive treatment naïve HBV patients initiating on TDF cases and 103 control ETV patients, matched by age, gender, and GFR groups (unimpaired: ≥ 80 and mild impairment: 50 ≤ eGFR < 80 mL/min). eGFR was based on Cockcroft-Gault and MDRD formula.

— Eighty-two MOH patients (mean age 44.5; 20 M, 62 F) and 35 episodic headache (mean age 40.2; 8 M, 27 F), were compared to 37 SA (mean age 32.5; 29 M, 8 F) and 37 healthy controls (mean age: 32.49; 20 M, 17 F). International Classification of Headache Disorders 2nd Edition criteria were employed. Chi-square test, Kruskal-Wallis test, and post hoc comparisons were used for statistics. Results.— MOH patients Fer-1 molecular weight scored higher on Hypochondriasis, Depression (only

females), Hysteria (only females) (P < .000). MOH did not show higher scores than episodic headache or healthy controls in dependency scales, while SA did. Conclusion.— The data obtained show that MOH and SA do not share common personality characteristics linked to dependence. Although further studies are needed to understand if such a difference is related to instrumental characteristics or to yet undiscovered psychobiological

characteristics of MOH patients; however, we hypothesize that the detected difference may rely on the fact that drug dependence in the 2 groups is promoted by entirely different needs: pleasure seeking in the SA group, pain avoidance in the MOH group. “
“(Headache 2011;51:664-673) Objective.— To evaluate the impact of a sumatriptan/naproxen sodium combination tablet on patient satisfaction, productivity, and Selleckchem Navitoclax functional disability in menstrual migraine treated during the mild pain phase of a single menstrual migraine attack associated with dysmenorrhea. Background.— Menstrual migraineurs with dysmenorrhea

represent a unique patient population not previously studied. When health outcomes end points are analyzed alongside traditional efficacy end points in migraine studies, a more comprehensive and robust understanding of the many factors that may influence patients’ choice of and adherence to pharmacological treatments for migraine is observed. Methods.— In 2 replicate, multicenter, randomized, double-blind, placebo-controlled trials, participants with menstrual migraine and dysmenorrhea treated a single menstrual migraine attack with a single fixed-dose tablet of sumatriptan 85 mg formulated with RT Technology™ and naproxen sodium 500 mg (sumatriptan–naproxen MCE sodium) or placebo. Results.— Participants randomized to sumatriptan–naproxen sodium were significantly more satisfied than those randomized to placebo at 24 hours post dose, as demonstrated by higher satisfaction subscale scores for efficacy (P < .001 for both studies), functionality (P = .003 for study 1; P < .001 for study 2), and ease of use (P = .027 for study 1; P = .011 for study 2). There was little bothersomeness of side effects associated with either treatment. Use of sumatriptan–naproxen sodium was also associated with lower reported “lost-time equivalents” in work and leisure time (pooled analysis, P = .003) and lower rates of functional disability (P = .05, study 1; P < .001, study 2) compared with placebo. Conclusion.

— Eighty-two MOH patients (mean age 44.5; 20 M, 62 F) and 35 episodic headache (mean age 40.2; 8 M, 27 F), were compared to 37 SA (mean age 32.5; 29 M, 8 F) and 37 healthy controls (mean age: 32.49; 20 M, 17 F). International Classification of Headache Disorders 2nd Edition criteria were employed. Chi-square test, Kruskal-Wallis test, and post hoc comparisons were used for statistics. Results.— MOH patients Venetoclax mouse scored higher on Hypochondriasis, Depression (only

females), Hysteria (only females) (P < .000). MOH did not show higher scores than episodic headache or healthy controls in dependency scales, while SA did. Conclusion.— The data obtained show that MOH and SA do not share common personality characteristics linked to dependence. Although further studies are needed to understand if such a difference is related to instrumental characteristics or to yet undiscovered psychobiological

characteristics of MOH patients; however, we hypothesize that the detected difference may rely on the fact that drug dependence in the 2 groups is promoted by entirely different needs: pleasure seeking in the SA group, pain avoidance in the MOH group. “
“(Headache 2011;51:664-673) Objective.— To evaluate the impact of a sumatriptan/naproxen sodium combination tablet on patient satisfaction, productivity, and Cobimetinib datasheet functional disability in menstrual migraine treated during the mild pain phase of a single menstrual migraine attack associated with dysmenorrhea. Background.— Menstrual migraineurs with dysmenorrhea

represent a unique patient population not previously studied. When health outcomes end points are analyzed alongside traditional efficacy end points in migraine studies, a more comprehensive and robust understanding of the many factors that may influence patients’ choice of and adherence to pharmacological treatments for migraine is observed. Methods.— In 2 replicate, multicenter, randomized, double-blind, placebo-controlled trials, participants with menstrual migraine and dysmenorrhea treated a single menstrual migraine attack with a single fixed-dose tablet of sumatriptan 85 mg formulated with RT Technology™ and naproxen sodium 500 mg (sumatriptan–naproxen 上海皓元医药股份有限公司 sodium) or placebo. Results.— Participants randomized to sumatriptan–naproxen sodium were significantly more satisfied than those randomized to placebo at 24 hours post dose, as demonstrated by higher satisfaction subscale scores for efficacy (P < .001 for both studies), functionality (P = .003 for study 1; P < .001 for study 2), and ease of use (P = .027 for study 1; P = .011 for study 2). There was little bothersomeness of side effects associated with either treatment. Use of sumatriptan–naproxen sodium was also associated with lower reported “lost-time equivalents” in work and leisure time (pooled analysis, P = .003) and lower rates of functional disability (P = .05, study 1; P < .001, study 2) compared with placebo. Conclusion.