The binding was only partially possible to inhibit with the addition of each molecule, however, and was therefore considered primarily unspecific. Thirteen patients with a current negative Bethesda titre had a previous selleckchem history of inhibitors, but no exposure to ITI-therapy (see Fig. 1). Six (46.2%) of these subjects had experienced high-responding

inhibitors with a mean peak titre of 15.6 BU mL−1 (range: 5.0–37.5 BU mL−1, median: 11.5 BU mL−1), whereas the others were low-responders. In two of the plasma samples of the latter subjects, an antibody response was detected in the ELISA assay, whereas this was not the case for the others. The median age did not differ significantly (P = 0.29) in patients without (median: 13.5 years, mean: 15.7 years, range: 1–68 years) and with (median: 14.0 years, mean: 23.2 years, range: 0–74 years) Bethesda-negative selleck kinase inhibitor ELISA-positive antibodies. However, within the subgroup without a history of inhibitory antibodies (n = 122), there was a significant difference in median age of patients with NNA (median: 30.0 years, mean: 28.0 years, range: 1–65 years) compared with patients without NNA (median: 14.0 years, mean: 17.0 years, range: 0–74 years) (P = 0.021). This was not the case in the subgroup with a history of inhibitors (n = 79) (P = 0.43). No significant difference in NNA prevalence was

found, in either the total cohort (n = 201) or any of the two subgroups (with and without history of inhibitors, see Fig. 1), when comparing patients carrying a high-risk mutation, defined as inversions, nonsense mutations or large deletions, with those selleck chemical with a low-risk mutation. Likewise, there was no correlation between race

and NNA development in any cohort analysed (data not shown). As noted above, 53 (67.9%) families had been previously characterized as discordant with respect to an inhibitory antibody response, 8 (10.3%) families concordant with a positive inhibitor titre found in all siblings and 17 families (21.8%) concordant without a history of inhibitors. However, when considering the total FVIII antibody response, the number of discordant families was reduced to 47 (60.3%) and the number of families with an antibody response in all siblings increased to 20 (25.6%), as 10 of the discordant and two of the concordant negative (i.e. no previous antibody response) families showed a FVIII antibody response in all subjects. For example, in one family with three siblings carrying a small deletion mutation, only one had a history of inhibitory FVIII antibodies, but with inclusion of results from the ELISA assays, all three brothers showed an antigenic response towards FVIII (data not shown). In four of the 17 families without a previous inhibitor, at least one sibling had a positive antibody response. In our cohort of 201 patients with severe haemophilia A, the prevalence of NNA (i.e.

99) and rtN238T (0.71%) related with low sensitivity to adefovir (ADV), and the other two displayed variants, such as rtA211T (0.57%), rtQ215H (3.91%), rtA219S (13.32%), rtA223T (0.71) and rtA223S (0.46%), likely related to ADV. Conclusions: After more than 7 years’ complete viral suppression and despite find more relative reductions in HBsAg level, none of the 7 HBeAg-ve patients cleared HBsAg after discontinuing TDF. After TDF, there is an increase in HBV reverse transcriptase variability mainly due to variants with low sensitivity to ADV, which seems to reflect

a cross-resistance mechanism between ADV and TDF. This phenomenon could reflect evolutive pressure of TDF over the cccDNA reservoir during suppression of detectable viral replication. Study funded by Instituto de Salud Carlos III, grant PI 1 1/01973, co-financed by the European Regional Development Fund (ERDF). Disclosures:

Maria Buti – Advisory Committees or Review Panels: Boerhinger selleck Inghelm, Boer-hinger Inghelm; Speaking and Teaching: MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen, MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen Rafael Esteban – Speaking and Teaching: MSD, BMS, Novartis, Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen The following people have nothing to disclose: David Tabernero, Francisco Rodriguez-Frias, Rosario Casillas, Josep Gregori, Carolina Gonzalez, Irene Bel-monte Mula, Maria Homs, Maria Blasi, Josep Quer, Leonardo Nieto, Silvia Camos, selleck screening library Andrea Caballero We recently reported that despite antiviral treatment, HBV ccc DNA persists in hepatocellular carcinoma (HCC) and is correlated to the absence of vascular invasion. The tumoral (T) and non-tumoral(NT) liver transcriptomes

are now available. Patients and methods. 63 HBsAg-positive patients ( anti-HCV, anti-HDV and anti-HIV negative), resected for HCC. Most were cirrhotic (82% of cases) with low viremia under antiviral therapy (79%). Replication in T and NT was assessed by detection of full length HBV DNA, quantification of HBV ccc DNA or of total HBV DNA. Agilent micro arrays were used for transcriptomic experiments. Results. HBV ccc DNA was strongly correlated with transcriptome analysis. Principal component analysis (PCA) comparing differential gene expression between T and NT demonstrated in the first dimension, a clustering according to the tumoral vascular invasion and in the second dimension, a clustering according to the detection of HBV ccc DNA in T. Fatty acid metabolism, complement and coagulation, retinol metabolism and PPAR pathways were upregulated in absence of vascular invasion. Vascular smooth muscle contraction, ECM-receptor interaction and Gap junction pathways were upregulated in case of tumoral replication of HBV. Comparisons with other data on HCC showed in HCC not replicating HBV, an enrichment of genes related to vascular invasion. Conclusion. HBV replication in the HCC correlated to unfrequent vascular invasion, better prognosis and specific pathways.

When corrected for age, this difference was borderline significant (P-value 0.05). The cumulative incidences of malignancies were similar in both groups (9% vs. 10%). Diabetes mellitus, on the other hand, this website occurred significantly more often in HIV-positive than in HIV-negative patients (12% vs. 7%, adjusted

P-value 0.006). All but one of the HIV-positive patients were on HAART when their diabetes was diagnosed. The prevalence of chronic hepatitis C infection was not associated with HIV status. Body mass indexes (BMI) could be calculated for 42 HIV-positive (72%) and 134 HIV-negative haemophilia patients (88%). Mean BMI was significantly lower in the HIV-positive patients (22.1 vs. 25.7 kg m−2, adjusted P-value < 0.001), and the prevalences of overweight (BMI 25.1–30.0 kg m−2) and obesity (BMI >30.0 kg m−2) were also much lower in these patients (10% and 2% vs. 45% and 10% respectively). Thirty-one HIV-positive patients (52%) were deceased at the end of follow-up. Causes of death are shown in Table 3. Death was reported to be solely AIDS related in 19 patients (61%) and caused by a combination Raf inhibitor of HIV and hepatitis C in three patients (10%). Mean age at death was 36.9 years (range: 14–65 years). All but two AIDS-related deaths occurred in patients who were not on HAART. Only the two lymphoma patients were on HAART at time of diagnosis, but the second patient had

started this treatment only a few months earlier. In one other patient on HAART, death was reported to be caused by a combination of HIV and hepatitis C. Median interval between HIV seroconversion and death was 11 years (range: 4–26 years). No fatal non-virus related malignancies occurred in our cohort, nor were there any fatal ischaemic cardiovascular

events. Interestingly, seven of nine HIV-infected haemophilia B patients (78%) were deceased, but only 24 of 51 HIV-infected check details haemophilia A patients (47%). Death was solely or partially AIDS related in five haemophilia B patients (71%) and in 17 haemophilia A patients (71%). Median interval between HIV seroconversion and death was similar across haemophilia types (10 years in haemophilia B and 11 years in haemophilia A, P-value 0.21). In comparison, 28 of the 152 HIV-negative severe controls (18%) were deceased at the end of follow-up. Main causes of death in these patients were intracranial bleeding, malignancies, hepatitis C, other bleedings and infections. Compared with the HIV-negative patients, the age-adjusted odds ratio for dying was 4.1 in HIV-positive patients (95% CI: 1.9–8.7, P-value < 0.001). The cumulative survival since 1980 for both the HIV-positive and HIV-negative patients with severe haemophilia is shown in Fig. 2. Fifty patients (83%) ever received antiretroviral treatment, 32 of whom were treated with HAART. Median month of start of HAART was January 1997 (range: January 1996–April 2008). Of the 27 patients who were still alive and treated at our centre in 2010, 25 (93%) were on HAART.

This retrospective study included 21 patients who underwent surgical resection for HCC disease recurrence

after RFA. Clinicopathological findings, including patterns of recurrence, immunohistochemical expression of proliferation markers (Ki-67 and p27Kip1) and survival outcome were PI3K inhibitor assessed. The median time interval after RFA until the diagnosis of intrahepatic and/or extrahepatic tumor progression was 12 months (range, 3–84). Radical surgical resection was attempted for intrahepatic local recurrence in 16 patients (18 lesions), for peritoneal dissemination in four, for lymph node metastases in three and for adrenal metastasis in two. In 14 of the 21 (67%) patients, the recurrent HCC were histologically diagnosed as of poorly differentiated type. Their average Ki-67 and p27Kip1 labeling indices were significantly higher (P = 0.020) and lower (P < 0.001), respectively, compared with values for the 108 HCC surgically resected at the initial treatment. Portal involvement was significantly higher (P = 0.01) in recurrent tumors after RFA (72%) than in HCC surgically resected at the initial treatment (43%). The mortality rate of salvage surgery was 0%, with cumulative survival rates at 1 and 3 years of 58.9% and 35.7%, respectively.

The recurrent tumors after RFA have characteristics of poor differentiation degree and abnormalities in cell-cycle regulators and are associated with aggressive vascular selleck screening library invasiveness. “
“In the present study, the potential benefits of oral carnitine

in preventing antituberculosis drug-induced hepatotoxicity (ATDH) were evaluated. Fifty-four patients in the carnitine and 62 see more patients in the placebo group completed the study. The carnitine group received 1000 mg oral carnitine solution twice daily for 4 weeks. The placebo group received 10 mL of oral placebo solution twice daily for 4 weeks. ATDH was defined as an increase in the serum level of aspartate aminotransferase or alanine aminotransferase greater than three or five times of the upper limit of normal with or without clinical symptoms of hepatotoxicity, respectively. During the study period, 29 (25%) patients experienced ATDH. Among these patients, nine (16.7%) and 20 (32.3%) were in the carnitine and placebo groups, respectively (P = 0.049). Based on multivariate logistic regression model, age over 35 years old (odds ratio [OR] = 7.01, P = 0.002), human immunodeficiency virus infection (OR = 40.4, P < 0.001), diabetes mellitus (OR = 37.6, P = 0.001), and placebo treatment (OR = 0.1, P = 0.01) were identified as predisposing factors for ATDH. Results of our preliminary clinical trial suggested that cotreatment with 2000 mg oral L-carnitine solution daily for 4 weeks significantly decreased the rate of ATDH. "
“Background and Aims:  An adequate range of colonic observations for precise evaluation of inflammation in ulcerative colitis (UC) patients has not been reported.

This retrospective study included 21 patients who underwent surgical resection for HCC disease recurrence

after RFA. Clinicopathological findings, including patterns of recurrence, immunohistochemical expression of proliferation markers (Ki-67 and p27Kip1) and survival outcome were KPT-330 in vitro assessed. The median time interval after RFA until the diagnosis of intrahepatic and/or extrahepatic tumor progression was 12 months (range, 3–84). Radical surgical resection was attempted for intrahepatic local recurrence in 16 patients (18 lesions), for peritoneal dissemination in four, for lymph node metastases in three and for adrenal metastasis in two. In 14 of the 21 (67%) patients, the recurrent HCC were histologically diagnosed as of poorly differentiated type. Their average Ki-67 and p27Kip1 labeling indices were significantly higher (P = 0.020) and lower (P < 0.001), respectively, compared with values for the 108 HCC surgically resected at the initial treatment. Portal involvement was significantly higher (P = 0.01) in recurrent tumors after RFA (72%) than in HCC surgically resected at the initial treatment (43%). The mortality rate of salvage surgery was 0%, with cumulative survival rates at 1 and 3 years of 58.9% and 35.7%, respectively.

The recurrent tumors after RFA have characteristics of poor differentiation degree and abnormalities in cell-cycle regulators and are associated with aggressive vascular R428 invasiveness. “
“In the present study, the potential benefits of oral carnitine

in preventing antituberculosis drug-induced hepatotoxicity (ATDH) were evaluated. Fifty-four patients in the carnitine and 62 check details patients in the placebo group completed the study. The carnitine group received 1000 mg oral carnitine solution twice daily for 4 weeks. The placebo group received 10 mL of oral placebo solution twice daily for 4 weeks. ATDH was defined as an increase in the serum level of aspartate aminotransferase or alanine aminotransferase greater than three or five times of the upper limit of normal with or without clinical symptoms of hepatotoxicity, respectively. During the study period, 29 (25%) patients experienced ATDH. Among these patients, nine (16.7%) and 20 (32.3%) were in the carnitine and placebo groups, respectively (P = 0.049). Based on multivariate logistic regression model, age over 35 years old (odds ratio [OR] = 7.01, P = 0.002), human immunodeficiency virus infection (OR = 40.4, P < 0.001), diabetes mellitus (OR = 37.6, P = 0.001), and placebo treatment (OR = 0.1, P = 0.01) were identified as predisposing factors for ATDH. Results of our preliminary clinical trial suggested that cotreatment with 2000 mg oral L-carnitine solution daily for 4 weeks significantly decreased the rate of ATDH. "
“Background and Aims:  An adequate range of colonic observations for precise evaluation of inflammation in ulcerative colitis (UC) patients has not been reported.

Dimorphism might therefore be expected for some taxa if the herd recognition hypothesis was correct. To conclude, neither the presence of a fairly random pattern of diversification in exaggerated structures, nor the lack of sexual dimorphism, represent clear support MI-503 clinical trial for the species recognition hypothesis over others. Padian & Horner (2011a) argued that the presence of exaggerated structures in sympatric, closely related taxa supports their role in species

recognition. However, it has been noted that ‘mating signals of sympatric species often are more distinct from one another than are other signals produced by the same species’ and, furthermore, that ‘species confined to different regions have no possibility of confusing their signals’ (both quotes by Wells & Henry, 1998). In short, we would expect that if these features

functioned in species recognition, they would be more divergent between sympatric species, and less divergent between allopatric ones. However, this is clearly not true for a number of examples in the dinosaur fossil record. Wuerhosaurus (or Stegosaurus) homheni is the only stegosaur recognized in the Lower Cretaceous Lianmuging Formation of China (Maidment et al., 2008). Given the distinctive bauplan of stegosaurs relative to potential sympatric dinosaurs, it is unlikely that individuals Wnt tumor would struggle selleckchem to identify conspecifics simply because they lacked dorsal plates and tail spikes. This and other examples (e.g. the lone Asian spinosaurine,

Ichthyovenator, Allain et al., 2012) render it difficult to interpret species recognition as a viable primary explanation for the evolution of exaggerated structures among these taxa. Main et al. (2005) noted of stegosaur anatomy that while ‘we have no independent evidence of mate competition, we can use the features of their plates to identify species’. However, this is not always true: disagreement continues over stegosaur taxonomy, with variation in plate and spike form being interpreted as within intraspecific variation by some, but exceeding it by others (Maidment et al., 2008). Similar problems exist for other lineages. An additional argument against the use of exaggerated structures in species recognition is that some structures differ little between sympatric species. The Upper Cretaceous Inner Mongolian locality of Bayan Mandahu, for example, has yielded the apparently contemporaneous neoceratopsians Protoceratops hellenikorhinus, Bagaceratops rozhdestvenskyi and Magnirostris dodsoni (Lambert et al., 2001). If some of these taxa are synonymous, then likely only one species occupied any one locality at any one time, and we return to the paradox of a character for ‘species recognition’ when there is no possibility of confusion.

Thirty-nine and 30 patients received RFA 1 and 2-4 times, respectively. After treatments, HCC recurrence was evaluated with dynamic CT or MRI every 3-4 months. All patients gave written informed consent to participate in the study in accordance with the Helsinki declaration, and this study was approved by the regional ethics committee (Medical Ethics Committee of Kanazawa University). Blood samples were tested for hepatitis B surface antigen and hepatitis C virus (HCV) antibody using commercial immunoassays (Fuji Rebio, Tokyo, Japan). The patients with HCV antibody were tested for serum HCV RNA by real-time PCR (Roche, Tokyo, Japan), and 49 of PLX4032 clinical trial 52 patients with HCV antibody were HCV RNA–positive.

HLA-based typing of PBMCs from patients and normal blood donors was performed using reverse sequence-specific oligonucleotide analysis with polymerase chain reaction (PCR-RSSO). The serum alpha-fetoprotein (AFP) level was measured via enzyme immunoassay (AxSYM AFP, Abbott Japan, Tokyo, Japan), and the pathological grading of tumor cell differentiation was assessed according to the Maraviroc mw general rules for the clinical and pathological study of primary liver cancer.8

The severity of liver disease was evaluated according to the criteria of Desmet et al. using biopsy specimens of liver tissue, where F4 was defined as cirrhosis.9 Fifty-five patients who participated in the present study received liver biopsy with RFA. Another 14 patients received liver biopsy 1-3 years before RFA. Eleven peptides that we

previously identified as being useful for analysis of immune response in HLA-A24–positive HCC patients were selected.10-13 Human immunodeficiency virus (HIV) envelope-derived peptide (HIVenv584)14 and cytomegalovirus (CMV) pp65-derived peptide (CMVpp65328)15 were also selected as control peptides. Peptides were synthesized at Sumitomo Pharmaceuticals selleck chemicals (Osaka, Japan). They were identified using mass spectrometry, and their purities were determined to be >90% by analytical high-performance liquid chromatography. PBMCs were isolated before and 2-4 weeks after HCC treatments as described.11 In the patients who received RFA 2-4 times, PBMCs were obtained 2-4 weeks after the final treatment. In some patients, PBMCs were also obtained 24 weeks after RFA. PBMCs were resuspended in Roswell Park Memorial Institute 1640 medium containing 80% fetal calf serum and 10% dimethyl sulfoxide and cryopreserved until use. Interferon-γ (IFN-γ) ELISPOT assays were performed as described.11 Negative controls consisted of an HIV envelope–derived peptide (HIVenv584).14 Positive controls consisted of 10 ng/mL phorbol 12-myristate 13-acetate (PMA, Sigma) or a CMVpp65-derived peptide (CMVpp65328).15 The colored spots were counted with a KS ELISpot Reader (Zeiss, Tokyo, Japan). The number of specific spots was determined by subtracting the number of spots in the absence of an antigen from the number in its presence.

Accordingly, curative treatments, like orthotopic liver transplantation (OLT), resection, or radiofrequency ablation (RFA) are reserved for patients with early stage HCC (BCLC stage 0/A). Unfortunately, HCC is commonly diagnosed at intermediate (BCLC stage B) or advanced (BCLC stage C) tumor stages6, 7 where only palliative treatment options can be offered, resulting in a limited overall survival (OS) of 11-20 months. Transarterial chemoembolization (TACE) is the recommended treatment modality selleckchem for asymptomatic, large, or multifocal HCC without macrovascular

invasion or extrahepatic metastasis (intermediate HCC, BCLC stage B). As most patients with HCC also suffer from liver cirrhosis, not only tumor characteristics but also the degree of liver dysfunction are of prognostic importance for patients undergoing TACE. Several studies showed8 that baseline tumor characteristics like tumor size or extent, alpha-fetoprotein (AFP) values, as well as baseline Child-Pugh score, presence of ascites, and several baseline lab values, e.g., AST9 are associated with OS of HCC patients. Furthermore, tumor-related

dynamics after TACE are important for patient prognosis, as radiologic and biochemical (AFP) tumor responses have been associated with improved patient outcome.10-12 Finally, deterioration buy AZD3965 of liver function after TACE may negatively impact the patient prognosis and liver function may further worsen after repeated TACE sessions or even find more obviate any consequent antitumor treatment. The aim of this study was to establish a clinically usable point score to guide the decision for retreatment with TACE in patients with HCC. Using a stepwise multivariate regression model we developed a novel point score predicting patient outcome with respect to patient characteristics prior to the second TACE as well as the dynamic of tumor and liver-function related parameters after the first TACE session. All patients, >18 years old at the time of the first TACE cycle, diagnosed with HCC by histology or dynamic imaging (computed

tomography [CT] / magnetic resonance imaging [MRI] scans) according to the European Association for the Study of the Liver (EASL) diagnostic criteria4 who were treated with conventional TACE (cTACE), transarterial embolization (TAE), or TACE with drug-eluting beads (DEB-TACE) (hereafter summarized and referred to as TACE) at the Department of Gastroenterology and Hepatology of the Medical University of Vienna between January 1999 and December 2009 (n = 231) were screened for eligibility (Fig. 1). Patients with HCC at BCLC stage A or B and preserved liver function (Child-Pugh stage A or B) who received at least two TACE sessions within 3 months (≤90 days) were included and formed the training cohort for all further analysis.

1 log copies/mL on pretreatment screening tests, NA therapy should be commenced without delay. Patients with

resolved HBV infection and HBV DNA levels <2.1 log copies/mL on pretreatment screening tests should undergo regular monitoring of HBV DNA levels during and after their immunosuppressive therapy or chemotherapy. If HBV DNA levels exceed 2.1 log copies/mL during monitoring, preemptive NA therapy should be commenced. Entecavir is the recommended Rapamycin order NA. The criteria for cessation of NA therapy are the same as for cessation of NA therapy in HBsAg positive patients. For patients with resolved HBV infection, NA therapy should be continued for at least 12 months after completion of immunosuppressive therapy or chemotherapy, although cessation of NAs may be considered during this period if continued ALT normalization and HBV DNA negative conversion are seen. Close follow-up including HBV DNA monitoring is necessary for at least 12 months after cessation of NA therapy. If HBV

DNA levels exceed 2.1 log copies/mL during the follow-up period, NA therapy should be recommenced immediately. HBV reactivation is a potential problem in recipients of a liver transplant from an HBsAg negative and anti-HBc antibody positive donor. In a report from a time before prophylactic click here HBIG administration became standard, HBV reactivation occurred in 15 out of 16 recipients of liver transplants from anti-HBc antibody positive donors, one of whom died from FCH.[332] It is preferable to exclude anti-HBc antibody positive donors, but a strategy is needed selleck chemicals llc when transplantation of a liver from such a donor cannot be avoided. One such strategy is to administer HBIG during the transplantation procedure, and maintain anti-HBs antibody

levels postoperatively. Postoperative administration of NA therapy, or NA+HBIG combination therapy, is also considered useful.[333, 334] Early commencement of NA therapy following HBV reactivation has also been reported to be effective.[335] HBV reactivation is seen in a high proportion (50–94%) of HBsAg positive patients undergoing transplantation of kidneys and other organs.[336-339] Following HBV reactivation, rapid progression is seen from chronic hepatitis B to liver cirrhosis, which becomes the cause of death. Prophylactic NA therapy is recommended for HBsAg positive and/or anti-HBc antibody positive patients, commencing prior to the transplantation procedure. HBV reactivation is seen in a high proportion (≥50%) of HBsAg positive patients undergoing of hematopoietic stem cell transplantation.[340] The rate of HBV reactivation is 14–20% in patients with resolved HBV infection.[341, 342] The risk of HBV reactivation is higher with allogeneic bone marrow transplantation than with autologous bone marrow transplantation.

If MOH shares some neurophysiological features with addiction, long-lasting functional alterations of the mesocorticolimbic dopamine system related to medication

overuse should be present. We collected functional magnetic resonance imaging data during the execution of a decision-making under risk paradigm in 8 MOH patients immediately after beginning medication withdrawal, in 8 detoxified MOH patients at 6 months after beginning medication withdrawal, in 8 chronic migraine patients, and in 8 control subjects. Our results revealed that MOH patients present: (1) reduced buy PD98059 task-related activity in the substantia nigra/ventral tegmental area complex and increased activity in the ventromedial prefrontal cortex, when compared with controls; (2) reduced activity in the substantia nigra/ventral tegmental area complex, when compared with chronic migraine patients; (3) increased activity in the ventromedial prefrontal cortex, when compared with detoxified MOH patients. Our study showed that MOH patients present dysfunctions

in the mesocorticolimbic dopamine circuit, in particular in the ventromedial prefrontal cortex and in the substantia nigra/ventral tegmental area complex. The ventromedial prefrontal find more cortex dysfunctions seem to be reversible and attributable to the acute/chronic headache, whereas the substantia nigra/ventral tegmental area complex dysfunctions are persistent and possibly related to medication click here overuse. These dysfunctions might be the expression of long-lasting neuroadaptations related to the overuse of medications and/or a pre-existing neurophysiological condition leading to vulnerability to medication overuse. The observed persistent dysfunctions in the midbrain dopamine suggest that MOH may share some neurophysiological

features with addiction. “
“Objective.— Examine whether acceptance and commitment additive therapy is effective in reducing the experience of sensory pain, disability, and affective distress because of chronic headache in a sample of outpatient Iranian females. Background.— Chronic headaches have a striking impact on sufferers in terms of pain, disability, and affective distress. Although several Acceptance and Commitment Therapy outcome studies for chronic pain have been conducted, their findings cannot be completely generalized to chronic headaches because headache-related treatment outcome studies have a different emphasis in both provision and outcomes. Moreover, the possible role of Iranian social and cultural contexts and of gender-consistent issues involved in Acceptance and Commitment Therapy outcomes deserve consideration. Methods.— This study used a randomized pretest–post-test control group design.