The start date for analyses was the date of liver biopsy, with any events occurring in the first 6 months excluded. Patients were monitored every 3-6 months buy VX-809 and followed up until death or liver transplantation, whichever occurred first, or until data analysis. For those lost to follow-up, up-to-date clinical information was sought by

the following: (1) contact with the primary care physician; (2) telephone interview; and (3) checking the respective death and transplant registries. Patients were censored at time of death or transplantation or last clinic visit, and those lost to follow-up were censored at the time last seen. All clinical outcomes were confirmed by a physician at each center, utilizing patient records and physician diagnoses. The following outcomes

were assessed: (1) liver complications, including liver failure, gastroesophageal varices (± hemorrhage), ascites, encephalopathy, hepatopulmonary syndrome, and HCC; (2) liver-related death or liver transplantation (for calculation of survival probability, transplantation was considered as an equivalent end-point); (3) all-cause mortality; and (4) total ABT-888 research buy vascular events (including myocardial infarction, stroke, and vascular deaths).13 HCC was diagnosed if the following were present: (1) pathological changes consistent with HCC identified by histological examination of liver tissue obtained by fine-needle aspiration, liver biopsy, or liver explant at transplantation or autopsy or (2) one or more hepatic space-occupying lesions that had vascular patterns typical of HCC by angiography, CYTH4 triple-phase computed tomography, or magnetic resonance imaging. All patients were followed according to standards of care and guidelines without experimental or therapeutic interventions for NAFLD or HCV. Weight management was performed with lifestyle intervention, such as dietary modification, and exercise was recommended at outpatients in overweight/obese patients. Other treatments, such as oral hypoglycemics, cholesterol-lowering

medications, and antihypertensive medications, were only given in the context of management of concomitant diabetes mellitus, hypercholesterolemia, or hypertension, respectively. Neither pharmacological nor lifestyle interventions were recorded systematically after baseline. Statistical analyses were performed using SPSS version 13.0 (SPSS, Inc., Chicago IL). Results are reported as means ± standard deviation (SD) or frequency (i.e., percentage), as appropriate. Continuous variables were compared using the two-tailed Student’s t-test. Categorical data were compared using the chi-square test. Variables with a P value of ≤0.1 on univariate analysis were further analyzed by multiple logistic regression to determine the independent determinants of outcome variables.

Analysis of the 43 incident de novo inhibitors found no significant association between putative risk factors and inhibitor development in PTPs. Taken together, the studies provide reliable evidence that switching FVIII products in PUPs and PTPs has no significant effect on inhibitor development. Hence, if switching products offers added value for the patient or society as a whole, the practice can be safely adopted. The inability to draw conclusions from cohort studies and systematic reviews about FVIII source as a risk factor for inhibitor onset PD0325901 nmr pointed to the need for a randomized study. Randomized controlled trials (RCTs) are the

foundation of evidence-based medicine as they provide the highest level of evidence and grade of recommendations for therapeutic choices. Treatment of haemophilia is based on very selleck few RCTs, in part because of the relative rarity of the disease and ethical aspects of randomization but also because of the excellent relationship between plasma FVIII levels and clinical outcomes. Throughout the years some important treatment standards have been established without the need for RCTs. These include: the efficacy and safety of virally inactivated plasma-derived factors (1980s); the efficacy of desmopressin in mild haemophilia and von Willebrand disease (1980s); and the efficacy and safety of recombinant factors (1990s). In terms

of RCTs available for treatment of haemophilia,

a few studies conducted in the early 1980s investigated the use of bypassing products in patients with inhibitors to FVIII. More recently, prophylaxis was established as the evidence-based standard-of-care for patients at risk of inhibitor development on the basis of two RCTs which compared prophylaxis with episodic (on demand) treatment [17, 18]. Lastly, the prospective, randomized International Immune Tolerance Study many compared high-dose and low-dose factor FVIII regimens in ‘good risk’ patients with high-titre inhibitors and found similar rates of inhibitor eradication [19]. Notwithstanding these few examples, the number of RCTs in haemophilia is low compared with other diseases. Despite the difficulties envisaged in designing and conducting a RCT in haemophilia, a decision to perform such a study was taken in order to address more definitively the unresolved issue of relative risk of inhibitor development in patients exposed to pdFVIII or rFVIII concentrates. Initiated in 2010, this international, randomized clinical trial is known by the acronym SIPPET: Study on Inhibitors in Plasma-Product Exposed Toddlers. In SIPPET, PUPs or minimally treated patients with severe haemophilia A are randomized to receive a FVIII product from one of two classes (recombinant or plasma-derived) for up to 50 exposure days (Fig. 2).

Analysis of the 43 incident de novo inhibitors found no significant association between putative risk factors and inhibitor development in PTPs. Taken together, the studies provide reliable evidence that switching FVIII products in PUPs and PTPs has no significant effect on inhibitor development. Hence, if switching products offers added value for the patient or society as a whole, the practice can be safely adopted. The inability to draw conclusions from cohort studies and systematic reviews about FVIII source as a risk factor for inhibitor onset http://www.selleckchem.com/products/pci-32765.html pointed to the need for a randomized study. Randomized controlled trials (RCTs) are the

foundation of evidence-based medicine as they provide the highest level of evidence and grade of recommendations for therapeutic choices. Treatment of haemophilia is based on very Ribociclib few RCTs, in part because of the relative rarity of the disease and ethical aspects of randomization but also because of the excellent relationship between plasma FVIII levels and clinical outcomes. Throughout the years some important treatment standards have been established without the need for RCTs. These include: the efficacy and safety of virally inactivated plasma-derived factors (1980s); the efficacy of desmopressin in mild haemophilia and von Willebrand disease (1980s); and the efficacy and safety of recombinant factors (1990s). In terms

of RCTs available for treatment of haemophilia,

a few studies conducted in the early 1980s investigated the use of bypassing products in patients with inhibitors to FVIII. More recently, prophylaxis was established as the evidence-based standard-of-care for patients at risk of inhibitor development on the basis of two RCTs which compared prophylaxis with episodic (on demand) treatment [17, 18]. Lastly, the prospective, randomized International Immune Tolerance Study Molecular motor compared high-dose and low-dose factor FVIII regimens in ‘good risk’ patients with high-titre inhibitors and found similar rates of inhibitor eradication [19]. Notwithstanding these few examples, the number of RCTs in haemophilia is low compared with other diseases. Despite the difficulties envisaged in designing and conducting a RCT in haemophilia, a decision to perform such a study was taken in order to address more definitively the unresolved issue of relative risk of inhibitor development in patients exposed to pdFVIII or rFVIII concentrates. Initiated in 2010, this international, randomized clinical trial is known by the acronym SIPPET: Study on Inhibitors in Plasma-Product Exposed Toddlers. In SIPPET, PUPs or minimally treated patients with severe haemophilia A are randomized to receive a FVIII product from one of two classes (recombinant or plasma-derived) for up to 50 exposure days (Fig. 2).

It was slowly injected through the catheter until GFV and their feeding vessels (posterior gastric vein, short gastric vein, or left gastric vein) were visualized. Transvenous administration of 4000 U human haptoglobin (Haptoglobin; Mitsubishi Pharma, Osaka, Japan) was performed to prevent renal failure and hemolysis due to the injection of 5% EOI18. The balloon was left inflated overnight. The next day venography was used to confirm the blood flow interruption in the shunt

and embolization of the gastric varix. Then the balloon was deflated, and the balloon catheter was removed. If embolization was insufficient, additional administration of EOI was performed. Four weeks after the treatment, abdominal contrast-enhanced CT was performed and total obliteration of GFV and SRS was confirmed (Fig. 1). CX-4945 datasheet Endoscopic examinations were performed in all patients every 6 months after the study began. If esophageal varices worsened and became risky, prophylactic endoscopic variceal ligation (EVL) was performed. Abdominal CT was performed every 12 months, and it was confirmed that HCC did not occur in

a 36-month period. The end-point of this study was death of the patient or, in the SRS (+) group, performance of MK-8669 clinical trial B-RTO or endoscopic injection therapy with cyanoacrylate for aggravated GFV in a period of ≥ 36 months. Both of the treatments affect SRS and the study was completed in 5 years from the beginning in each patient. The data in the tables are shown as mean ± standard deviation, and the data in the figures are shown as mean ± standard error of the mean. anova was used for patient background including age, sex, underlying disease, Child–Pugh classification, and Child–Pugh score. Analysis was performed using a t-test for the variceal form and SRS diameter. Analysis

was performed using the Tukey–Kramer test for the comparison of total bilirubin levels, albumin levels, prothrombin times, and Child–Pugh scores among the three groups. For comparison of variables within a group, a paired t-test was used for analysis. Analysis was performed using the Kaplan–Meier method for cumulative survival rates. The differences D-malate dehydrogenase among groups were compared using a log–rank test. anova was used to analyze deaths and aggravation of varices during the follow-up period. A P-value of ≤ 0.05 was established as significant. Statistical analysis was performed using spss 10.0J (spss, Chicago, IL, USA). Table 1 shows the ages, sexes, causes of liver cirrhosis, Child–Pugh classifications, and Child–Pugh scores of the SRS (−), SRS (+) and B-RTO groups. The table also shows the endoscopic variceal forms and SRS diameters of the SRS (+) and B-RTO groups. There were no significant differences in any parameters among the groups.

Target genes regulated by MEG3 were detected with the Dual Luciferase reporter system and their expression levels were confirmed using qRT-PCR and Western blotting. Results: In contrast to matched adjacent non-neoplastic tissues, the expression of MEG3 was absent or decreased in most HCC tissues as well as in HepG2 cells. Low expression levels of MEG3 were associated with advanced pathologic stage, tumor size and a relatively

poor prognosis in HCC patients. Hypermethylation of MEG3 differentially methylated regions was identified by MSP in both HCC tissues and HepG2 cells and MEG3 expression was increased with the inhibition of DNA methyltransferase with 5-aza-2′-deoxycytidine treatment. MEG3 was overexpressed by transfection with pcDNA3.1-MEG3 in HepG2 cells. qRT-PCR analysis revealed that MEG3 expression was increased

by 51-fold in HepG2 cells, Hydroxychloroquine price compared with the empty vector group. Overexpression of MEG3 decreased cell proliferation and increased 11% cell apoptosis ratio in vitro. MEG3 activated P53 and ILF-3 in HepG2 cells. Conclusion: Our data suggest that MEG3 is epigenetically silenced due to promoter hypermethylation, which may contribute to the development of HCC. MEG3 plays Fulvestrant order a tumor suppressor role by activating P53 and ILF-3 gene. Key Word(s): 1. MEG3; 2. hepatocellular arcinoma; 3. methylation; 4. prognosis; 5. p53 Presenting Author: LING FEI WU Additional Authors: MENG QI XIANG, WEI DENG, LI XUAN

LIU, XIAO TAO ZHOU, PEI RUI CHEN, LING FEI WU Corresponding Author: LING FEI WU Affiliations: Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Digestive enzyme Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med Objective: To investigate the role of DNA methyltransferases (DNMTs) and methylation on adenosine (ADO)-induced apoptosis in human hepatocellular carcinoma HepG2 cells. Methods: HepG2 cells were treated with different concentrations of ADO alone or in combination with homocysteine (HCY) for different durations. 5-aza-2′-deoxycytidine (5-Aza-CdR) as a positive control. Cell proliferation inhibition rates were evaluated by CCK8 assay. Cell apoptosis was detected by AnnexinV-FITC/PI staining. The mitochondrial membrane potentials were measured by flow cytometry. The mRNA and protein expression of DNMT1, DNMT3a, DNMT3b, MDM-2, P53, caspase-3, caspase-9 and cytochrome C were detected by qRT-PCR and Western blotting, respectively. The mRNA expression of lncRNA-MEG3 was also detected by qRT-P CR. Results: ADO alone or in combination with HCY significantly suppressed the cell proliferation of HepG2 cells in a dose- and time-dependent manner.

Target genes regulated by MEG3 were detected with the Dual Luciferase reporter system and their expression levels were confirmed using qRT-PCR and Western blotting. Results: In contrast to matched adjacent non-neoplastic tissues, the expression of MEG3 was absent or decreased in most HCC tissues as well as in HepG2 cells. Low expression levels of MEG3 were associated with advanced pathologic stage, tumor size and a relatively

poor prognosis in HCC patients. Hypermethylation of MEG3 differentially methylated regions was identified by MSP in both HCC tissues and HepG2 cells and MEG3 expression was increased with the inhibition of DNA methyltransferase with 5-aza-2′-deoxycytidine treatment. MEG3 was overexpressed by transfection with pcDNA3.1-MEG3 in HepG2 cells. qRT-PCR analysis revealed that MEG3 expression was increased

by 51-fold in HepG2 cells, PS-341 supplier compared with the empty vector group. Overexpression of MEG3 decreased cell proliferation and increased 11% cell apoptosis ratio in vitro. MEG3 activated P53 and ILF-3 in HepG2 cells. Conclusion: Our data suggest that MEG3 is epigenetically silenced due to promoter hypermethylation, which may contribute to the development of HCC. MEG3 plays Apitolisib order a tumor suppressor role by activating P53 and ILF-3 gene. Key Word(s): 1. MEG3; 2. hepatocellular arcinoma; 3. methylation; 4. prognosis; 5. p53 Presenting Author: LING FEI WU Additional Authors: MENG QI XIANG, WEI DENG, LI XUAN

LIU, XIAO TAO ZHOU, PEI RUI CHEN, LING FEI WU Corresponding Author: LING FEI WU Affiliations: Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Etomidate Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med Objective: To investigate the role of DNA methyltransferases (DNMTs) and methylation on adenosine (ADO)-induced apoptosis in human hepatocellular carcinoma HepG2 cells. Methods: HepG2 cells were treated with different concentrations of ADO alone or in combination with homocysteine (HCY) for different durations. 5-aza-2′-deoxycytidine (5-Aza-CdR) as a positive control. Cell proliferation inhibition rates were evaluated by CCK8 assay. Cell apoptosis was detected by AnnexinV-FITC/PI staining. The mitochondrial membrane potentials were measured by flow cytometry. The mRNA and protein expression of DNMT1, DNMT3a, DNMT3b, MDM-2, P53, caspase-3, caspase-9 and cytochrome C were detected by qRT-PCR and Western blotting, respectively. The mRNA expression of lncRNA-MEG3 was also detected by qRT-P CR. Results: ADO alone or in combination with HCY significantly suppressed the cell proliferation of HepG2 cells in a dose- and time-dependent manner.

2.15 cells, and interestingly, numerous tubules extended outward from the MVBs with a 10-fold greater frequency in the HepG2.2.15 cells than the parental HepG2. These tubules also formed in Huh7 cells trans-fected with the HBV genome while siRNA-mediated knockdown of Rab7 decreased tubule formation significantly. From these findings, we conclude that MVB dynamics are induced by HBV and are Rab7-dependent. Importantly, Rab7 knockdown decreased the colocalization selleck inhibitor of viral proteins and lysosomes, and increased the viral secretion. Although it was found that HBe activated Rab7, there was no evidence of direct interaction

between HBe and Rab7. As Rab7 is regulated by the GTPase activating protein (GAP) TBC1D15, we tested for interactions between HBe and TBC1D15. The results of IP showed an interaction between myc-HBe and FLAG-TBC1D15, while GST-HBe pulldown supported the results. In support of these biochemical findings cells expressing myc-HBe and FLAG-TBC1D15 exhibited a substantial colocalization. Conclusion: These findings suggest that HBV may activate Rab7 through the interaction between HBe and the Rab7 GAP, TBC1D15.

This activation induces tubules extending from MVBs/APs and promotes the fusion with lysosomes resulting in the degradation of HBV particles in MVBs/APs. SB525334 supplier HBV is known as a ‘stealth’ virus, and the Rab7 activation by HBe, which attenuates the HBV secretion, may lead to a weakened immune responses for persistent infection. Disclosures: The following people have nothing to disclose: Jun Inoue, Eugene W. Krueger, Jing Chen, Hong Cao, Tooru Shimosegawa, Mark A. McNiven Background: UPA-SCID chimeric mice with humanized livers (SCID-MhL) are a useful tool for studying HBV infection in the absence of an adaptive immune response. Aims: To estimate HBV clearance rate from circulation post-inoculation (p.i.) and characterize subsequent HBV kinetics from inoculation to steady state in the uPA-SCID model. Methods: Twenty-nine mice (25 SCID-MhL,

4 without humanized livers, SCID-M) PAK5 were inoculated with HBV serum (Fig.1). Viral levels were frequently measured from blood up to 60 days p.i. HBV half-life (t1/2) was estimated during the 1st phase (Fig.1) using a linear mixed-effects model. HBV DNA was measured using Real-Time quantitative PCR with limit of detection of 3 log cps/mL. Results: While in SCID-M HBV was rapidly cleared (Fig.1, dashed line), a productive infection was established in SCID-MhL (Fig.1, solid line). After an initial viral decline and eclipse phase (Fig.1 phases 1-3), the virus resurged and eventually stabilized at steady state unexpectedly via a multiphasic kinetic pattern (Fig.1, phases 4-7). Interestingly, during the first 6hr p.i. HBV declined more rapidly in SCID-M [t1/2=37 min (95%CI:35-39 min)] compared to repopulated SCID-MhL [t1/2=63 min (95%CI:59-67 min)] (p<0.001).

She was interested in retreatment due to her esthetic and masticatory functional problems. The intraoral examination presented class III malocclusion with an anterior edge-to-edge relationship (Fig 1). Occlusal contacts were present on the maxillary anterior teeth only. The maxillary central incisors displayed some gingival recession and grade 1 mobility. The maxillary right posterior teeth, mandibular right canine, and first and second premolars had been prepared, but not restored. The mandibular right first molar was missing.

Brackets had been prepared on the left mandibular first and second premolars for vertical control. At clinical examination, the patient showed a severely

decreased lower facial height and INCB024360 nmr mandibular prognathism with significant overclosure in maximal intercuspal position (Fig 1). The maxillary teeth were not exposed when the patient attempted to smile. The interocclusal distance at rest position was 13 mm, and the general facial appearance improved with the mandible in the physiological rest position. Cephalometric evaluation demonstrated decreased lower facial height, decreased mandibular plane angle, and sagittal and vertical deficiency of the maxilla with relative mandibular protrusion. The panoramic radiograph showed distinct features of CCD: the parallel-sided ascending ramus of the mandible, the upward-pointed coronoid process, Z-VAD-FMK and the downward-tilting zygomatic arch (Fig 2). The goal of treatment was to improve facial esthetics by increasing the OVD in order to obtain an esthetic upper tooth/lip relationship and to achieve satisfactory masticatory function. Ergoloid To obtain these ends, LeFort I osteotomy followed by prosthetic rehabilitation was presented as a treatment option; however, the patient refused orthognathic surgery because of fear of extensive surgery. Therefore, the alternative treatment option

was limited to prosthetic rehabilitation. The treatment plan for the patient was divided into two phases. The first phase was the fabrication of the maxillary and mandibular interim prostheses to evaluate facial esthetics and function. Adequate OVD was to be verified after trials with interim prostheses. The second phase consisted of the fabrication of definitive prostheses. The prosthetic options considered for the mandible were implant-supported fixed dental prostheses (FDPs) for the missing teeth and metal ceramic restorations. The advantages and disadvantages of maxillary overdenture and FDPs as prosthetic options for the maxilla were considered. Facial parameters such as lip support, smile line, and upper lip length were evaluated with interim prostheses for decision making. The decision was to be finalized after evaluation of the interim prostheses.

5D) and localized primarily in periportal regions. Biochemical analysis confirmed that hepatic TG content was reduced in L-Fabp−/− mice, with this website no difference in hepatic cholesterol, free cholesterol, phospholipid, or FA (Fig. 5E). The decreased abundance of LDs in TFF-fed L-Fabp−/− mice was accompanied by decreased expression of perilipin 4 (Plin4), perilipin 5 (Plin 5), and Cidec (Fsp27) (Fig. 5F). These findings suggest that TFF-fed L-Fabp−/− mice exhibit reduced

hepatic steatosis with attenuated LD formation compared to C57BL/6J control mice. There was no consistent change in the expression of genes mediating hepatic FA oxidation either by diet or genotype (Fig. 5G) and both genotypes exhibited comparable up-regulation of lipogenic genes in response to TFF feeding. We also examined the possibility that the shift in LD accumulation with TFF feeding reflected alterations in autophagy in L-Fabp−/− mice. We found that TFF feeding induced a significant change in the ratio of LC3II/LC3-I, implying increased autophagy (Fig. 5H), but these changes were comparable in both genotypes (Fig. 5I). Accordingly, the mechanisms underlying the attenuated accumulation

of hepatic triglyceride likely reflect a combination of subtle shifts in FA utilization rather than changes in Selleck BAY 80-6946 a single pathway. Since Ad-L-Fabp transduction attenuated the activation of HSCs in vitro, we reasoned that the development of hepatic fibrosis might be augmented in TFF-fed L-Fabp−/− mice, despite the reduction in

hepatic triglyceride content. However, this was not the case. L-Fabp−/− mice exhibited reduced mRNA abundance of profibrogenic genes, including tissue inhibitor of metalloproteinase 1 (TIMP1), connective tissue growth factor (CTGF) (αI(I)Col and α4(I)Col), with a trend towards decreased expression of α-SMA (Fig. 6A). These findings were confirmed histologically, with fewer collagen fibrils in TFF-fed L-Fabp−/− mice compared to controls (Fig. 6B) and blinded evaluation revealed reduced fibrotic foci (Fig. 6C). These results collectively demonstrate both attenuated steatosis and reduced fibrogenesis in TFF-fed L-Fabp−/− mice. The central observations of this report demonstrate that L-Fabp plays a cell-specific role in regulating IKBKE elements of lipid metabolism in murine hepatocytes and stellate cells, with implications for HSC activation in vitro and for the development and progression of diet-induced NAFLD. The finding that L-Fabp mRNA is abundantly expressed in freshly isolated HSCs, with a coordinated decrease in mRNA expression after 3 days in culture, and that these changes are temporally related to LD depletion and HSC activation, along with reversal of these phenotypes upon Ad-L-Fabp transduction, collectively demonstrate a functional role for L-Fabp in both HSC lipid metabolism and HSC activation. The TFF feeding experiments extend earlier studies which demonstrated that L-Fabp−/− mice are protected against diet-induced obesity and hepatic steatosis.

By this method we identified 1536 patients. Only patients with available clinical and biochemical components of the new simplified criteria at baseline were included.17 Thus, information on the presence of autoantibodies, immunoglobulin G (IgG) or gammaglobulins, viral serologies, and a liver biopsy were obtained before initiation of immunosuppressive therapy. Patients seen at the Mayo Clinic only for a second opinion, but who were diagnosed earlier and who had already started treatment, were excluded. Also, patients undergoing transplants for AIH and patients with decompensated liver disease at presentation C59 wnt research buy were excluded as well

as pediatric cases (younger than 16 years of age). The reason for excluding patients with liver failure or those who required transplantation was because the diagnosis of AIH is more uncertain

in these conditions. Some features of AIH such as autoantibodies can be present in patients with liver failure and decompensated liver disease, probably secondary to the chronic liver injury. Furthermore, most patients with decompensated liver disease had been started on treatment for AIH elsewhere, and therefore Vincristine in vivo there was often a lack of important biochemical parameters such as gammaglobulins or IgG and autoantibodies, making a diagnostic score almost impossible. Furthermore, patients with a diagnosis of primary biliary cirrhosis and primary sclerosing cholangitis were excluded, as were patients with clinical suspicion of overlap syndromes (AIH/primary biliary cirrhosis and AIH/primary sclerosing cholangitis). A retrospective review was performed on patients fulfilling the inclusion criteria. The following variables

were obtained by the chart review: age, sex, date of liver biopsy, titers of antinuclear antibodies, smooth muscle antibodies, liver kidney microsomal, antimitochondrial antibodies, antinuclear cytoplasmic antibodies, IgG, gammaglobulins, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, albumin, and international normalized ratio at baseline. Furthermore, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, Flavopiridol (Alvocidib) total bilirubin, albumin, international normalized ratio, IgG, gamma globulins at 1 to 2 weeks, 2 months, 6 months, 1 year, and at last follow-up after start of immunosuppressive treatment were recorded. The presence of a suspicion of drug etiology in triggering the AIH was recorded. The liver biopsy results were analyzed, and histology compared between the DIAH patients and age (±5 years of age at the diagnosis of AIH) and sex-matched patients (n = 24) randomly chosen from the rest of the AIH patients. Sex was balanced, and no significant age difference was found at diagnosis. Furthermore, patients with nitrofurantoin-induced and minocycline-induced AIH were compared. All biopsy materials were reviewed by a single liver pathologist (S.O.S.), blinded to the clinical context of the biopsy as well as the patient’s outcomes.