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Sofosbuvir-based regimens can be used in ESRD patients on dialysis with good efficacy.

Objective: A randomized, double blind, split mouth, controlled clinical trial was conducted to evaluate the effect of two desen sitizing agents on reduction of Dentin Hypersensitivity (DH). Material and Methodology:A sample of 73 teeth from 13 patients, among which at least 3 teeth had dentin hypersensitivity, was randomly allocated into 3 treatment groups: Group A: treated with 30% ethenolic extract of Indian Propolis, Group B: treated with GC tooth mousse, and Group C: treated with sterile water. A Verbal Rating Scale (VRS) was used to record the degree of hypersensitivity, based on patient's response to tactile and air blast stimuli. The baseline scores were obtained. Each intervention group received applications of their respective agents consecutively on 1 st , 7 th , 14 th and 21 st days. After each application, the scores were recorded.Results: Both the 30% Indian Propolis and GC tooth mousse showed significant reductions in dentin hypersensitivity.Conclusion: GC tooth mousse was found to be significantly better in reducing the dentinal hypersensitivity as compared to Propolis and sterile water (p< 0.01).

BackgroundIn the SELECT-MONOTHERAPY trial, upadacitinib (UPA), an oral JAK1-selective inhibitor, showed efficacy when used as monotherapy over 14 weeks (wks) in rheumatoid arthritis (RA) patients (pts) with an inadequate response to methotrexate (MTX).1 ObjectivesSafety and efficacy of UPA monotherapy were assessed through 48 wks in an ongoing long-term extension period of SELECT-MONOTHERAPY.MethodsAt baseline (BL), pts on stable MTX were randomized to either continue MTX (cMTX, given as a blinded study drug) or switch to once-daily (QD) UPA at 15 (UPA15) or 30 mg (UPA30) monotherapy for 14 wks. From Wk14, the start of a long-term blinded extension, pts randomized to cMTX were switched to UPA15 or 30mg per pre-specified assignment at BL, pts randomized to UPA15 or 30 continued their initial treatment. No dose adjustments for UPA were allowed. Starting at Wk26, for pts who did not achieve CDAI ≤10, background csDMARDS could be initiated. Efficacy data up to the Wk48 visit are reported “As Observed”. Adverse events (AE) per 100 pt yrs (PYs) are summarized up to May 25 2018.ResultsOf 648 pts randomized at BL, 598 (92%) completed 14 wks and continued on to the extension period. By May 25 2018, 16% discontinued study drug; 5% due to AE, 0.5% due to lack of efficacy, 4% withdrew consent, 1% were lost to follow-up, and 6% due to other reasons. Cumulative exposures to UPA15 and UPA30 were 336.0 PYs and 337.1 PYs, respectively. Starting from Wk26, background csDMARDs were initiated for approximately 18% of pts.Based on As Observed data, for pts on UPA from BL through Wk48 on UPA15 [250/300 (83%)] and UPA30 [251/298 (84%)], clinical and functional outcomes continued to improve, or were maintained (Table 1). For pts continuing UPA15 and 30, DAS28-CRP<2.6 was 55% and 68%, and CDAI≤2.8 was 28% and 42%, respectively. Pts who were switched from cMTX to UPA15 or 30 at Wk14 had similar responses at Wk 48.The most frequently reported treatment-emergent AEs were urinary tract infection, blood creatine phosphokinase increase, upper respiratory tract infection, nasopharyngitis, worsening of RA, herpes zoster (HZ), alanine aminotransferase increase, and bronchitis. The most frequently reported serious AE was pneumonia (8 events). Events/100PYs were numerically higher in the UPA30 vs UPA15 arm for HZ, and hepatic disorders, and were comparable for serious infections and malignancies excluding non-melanoma skin cancer (Table 2). Adjudicated venous thromboembolic events (VTE) were observed only on UPA15 (2 pts with deep vein thrombosis and 2 pts with pulmonary embolism; all patients had at least one risk factor for VTE).ConclusionUPA 15 or 30 monotherapy resulted in similar improvements in signs and symptoms and physical function through 48 wks. The overall benefit-risk profile of both doses of UPA was favorable based on safety and efficacy data through Wk48 but will be confirmed through an integrated safety analysis across all the ph 3 trials.Abstract THU0191 –Table 1Abstract THU0191 –Table 2Reference[1] Smolen, et al. Arthritis and Rheu...

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DESCRITORES KEYWORDSEpidemiologia; Cárie dentária; Estudantes; Dieta cariogênica. Epidemiology; Dental caries; Students; Diet, cariogenic. Resultados: Uma elevada frequência de consumo de alimentos açucarados foi registrada para os estudantes das escolares parti culares, os quais apresentaram maior prevalência de cárie quando comparado aos estudantes de escolas públicas (P=0,000). Entretanto, verifi cou-se diferença estati sti camente signifi cante (P=0,000) no método de higienização dos dentes entre os escolares. Conclusão: Verifi cou-se que estudantes de escolas parti culares têm maior prevalência de cárie dentária quando comparado àqueles de escolas públicas em decorrência de consumirem maior quanti dade de doces e de alimentos açucarados entre as refeições por possuírem maior status sócio-econômico. Objecti ve:To fi nd out the eff ect of cariogenic food exposure on prevalence of dental caries among fee and non fee paying school children in Udaipur, India. Method: A cross secti onal study was conducted in non-fee paying and fee paying school children in Udaipur. A total of 281 children were examined. Response rate was 93.6%. An examinati on was performed using Type III examinati on procedure. To record the caries experience decayed, missing, fi lled (DMF) caries index was used. Stepwise Multi ple Regression Analysis and ANOVA and Chi square analysis was applied by using S.P.S.S. soft ware. Results:The highest frequency of sweet consumpti on was recorded in fee paying subjects, who also had stati sti cally signifi cant higher caries prevalence than in non fee paying subjects (P=0.000). However there was signifi cant diff erence (P=0.000) in method of cleansing of the teeth between fee and non fee paying subjects. Conclusion: It was found that fee paying subjects in India are having more dental caries prevalence as compared to non fee-paying because fee-paying subjects are consuming more sweets, more in between sugary meal, bakery products as they belong to high socio-economic status.Pesq Bras Odontoped Clin Integr, João Pessoa, 10(3):331-336, set./dez. 2010

BackgroundFor patients with RA who are refractory to biologic DMARDs (bDMARDs), such as tumor necrosis factor inhibitors (TNFis), optimal disease control is less likely to be achieved with subsequent therapy.1 In line with recommendations from EULAR and ACR, switching to a treatment with a different mechanism of action is appropriate for these patients.ObjectivesTo describe the efficacy and safety of upadacitinib (UPA) 15 mg once daily in patients with RA and an inadequate response or intolerance to TNFis (TNFi-IR).MethodsA post hoc subgroup analysis was conducted in TNFi-IR patients who were treated with UPA 15 mg once daily in three Phase 3 clinical trials: SELECT-BEYOND,2 -CHOICE,3 and -COMPARE.4 For COMPARE, only patients treated with adalimumab and switched to UPA as rescue therapy were included. ≥20/50/70% improvement in ACR criteria, DAS28(CRP), CDAI, and SDAI, as well as change from baseline in HAQ-DI and other patient-reported outcomes (PROs) were reported through 24 weeks. Non-responder imputation was used for all missing categorical outcomes; as observed (COMPARE) or multiple imputation (CHOICE, BEYOND) were used for missing continuous outcomes. Pooled safety results were presented as exposure-adjusted event rates (EAERs) with a cut-off of June 30, 2021.Results568 TNFi-IR patients were included: 146 from BEYOND, 263 from CHOICE, and 159 from COMPARE. Mean duration since RA diagnosis was longer for BEYOND and CHOICE versus COMPARE; cardiovascular (CV) risk factors were common among this refractory population (Table 1). ACR20/50/70 and disease activity outcomes observed in the TNFi-IR population were generally consistent with the overall BEYOND2 and CHOICE3 bDMARD-IR populations, and consistent across the three studies in the TNFi-IR subgroups (Figure 1). Improvements in PROs including HAQ-DI, fatigue, pain, and morning stiffness over 24 weeks were observed (data not shown). Pooled safety results reporting 1574.8 patient-years (PY) of exposure in the TNFi-IR subgroup showed similar results to the overall BEYOND2 and CHOICE3 bDMARD-IR study populations, with EAERs of 3.1 events/100 PY for herpes zoster and 0.8 events/100 PY for adjudicated major adverse CV events, adjudicated venous thromboembolism (VTE), and malignancy excluding non-melanoma skin cancer. The EAER of any AE leading to death was 1.4 events/100 PY.Table 1.Baseline characteristics of TNFi-IR patients treated with UPA 15 mgn (%), unless specifiedSELECT-BEYOND (n=146)SELECT-CHOICE (n=263)SELECT-COMPARE (ADA → UPA) (n=159)Female122 (83.6)219 (83.3)133 (83.6)Mean (SD) age, years56.6 (11.0)55.5 (11.1)53.9 (10.6)Mean (SD) duration of RA diagnosis, years13.2 (9.5)12.5 (9.4)8.2 (8.5)Concomitant csDMARDs MTX alone100 (70.4)195 (74.1)159 (100.0) MTX and other csDMARDs20 (14.1)25 (9.5)0 csDMARDs other than MTX22 (15.5)38 (14.4)0Concomitant oral steroids73 (50.0)140 (53.2)98 (61.6)1 prior bDMARD68 (46.6)172 (65.4)142 (89.3)2 prior bDMARDs40 (27.4)62 (23.6)17 (10.7)a≥3 prior bDMARDs38 (26.0)29 (11.0)0Failed ≥1 prior TNFi due to lack of efficacyb131 (89.7)223 (84.8)159 (100.0)History of VTE / CV event3 (2.1) / 28 (19.2)6 (2.3) / 20 (7.6)4 (2.5) / 14 (8.8)CV risk factors Hypertension72 (49.3)109 (41.4)68 (42.8) Diabetes mellitus22 (15.1)34 (12.9)17 (10.7) Smoking (current former past)68 (46.6)109 (41.5)55 (34.6) Elevated LDL-C (≥3.36 mmol/L)38 (26.0)52 (20.0)48 (30.2) Low HDL-C (≤1.55 mmol/L)80 (54.8)171 (65.0)88 (55.3)aThese patients received one bDMARD before entry into SELECT-COMPARE.bRemaining patients were intolerant to ≥1 prior TNFi.ConclusionIn this post hoc subgroup analysis, TNFi-IR patients treated with UPA 15 mg achieved clinically meaningful efficacy responses over 24 weeks, with safety consistent with the overall bDMARD-IR patient population in the Phase 3 program.References[1]Rendas-Baum R, et al. Arthritis Res Ther 2011;13:R25;[2]Genovese C, et al. Lancet 2018;391:2513–24;[3]Rubbert-Roth A, et al. NEJM 2020;383:1511–21;[4]Fleischmann R, et al. Ann Rheum Dis 2019;78:1454–62.AcknowledgementsAbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation of the data; and participated in the writing, review, and approval of the abstract. AbbVie and the authors thank all study investigators for their contributions and the patients who participated in this study. No honoraria or payments were made for authorship. Medical writing support was provided by Amy Wilson, MSc, of 2 the Nth (Cheshire, UK), and was funded by AbbVie.Disclosure of InterestsRoy M. Fleischmann Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Eli Lilly, Galvani, Gilead, GSK, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Biosplice, Bristol-Myers Squibb, Flexion, Gilead, Horizon, Eli Lilly, Galvani, Janssen, Novartis, Pfizer, Sanofi-Aventis, Selecta, Teva, UCB, Viela, and Vorso, Louis Bessette Speakers bureau: AbbVie, Amgen, Bristol-Meyers Squibb, Celgene, Eli Lilly, Fresenius Kabi, Gilead, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi-Aventis, Teva, and UCB, Consultant of: AbbVie, Amgen, Bristol-Meyers Squibb, Celgene, Eli Lilly, Fresenius Kabi, Gilead, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi-Aventis, Teva, and UCB, Grant/research support from: AbbVie, Amgen, Bristol-Meyers Squibb, Celgene, Eli Lilly, Fresenius Kabi, Gilead, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi-Aventis, Teva, and UCB, Jeffrey Sparks Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead, Inova Diagnostics, Janssen, Optum, and Pfizer, Stephen Hall Consultant of: AbbVie, Amgen, Bristol-Meyers Sqibb, Eli Lilly, Gilead, Janssen, Merck, Novartis, and UCB, Grant/research support from: AbbVie, Amgen, Bristol-Meyers Sqibb, Eli Lilly, Gilead, Janssen, Merck, Novartis, and UCB, Manish Jain Consultant of: AbbVie, Amgen, Eli Lilly, Novartis, and Pfizer, Grant/research support from: AbbVie, Amgen, Eli Lilly, Novartis, and Pfizer, Adriana Kakehasi Speakers bureau: AbbVie, Amgen, Eli Lilly, Fresenius Kabi, Janssen, Novartis, Pfizer, Sandoz, and UCB, Consultant of: AbbVie, Amgen, Eli Lilly, Fresenius Kabi, Janssen, Novartis, Pfizer, Sandoz, and UCB, Grant/research support from: AbbVie, Amgen, Eli Lilly, Fresenius Kabi, Janssen, Novartis, Pfizer, Sandoz, and UCB, Yanna Song Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Sebastian Meerwein Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Ryan DeMasi Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Jessica Suboticki Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Andrea Rubbert-Roth Consultant of: AbbVie, AbbVie Deutschland, Amgen, Bristol-Myers Squibb, Chugai Pharmaceuticals, Eli Lilly, F. Hoffman-La Roche, Gilead Sciences, Janssen Global Services, Novartis, and Sanofi Pasteur

BackgroundUpadacitinib (UPA), a selective JAK1 inhibitor, has demonstrated efficacy and safety in patients with rheumatoid arthritis (RA) as monotherapy and in combination with conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) such as methotrexate (MTX).1,2 However, UPA monotherapy has not been compared directly with UPA combination therapy in the Phase 3 program.ObjectivesTo compare the efficacy of UPA monotherapy and UPA in combination with MTX using data from two Phase 3 trials of RA patients with an inadequate response (IR) to prior MTX therapy.MethodsIn SELECT-MONOTHERAPY, 648 MTX-IR patients were randomized to receive UPA 15 mg or 30 mg monotherapy once daily (QD), or continue with MTX monotherapy (cMTX; given as a blinded study drug), for 14 weeks. In SELECT-NEXT, 661 csDMARD-IR patients were randomized to receive UPA 15 mg or 30 mg QD or placebo (PBO) for 12 weeks on a background of csDMARDs. Only patients receiving concomitant MTX (with or without additional csDMARDs) at baseline in SELECT-NEXT were included in this analysis. The primary endpoints of both studies were the proportion of patients achieving ACR20 and DAS28(CRP) ≤3.2. Additional endpoints included ACR50/70, DAS28(CRP) <2.6, CDAI remission (≤2.8), CDAI low disease activity (LDA; ≤10), and change from baseline in HAQ-DI. Logistic regression or ordinary least squares analyses were used to compare outcomes with monotherapy versus combination therapy, adjusting for demographics and baseline disease characteristics.ResultsA total of 1114 patients were included in the analysis, of whom 648 received monotherapy in SELECT-MONOTHERAPY and 466 received combination therapy in SELECT-NEXT. Of the patients receiving combination therapy, 338 (72.5%) were receiving MTX background therapy only and 128 (27.5%) were receiving MTX plus other csDMARDs. Baseline characteristics were generally similar between the study cohorts; the majority of patients in both studies were female and of white ethnicity, with a mean age of approximately 55 years and a mean MTX dose of approximately 17 mg/week. Consistent with previously reported results from SELECT-MONOTHERAPY1 and SELECT-NEXT,2 both UPA monotherapy and UPA combination therapy led to significant improvements in efficacy outcomes versus cMTX/PBO+MTX (Table). No significant differences were observed between UPA monotherapy and UPA combination therapy across a range of clinical endpoints, including ACR20/50/70 responses and measures of LDA and remission. In addition, improvements in quality of life as measured by HAQ-DI were similar with UPA monotherapy and combination therapy. Efficacy was comparable between the two UPA doses in the combination therapy group, whereas in the monotherapy group numerically higher responses were observed with UPA 30 mg versus UPA 15 mg.ConclusionIn MTX-IR patients with RA, the efficacy of UPA appears comparable when administered as monotherapy or when given in combination with MTX.References1Smolen J, et al. Ann Rheum Dis 2018;77:67?8;2Burmester GR, et al. Lancet 20...