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383 results on '"Dieterich D"'

1. Cost- Effectiveness of Avatrombopag for the Treatment of Thrombocytopenia in Patients with Chronic Liver Disease

Author

Mladsi D, Barnett C, Aggarwal K, Vredenburg M, Dieterich D, and Kim R

Subjects
liver diseases platelet transfusion, thrombocytopenia, cost-effectiveness, Medicine (General), R5-920, Therapeutics. Pharmacology, RM1-950
Abstract

Deirdre Mladsi,1 Christine Barnett,1 Kavita Aggarwal,2 Michael Vredenburg,2 Douglas Dieterich,3 Ray Kim4 1RTI Health Solutions Research, Triangle Park, NC, USA; 2Dova Pharmaceuticals, Durham, NC, USA; 3Icahn School of Medicine, New York, NY, USA; 4School of Medicine, Stanford University, Stanford, CA, USACorrespondence: Deirdre MladsiRTI Health Solutions Research, Triangle Park, NC 27709-2194 Tel +1 919 541 7094Fax +1 919 541 7222Email dmladsi@rti.orgBackground and Aim: Thrombocytopenia is common in people with chronic liver disease, who frequently undergo invasive procedures. To minimize the risk of bleeding, prophylactic platelet transfusions have traditionally been used but carry many risks. The aim of this study was to evaluate the cost-effectiveness of avatrombopag compared with platelet transfusion and lusutrombopag as a treatment for thrombocytopenia in adult patients with chronic liver disease scheduled to undergo a medical procedure.Methods: A decision-tree model was developed from a US payer perspective to capture acute events observed in phase 3 global randomized controlled clinical trials and, to support exploratory analyses, potential longer-term complications resulting from a major bleed or thromboembolic event. Treatment costs were taken from publicly available data sources. The interventions were evaluated in the overall trial populations and in subpopulations with higher and lower baseline platelet counts. Results were presented as incremental cost per platelet transfusion avoided. One-way and probabilistic sensitivity analyses were conducted.Results: In the overall population, avatrombopag reduced the need for platelet transfusions and produced cost-savings compared with platelet transfusion (80% fewer prophylactic platelet transfusions, $4250 lower costs) and lusutrombopag (42% fewer prophylactic platelet transfusions, $5819 lower costs). Similar results were seen in both the higher and lower platelet count subpopulations. The one-way and probabilistic sensitivity analyses found that the use of avatrombopag is cost-saving with the incremental cost-effectiveness ratio in quadrant IV (decreased costs, prophylactic platelet transfusions avoided).Conclusion: The use of avatrombopag is expected to be cost-saving while reducing the need for prophylactic platelet transfusions compared with platelet transfusion and lusutrombopag.Keywords: liver diseases platelet transfusion, thrombocytopenia, cost-effectiveness

Published
2020

24. Telaprevir for previously untreated chronic hepatitis C virus infection

Author

Jacobson I. M., McHutchison J. G., Dusheiko G., Di Bisceglie A. M., Reddy K. R., Bzowej N. H., Marcellin P., Muir A. J., Ferenci P., Flisiak R., George J., Rizzetto M., Shouval D., Sola R., Terg R. A., Yoshida E. M., Adda N., Bengtsson L., Sankoh A. J., Kieffer T. L., George S., Kauffman R. S., Zeuzem S., ADVANCE Study Team: Gadano A., Terg R., Bell S., Cheng W., Crawford D., Dore G., MacDonald G., Roberts S., Gschwantler M., Laferl H., Maieron A., Heathcote J., Kaita K., Myers R., Sherman M., Yoshida E., Barange K., Couzigou P., Pawlotsky J. M., Pol S., Serfaty L., Trépo C., Zarski J. P., Berg T., Buggisch P., Diepolder H., Goeser T., Mauss S., Rasenack J., Schmidt W., Wedemeyer H., Baruch Y., Ben Ari Z., Maor Y., Safadi R., Zuckerman E., Colombo M., Baka Cwierz B., Gladysz A., Janczewska Kazek E., Jablkowski M., Krycka W., Diago M., Esteban Mur R., Sanchez Tapias J., Brown A., Fox R., Afdhal N., Arora S., Bennett M., Bernstein D., Bloomer J., Bochan M., Bonkovsky H., Brady C., Brown R., Bzowej N., Cochran J., Chasen R., Davis G., De Jesus E., Di Bisceglie A., Dienstag J., Dieterich D., Etzkorn K., Everson G., Fried M., Freilich B., Ghalib R., Gitlin N., Godofsky E., Gordon S., Hassanein T., Jacobson I., Javadi F., Jonas M., Kilby A., Kwo P., Lawitz E., Lebovics E., Lee W., Luketic V., Maillard M., Monto A., Morgan T., Min A., Murphy M., Nelson D., Northup P., Nyberg L., Pockros P., Poordad F., Poulos J., Reddy R., Rodriguez Torres M., Satyanarayana R., Schiff E., Schwartz H., Shaikh O., Sheikh M., Sherman K., Smith J., Strohecker J., Sulkowski M., Szabo G., Te H., Terrault N., Tsai N., Vargas H., Vierling J., Wruble L., Younossi Z., Zein N., ANDREONE, PIETRO, Jacobson I.M., McHutchison J.G., Dusheiko G., Di Bisceglie A.M., Reddy K.R., Bzowej N.H., Marcellin P., Muir A.J., Ferenci P., Flisiak R., George J., Rizzetto M., Shouval D., Sola R., Terg R.A., Yoshida E.M., Adda N., Bengtsson L., Sankoh A.J., Kieffer T.L., George S., Kauffman R.S., Zeuzem S., ADVANCE Study Team: Gadano A., Terg R., Bell S., Cheng W., Crawford D., Dore G., MacDonald G., Roberts S., Gschwantler M., Laferl H., Maieron A., Heathcote J., Kaita K., Myers R., Sherman M., Yoshida E., Barange K., Couzigou P., Pawlotsky J.M., Pol S., Serfaty L., Trépo C., Zarski J.P., Berg T., Buggisch P., Diepolder H., Goeser T., Mauss S., Rasenack J., Schmidt W., Wedemeyer H., Baruch Y., Ben-Ari Z., Maor Y., Safadi R., Zuckerman E., Andreone P., Colombo M., Baka-Cwierz B., Gladysz A., Janczewska-Kazek E., Jablkowski M., Krycka W., Diago M., Esteban-Mur R., Sanchez-Tapias J., Brown A., Fox R., Afdhal N., Arora S., Bennett M., Bernstein D., Bloomer J., Bochan M., Bonkovsky H., Brady C., Brown R., Bzowej N., Cochran J., Chasen R., Davis G., De Jesus E., Di Bisceglie A., Dienstag J., Dieterich D., Etzkorn K., Everson G., Fried M., Freilich B., Ghalib R., Gitlin N., Godofsky E., Gordon S., Hassanein T., Jacobson I., Javadi F., Jonas M., Kilby A., Kwo P., Lawitz E., Lebovics E., Lee W., Luketic V., Maillard M., Monto A., Morgan T., Min A., Murphy M., Nelson D., Northup P., Nyberg L., Pockros P., Poordad F., Poulos J., Reddy R., Rodriguez-Torres M., Satyanarayana R., Schiff E., Schwartz H., Shaikh O., Sheikh M., Sherman K., Smith J., Strohecker J., Sulkowski M., Szabo G., Te H., Terrault N., Tsai N., Vargas H., Vierling J., Wruble L., Younossi Z., and Zein N.

Subjects
Adult, Male, medicine.medical_specialty, CHRONIC HEPATITIS C, Telaprevir, ANTIVIRAL TREATMENT, Serine Proteinase Inhibitors, Hepatitis C virus, Hepacivirus, Interferon alpha-2, medicine.disease_cause, Gastroenterology, Antiviral Agents, Polyethylene Glycols, chemistry.chemical_compound, Young Adult, Double-Blind Method, Internal medicine, Boceprevir, medicine, Humans, Beclabuvir, Aged, business.industry, Ribavirin, Danoprevir, Interferon-alpha, virus diseases, General Medicine, Hepatitis C, Sequence Analysis, DNA, Hepatitis C, Chronic, Middle Aged, Viral Load, medicine.disease, Ombitasvir, Recombinant Proteins, digestive system diseases, Logistic Models, chemistry, Immunology, RNA, Viral, Drug Therapy, Combination, Female, business, Oligopeptides, medicine.drug
Abstract

A B S T R AC T Background In phase 2 trials, telaprevir, a hepatitis C virus (HCV) genotype 1 protease inhibitor, in combination with peginterferon–ribavirin, as compared with peginterferon–ribavirin alone, has shown improved efficacy, with potential for shortening the duration of treatment in a majority of patients. Methods In this international, phase 3, randomized, double-blind, placebo-controlled trial, we assigned 1088 patients with HCV genotype 1 infection who had not received previous treatment for the infection to one of three groups: a group receiving telaprevir combined with peginterferon alfa-2a and ribavirin for 12 weeks (T12PR group), followed by peginterferon–ribavirin alone for 12 weeks if HCV RNA was undetectable at weeks 4 and 12 or for 36 weeks if HCV RNA was detectable at either time point; a group receiving telaprevir with peginterferon–ribavirin for 8 weeks and placebo with peginterferon–ribavirin for 4 weeks (T8PR group), followed by 12 or 36 weeks of peginterferon–ribavirin on the basis of the same HCV RNA criteria; or a group receiving placebo with peginterferon–ribavirin for 12 weeks, followed by 36 weeks of peginterferon–ribavirin (PR group). The primary end point was the proportion of patients who had undetectable plasma HCV RNA 24 weeks after the last planned dose of study treatment (sustained virologic response). Results Significantly more patients in the T12PR or T8PR group than in the PR group had a sustained virologic response (75% and 69%, respectively, vs. 44%; P

Published
2011

34. High baseline bilirubin and low albumin predict liver decompensation and serious adverse events in HCV-infected patients treated with sofosbuvir-containing regimens

Author

Perumalswami, P. V., primary, Patel, N., additional, Bichoupan, K., additional, Ku, L., additional, Yalamanchili, R., additional, Harty, A., additional, Motamed, D., additional, Khaitova, V., additional, Chang, C., additional, Grewal, P., additional, Liu, L., additional, Schiano, T. D., additional, Woodward, M., additional, Dieterich, D. T., additional, and Branch, A. D., additional

Published
2016
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35. Simeprevir (TMC435) with pegylated interferon/ribavirin in patients coinfected with HCV genotype 1 and HIV-1: a phase 3 study

Author

Dieterich D, Rockstroh JK, Orkin C, Gutiérrez F, Klein MB, Reynes J, Shukla U, Jenkins A, Lenz O, Ouwerkerk-Mahadevan S, Peeters M, De La Rosa G, Tambuyzer L, and Jessner W

Subjects
coinfection, hepatitis C virus, human immunodeficiency virus type 1, simeprevir, viruses, virus diseases, digestive system diseases
Abstract

Simeprevir is an oral, once-daily, hepatitis C virus (HCV) NS3/4A protease inhibitor for the treatment of chronic HCV genotype 1 infection. Human immunodeficiency virus (HIV) coinfection accelerates progression of liver disease. This uncontrolled, open-label trial explored the safety and efficacy of simeprevir in patients with HCV genotype 1/HIV type 1 (HIV-1) coinfection.

Published
2014

44. Experimental and Investigational Targeted Therapies for the Management of Fibrosis in NASH: An Update

Author

Huisman TM, Dieterich DT, and Friedman SL

Subjects
liver fibrosis, novel treatments, nash, pharmacotherapies, antifibrotic therapy, cirrhosis, hepatic stellate cell, Therapeutics. Pharmacology, RM1-950
Abstract

Tsipora M Huisman, Douglas T Dieterich, Scott L Friedman Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USACorrespondence: Scott L FriedmanIcahn School of Medicine at Mount Sinai, Box 1123, 1425 Madison Ave, Room 1170C, New York, NY, 10025, USAEmail Scott.friedman@mssm.eduAbstract: There have been major advances in the treatment of HBV and HCV with anti-viral treatments, which is reducing the prevalence of fibrosis due to these viruses and obviating the need for anti-fibrotic therapies in these diseases. At the same time, however, the prevalence of non-alcoholic fatty liver disease (NAFLD) has been increasing, of which a substantial fraction of patients have non-alcoholic steatohepatitis (NASH), which may progress to cirrhosis. Accordingly, NASH is emerging as the leading indication for liver transplantation in North America and Europe. Progress in uncovering pathogenic determinants of fibrosis in NASH include metabolic dysregulation in hepatocytes that induce inflammation and cytokine secretion leading to cell injury and apoptosis, among others. These pathogenic events converge upon hepatic stellate cells, which are the primary fibrogenic cell in liver, and represent a target of new therapeutic candidates that are currently being evaluated in animal models and clinical trials. This review highlights key experimental and investigational therapies for NASH fibrosis, whose evaluation will be accelerated as new non-invasive markers of fibrosis are established. While no drugs are approved yet for NASH fibrosis, there is growing optimism that new pharmacotherapies are likely to emerge within the next 3 years that will favorably alter the natural history of disease.Keywords: liver fibrosis, novel treatments, NASH, pharmacotherapies, antifibrotic therapy, cirrhosis, hepatic stellate cell

Published
2021

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