13 results on '"Gevers T. J. G."'
Search Results
2. Systematic review of response criteria and endpoints in autoimmune hepatitis by the International Autoimmune Hepatitis Group
- Author
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Pape, S, Snijders, R, Gevers, T, Chazouilleres, O, Dalekos, G, Hirschfield, G, Lenzi, M, Trauner, M, Manns, M, Vierling, J, Montano-Loza, A, Lohse, A, Schramm, C, Drenth, J, Heneghan, M, Almasio, P, Alvarez, F, Andrade, R, Arikan, C, Assis, D, Bardou-Jacquet, E, Biewenga, M, Cancado, E, Cazzagon, N, Colloredo, G, Cuarterolo, M, Debray, D, Robles-Diaz, M, Dyson, J, Efe, C, Engel, B, Ferri, S, Fontana, R, Gatselis, N, Gerussi, A, Halilbasic, E, Halliday, N, van Hoek, B, Horby Jorgensen, M, Indolfini, G, Iorio, R, Jeong, S, Jones, D, Kelly, D, Kerkar, N, Lacaille, F, Lammert, C, Leggett, B, Levy, C, Liberal, R, Lleo, A, Ines Lopez, S, de Martin, E, Mclin, V, Mieli-Vergani, G, Milkiewicz, P, Mohan, N, Muratori, L, Nebbia, G, van Nieuwkerk, C, Oo, Y, Ortega, A, Pares, A, Pop, T, Pratt, D, Purnak, T, Ranucci, G, Rushbrook, S, Stattermayer, A, Swain, M, Tanaka, A, Taubert, R, Terrabuio, D, Terziroli, B, Valentino, P, van den Brand, F, Villamil, A, Wahlin, S, Ytting, H, Zachou, K, Zeniya, M, Pape S., Snijders R. J. A. L. M., Gevers T. J. G., Chazouilleres O., Dalekos G. N., Hirschfield G. M., Lenzi M., Trauner M., Manns M. P., Vierling J. M., Montano-Loza A. J., Lohse A. W., Schramm C., Drenth J. P. H., Heneghan M. A., Almasio P., Alvarez F., Andrade R., Arikan C., Assis D., Bardou-Jacquet E., Biewenga M., Cancado E., Cazzagon N., Colloredo G., Cuarterolo M., Dalekos G., Debray D., Robles-Diaz M., Drenth J., Dyson J., Efe C., Engel B., Ferri S., Fontana R., Gatselis N., Gerussi A., Halilbasic E., Halliday N., Heneghan M., Hirschfield G., van Hoek B., Horby Jorgensen M., Indolfini G., Iorio R., Jeong S., Jones D., Kelly D., Kerkar N., Lacaille F., Lammert C., Leggett B., Levy C., Liberal R., Lleo A., Lohse A., Ines Lopez S., de Martin E., McLin V., Mieli-Vergani G., Milkiewicz P., Mohan N., Muratori L., Nebbia G., van Nieuwkerk C., Oo Y., Ortega A., Pares A., Pop T., Pratt D., Purnak T., Ranucci G., Rushbrook S., Stattermayer A., Swain M., Tanaka A., Taubert R., Terrabuio D., Terziroli B., Valentino P., van den Brand F., Villamil A., Wahlin S., Ytting H., Zachou K., Zeniya M., Pape, S, Snijders, R, Gevers, T, Chazouilleres, O, Dalekos, G, Hirschfield, G, Lenzi, M, Trauner, M, Manns, M, Vierling, J, Montano-Loza, A, Lohse, A, Schramm, C, Drenth, J, Heneghan, M, Almasio, P, Alvarez, F, Andrade, R, Arikan, C, Assis, D, Bardou-Jacquet, E, Biewenga, M, Cancado, E, Cazzagon, N, Colloredo, G, Cuarterolo, M, Debray, D, Robles-Diaz, M, Dyson, J, Efe, C, Engel, B, Ferri, S, Fontana, R, Gatselis, N, Gerussi, A, Halilbasic, E, Halliday, N, van Hoek, B, Horby Jorgensen, M, Indolfini, G, Iorio, R, Jeong, S, Jones, D, Kelly, D, Kerkar, N, Lacaille, F, Lammert, C, Leggett, B, Levy, C, Liberal, R, Lleo, A, Ines Lopez, S, de Martin, E, Mclin, V, Mieli-Vergani, G, Milkiewicz, P, Mohan, N, Muratori, L, Nebbia, G, van Nieuwkerk, C, Oo, Y, Ortega, A, Pares, A, Pop, T, Pratt, D, Purnak, T, Ranucci, G, Rushbrook, S, Stattermayer, A, Swain, M, Tanaka, A, Taubert, R, Terrabuio, D, Terziroli, B, Valentino, P, van den Brand, F, Villamil, A, Wahlin, S, Ytting, H, Zachou, K, Zeniya, M, Pape S., Snijders R. J. A. L. M., Gevers T. J. G., Chazouilleres O., Dalekos G. N., Hirschfield G. M., Lenzi M., Trauner M., Manns M. P., Vierling J. M., Montano-Loza A. J., Lohse A. W., Schramm C., Drenth J. P. H., Heneghan M. A., Almasio P., Alvarez F., Andrade R., Arikan C., Assis D., Bardou-Jacquet E., Biewenga M., Cancado E., Cazzagon N., Colloredo G., Cuarterolo M., Dalekos G., Debray D., Robles-Diaz M., Drenth J., Dyson J., Efe C., Engel B., Ferri S., Fontana R., Gatselis N., Gerussi A., Halilbasic E., Halliday N., Heneghan M., Hirschfield G., van Hoek B., Horby Jorgensen M., Indolfini G., Iorio R., Jeong S., Jones D., Kelly D., Kerkar N., Lacaille F., Lammert C., Leggett B., Levy C., Liberal R., Lleo A., Lohse A., Ines Lopez S., de Martin E., McLin V., Mieli-Vergani G., Milkiewicz P., Mohan N., Muratori L., Nebbia G., van Nieuwkerk C., Oo Y., Ortega A., Pares A., Pop T., Pratt D., Purnak T., Ranucci G., Rushbrook S., Stattermayer A., Swain M., Tanaka A., Taubert R., Terrabuio D., Terziroli B., Valentino P., van den Brand F., Villamil A., Wahlin S., Ytting H., Zachou K., and Zeniya M.
- Abstract
Background & Aims: Autoimmune hepatitis (AIH) has been well characterised and codified through the development of diagnostic criteria. These criteria have been adapted and simplified and are widely used in clinical practice. However, there is a need to update and precisely define the criteria for both treatment response and treatment. Methods: A systematic review was performed and a modified Delphi consensus process was used to identify and redefine the response criteria in autoimmune hepatitis. Results: The consensus process initiated by the International Autoimmune Hepatitis Group proposes that the term ‘complete biochemical response’ defined as ‘normalization of serum transaminases and IgG below the upper limit of normal’ be adopted to include a time point at 6 months after initiation of treatment. An insufficient response by 6 months was a failure to meet the above definition. Non-response was defined as ‘<50% decrease of serum transaminases within 4 weeks after initiation of treatment’. Remission is defined as liver histology with a Hepatitis Activity Index <4/18. Intolerance to treatment was agreed to stand for ‘any adverse event possibly related to treatment leading to potential drug discontinuation’. Conclusions: These definitions provide a simple and reproducible framework to define treatment response and non-response, irrespective of the therapeutic intervention. A consensus on endpoints is urgently required to set a global standard for the reporting of study results and to enable inter-study comparisons. Future prospective database studies are needed to validate these endpoints. Lay summary: Consensus among international experts on response criteria and endpoints in autoimmune hepatitis is lacking. A consensus on endpoints is urgently required to set a global standard for the reporting of study results and to enable the comparison of results between clinical trials. Therefore, the International Autoimmune Hepatitis Group (IAIHG) herein presents
- Published
- 2022
3. Antiviral therapy in chronic hepatitis E: a systematic review
- Author
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Peters van Ton, A. M., Gevers, T. J. G., and Drenth, J. P. H.
- Published
- 2015
- Full Text
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4. Somatostatin analogues improve health-related quality of life in polycystic liver disease: a pooled analysis of two randomised, placebo-controlled trials
- Author
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Neijenhuis, M. K., Gevers, T. J. G., Nevens, F., Hogan, M. C., Torres, V. E., Kievit, W., and Drenth, J. P. H.
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- 2015
- Full Text
- View/download PDF
5. The long-term outcome of patients with polycystic liver disease treated with lanreotide
- Author
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Chrispijn, M., Nevens, F., Gevers, T. J. G., Vanslembrouck, R., van Oijen, M. G. H., Coudyzer, W., Hoffmann, A. L., Dekker, H. M., de Man, R. A., van Keimpema, L., and Drenth, J. P. H.
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- 2012
- Full Text
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6. Clinical predictors of escalating care in hepatic and renal cyst infection in autosomal dominant polycystic kidney and liver disease
- Author
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Marten Lantinga, Sevaux, R. G. L., Gevers, T. J. G., Oyen, W. J. G., Fijter, J. W., Soonawala, D., Zietse, R., Salih, M., Casteleijn, N. F., Spithoven, E. M., Meijer, E., Gansevoort, R. T., Drenthl, J. P. H., Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), and Internal Medicine
- Abstract
BACKGROUND: Cyst infection may occur in autosomal dominant polycystic kidney disease (ADPKD) and autosomal dominant polycystic liver disease (ADPLD). Antimicrobial agents often fail to control infection, leading to invasive action. We aimed to identify factors predicting escalation of care. METHODS: ADPKD and ADPLD patients were identified from local/national databases (2001-2013). Records were screened for patients meeting criteria for cyst infection (positive cyst aspirate and/or clinical findings). Factors that predict escalated care were identified with multivariate modified Poisson regression. RESULTS: We screened 1773 patients. A total of 77 patients with cyst infection (4.3%) were included for analysis (hepatic 36%; male 49%; age 54 ±; 13 years; ADPKD 95%; dialysis 9%, diabetes 18%, renal transplant 56%, eGFR [IQR 24-78] ml/min/1.73 m2 (excluding patients with a history of renal transplant or receiving dialysis)). A pathogen was identified in 71% of cases. Escherichia coli was the most common pathogen and accounted for 69% of cases. Initial treatment was limited to antibiotics in 87% of patients (n = 67), 40% included a fluoroquinolone. Ultimately, 48% of patients underwent some form of invasive action (escalation of care). Increasing white blood cell count (WBC) (RR 1.04 95%-CI 1.01-1.07, p = 0.008) was associated with escalating care, whereas an increase in time between transplant and infection (RR 0.92 95% CI 0.86-0.97, p = 0.005) and E. coli isolation (RR 0.55 95% CI 0.34-0.89, p = 0.02) were protective. CONCLUSION: High serum WBC, isolation of atypical pathogens and early infection after transplantation are factors that increase the risk of escalation of care in hepatic and renal cyst infection patients.
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- 2018
7. Systematic review: the management of hepatic cyst infection
- Author
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Lantinga, M. A., primary, Geudens, A., additional, Gevers, T. J. G., additional, and Drenth, J. P. H., additional
- Published
- 2014
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8. The long-term outcome of patients with polycystic liver disease treated with lanreotide
- Author
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Chrispijn, M., primary, Nevens, F., additional, Gevers, T. J. G., additional, Vanslembrouck, R., additional, van Oijen, M. G. H., additional, Coudyzer, W., additional, Hoffmann, A. L., additional, Dekker, H. M., additional, de Man, R. A., additional, van Keimpema, L., additional, and Drenth, J. P. H., additional
- Published
- 2011
- Full Text
- View/download PDF
9. Systematic review: the management of hepatic cyst infection.
- Author
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Lantinga, M. A., Geudens, A., Gevers, T. J. G., and Drenth, J. P. H.
- Subjects
CYSTIC kidney disease ,POLYCYSTIC kidney disease treatment ,AUTOMATIC extracting (Information science) ,DIABETES ,TRANSPLANTATION of organs, tissues, etc. ,THERAPEUTICS - Abstract
Background Cyst infection is a severe complication of hepatic cystic disease. However, an evidence-based treatment strategy is not available. Aim To assess the available treatment strategies and provide a treatment advice for de novo hepatic cyst infection. Methods We systematically searched PubMed (1948-2014), EMBASE (1974-2014), and the Cochrane Library (until 2014) for studies involving humans (≥18 years) treated for a hepatic cyst infection. We extracted data on patient characteristics, treatment and follow-up. Results We identified 41 articles; all were case series or case reports, implicating a high risk of bias. We included 54 hepatic cyst infection cases (male 39%; mean age 63 ± 12 years; diabetes 6%; dialysis 19%; transplant recipients 30%). Initial therapy consisted of antimicrobial (56%), percutaneous (31%) or surgical treatment (13%). We identified 42 antimicrobial regimens consisting of 23 different combinations. Most used antibiotic classes were quinolones (34%) and cephalosporins (34%). Antimicrobials failed in 70% of cases, eventually requiring percutaneous or surgical treatment in, respectively, 37% and 27%. Recurrent hepatic cyst infection was frequent (20%). Median time to recurrence was 8 weeks ( IQR 3-24 weeks). In 46%, recurrence occurred in renal transplant recipients. Cyst infection related deaths occurred in 9%, of whom 40% were on dialysis. Conclusions The literature shows that treatment of hepatic cyst infection is highly heterogeneous. We recommend first line treatment with oral ciprofloxacin. In case of failure, percutaneous cyst drainage needs to be considered. [ABSTRACT FROM AUTHOR]
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- 2015
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10. Clinical predictors of escalating care in hepatic and renal cyst infection in autosomal dominant polycystic kidney and liver disease.
- Author
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Lantinga MA, de Sévaux RGL, Gevers TJG, Oyen WJG, de Fijter JW, Soonawala D, Zietse R, Salih M, Casteleijn NF, Spithoven EM, Meijer E, Gansevoort RT, and Drenth On Behalf Of The Dipak Consortium JPH
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- Aged, Cysts genetics, Escherichia coli isolation & purification, Escherichia coli Infections blood, Escherichia coli Infections surgery, Female, Humans, Kidney Transplantation, Leukocyte Count, Liver Diseases genetics, Male, Middle Aged, Retrospective Studies, Time Factors, Anti-Bacterial Agents therapeutic use, Cysts complications, Escherichia coli Infections drug therapy, Liver Diseases complications, Polycystic Kidney, Autosomal Dominant complications
- Abstract
Background: Cyst infection may occur in autosomal dominant polycystic kidney disease (ADPKD) and autosomal dominant polycystic liver disease (ADPLD). Antimicrobial agents often fail to control infection, leading to invasive action. We aimed to identify factors predicting escalation of care., Methods: ADPKD and ADPLD patients were identified from local/national databases (2001-2013). Records were screened for patients meeting criteria for cyst infection (positive cyst aspirate and/or clinical findings). Factors that predict escalated care were identified with multivariate modified Poisson regression., Results: We screened 1773 patients. A total of 77 patients with cyst infection (4.3%) were included for analysis (hepatic 36%; male 49%; age 54 ±; 13 years; ADPKD 95%; dialysis 9%, diabetes 18%, renal transplant 56%, eGFR [IQR 24-78] ml/min/1.73 m2 (excluding patients with a history of renal transplant or receiving dialysis)). A pathogen was identified in 71% of cases. Escherichia coli was the most common pathogen and accounted for 69% of cases. Initial treatment was limited to antibiotics in 87% of patients (n = 67), 40% included a fluoroquinolone. Ultimately, 48% of patients underwent some form of invasive action (escalation of care). Increasing white blood cell count (WBC) (RR 1.04 95%-CI 1.01-1.07, p = 0.008) was associated with escalating care, whereas an increase in time between transplant and infection (RR 0.92 95% CI 0.86-0.97, p = 0.005) and E. coli isolation (RR 0.55 95% CI 0.34-0.89, p = 0.02) were protective., Conclusion: High serum WBC, isolation of atypical pathogens and early infection after transplantation are factors that increase the risk of escalation of care in hepatic and renal cyst infection patients.
- Published
- 2018
11. Full-dose sofosbuvir and daclatasvir for chronic hepatitis C infection in haemodialysis patients.
- Author
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Gevers TJ, Burger D, Schipper-Reintjes E, Kooistra MP, and Richter C
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- Antiviral Agents therapeutic use, Carbamates, Female, Genotype, Hepacivirus genetics, Hepatitis C, Chronic blood, Hepatitis C, Chronic complications, Humans, Kidney Failure, Chronic complications, Liver Cirrhosis complications, Male, Middle Aged, Pyrrolidines, RNA, Viral blood, Sustained Virologic Response, Valine analogs & derivatives, Viral Load, Antiviral Agents administration & dosage, Hepatitis C, Chronic drug therapy, Imidazoles therapeutic use, Kidney Failure, Chronic therapy, Renal Dialysis, Ribavirin therapeutic use, Sofosbuvir administration & dosage
- Published
- 2016
12. Hepatic and renal manifestations in autosomal dominant polycystic kidney disease: a dichotomy of two ends of a spectrum.
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van Gulick JJ, Gevers TJ, van Keimpema L, and Drenth JP
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- Humans, Hypertension etiology, Liver Diseases therapy, Polycystic Kidney, Autosomal Dominant diagnosis, Polycystic Kidney, Autosomal Dominant genetics, Polycystic Kidney, Autosomal Dominant therapy, Kidney Failure, Chronic etiology, Liver Diseases etiology, Polycystic Kidney, Autosomal Dominant complications
- Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is a multisystem disorder. It is the most common genetic cause of end-stage renal disease. One frequent extra-renal manifestation is hepatic cyst formation. The majority of ADPKD patients develop complications as a result of renal cyst formation; however, a small proportion develop extensive hepatic disease with minor renal features. Both phenotypes seem to represent the spectrum of ADPKD. This review discusses the current understanding of the pathogenesis of the disease, its manifestations and the mechanisms of cyst formation. Furthermore, it focuses on monitoring the disease and the treatment options currently available.
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- 2011
13. Treatment extension benefits HCV genotype 1 patients without rapid virological response: a systematic review.
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Gevers TJ, Slavenburg S, van Oijen MG, and Drenth JP
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- Antiviral Agents therapeutic use, Confidence Intervals, Drug Therapy, Combination, Genotype, Hepatitis C genetics, Humans, Interferon alpha-2, Interferon-alpha therapeutic use, Polyethylene Glycols therapeutic use, Recombinant Proteins, Ribavirin therapeutic use, Risk, Time Factors, Treatment Outcome, Hepatitis C drug therapy
- Abstract
Background: Current guidelines recommend 48 weeks of treatment with pegylated interferon and ribavirin for patients infected with chronic hepatitis C virus (HCV) genotype 1. Several clinical trials have investigated the efficacy of treatment duration longer than 48 weeks, but yielded discordant results., Methods: We performed a structured search of PubMed, Web of Science and the Cochrane library to identify randomised clinical trials in HCV genotype 1 patients who were treated either for 48 or 72 weeks. Sustained viral response (SVR) data were pooled and a sample size weighted pooled proportion was calculated., Results: We identified five studies matching our criteria. Studies randomised at baseline (n=1), at absence of rapid virological response (RVR) at week 4 (n=1), at early virological response at week 12 (EVR) (n=1) or at slow response at week 24 (n=2). In the RCT that randomised at absence of RVR, SVR was significantly higher in the extended treatment arm (57 vs 42%, p=0.02) with an RR of 1.35 (95% CI 1.04 to 1.75). This tendency was also observed in the studies that randomised at slow response (44 vs 35%), although no longer statistically significantly different., Conclusion: Prolonged 72-week treatment should be considered in HCV genotype 1 patients without RVR at week 4, as this increased SVR.
- Published
- 2011
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