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17. Pulse versus daily oral cyclophosphamide for induction of remission in ANCA-associated vasculitis: long-term follow-up

Author

Harper, L1, Morgan, Md, Walsh, M, Hoglund, P, Westman, K, Flossmann, O, Tesar, V, Vanhille, P, de Groot, K, Luqmani, R, Flores Suarez LF, Watts, R, Pusey, C, Bruchfeld, A, Rasmussen, N, Blockmans, D, Savage, Co, Jayne, D, EUVAS i. n. v. e. s. t. i. g. a. t. o. r. s. Abramowicz, D, Wissing, M, Madhoun, P, Stolear, J, Ekstrand, A, Chabova, V, Rychlik, I, Bataille, P, Puechal, X, Leblau, J, Esnault, Vl, Gross, Wl, Weidner, S, Rupprecht, H, Schneider, M, Specker, C, Schmitt, W, van der Woude, F, Vischedyck, M, Feighery, C, Garibotto, Giacomo, Sinico, Ra, Santostefano, M, Dadoniene, J, Hagen, Ec, Oudejans, I, Verburgh, C, Ballarin, J, Mirapeix, E, Valles, M, Pettersson, E, Eriksson, P, Selga, D, Segelmark, M, Sterner, G, Lundberg, I, Svenungsson, E, Chizzolini, C, Adu, D, de Souza, R., and Chizzolini, Carlo

Subjects
Male, Time Factors, Administration, Oral, Kidney, law.invention, Cyclophosphamide/administration & dosage, Randomized controlled trial, law, Risk Factors, Secondary Prevention, Immunology and Allergy, ddc:616, Aged, 80 and over, ANCA, Remission Induction, Middle Aged, Female, Vasculitis, Immunosuppressive Agents, medicine.drug, Systemic vasculitis, Adult, medicine.medical_specialty, Cyclophosphamide, Adolescent, Kidney/physiology, Immunology, General Biochemistry, Genetics and Molecular Biology, Antibodies, Antineutrophil Cytoplasmic, Young Adult, Rheumatology, Internal medicine, medicine, Kidney Function, Humans, Adverse effect, Immunosuppressive Agents/administration & dosage, Aged, Retrospective Studies, business.industry, Vasculitis/drug therapy/immunology/mortality, Antibodies, Antineutrophil Cytoplasmic/immunology, Retrospective cohort study, medicine.disease, Surgery, Regimen, Pulse Therapy, Drug, business, Follow-Up Studies
Abstract

INTRODUCTION: The previously reported randomised controlled trial of a consensus regimen of pulse cyclophosphamide suggested that it was as effective as a daily oral (DO) cyclophosphamide for remission induction of antineutrophil cytoplasm autoantibodies-associated systemic vasculitis when both were combined with the same glucocorticoid protocol (CYCLOPS study (Randomised trial of daily oral versus pulse Cyclophosphamide as therapy for ANCA-associated Systemic Vasculitis published de groot K, harper L et al Ann Int Med 2009)). The study had limited power to detect a difference in relapse. This study describes the long-term outcomes of patients in the CYCLOPS study. METHODS: Long-term outcomes were ascertained retrospectively from 148 patients previously recruited to the CYCLOPS Trial. Data on survival, relapse, immunosuppressive treatment, cancer incidence, bone fractures, thromboembolic disease and cardiovascular morbidity were collected from physician records retrospectively. All patients were analysed according to the group to which they were randomised. RESULTS: Median duration of follow-up was 4.3 years (IQR, 2.95-5.44 years). There was no difference in survival between the two limbs (p=0.92). Fifteen (20.8%) DO and 30 (39.5%) pulse patients had at least one relapse. The risk of relapse was significantly lower in the DO limb than the pulse limb (HR=0.50, 95% CI 0.26 to 0.93; p=0.029). Despite the increased risk of relapse in pulse-treated patients, there was no difference in renal function at study end (p=0.82). There were no differences in adverse events between the treatment limbs. DISCUSSION: Pulse cyclophosphamide is associated with a higher relapse risk than DO cyclophosphamide. However, this is not associated with increased mortality or long-term morbidity. Although the study was retrospective, data was returned in 90% of patients from the original trial.

Published
2016

18. Diagnostic value of standardized assays for anti-neutrophil cytoplasmic antibodies in idiopathic systemic vasculitis

Author

Hagen, E, Daha, M, Hermans, J, Andrassy, K, Csernok, E, Gaskin, G, Lesavre, P, Lüdemann, J, Rasmussen, N, Sinico, R, Wiik, A, Van Der Woude, F, Van Der Woude, F., SINICO, RENATO ALBERTO, Hagen, E, Daha, M, Hermans, J, Andrassy, K, Csernok, E, Gaskin, G, Lesavre, P, Lüdemann, J, Rasmussen, N, Sinico, R, Wiik, A, Van Der Woude, F, Van Der Woude, F., and SINICO, RENATO ALBERTO

Abstract

Diagnostic value of standardized assays for anti-neutrophil cytoplasmic antibodies in idiopathic systemic vasculitis. Anti-neutrophil cytoplasmic antibodies (ANCA) are widely used as diagnostic markers for Wegener's granulomatosis (WG), microscopic polyangiitis (MPA), Churg-Strauss syndrome (CSS) and idiopathic rapidly progressive glomerulonephritis (iRPGN). The objective of this study was to evaluate the diagnostic value of ANCA measurement by the indirect immunofluorescence (IIF) test, and by anti-PR3 and anti-MPO ELISA performed in different locations, in patients with idiopathic small vessel vasculitis. Fourteen centers participated in a standardization study of ANCA assays, and entered a total number of 169 newly diagnosed and 189 historical patients with idiopathic systemic vasculitis or iRPGN. Patients were classified according to a pre-defined diagnostic classification system. Results were compared with those of 184 disease controls and 740 healthy controls, The IIF test was performed according to standard methodology; ELISAs had been standardized among the participants in a previous phase of the study. The sensitivities of assays in patients were as follows. The sensitivity in WG was: cANCA 64%, pANCA 21%, anti-PR3 66%, anti-MPO 24%. In MPA the sensitivity was: cANCA 23%, pANCA 58%, anti-PR3 26%, anti-MPO 58%. Sensitivity in iRPGN was: cANCA 36%, pANCA 45%, anti-PR3 50%, anti-MPO 64%. The specificity of assays (related to disease controls) was: cANCA 95%, pANCA 81%, anti-PR3 87%, anti-MPO 91%. When the results of the IIF test were combined with those of the ELISAs (cANCA/anti-PR3 positive, pANCA/anti-MPO positive), the diagnostic specificity increased to 99%. The sensitivity of the combination of cANCA + anti-PR3 or pANCA + anti-MPO for WG, MPA or iRPGN was 73%, 67% and 82%, respectively. From this study we conclude that the value of the IIF test for ANCA detection can be greatly increased by the addition of a well standardized antigen-specific ELISA. In a

Published
1998

19. Development and standardization of solid phase assays for the detection of anti-neutrophil cytoplasmic antibodies (ANCA). A report on the second phase of an international cooperative study on the standardization of ANCA assays

Author

Hagen, E, Andrassy, K, Csernok, E, Daha, M, Gaskin, G, Gross, W, Hansen, B, Heigl, Z, Hermans, J, Jayne, D, Kallenberg, C, Lesavre, P, Lockwood, C, Lüdemann, J, Mascart Lemone, F, Mirapeix, E, Pusey, C, Rasmussen, N, Sinico, R, Tzioufas, A, Wieslander, J, Wiik, A, Van der Woude, F, Van der Woude, F., SINICO, RENATO ALBERTO, Hagen, E, Andrassy, K, Csernok, E, Daha, M, Gaskin, G, Gross, W, Hansen, B, Heigl, Z, Hermans, J, Jayne, D, Kallenberg, C, Lesavre, P, Lockwood, C, Lüdemann, J, Mascart Lemone, F, Mirapeix, E, Pusey, C, Rasmussen, N, Sinico, R, Tzioufas, A, Wieslander, J, Wiik, A, Van der Woude, F, Van der Woude, F., and SINICO, RENATO ALBERTO

Abstract

Anti-neutrophil cytoplasmic antibodies (ANCA) are diagnostic markers for systemic vasculitis. They are classically detected by an indirect immunofluorescence test using normal donor neutrophils as substrate. This assay lacks antigenic specificity and is not quantitative. The 'EC/BCR Project for ANCA Assay Standardization' is an international collaboration study with the aim to develop and standardize solid phase assays for ANCA detection. In this part of the study the isolation and characterization of proteinase-3 and myeloperoxidase, the two main target molecules for ANCA, and the development and standardization of ELISAs with these antigens are described. Six laboratories successfully isolated purified proteinase-3 preparations that could be used. Three of these preparations, together with one myeloperoxidase preparation, were subsequently used for ANCA testing by ELISA. The ELISA technique was standardized in two rounds of testing in the 14 participating laboratories. The coefficient of variation of these new assays decreased from values of approx. 50% in the first round to approx. 20% in the second round. We conclude that purified proteinase-3 and myeloperoxidase can be used in standardized ELISAs for ANCA detection. Whether such procedures offer advantages over the IIF test will be determined in a prospective clinical study

Published
1996

20. The value of indirect immunofluorescence and solid phase techniques for ANCA detection

Author

Hagen, E, Andrassy, K, Chernok, E, Daha, M, Gaskin, G, Gross, W, Lesavre, P, Ludemann, J, Pusey, C, Rasmussen, N, Savage, C, Sinico, R, Wiik, A, Van der Woude, F, Van der Woude, F., SINICO, RENATO ALBERTO, Hagen, E, Andrassy, K, Chernok, E, Daha, M, Gaskin, G, Gross, W, Lesavre, P, Ludemann, J, Pusey, C, Rasmussen, N, Savage, C, Sinico, R, Wiik, A, Van der Woude, F, Van der Woude, F., and SINICO, RENATO ALBERTO

Abstract

This study describes the results of phase I of an international effort to develop and standardize assays for the detection of anti-neutrophil cytoplasmic antibodies (ANCA). 12 sera, four of which were selected for their potential to cause problems in the detection of various ANCA specificities, were analyzed in the standard indirect immunofluorescence (IIF) test and in ELISAs for ANCA routinely performed in the seven participating laboratories. The IIF methodology differed with respect to the dilution of the serum being screened and the concentration of the conjugate used. Results from sera with high ANCA titers were similar, although the quantitative values could not be compared. In sera containing rheumatoid factor and anti-nuclear antibodies (ANA), ANCA-unrelated staining patterns were observed. Six antigen preparations were used in ELISA for the detection of cANCA. In ELISA with purified proteinase-3 all three cANCA sera were positive, but not anti-myeloperoxidase (MPO) or anti-lactoferrin (LF) positive sera. The other assays were less sensitive or gave inconsistent results. Various preparations of purified MPO and LF used in ELISA were readily recognized by anti-MPO and anti-LF positive sera. From this study it can be concluded that the IIF test, although performed with different methods, shows comparable results using strongly positive sera. In general solid phase assays for cANCA detection are not well standardized and need improvement although the purified proteinase-3 ELISA is possibly an exception. MPO and LF can be used in ELISA procedures for the detection of pANCA-related antibodies.

Published
1993

21. Study of Heart and Renal Protection (SHARP): Randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease.

Author

Reaich R., Schouten D., Rashid H., Birtcher K., Cantu J., Tait C., Taun W., Fadem S., Das D., Khosla U., Brown C., Brown T., Buquing J., Cromwell H., Dickson N., Najimipour B., Robeson J., Tabibi W., Mulloy L., Bailey K., Burton B., Fall P., Jagadeesan M., Paulson W., Szerlip H., White J., Faulkner M., Adeleye O., Boatright D., Mensah D., Nwankwo U., Crutcher L., Cummings C., Floyd M., Putatunda B., Ross J., Sanford V., Thadani U., Haragsim L., Parker B., Rogan L., Thresher M., Turner J., Dworkin L., Mignano D., O'Mara A., Shemin D., Bakris G., Basta E., Chua D., Neri G., Ahmed I., Elliott W., Fondren L., Hasabou N., Khosla N., Mazin A., Riehle J., Kovesdy C., Mendoza J., Ahmadzadeh S., Iranmanesh A., Lewis M., Lu J., Benabe J., Gonzalez-Melendez E., Padilla B., Serrano J., Russ T., Athmann L., Funke L., Larson P., Roach D., Salveson B., Nogueira J., Hanes D., Hise M., Light P., Copland E., Fink J., Hakim M., Hough K., McMinn S., Weir M., Young C., Kershaw G., Hill I., White B., Plumb T., Florescu M., Groggel G., Martin M., Rao V., Denu-Ciocca C., Candiani C., Cooper J., Gordon B., Joy M., Kiser M., Lambeth C., Rosas S., Cochetti P., Robinson J., Schankel K., Teng H., Weise W., Geneidy A., Murray P., Solomon R., De Waal D., LaPointe S., Schoenknecht A., Campese V., Habashy M., Ananthakrisna R., Bedwani D., Fazli U., Fetrat M., Frampton Q., Kaldas B., Kazarian V., Pitts L., Sadeghi A., Yeasmin N., Young E., Fissell R., Belanger K., Ricci N., Farwell W., Bowman T., Dhingra R., Pesenson A., Ambrosino J., Chittamooru S., Kaufman J., Ramos M., Yap C., Nakhle S., Aligaen L., Duren D., Laine B., Moore S., Tuazon H., Coyne D., Audrain J., Bryant B., Dombek S., Freeman S., Klein P., Germain M., Berkowitz A., Bokhari A., Braden G., Diaz A., Greco B., Mulhern J., O'Shea M., Poindexter A., Poppel D., Ryan M., Sweet S., Ye J., Osterman J., Lin T., Mays B., Rizvi A., Sonnier C., Twining C., Wang S., Hix M., Schenck J., Baigent C., Landray M., Reith C., Dasgupta T., Emberson J., Herrington W., Lewis D., Mafham M., Collins R., Bray C., Chen Y., Baxter A., Young A., Hill M., Knott C., Cass A., Feldt-Rasmussen B., Fellstrom B., Grobbee R., Gronhagen-Riska C., Haas M., Holdaas H., Hooi L.S., Jiang L., Kasiske B., Krairittichai U., Levin A., Massy Z., Tesar V., Walker R., Wanner C., Wheeler D., Wiecek A., Majoni W., Simpson D., Strony J., Musliner T., Agodoa L., Armitage J., Chen Z., Craig J., De Zeeuw D., Gaziano M., Grimm R., Krane V., Neal B., Ophascharoensuk V., Pedersen T., Sleight P., Tobert J., Tomson C., Sandercock P., Keech A., Whelton P., Yusuf S., Peto R., Parish S., Dolph L., Bahu T., Booth-Davey E., Brewster A., Yau F., Denis E., Frederick K., Haywood D., Heineman J., Howard S., Jayne K., Madgwick Z., Michell S., Murphy K., Ning L., Nolan J., Nunn M., Roberts J., Wickman M., Bowman L., Bulbulia R., Haynes R., Rahimi K., Rahman N., Ait-Sadi R., Barton I., Zhu W., Clark S., Kourellias K., Radley M., Brown K., Worthing D., Coates G., Goodenough B., Lucas N., Carreras A., Currie R., Donaldson O., Fjalling E., Gallagher M., Gibson K., Goddard J., Healy J., Hones L., Jardine M., Kwong I., Merai M., Murray S., Perkovic V., Rendina A., Gallo K., Caron S., Carlson K., Foley K., Matzek S., Mewhort L., O'Donoghue S., Perel-Winkler A., Terins T., Nie Q., Yu H., Ge L., Hao D., Li L., Pang X., Wei X., Yan G., Certikova Chabova V., Holst H., Molvadgaard T., Munksgaard D., Peltonen Y., Liabeuf S., Lebel C., Ouabou L., Bauer B., Bergmann K., Beusch M., Cavitt D., Drechsler C., Dulau I., Hugen K., Kempf S., Kuchenmeister B., Pscheidl V., Schmiedeke D., Schwarz M., Speerschneider K., Stahl B., Lim B.C., Nadia H., Zishareena M.F., Vasuthavan S., Ganesapillai A.T., Yuen S., Grobbee D., Bobbink I., Groot K., Sikking I., Raley J., Colban M., Smerud K., Trygg N., Waagaard E., Westad H., Rotkegel S., Spiechowicz U., Domoradzka M., Gawlowska M., Flygar A., Odmark I., Pettersson A., Blackwood S., Barclay J., Benham J., Brown R., Cureton L., Jackson D., Kennedy I., Leaper C., Taylor A., Winter C., Wise C., Nash M., Taylor Bennett A., Donaldson D., Chalmers K., Corderoy H., Bartkoske M., Bjerk C., Camarena A., Herskovitz L., Heuer C., Levin J., Robinson R., Wicklund B., Bentzel D., Cohen S., Costa C., Scranton R., Auwardt R., Boyer M., Cogdell P., Menahem S., Sheldrake J., Mount P., Fraenkel M., Bisscheroux P., Dempester J., Gleeson P., Harris G., Holmes C., Hyett K., Linton A., Miach P., Booth D., Druce L., Mantha M., Borg E., Green S., Killen J., Lynch Y., Colquhoun D., Herzig K., Row G., Addison J., Asa J., Beatson G., Calvird D., Edmunds J., Ferreira-Jardim A., Gwynne A., Mackay D., McLoughlin L., Wightwick C., Williams L., Ferrari P., Barry J., Hodson S., Zakrzewska W., Meagher E., Mulcahy M., Parnham A., Carney S., Garvey L., Gillies A., Hayes S., Mathew M., Fassett R., Anderson L., Clingeleffer C., Curnock A., Mayne L., Richardson D., Smith M., Smith S., Suranyi M., Howlin K., Chow J., Cleland B., Rayment G., Spicer T., Wong J., Wong M., Packham D., Alison C., Fraser I., Mitchell J., Nagle J., Brown F., Ellery C., Monkhouse J., Nandkumar J., Reith-Myers L., Gray N., Cocks C., Courtney M., Hollett P., Johnston C., Larsen H., Pollock A., Stewart S., Styles G., Wyndham R., Fanning M., Gibson W., Jackson S., Mannering M., Mercado E., Oliphant R., Sud K., Ubera N., Wood C., Karrasch J., Brinkley T., Estensen K., Moroney A., Sutton J., Warren R., Saltissi D., Jahke H., Roach H., Saltissi J., Wiederroth O'Brien M., Johnson D., Bali V., Evans M., Franzen K., Halbish S., Helyar J., Martin A., Mudge D., Sonnenburg K., Sudak J., Roger S., Almeida S., Andrews H., Bohringer L., Bouwhuis L., Brady L., Carpenter A., Warren S., Elias T., Bannister K., Chew G., Clarke J., Faull R., Hooper A., Jeffs L., Napier A., Peh C., Pirone K., Skilton F., Ranganathan D., Best J., Hart L., Healy H., Morgan C., Ratanjee S., Salisbury A., Jose M., Freeman J., Hamilton R., Kirkland G., Read G., Anderson H., Boekel K., Farrell M., Foreman A., Iliev K., Pedagogos E., Raspudic T., Pollock C., Cooper B., Kesselhut J., Macadam C., Pearse J., Rowland C., Tully H., Irish A., Dogra G., Coutts P., Hayes L., Khoo D., Nathoo B., Shakespeare K., Warger A., Gillin A., Burman J., George C., Sherwood S., Snelling P., Stevens C., Hutchison B., Luxton G., Devenny N., Herson H., Pellicano S., Kelly J., Coutelas J., Garlinge C., McClelland A., Pirabhahar S., Saleh H., Langham R., Englebright B., Giang M., Lanteri M., Mullins K., Turner C., Collett P., Stokoe S., Sutherland K., Talafua D., Talaulikar G., Clarkson A., Rees C., Carney G., Falk M., Gracey D., Jadeer A., Johnson P., Karpe K., Singer R., Walters G., McDonald S., Burgess J., Fischer K., Gentgall M., Hockley M., Veitch D., De Jersey P., Gillam A., Hartig V., Holland K., McArdle J., Washington W., Rangan G., Mikaheal M., Murie P., Perez N., Punnoose N., Smolonogov T., Taler N., Williams G., Wen C., Kohlhagen J., Wessels J., Johnson S., Reid A., Ryan J., Taprell D., Auinger M., Eigner M., Kodras K., Leithner C., Magpantay L., Marterer C., Prager R., Prinz C., Seiringer E., Kramar R., Mitter E., Stummvoll H., Dieplinger G., Wenzel R., Stolz G., Drose S., Edlinger E., Headlam-Leitner E., Miska H., Then M., Weninger S., Lhotta K., Neyer U., Dickie H., Smodek S., Sprenger-Mahr H., Rosenkranz A., Zitt E., Mayr B., Schinner A., Soltys G., Begin V., Brunet S., Cournoyer S., Gelinas M., Giroux C., Martineau J., Roy M., Savoie L., Agharazii M., Blouin J., Desmeules S., Langlois S., Samson F., Wong G., Constantini L., Jing J., Malko J., Rivers C., Rochester D., Skilling C., Wadgymar A., Wu G., Kates D., Husch J., Mantle M., Turri L., Barrett B., Curtis B., Greeley B., Hannaford M., Harnett J., Kelly M., Langille E., Morgan J., Murphy S., Karim M., Arbo T., Carpenito G., Chan V., DaRoza G., Friesen M., Kraus D., Lam S., Lange B., Minhas S., Starko R., Torng S., Vela K., Madore F., Roy P., Troyanov S., Bonnardeaux A., Lauzon L., Pichette V., Yeates K., Mahoney K., Myers C., Pilkey R., Moist L., Edgar M., House A., Kortas C., Mindorff S., Tam P., Chow S., Fung J., Nagai G., Ng P., Sikaneta T., Ting R., Forzley B., Clouatre Y., Cooper S., DaCosta H., Granger S., Valley S., Karunakaran S., Abdulhadi M., Altwasser C., Anderson S., Bergquist L., Wijeyesinghe C., Berst L., Horgan K., Coles K., Lotter T., Robson L., Barre P., Golden J., Golden M., Tanguay N., Rigatto C., Armstrong S., Fine A., Fontaine B., Friesen D., Henry S., Kraushar M., Reslerova M., Verrelli M., Rabbat C., Clase C., Suva G., Winegard N., Goldstein M., Curvelo S., Donnelly S., Huckle J., Marticorena R., Chan-Yan C., Chiu A., DeLuca L., Flamer D., Gill J., Jamal A., Jung B., Kiaii M., Landsberg D., Rozen N., Taylor P., Werb R., Pylypchuk G., Ahmed A., Barton J., Hundseth M., Kappel J., Keindel I., Klassen J., Pylypchuk S., Rindall M., Tobe S., Naimark D., Agelopoulos M., Chessman M., Hladunewich M., Perkins N., Sainsbury S., McCready W., Adams B., Tonelli M., Caldwell S., Kumar U., McMahon A., Nikitin S., Restall J., Treit S., Wysocki Y., Duncan J., Copland M., Jastrzebski J., Keown P., Kwan S., Rogers D., Shapiro J., Singh S., Sioson L., Yee K., Yeung C., Zacharias J., Bueti J., Dizon B., Lam H., Miller L., Ross M., Zarrillo M., Li Z., Wang C., Liu L., Hong M., Zheng H., Zuo W., Ge Z., Liu Q., Li Y., Sun K., Zhao R., Sun G., Wang F., Cui Z., Lou F., Du Y., Song L., Huang H., Song Z., Wang J., Zhou L., Wu R., Xiao R., Zhang Q., Duan N., Ju N., Wang A., Xu Z., Lu Z., Zhang Y., Zhao L., Zhang C., Mo Z., Xie Y., Xiong J., Chen J., Guo L., Zhao S., Peiskerova M., Jancova E., Kazderova M., Kobrova L., Gorun P., Kmentova T., Burgelova M., Lyerova L., Viklicky O., Berdych M., Nydlova Z., Jelinkova G., Moltas J., Pauzar T., Knetl P., Cahova J., Simkova J., Zakova M., Vankova S., Safarova R., Hruby M., Karlova R., Prikaska V., Sellenberg P., Vesela E., Malanova L., Vlasak J., Kaprova P., Novakova D., Kotherova K., Studenovska M., Christensen J., Solling J., Jepsen M., Kristensen V., Aerenlund H., Braemer-Jensen M., Kamper A., Raaschou S., Heaf J., Dreyer J., Freese P., Holm M., Munch M., Gade-Rasmussen E., Bredmose K., Daugaard H., Nielsen J., Friedberg M., Jensen D., Munk Plum M., Solling K., Dieperink H., Arp Nielsen L., Friborg E., Gloe-Jakobsen A., Thye Ronn P., Rasmussen K., Andersen C., Johansen A., Odum L., Ostergaard O., Pedersen L., Lykkegaard S., Aundal M., Faureholm Huess S., Danielsen H., Madsen J., Nyvang M., Ekstrand A., Boman H., Hartman J., Lipponen A., Lithovius R., Rauta V., Salmela A., Saloranta K., Forslund T., Koskiaho P., Jaaskelainen K., Kanninen M., Laine K., Asola M., Huhti J., Pentti M., Metsarinne K., Heiro M., Koivuviita N., Saarinen M., Tertti R., Choukroun G., Fournier A., Ducloux D., Marechal F., Simula Faivre D., Combe C., Douillet M., Lamblot T., Nardi H., Vendrely B., Bourbigot B., Ferlandin S., Zaoui P., Jouet C., Geffroy-Guiberteau S., Bugnazet L., Aldigier J., El Hamel-Belili C., Giraud S., Dussol B., Berland Y., Chollet M., Sichez H., Cristol J., Canaud B., Morena M., Rodriguez A., Kessler M., Mizejewski B., Risse B., Urena Torres P., Bou-Bekr M.A., Arezki C., Ras El Qdim P., Vela C., Borsato F., Talairach A., Normand M., Normand V., Rieu P., Gauthier B., Vigneron-Foy C., Wolak A., Menoyo V., Alos L., Caillette-Beaudoin A., Berger V., Al-Sarraf S., Konnerth I., Urban C., Weiner S., Boesken W., Jochum E., Kiefer C., Wagner A., Krumme B., Bohler J., Bonow B., Hohenstatt U., Mettang T., Rockel A., Langanke J., Lipponer H., Dunschen-Weimar G., Dunst R., Hubel E., Petrik R., Rengel R., Schmidgen M., Mayr H., Garschhammer C., Weirauch S., Anger H., Goock T., Mai A., Bast I., Suptitz C., Iwig B., Florschutz K., Hasselbacher R., Sauerbrey G., Delrieux S., Rau S., Poley M., Laux R., Schonfelder O., Kunowski G., Fuchs G., Hoffmann K., Schurger R., Brensing K., Guven Z., Immenkamp C., Kottmann C., Schmitt H., Schulz M., Arnold P., Knaup R., Schneider H., Siemsen H., Pyriki P., Korkemeyer F., Pyriki R., Siebrecht A., Schulz E., Krumwiede A., Kruse D., Lucke S., Keim H., Fink H., Fischer S., Klingbeil A., Kuhlmei K., Ortwein-Horn N., Merker L., Bayer B., Benamar K., Emmert S., Floten E., Holzheuer K., Lummer M., Ossendorf E., Scholz M., Oppitz M., Georgiew L., Tripps C., Wendehake M., Lange D., Pingel V., Brause M., Schanze W., Duygulu E., Dellanna F., Heinemann-Nieberding S., Sturmer C., Wieczorek K., Zarga O., Kullmer B., Kullmer S., Akin M., Gondolf M., Schutterle S., Walker G., Bertsch R., Seul M., Allendorff J., Siehler R., Stemmler S., Baldus M., Adler A., Harter S., Wurmell W., Moller M., Hame C., Muller M., Schreiber M., Schurfeld C., Millington-Herrmann M., Benschneider A., Gaffal J., Sprunken U., Bohling M., Wunderlich S., Schramm L., Kollenbrath C., Netzer K., Sieber T., Zimmermann J., Bellersen M., Uerkvitz M., David-Walek T., Hauschildt B., Leimenstoll G., Lonnemann G., Hilfenhaus M., Benedetto C., Stockmann S., Ichtiaris P., Jungmann A., Neumeier K., Stoof A., Bohmer K., Kirpal A., 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Weyer J., Heine C., Kirste P., Zemann B., Alscher D., Rumpf D., Wullen B., Bengel A., Friedrich B., Kirschner T., Knodler U., Machleidt C., Niederstrasser K., Noack E., Wilhelm J., Heuer H., Dulea J., Piolot R., Rudke M., Treinen G., Elberg B., Hanke J., Nitschke T., Rosendahl C., Schmitz A., Schrader J., Kulschewski A., Lubcke C., Hammersen F., Luders S., Venneklaas U., Muhlfeld A., Arabi Al-Khanne F., Ketteler M., Politt D., Schuster C., Eitner F., Goretz U., Heidenreich S., Janssen U., Kranz A., Moormann E., Schneider B., Weber W., Frei U., Jovanovic T., Asmus H., Canaan-Kuhl S., Pannier L., Petersen S., Pluer M., Schaeffner E., Schafer C., Warncke S., Schmieder R., Donhauser C., Schulze B., Koziolek M., Bechtel W., Kurz B., Strutz F., Bramlage C., Dreyer S., Mommeyer E., Niemann J., Scheel A., Troche-Polzien I., Weber F., Heine G., Girndt M., Lizzi F., Rogacev K., Lindner T., Achenbach H., Peschel K., Beige J., Jentho S., Kreyssig C., Prill K., Renders L., Walcher J., Cerny S., 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Mathisen U., Pedersen M., Rumsfeld M., Toft I., Berget K., Landsverk K., Tveiten G., Wamstad H., Klinger M., Krajewska M., Golebiowski T., Kusztal M., Spiechowicz-Zaton U., Rutkowski B., Renke M., Tylicki L., Czekalski S., Koziol L., Wanic-Kossowska M., Wasik-Olejnik A., Nowicki M., Dryja P., Kurnatowska I., Zawiasa A., Ciszek M., Gomolka M., Mysliwiec M., Brzosko S., Mazerska M., Hruby Z., Koscielniak K., Stanek-Piotrowska M., Mesjasz J., Rudka R., Baranski M., Jupowiecki J., Klein D., Switalski M., Kuriga M., Ostrowski M., Lidman A., Linde T., Waltersson K., Weiss L., Andersson G., Lindell C., Welander G., Jacobson S., Edensjo P., Wallin J., Linder M., Karsberg M., Hellgren K., Lonn I., Frisenette-Fich C., Johansson A., Lundstrom A., Mauritz N., Stahl-Nilsson A., Tobafard N., Hellberg O., Ejemar E., Von Schmalensee N., Gunne T., Eriksson A., Ostberg S., Svensson C., Mulec H., Jacobsson A., Karlsson M., Onnermalm L., Osagie S., Ekengren U., Larsson M., Lindberger K., Olofsson A., 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Reaich R., Schouten D., Rashid H., Birtcher K., Cantu J., Tait C., Taun W., Fadem S., Das D., Khosla U., Brown C., Brown T., Buquing J., Cromwell H., Dickson N., Najimipour B., Robeson J., Tabibi W., Mulloy L., Bailey K., Burton B., Fall P., Jagadeesan M., Paulson W., Szerlip H., White J., Faulkner M., Adeleye O., Boatright D., Mensah D., Nwankwo U., Crutcher L., Cummings C., Floyd M., Putatunda B., Ross J., Sanford V., Thadani U., Haragsim L., Parker B., Rogan L., Thresher M., Turner J., Dworkin L., Mignano D., O'Mara A., Shemin D., Bakris G., Basta E., Chua D., Neri G., Ahmed I., Elliott W., Fondren L., Hasabou N., Khosla N., Mazin A., Riehle J., Kovesdy C., Mendoza J., Ahmadzadeh S., Iranmanesh A., Lewis M., Lu J., Benabe J., Gonzalez-Melendez E., Padilla B., Serrano J., Russ T., Athmann L., Funke L., Larson P., Roach D., Salveson B., Nogueira J., Hanes D., Hise M., Light P., Copland E., Fink J., Hakim M., Hough K., McMinn S., Weir M., Young C., Kershaw G., Hill I., White B., Plumb 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N., Carreras A., Currie R., Donaldson O., Fjalling E., Gallagher M., Gibson K., Goddard J., Healy J., Hones L., Jardine M., Kwong I., Merai M., Murray S., Perkovic V., Rendina A., Gallo K., Caron S., Carlson K., Foley K., Matzek S., Mewhort L., O'Donoghue S., Perel-Winkler A., Terins T., Nie Q., Yu H., Ge L., Hao D., Li L., Pang X., Wei X., Yan G., Certikova Chabova V., Holst H., Molvadgaard T., Munksgaard D., Peltonen Y., Liabeuf S., Lebel C., Ouabou L., Bauer B., Bergmann K., Beusch M., Cavitt D., Drechsler C., Dulau I., Hugen K., Kempf S., Kuchenmeister B., Pscheidl V., Schmiedeke D., Schwarz M., Speerschneider K., Stahl B., Lim B.C., Nadia H., Zishareena M.F., Vasuthavan S., Ganesapillai A.T., Yuen S., Grobbee D., Bobbink I., Groot K., Sikking I., Raley J., Colban M., Smerud K., Trygg N., Waagaard E., Westad H., Rotkegel S., Spiechowicz U., Domoradzka M., Gawlowska M., Flygar A., Odmark I., Pettersson A., Blackwood S., Barclay J., Benham J., Brown R., Cureton L., Jackson D., Kennedy I., Leaper C., Taylor A., Winter C., Wise C., Nash M., Taylor Bennett A., Donaldson D., Chalmers K., Corderoy H., Bartkoske M., Bjerk C., Camarena A., Herskovitz L., Heuer C., Levin J., Robinson R., Wicklund B., Bentzel D., Cohen S., Costa C., Scranton R., Auwardt R., Boyer M., Cogdell P., Menahem S., Sheldrake J., Mount P., Fraenkel M., Bisscheroux P., Dempester J., Gleeson P., Harris G., Holmes C., Hyett K., Linton A., Miach P., Booth D., Druce L., Mantha M., Borg E., Green S., Killen J., Lynch Y., Colquhoun D., Herzig K., Row G., Addison J., Asa J., Beatson G., Calvird D., Edmunds J., Ferreira-Jardim A., Gwynne A., Mackay D., McLoughlin L., Wightwick C., Williams L., Ferrari P., Barry J., Hodson S., Zakrzewska W., Meagher E., Mulcahy M., Parnham A., Carney S., Garvey L., Gillies A., Hayes S., Mathew M., Fassett R., Anderson L., Clingeleffer C., Curnock A., Mayne L., Richardson D., Smith M., Smith S., Suranyi M., Howlin K., Chow J., Cleland B., Rayment G., Spicer T., Wong J., Wong M., Packham D., Alison C., Fraser I., Mitchell J., Nagle J., Brown F., Ellery C., Monkhouse J., Nandkumar J., Reith-Myers L., Gray N., Cocks C., Courtney M., Hollett P., Johnston C., Larsen H., Pollock A., Stewart S., Styles G., Wyndham R., Fanning M., Gibson W., Jackson S., Mannering M., Mercado E., Oliphant R., Sud K., Ubera N., Wood C., Karrasch J., Brinkley T., Estensen K., Moroney A., Sutton J., Warren R., Saltissi D., Jahke H., Roach H., Saltissi J., Wiederroth O'Brien M., Johnson D., Bali V., Evans M., Franzen K., Halbish S., Helyar J., Martin A., Mudge D., Sonnenburg K., Sudak J., Roger S., Almeida S., Andrews H., Bohringer L., Bouwhuis L., Brady L., Carpenter A., Warren S., Elias T., Bannister K., Chew G., Clarke J., Faull R., Hooper A., Jeffs L., Napier A., Peh C., Pirone K., Skilton F., Ranganathan D., Best J., Hart L., Healy H., Morgan C., Ratanjee S., Salisbury A., Jose M., Freeman J., Hamilton R., Kirkland G., Read G., Anderson H., Boekel K., Farrell M., Foreman A., 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Szymanski J., Almond M., Bourton L., Bromwich C., Dawson S., Mason S., Oliveira D., Ramkhelawon R., Tuazon J., Andrews P., Archer K., Moore A., Thomas G., Velazquez C., Mumtaz R., Roberts R., Farquhar F., Ott J., Fenwick S., Callaway A., Garrett P., Dees L., McDonagh U., Garner S., Zehnder D., Aldridge N., Dyer C., Gomez M., Hewins S., McCarthy K., Rush J., Spencer S., Harvey M., Mills H., Drew P., Henry M., Wilberforce S., Worth D., Adair Z., Hartley J., Jibani M., Jones D., Swan S., Shamp T., Alcorn H., Bookey J., Cannon C., Jarvis K., Muesing C., Murphy M., Muster H., Planting M., Strand C., Middleton J., Gitter K., Mace N., Schumm D., Pogue V., Alimohammadi B., Arora P., Herbert L., Cheng J., Dowie D., Mohan S., Peters G., Tuttle K., Albritton S., Benedetti R., Joshi S., Lund B., Shuler L., Trevino M., Mai K., Osborn T., Parekh R., Eustace J., Novak G., Patterson S., Lindsey C., Hill T., Liston M., Wiegmann T., Nagaria A., Hurd C., Hurst A., Omoscharka E., Parks S., and Price V.

Abstract

Background: Lowering low-density lipoprotein (LDL) cholesterol with statin therapy has been shown to reduce the incidence of atherosclerotic events in many types of patient, but it remains uncertain whether it is of net benefit among people with chronic kidney disease (CKD). Method(s): Patients with advanced CKD (blood creatinine >=1.7 mg/dL [>= 150 mumol/L] in men or >=1.5 mg/dL [ >= 130 mumol/L] in women) with no known history of myocardial infarction or coronary revascularization were randomized in a ratio of 4:4:1 to ezetimibe 10 mg plus simvastatin 20 mg daily versus matching placebo versus simvastatin 20 mg daily (with the latter arm rerandomized at 1 year to ezetimibe 10 mg plus simvastatin 20 mg daily vs placebo). The key outcome will be major atherosclerotic events, defined as the combination of myocardial infarction, coronary death, ischemic stroke, or any revascularization procedure. Results A total of 9,438 CKD patients were randomized, of whom 3,056 were on dialysis. Mean age was 61 years, two thirds were male, one fifth had diabetes mellitus, and one sixth had vascular disease. Compared with either placebo or simvastatin alone, allocation to ezetimibe plus simvastatin was not associated with any excess of myopathy, hepatic toxicity, or biliary complications during the first year of follow-up. Compared with placebo, allocation to ezetimibe 10 mg plus simvastatin 20 mg daily yielded average LDL cholesterol differences of 43 mg/dL (1.10 mmol/L) at 1 year and 33 mg/dL (0.85 mmol/L) at 2.5 years. Follow-up is scheduled to continue until August 2010, when all patients will have been followed for at least 4 years. Conclusions SHARP should provide evidence about the efficacy and safety of lowering LDL cholesterol with the combination of ezetimibe and simvastatin among a wide range of patients with CKD.Copyright © 2010, Mosby, Inc. All rights reserved.

Published
2010

22. Proteoglycan production by human glomerular visceral epithelial cells and mesangial cells in vitro

Author

van Det, N F, van den Born, J, Tamsma, J T, Verhagen, N A, van den Heuvel, L P, Berden, J H, Bruijn, J A, Daha, M R, van der Woude, F J, Groningen Kidney Center (GKC), and Groningen Institute for Organ Transplantation (GIOT)

Subjects
Adult, Adolescent, Transcription, Genetic, Molecular Sequence Data, Enzyme-Linked Immunosorbent Assay, Chondroitin Sulfate Proteoglycans/analysis, RNA/genetics, Sulfur Radioisotopes, Tritium, Polymerase Chain Reaction, Glomerular Mesangium/metabolism, Leucine/metabolism, Humans, Proteoglycans/biosynthesis, Child, Heparitin Sulfate/biosynthesis, Cells, Cultured, Chromatography, High Pressure Liquid, Aged, Glucosamine/metabolism, Base Sequence, RNA, Messenger/analysis, Infant, Middle Aged, carbohydrates (lipids), Epithelium/metabolism, Sulfates/metabolism, Kidney Glomerulus/cytology, Child, Preschool, DNA, Complementary/biosynthesis, Heparan Sulfate Proteoglycans
Abstract

Proteoglycans metabolically labelled with [35S]sulphate and [3H]glucosamine or [3H]leucine were isolated from the incubation medium and cell layer of human adult mesangial cells and glomerular visceral epithelial cells using sequential DEAE chromatography purification steps followed by gel-filtration chromatography. The proteoglycan composition of each peak was analysed by treatment with HNO2, chondroitinase ABC or chondroitinase AC followed by chromatography on Sephadex G-50 columns. Heparan sulphate proteoglycan (HSPG) and dermatan sulphate proteoglycan were detected in both the culture medium and cell layer of mesangial cells. Culture medium of glomerular visceral epithelial cells contained HSPG and a second proteoglycan with the properties of a hybrid molecule containing HS and chondroitin sulphate (CS). The cell layer contained HSPG and CSPG. Detailed analysis of the hybrid molecule revealed that it had an apparent molecular mass of 400 kDa. SDS/PAGE of hybrid molecules, after treatment with heparitinase and chondroitinase ABC, revealed a core protein of 80 kDa. Using 1.8% polyacrylamide/0.6% agarose-gel electrophoresis, we deduced that the HS and CS were independently attached to one core protein. Because glomerular-basement-membrane HSPG is thought to be derived from mesangial cells and glomerular visceral epithelial cells and this molecule is involved in several kidney diseases, we investigated its synthesis in more detail. Anti-(rat glomerular-basement-membrane HSPG) monoclonal antibodies (JM403) and anti-(human glomerular-basement-membrane HSPG) polyclonal antibodies (both antibodies known to react with the large basement-membrane HSPG, perlecan) reacted strongly with HSPG obtained from both mesangial cells and glomerular visceral epithelial cells. However, the hybrid molecule did not react with these antibodies, suggesting that the HS side chain and the core protein were different from glomerular-basement-membrane HSPG. To quantify HS we performed an inhibition ELISA using mouse antibodies specific for glomerular-basement-membrane HS glycosaminoglycan side chains. Glomerular visceral epithelial cells produced significantly higher levels of HS (between 197.56 and 269.40 micrograms/72 h per 10(6) cells) than mesangial cells (between 29.8 and 45.5 micrograms/72 h per 10(6) cells) (three different cell lines; n = 3; P < 0.001). HS production by these cells was inhibited by cycloheximide, revealing that it was synthesized de novo. Expression of perlecan mRNA, demonstrated using reverse transcriptase PCR, was different in the two cell types. We conclude that glomerular visceral epithelial cells and mesangial cells have characteristic patterns of proteoglycan production. Glomerular visceral epithelial cells produced a hybrid proteoglycan containing CS and HS independently attached to its core protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1995

23. European therapeutic trials in ANCA-associated systemic vasculitis: Disease scoring, consensus regimens and proposed clinical trials EUROPEAN COMMUNITY STUDY GROUP ON CLINICAL TRIALS IN SYSTEMIC VASCULITIS ECSYSVASTRIAL (BMHl-Cr93-1078)

Author

Rasmussen, N. Jayne, D.R.W. Abramowicz, D. Andrassy, K. Bacon, P.A. Cohen Tervaert, J.W. Dadonlené, J. Feighery, C. Van Es, L.A. Ferrario, F. Gaskin, G. Gregorini, G. De Groot, K. Gross, W.L. Grönhagen-Riska, C. Guillevin, L. Hagen, E.C. Heigl, Z. Hermans, J. Kallenberg, C.G.M. Landais, P. Lesavre, P. Lockwood, C.M. Luqmani, R. Mirapeix, E. Pettersson, E. Pusey, C. Savage, C.O.S. Sinico, R.A. Specks, U. Tzioufas, A.G. Westman, K.W.A. Wiik, A. Van Der Woude, F.

Published
1995

24. Long-term renal injury in ANCA-associated vasculitis: an analysis of 31 patients with follow-up biopsies

Author

Hauer, H, Bajema, I, Hagen, E, Noël, L, Ferrario, F, Waldherr, R, van Houwelingen, H, Lesavre, P, Sinico, R, van der Woude, F, Gaskin, G, Verburgh, C, de Heer, E, Bruijn, J, Bruijn, J., SINICO, RENATO ALBERTO, Hauer, H, Bajema, I, Hagen, E, Noël, L, Ferrario, F, Waldherr, R, van Houwelingen, H, Lesavre, P, Sinico, R, van der Woude, F, Gaskin, G, Verburgh, C, de Heer, E, Bruijn, J, Bruijn, J., and SINICO, RENATO ALBERTO

Abstract

Background. We reported previously that in renal disease in relation to antineutrophil cytoplasm auto-antibodies (ANCA)-associated vasculitis, renal outcome correlates better with the percentage of normal glomeruli than with separate active lesions. This may imply that glomeruli, once affected by necrotizing and crescentic lesions, are irreversibly damaged. We quantified and evaluated the course of renal lesions in the present study. Methods. We retrospectively analysed 31 patients with renal disease in relation to ANCA-associated vasculitis, all treated with immunosuppressive drugs. In all patients, a renal biopsy was performed at diagnosis. A follow-up biopsy was performed in all patients on the indication of a suspected renal relapse, after a mean interval of 31 months. Results. The mean percentage of normal glomeruli in the renal biopsy did not change over time (29% in the initial and 30% in the follow-up biopsy). The mean percentage of glomeruli with crescents, however, significantly decreased from 57 to 30% (P < 0.001). The percentage of glomerulosclerosis significantly increased from 12 to 39% (P < 0.001). The data were independent of diagnosis, gender, age, time interval between the biopsies, and treatment. Conclusions. This is the first study to quantify glomerular changes between two time points in patients with renal vasculitis. Our results suggest that, on average, no new glomeruli are recruited into the active disease process. The sum of the percentage of crescentic and sclerotic glomeruli in the initial biopsies is larger than the percentage of sclerotic glomeruli in the follow-up biopsies. Thus, therapy seems not only to prevent normal glomeruli from being recruited into the active disease process for a certain time, but seems also to allow part of the active lesions to revert into a normal phenotype, although another part of the active lesions will be transformed to a chronic phenotype

Published
2002

39. European therapeutic trials in ANCA-associated systemic vasculitis: disease scoring, consensus regimens and proposed clinical trials EUROPEAN COMMUNITY STUDY GROUP ON CLINICAL TRIALS IN SYSTEMIC VASCULITIS ECSYSVASTRIAL (BMHl-Cr93-1078)

Author

Rasmussen, N, primary, Jayne, D R W, additional, Abramowicz, D, additional, Andrassy, K, additional, Bacon, P A, additional, Cohen Tervaert, J W, additional, Dadonlené, J, additional, Feighery, C, additional, van Es, L A, additional, Ferrario, F, additional, Gaskin, G, additional, Gregorini, G, additional, de Groot, K, additional, Gross, W L, additional, Grönhagen-Riska, C, additional, Guillevin, L, additional, Hagen, E C, additional, Heigl, Z, additional, Hermans, J, additional, Kallenberg, C G M, additional, Landais, P, additional, Lesavre, P, additional, Lockwood, C M, additional, Luqmani, R, additional, Mirapeix, E, additional, Pettersson, E, additional, Pusey, C, additional, Savage, C O S, additional, Sinico, R A, additional, Specks, U, additional, Tzioufas, A G, additional, Westman, K W A, additional, Wiik, A, additional, and van der Woude, F, additional

Published
1995
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42. Expression of glomerular extracellular matrix components in human diabetic nephropathy: decrease of heparan sulphate in the glomerular basement membrane RID=""ID="" Abbreviations: HS: Heparan sulphate; GBM: glomerular basement membrane; HSPG: heparan sulphate proteoglycan; NC: noncollagenous globular domain; IDDM, insulin-dependent diabetes mellitus; NIDDM, non-insulin-dependent diabetes mellitus

Author

Hermans, J., primary, Veerkamp, J. H., additional, Lemkes, H. H. P. J., additional, van der Woude, F. J., additional, Bruijn, J. A., additional, Assmann, K. J. M., additional, Tamsma, J. T., additional, van den Born, J., additional, Weening, J. J., additional, Berden, J. H. M., additional, Wieslander, J., additional, and Schrama, E., additional

Published
1994
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47. Atorvastatin interferes with activation of human CD4+ T cells via inhibition of small guanosine triphosphatase (GTPase) activity and caspase-independent apoptosis.

Author

Brinkkoetter, P.-T., Gottmann, U., Schulte, J., van der Woude, F. J., Braun, C., and Yard, B. A.

Subjects
CD4 antigen, CD antigens, T cells, LYMPHOCYTES, GUANOSINE triphosphatase, CLINICAL immunology, EXPERIMENTAL immunology
Abstract

Although a beneficial effect of hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, i.e. statins, on cell-mediated immunity has been suggested in vivo and in vitro, little is known about the molecular and biochemical events by which statins inhibit T cell proliferation. To address this question, we investigated the effects of atorvastatin (AT) on intracellular cytokine production, T cell activation markers, cell cycle progression and apoptosis in human CD4+ T cells. AT did not influence intracellular cytokine production after short-term stimulation of whole blood with phorbol myristate acetate (PMA)/ionomycin or superantigen (SEB). In contrast, AT influenced CD45RA to RO switching dose-dependently, as well as CD25 expression, and caused cell cycle arrest in the G1 phase after long-term T cell stimulation. This occurred in conjunction with a reduced expression of cyclin-dependent kinases 2 and 4 and p21wav1/cip1 and was paralleled by an increased protein expression of p27kip1. In addition to G1 arrest, increased apoptosis was observed in AT-treated cells. In line with this, the expression of Bcl-xl and pBad were decreased by AT. Apoptosis was independent of caspases 3 and 9 activation. The inhibitory effect of AT on T cell proliferation could be overcome by addition of mevalonic acid or geranylgeranyl pyrophosphate, but not by farnesyl pyrophosphate or squalen, suggesting reduced protein prenylation. Activation of Rho, Rac and Ras were strongly reduced in AT-treated T cells, suggesting that impaired geranylation of these molecules might underlie the inhibitory effect of AT on T cell proliferation. [ABSTRACT FROM AUTHOR]

Published
2006
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48. Reticuloendothelial Fc receptor function in SLE patients. II. Associations with humoral immune response parameters in vivo and in vitro.

Author

van der Woude, F. J., Kallenberg, C. O. M., Limburg, P. C., Beekhuis, H., Ouwehand, W., van der Giessen, M., Hoedemaeker, J., van der Hem, G. K., and The, T. H.

Subjects
*SYSTEMIC lupus erythematosus, *IMMUNE response, *IMMUNOGLOBULIN G, *B cells, *ANTIGENS, *CELL receptors, *PATIENTS
Abstract

We studied the relationship between reticuloendothelial Fc receptor function and some parameters of the humoral immune response in vivo and in vitro in 18 SLE patients. Fc receptor-mediated immune clearance correlated remarkably well with (a) a decrease of antigen specific IgG after immunization with a primary test antigen (α-Helix pomatia haemocyanin) (P < 0.01) and (b) the spontaneous IgG release in vitro of B cells obtained from peripheral blood (P < 0.01). These two parameters were significantly interrelated. Reticuloendothelial Fc receptor function was not related to serum IgG levels. The study provides evidence for an association between polyclonat B cell activation and Fe receptor-mediated immune clearance in SLE patients. The possible nature of this association is discussed. [ABSTRACT FROM AUTHOR]

Published
1984

49. Reticuloendothelial Fc receptor function in SLE patients. I. Primary HLA linked defect or acquired dysfunction secondary to disease activity?

Author

van der Woude, F. J., van der Giessen, M., Kallenberg, C. G. M., Ouwehand, W., Beekhuis, H., Beelen, J. M., van Son, W. J., Hoedemaeker, J., van der Hem, G. K., and The, T. H.

Subjects
*SYSTEMIC lupus erythematosus, *IMMUNE response, *ENZYME-linked immunosorbent assay, *GENETICS, *AUTOIMMUNE diseases, *PHENOTYPES, *PATIENTS
Abstract

Reticuloendothelial system (RES) Fc receptor-mediated immune clearance was measured in 18 patients with systemic lupus erythematosus (SLE). Only two patients, with major disease activity, had a prolonged T½ of the blood disappearance curve of injected IgG coated red cells in comparison to 22 healthy controls. Circulating immune complexes (CIC) were studied with three methods: PEG precipitation, Clq-ELISA and the indirect granulocyte phagocytosis test (IGFT). The T½ of the blood disappearance curve related significantly to the IGFT (r=0.55, P <0.05) and not to the PEG and Clq-ELISA test. Although HLA-DR3 phenotype frequency was significantly increased in our SLE population (P < 0.05), it was not related to Fc receptor function. Similarly, HLA-DR2 phenotype was not related to RES Fc receptor function. These data do not support the concept that a genetic HLA linked defect in reticuloendothelial Fc receptor function is a primary cause of SLE, predisposing the inflicted individual to immune complex deposition. However, Fc receptor-mediated immune clearance seems to be related to disease activity itself and to levels of CIC. [ABSTRACT FROM AUTHOR]

Published
1984

50. The current status of neutrophil cytoplasmic antibodies.

Author

Van Der Woude, F. J., Daha, M. R., and Van Es, L. A.

Subjects
*NEUTROPHILS, *GLOMERULONEPHRITIS, *IMMUNOGLOBULINS, *PATHOGENIC microorganisms, *VASCULITIS, *T cells
Abstract

Several studies in the past 10 years have demonstrated the occurrence of autoantibodies against cytoplasmic constituents in patients with vasculitis and glomerulonephritis. In this review the nomenclature of these antibodies is discussed and assays and clinical associations are summarized. Although the antigens involved are not completely identified, antibodies and T cells reactive with myeloid lysozomal enzymes may both play a significant role in pathogenesis. [ABSTRACT FROM AUTHOR]

Published
1989

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