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2. Analysis of Single Nucleotide Polymorphisms in Sarcoidosis and Chronic Beryllium Disease

Author

Frye, B., Gaede, K. I., Saltini, C., Rossman, M. D., Monos, D. S., Rosenman, K. D., Schuler, C. R., Weston, A., Wegner, R., Noth, R., Zissel, G., Schreiber, S., Nothnagel, M., Muller-Quernheim, J., Frye, B., Gaede, K. I., Saltini, C., Rossman, M. D., Monos, D. S., Rosenman, K. D., Schuler, C. R., Weston, A., Wegner, R., Noth, R., Zissel, G., Schreiber, S., Nothnagel, M., and Muller-Quernheim, J.

Published
2020

4. Hot of the breath: Mortality as a primary end-point in IPF treatment trials: the best is the enemy of the good

Author

Wells, Athol U, Behr, Juergen, Costabel, Ulrich, Cottin, Vincent, Poletti, Venerino, Richeldi, Luca, Albera, C, Ancochea, J, Antoniou, KM, Bonella, F, Bonniaud, P, Bouros, D, Bresser, P, Cordier, JF, Crestani, B, Domagala-Kulawik, J, Drent, M, Egan, JJ, Geiser, T, Grunewald, J, Grutters, J, Gudmundsson, G, Guenther, A, Harari, S, Harrison, NK, Hirani, N, Hodgson, U, Kahler, CM, Keane, MP, Kiter, G, Kneussl, M, Maher, TM, Mogulkoc, N, Muller-Quernheim, J, Neurohr, C, Nunes, H, Parfrey, H, Peros-Golubicic, T, Polychronopoulos, V, Prevot, G, Renzoni, ER, Robalo Cordeiro, C, Saltini, C, Skold, M, Spagnolo, P, Thomeer, M, Tomasseti, S, Valeyre, D, Vancheri, C, Wallaert, B, Wuyts, W, and Xaubet, A

Published
2012
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5. Analysis of Single Nucleotide Polymorphisms in Sarcoidosis and Chronic Beryllium Disease

Author

Frye, B., primary, Gaede, K.I., additional, Saltini, C., additional, Rossman, M.D., additional, Monos, D.S., additional, Rosenman, K.D., additional, Schuler, C.R., additional, Weston, A., additional, Wegner, R., additional, Noth, R., additional, Zissel, G., additional, Schreiber, S., additional, Nothnagel, M., additional, and Muller-Quernheim, J., additional

Published
2020
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13. The AIPO-SIMeR document on idiopathic pulmonary fibrosis

Author

Tomassetti, S, Albera, C, Aronne, D, Confalonieri, M, Harari, S, Luisetti, M, Poletti, V, Richeldi, L, Rottoli, P, Saltini, C, Vancheri, C, Vitulo, P, Pesci, A, Tomassetti S., Albera C., Aronne D., Confalonieri M., Harari S., Luisetti M., Poletti V., Richeldi L., Rottoli P., Saltini C., Vancheri C., Vitulo P., Pesci A., Tomassetti, S, Albera, C, Aronne, D, Confalonieri, M, Harari, S, Luisetti, M, Poletti, V, Richeldi, L, Rottoli, P, Saltini, C, Vancheri, C, Vitulo, P, Pesci, A, Tomassetti S., Albera C., Aronne D., Confalonieri M., Harari S., Luisetti M., Poletti V., Richeldi L., Rottoli P., Saltini C., Vancheri C., Vitulo P., and Pesci A.

Published
2015

15. The AIPO-SIMeR document on idiopathic pulmonary fibrosis

Author

Tomassetti S., Albera C., Aronne D., Confalonieri M., Harari S., Luisetti M., Poletti V., Richeldi L., Rottoli P., Saltini C., Vancheri C., Vitulo P., Pesci A., Tomassetti, S, Albera, C, Aronne, D, Confalonieri, M, Harari, S, Luisetti, M, Poletti, V, Richeldi, L, Rottoli, P, Saltini, C, Vancheri, C, Vitulo, P, and Pesci, A

Subjects
respiratory tract disease
Published
2015

17. HFE gene variants and iron induced O2 radical generation in idiopathic pulmonary fibrosis

Author

Sangiuolo F. (1), Puxeddu E. (1), Pezzuto G. (2), Cavalli F. (3), Longo G. (1), Comandini A. (2), Di Pierro D. (4), Pallante M. (1), Sergiacomi G. (5), Simonetti G. (5), Zompatori M. (6), Orlandi A. (7), Magrini A. (1), Amicosante M. (1), Mariani F. (8), Losi M. (2), Fraboni D. (9), Bisetti A. (10), and Saltini C. (1, 2, 3)

Subjects
IPF, nutritional and metabolic diseases, iron homeostasis, HFE, respiratory system, respiratory tract diseases
Abstract

In idiopathic pulmonary fibrosis (IPF), lung accumulation of excessive extracellular iron and macrophage haemosiderin may suggest disordered iron homeostasis leading to recurring microscopic injury and fibrosing damage. The current study population comprised 89 consistent IPF patients and 107 controls. 54 patients and 11 controls underwent bronchoalveolar lavage (BAL). Haemosiderin was assessed by Perls' stain, BAL fluid malondialdehyde (MDA) by high-performance liquid chromatography, BAL cell iron-dependent oxygen radical generation by fluorimetry and the frequency of hereditary haemochromatosis HFE gene variants by reverse dot blot hybridisation. Macrophage haemosiderin, BAL fluid MDA and BAL cell unstimulated iron-dependent oxygen radical generation were all significantly increased above controls (p

Published
2015
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18. Monitoring the quality of laboratories and the prevalence of resistance to antituberculosis drugs: Italy, 1998–2000

Author

Migliori, G. B., Fattorini, L., Vaccarino, R., Besozzi, G., Saltini, C., Orefici, G., Iona, E., Matteelli, A., Fiorentini, F., Codecasa, L. R., Casali, Lucio, Cassone, A., De Santis, A., Giorgio, V., Vinciguerra, P., Angarano, G., Petrozzi, L., Costa, D., Gozzellino, F., Perboni, A., Marchetti, D., Pascali, A., Falcone, F., Mariano, V., Rizza, F., Pretto, P., Turano, A., Carosi, G. P., Farris, A. G., Ligia, G. P., Orani, G., Farris, B., Foschi, C., Trucco, G., Aiolfi, S., Ceruti, T., Parpanesi, M., Calabro, S., Felisatti, G., Tortoli, E., Nutini, S., Montini, G., D'Ambrosio, V., Ceraminiello, A., Bernorio, S., Buono, L., Montesano, P., Vinci, E., Sabato, E., Gamba, S., Crepaldi, P., Magliano, E., Penati, V., Vaccarino, P., Astolfi, A., Bertoli, G., Rupianesi, F., Losi, M., Richeldi, L., Ferrara, Giovanni, Minuccio, E., Napolitano, G., Molinari, G. L., Saini, L., Garzone, A., Vertuccio, C., Marcias, S., Menozzi, M., Marone, P., Peona, V., Nascimbene, C., Pasi, A., Cascina, A., Monaco, A., Penza, O., Pasticci, Maria Bruna, Bistoni, F., Sposini, T., Colorizio, V., Confalonieri, M., Bottrighi, P., Macor, G., Moretti, G., Fatigante, R., Barbaro, A., Agati, G., Zaccara, F., Viola, S., Le Donne, R., Farinelli, G., Mancini, D., Ermeti, M., Longi, R., Tronci, M., Bisetti, A., Altieri, A., and Fadda, G.

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, Tuberculosis, Prevalence of resistance, Drug Resistance, Antitubercular Agents, Drug resistance, Proficiency testing, Drug, Immigrant, Susceptibility testing, Emigration and Immigration, Humans, Italy, Laboratories, Prevalence, Drug Resistance, Multiple, Bacterial, Tuberculosis, Multidrug-Resistant, Internal medicine, medicine, Ethambutol, business.industry, Public health, Isoniazid, Bacterial, Multidrug-Resistant, medicine.disease, Surgery, Streptomycin, business, Multiple, Rifampicin, medicine.drug
Abstract

In 1998 a network of 20 regional tuberculosis (TB) laboratories (the Italian Multicentre Study on Resistance to Antituberculosis drugs (SMIRA) network) was established in Italy to implement proficiency testing and to monitor the prevalence of drug resistance nationwide. The network managed 30% of all TB cases reported in Italy each year. The aim of the present report is to describe: 1) the accuracy of drug-susceptibility testing in the network; 2) the prevalence of drug resistance for the period 1998-2000. Data were collected from the network laboratories. Sensitivity to streptomycin and ethambutol increased from the first survey (1998-1999) to the second survey (2000) from 87.7 to 91.9%. Specificity, predictive values for resistance and susceptibility, efficiency and reproducibility were consistent in both surveys. In previously untreated cases, the prevalence of multidrug-resistance was the same in both surveys (1.2%), while a slight decrease from the first to the second survey was observed for monoresistance to rifampicin (from 0.8 to 0.4%) and isoniazid (from 2.9 to 2%). The significant association found between isoniazid resistance and immigration is a useful indicator for both clinicians managing individual tuberculosis cases and public health services planning control strategies.

Published
2003
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19. Design of immunogenic peptides from Mycobacterium tuberculosis genes expressed during macrophage infection

Author

Seghrouchni F, Contini S, Markova R, Drenska R, Sadki K, Baassi L, Todorova Y, Terzieva V, Cappelli G, Altieri AM, Alma MG, Benjouad A, Mariani F, Petrunov B, Colizzi V, El Aouad R, Saltini C, Amicosante M., BOCCHINO, MARIALUISA, Seghrouchni, F, Contini, S, Markova, R, Drenska, R, Sadki, K, Baassi, L, Todorova, Y, Terzieva, V, Bocchino, Marialuisa, Cappelli, G, Altieri, Am, Alma, Mg, Benjouad, A, Mariani, F, Petrunov, B, Colizzi, V, El Aouad, R, Saltini, C, and Amicosante, M.

Published
2009

20. An official American Thoracic Society statement: diagnosis and management of beryllium sensitivity and chronic beryllium disease

Author

Balmes, J, Abraham, J, Dweik, R, Fireman, E, Fontenot, A, Maier, L, Muller Quernheim, J, Ostiguy, G, Pepper, L, Saltini, C, Schuler, C, Takaro, T, Wambach, P, ATS Ad Hoc Committee on Beryllium Sensitivity, and Chronic Beryllium Disease

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, Pathology, Medical surveillance, Berylliosis, Inflammatory response, Beryllium exposure, Settore MED/10 - Malattie dell'Apparato Respiratorio, chemistry.chemical_element, Critical Care and Intensive Care Medicine, Lymphocyte proliferation test, Internal medicine, Occupational Exposure, medicine, Hypersensitivity, Humans, business.industry, medicine.disease, digestive system diseases, respiratory tract diseases, surgical procedures, operative, chemistry, Lung disease, Chronic Disease, Beryllium, business, Beryllium Disease
Abstract

Beryllium continues to have a wide range of industrial applications. Exposure to beryllium can lead to sensitization (BeS) and chronic beryllium disease (CBD).The purpose of this statement is to increase awareness and knowledge about beryllium exposure, BeS, and CBD.Evidence was identified by a search of MEDLINE. The committee then summarized the evidence, drew conclusions, and described their approach to diagnosis and management.The beryllium lymphocyte proliferation test is the cornerstone of both medical surveillance and the diagnosis of BeS and CBD. A confirmed abnormal beryllium lymphocyte proliferation test without evidence of lung disease is diagnostic of BeS. BeS with evidence of a granulomatous inflammatory response in the lung is diagnostic of CBD. The determinants of progression from BeS to CBD are uncertain, but higher exposures and the presence of a genetic variant in the HLA-DP β chain appear to increase the risk. Periodic evaluation of affected individuals can detect disease progression (from BeS to CBD, or from mild CBD to more severe CBD). Corticosteroid therapy is typically administered when a patient with CBD exhibits evidence of significant lung function abnormality or decline.Medical surveillance in workplaces that use beryllium-containing materials can identify individuals with BeS and at-risk groups of workers, which can help prioritize efforts to reduce inhalational and dermal exposures.

Published
2014

22. Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis

Author

Luca, Richeldi, du Bois, Roland M., Ganesh, Raghu, Arata, Azuma, Brown, Kevin K., Ulrich, Costabel, Vincent, Cottin, Flaherty, Kevin R., Hansell, David M., Yoshikazu, Inoue, Dong Soon Kim, Martin, Kolb, Nicholson, Andrew G., Noble, Paul W., Moisés, Selman, Hiroyuki, Taniguchi, Michèle, Brun, Florence Le Maulf, Mannaïg, Girard, Susanne, Stowasser, Rozsa Schlenker Herceg, Bernd, Disse, Collard, Harold R., Corte, T, Davies, H, Glaspole, I, Mulder, J, Veitch, E, De Vuyst, P, Liistro, G, Sibille, Y, Vincken, W, Wuyts, W, Fell, C, Hernandez, P, Kolb, M, Undurraga, A, Bai, C, Chen, P, Gao, Z, Kang, J, Li, H, Li, Z, Wan, H, Wang, H, Wen, F, Xiao, Q, Xu, Z, Zhang, W, Zheng, X, Zhu, H, Pauk, N, Reiterer, P, Vasakova, M, Hodgson, U, Bourdin, A, Cadranel, J, Camus, P, Chanez, P, Cottin, V, Crestani, B, Israel Biet, D, Jouneau, S, Lebargy, F, Marquette, C, Prévot, G, Valeyre, D, Wallaert, B, Bonnet, R, Costabel, U, Gläser, S, Grohé, C, Guenther, A, Hammerl, P, Höffken, G, Karagiannidis, C, Kirschner, J, Kirsten, A, Korn, S, Kreuter, M, Müller Quernheim, J, Neurohr, C, Pfeifer, M, Schönfeld, N, Wiewrodt, R, Antoniou, K, Daniil, Z, Diamantea, F, Koulouris, N, Mathioudakis, G, Ghosal, A, Kadappa Shivappa, S, Kawedia, M, Khatavkar, P, Kumar, A, Mehta, P, Singh, V, Srikanth, K, Thakker, H, Udwadia, Z, Egan, J, Fink, G, Kramer, M, Yigla, M, Agostini, Carlo, De Benedetto, F, Harari, S, Luppi, F, Paggiaro, P, Tavanti, L, Pesci, A, Poletti, V, Rottoli, P, Saltini, C, Sanduzzi Zamparelli, A, Vancheri, C, Bando, M, Hasegawa, Y, Hashimoto, K, Homma, S, Inase, N, Inoue, Y, Arai, T, Izumi, S, Kawamura, T, Kishi, K, Kondo, Y, Kuwano, K, Miura, Y, Nishioka, Y, Nishiyama, O, Ogura, T, Ohkouchi, S, Saito, T, Setoguchi, Y, Shindoh, J, Taguchi, Y, Tanakadate, M, Tomii, K, Sugita, Y, Yamaguchi, T, Yoshimori, K, Jeong, S, Kim, D, Kim, Y, Park, C, Song, J, Uh, S, Selman, M, Bresser, P, Grutters, J, Wijsenbeek, M, Arrobas, A, Cardoso, J, Costa, R, Morais, A, Neves, S, Serrado, M, Ilkovick, M, Vizel, A, Alfageme Michavila, I, Ancochea, J, Castillo Villegas, D, Molina Molina, M, Morell, F, Xaubet, A, Aktogu Ozkan, S, Kayacan, O, Ongen, G, Mogulkoc, N, Tuncay, E, Beirne, P, Bettinson, H, Burge, P, Dempsey, O, Maher, T, Millar, A, Spencer, L, Thickett, D, Alvarez, J, Andrews, C, Bajwa, O, Baker, A, Baughman, R, Belperio, J, Bradley, J, Collard, H, Cordova, F, Daniels, C, de Andrade, J, Dushay, K, Enelow, R, Ettinger, N, Gibson, K, Gotfried, M, Hajari Case, A, Hotchkin, D, Huggins, J, Kaye, M, Kershaw, C, Kureishy, S, Lancaster, L, Lederer, D, Mageto, Y, Masson, J, Meyer, K, Mohabir, P, Morrison, L, Nathan, S, Noth, I, Oelberg, D, Rahaghi, F, Riley, D, Rizzo, A, Rossman, M, Ruzi, J, Sachs, P, Schaumberg, T, Scholand, M, Schroeder, C, Seifer, F, Shea, J, Sinkowitz, D, Tabak, J, Taylor, J, Thompson, J, Thurm, C, Tita, J, Wencel, M, Westerman, J, Lasky, J, Demedts, M, Casteels, M, Loddenkemper, R, Michaelis, J, Roman, J, Tino, G, Luisetti, M., and Clinical sciences

Subjects
Male, medicine.medical_specialty, Vital capacity, Indoles, Exacerbation, Aged, Disease Progression, Double-Blind Method, Enzyme Inhibitors, Female, Humans, Idiopathic Pulmonary Fibrosis, Middle Aged, Protein Kinase Inhibitors, Protein-Tyrosine Kinases, Quality of Life, Treatment Outcome, Vital Capacity, Settore MED/10 - Malattie dell'Apparato Respiratorio, Medizin, Placebo, Gastroenterology, FEV1/FVC ratio, Idiopathic pulmonary fibrosis, chemistry.chemical_compound, Internal medicine, medicine, business.industry, Medicine (all), Hazard ratio, General Medicine, Pirfenidone, medicine.disease, Surgery, chemistry, Nintedanib, business, medicine.drug
Abstract

Background Nintedanib (formerly known as BIBF 1120) is an intracellular inhibitor that targets multiple tyrosine kinases. A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. Methods We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis. The primary end point was the annual rate of decline in forced vital capacity (FVC). Key secondary end points were the time to the first acute exacerbation and the change from baseline in the total score on the St. George’s Respiratory Questionnaire, both assessed over a 52-week period. Results A total of 1066 patients were randomly assigned in a 3:2 ratio to receive nintedanib or placebo. The adjusted annual rate of change in FVC was −114.7 ml with nintedanib versus −239.9 ml with placebo (difference, 125.3 ml; 95% confidence interval [CI], 77.7 to 172.8; P

Published
2014

24. Cost determinants of tuberculosis management in a low-prevalence country

Author

Bocchino, M., Greco, S., Rosati, Y., Mattioli, G., Marruchella, A., Mori, P., Bibbolino, C., Enrico Girardi, Squarcione, S., Saltini, C., Bocchino, Marialuisa, Greco, S, Rosati, Y, Mattioli, G, Marruchella, A, De Mori, P, Bibbolino, C, Girardi, E, Squarcione, S, and Saltini, C.

Subjects
Adult, Male, demography, Tuberculosi, Settore MED/10 - Malattie dell'Apparato Respiratorio, drug cost, review, Antitubercular Agents, Case outcome, Costs, Hospital care, Tuberculosis, medical record, sputum analysis, Antitubercular Agent, Outcome Assessment (Health Care), multidrug resistance, Retrospective Studie, drug tolerance, Prevalence, Humans, thorax radiography, Retrospective Studies, Aged, fever, Human immunodeficiency virus, health care cost, Health Care Costs, tuberculostatic agent, adult, female, hospital cost, hospitalization, human, major clinical study, male, priority journal, prognosis, tuberculosis, Female, Hospitalization, Italy, Middle Aged, Human
Abstract

Division of respiratory medicine in a specialised infectious disease hospital in Rome, Italy.

Published
2006

25. Efficacy of pirfenidone for idiopathic pulmonary fibrosis: An Italian real life study

Author

Harari, S, Caminati, A, Albera, C, Vancheri, C, Poletti, V, Pesci, A, Luppi, F, Saltini, C, Agostini, C, Bargagli, E, Sebastiani, A, Sanduzzi, A, Giunta, V, Della Porta, R, Bandelli, G, Puglisi, S, Tomassetti, S, Biffi, A, Cerri, S, Mari, A, Cinetto, F, Tirelli, F, Farinelli, G, Bocchino, M, Specchia, C, Confalonieri, M, PESCI, ALBERTO, BIFFI, ALICE, Confalonieri, M., Harari, S, Caminati, A, Albera, C, Vancheri, C, Poletti, V, Pesci, A, Luppi, F, Saltini, C, Agostini, C, Bargagli, E, Sebastiani, A, Sanduzzi, A, Giunta, V, Della Porta, R, Bandelli, G, Puglisi, S, Tomassetti, S, Biffi, A, Cerri, S, Mari, A, Cinetto, F, Tirelli, F, Farinelli, G, Bocchino, M, Specchia, C, Confalonieri, M, PESCI, ALBERTO, BIFFI, ALICE, and Confalonieri, M.

Abstract

Background In this retrospective Italian study, which involved all major national interstitial lung diseases centers, we evaluated the effect of pirfenidone on disease progression in patients with IPF. Methods We retrospectively studied 128 patients diagnosed with mild, moderate or severe IPF, and the decline in lung function monitored during the one-year treatment with pirfenidone was compared with the decline measured during the one-year pre-treatment period. Results At baseline (first pirfenidone prescription), the mean percentage forced vital capacity (FVC) was 75% (35-143%) of predicted, and the mean percentage diffuse lung capacity (DLCO) was 47% (17-120%) of predicted. Forty-eight patients (37.5%) had mild disease (GAP index stage I), 64 patients (50%) had moderate IPF (stage II), and 8 patients (6.3%) had severe disease (stage III). In the whole population, pirfenidone attenuated the decline in FVC (p = 0.065), but did not influence the decline in DLCO (p = 0.355) in comparison to the pre-treatment period. Stratification of patients into mild and severe disease groups based on %FVC level at baseline (>75% and ≤75%) revealed that attenuation of decline in FVC (p = 0.002) was more pronounced in second group of patients. Stratification of patients according to GAP index at baseline (stage I vs. II/III) also revealed that attenuation of decline in lung function was more pronounced in patients with more severe disease. Conclusions In this national experience, pirfenidone reduced the rate of annual FVC decline (p = 0.065). Since pirfenidone provided significant treatment benefit for patients with moderate-severe disease, our results suggest that the drug may also be effective in patients with more advanced disease., Background In this retrospective Italian study, which involved all major national interstitial lung diseases centers, we evaluated the effect of pirfenidone on disease progression in patients with IPF. Methods We retrospectively studied 128 patients diagnosed with mild, moderate or severe IPF, and the decline in lung function monitored during the one-year treatment with pirfenidone was compared with the decline measured during the one-year pre-treatment period. Results At baseline (first pirfenidone prescription), the mean percentage forced vital capacity (FVC) was 75% (35-143%) of predicted, and the mean percentage diffuse lung capacity (DLCO) was 47% (17-120%) of predicted. Forty-eight patients (37.5%) had mild disease (GAP index stage I), 64 patients (50%) had moderate IPF (stage II), and 8 patients (6.3%) had severe disease (stage III). In the whole population, pirfenidone attenuated the decline in FVC (p = 0.065), but did not influence the decline in DLCO (p = 0.355) in comparison to the pre-treatment period. Stratification of patients into mild and severe disease groups based on %FVC level at baseline (>75% and ≤75%) revealed that attenuation of decline in FVC (p = 0.002) was more pronounced in second group of patients. Stratification of patients according to GAP index at baseline (stage I vs. II/III) also revealed that attenuation of decline in lung function was more pronounced in patients with more severe disease. Conclusions In this national experience, pirfenidone reduced the rate of annual FVC decline (p = 0.065). Since pirfenidone provided significant treatment benefit for patients with moderate-severe disease, our results suggest that the drug may also be effective in patients with more advanced disease.

Published
2015

26. Development of a post-exposure paediatric anti HIV-AIDS vaccine based on the combined synthetic/recombinant HIV peptides and BCG for boosting innate and acquired immunity. North-South transfer in Biotechnology of Tuberculosis and AIDS. University of Rome 'Tor Vergata'. UNESCO Interdisciplinary Chair in Biotechnology. Vittorio Colizzi, Luc Montagnier, 2004

Author

AMICOSANTE M, ANDREONI M, ANSELMI A, CASTELLI G, CIARAMELLA A, COLIZZI V, D'ARRIGO R, ERCOLI L, FRAZIANO M, GARG SK, MARCHIONE P, MATTEI M, PALMIERI G, PERNO F, SALTINI C, SANTUCCI M, SUMERSKA T, ROSSI P, VENDETTI S, CAPPELLI G, CAVONE A, GRASSI M, MARIANI F, MIGNONE M, PERRETTA G, CASETTI R, HOREJSH D, MARTINI F, MONTESANO C, GIOIA C, POCCIA F, PUCILLO L, SACCHI A, DI SANO C, CAIRO C, GALLO R, REDFIELD R, PAUZA D, CHENAL H, MONTAGNIER L, OLIVIER R, TONI T, MAULE L, SIMPORE J., DI GIORGIO, Giuseppa, MARTINO, Andrea, BONANNO, Cesira, DIELI, Francesco, SALERNO, Alfredo, COLIZZI V., MONTAGNIER L., AMICOSANTE M, ANDREONI M, ANSELMI A, CASTELLI G, CIARAMELLA A, COLIZZI V, D'ARRIGO R, DI GIORGIO G, ERCOLI L, FRAZIANO M, GARG SK, MARCHIONE P, MATTEI M, PALMIERI G, PERNO F, SALTINI C, SANTUCCI M, SUMERSKA T, ROSSI P, VENDETTI S, CAPPELLI G, CAVONE A, GRASSI M, MARIANI F, MIGNONE M, PERRETTA G, CASETTI R, HOREJSH D, MARTINO A, MARTINI F, MONTESANO C, GIOIA C, POCCIA F, PUCILLO L, SACCHI A, BONANNO CT, DIELI F, DI SANO C, SALERNO A, CAIRO C, GALLO R, REDFIELD R, PAUZA D, CHENAL H, MONTAGNIER L, OLIVIER R, TONI T, MAULE L, and SIMPORE J

Published
2004

28. Treatment of idiopathic pulmonary fibrosis with ambrisentan: a parallel, randomized trial

Author

Raghu, G, Behr, J, Brown, K, Egan, J, Kawut, S, Flaherty, K, Martinez, F, Nathan, S, Wells, A, Collard, H, Costabel, U, Richeldi, L, de Andrade, J, Khalil, N, Morrison, L, Lederer, D, Shao, L, Li, X, Pedersen, P, Montgomery, A, Chien, J, O'Riordan, T, Amin, D, Baker, A, Baratz, D, Baughman, R, Cagino, A, Chan, A, Chapman, J, Cordova, F, Edelman, J, Enelow, R, Ettinger, N, Glassberg, M, Golden, J, Ilowite, J, Kreider, M, Kureishy, S, Lancaster, L, Limper, A, Strek, M, Padilla, M, Fisher, M, Riley, D, Mohabir, P, Safdar, Z, Sahn, S, Schaumberg, T, Scholand, M, Smith, C, Sussman, R, Yung, G, Saggar, R, Geffen, D, Zibrak, J, Alvarez, J, Chan, K, Ruzi, J, Mcconnell, J, Mehta, J, Verghese, G, Talwar, A, Haddad, T, Sood, N, Goldberg, H, Sundar, K, Ziedalski, T, Gibson, K, Chan, C, Lien, D, Fell, C, Fox, G, Poirier, C, Provencher, S, Wilcox, P, Vilayi Weiler, Z, Kramer, M, Yigla, M, Baloira, A, Parakova, Z, Kra, H, Schwarz, Y, Martinez, C, Ben Dov, I, Kahler, C, Xaubet, A, Skrickova, J, Kolek, V, Parfrey, H, Echave Sustaeta, J, Wuyts, W, Geiser, T, Muller Quernheim, J, Whyte, M, Pfeifer, M, Grohe, C, Bourdin, A, Olschewski, H, Sibille, Y, Snizek, T, Vytiska, J, Pesek, M, Crestani, B, Wallaert, B, Chanez, P, Biet, D, Pompidou, G, Dromer, C, Gläser, S, Wagner, U, Witt, C, Herth, F, Hoeffken, G, Coswig, F, Breuer, R, Kerem, E, Adir, Y, Agostini, C, Cremona, G, Vitulo, P, Poletti, V, Rottoli, P, Rybacki, C, Piotrowski, W, Morera, J, Hattotuwa, K, Warburton, C, Corris, P, Leonard, C, Booth, H, Britton, M, Marchand Adam, S, Marquette, C, Tamm, M, Lazor, R, Chalmers, G, Hirani, N, De Vuyst, P, Saltini, C, Harari, S, Maher, T, Campos, F, Ramirez, A, Wehbe, L, Altieri, H, Fuchigami, A, Salinas, C, Mattos, W, Posadas, R, Fiss, E, Diaz Castanon, J, Munoz, S, Ramirez, L, Chercoff, J, Fritscher, C, Cardoso, A, Moreira, M, Steidle, L, Arakaki, J, Florenzano, M, Leon, L, Bernardini, S, Gilberto, A, Duque, C, Awad, C, Severiche, D, Lucro, D, Grimaldos, F, Rubin, A, Barrera, C, Ore, D, Heredia, C, Mazzei, J, Matiz, C, Glanville, A, Hopkins, P, Smallwood, D, Veitch, E, Musk, M, Glaspole, I, Wood Baker, R, Veale, A, and Costabel, Ulrich (Beitragende*r)

Subjects
Adult, Male, medicine.medical_specialty, Ambrisentan, Endothelin A Receptor Antagonists, Settore MED/10 - Malattie dell'Apparato Respiratorio, Medizin, Placebo, Idiopathic pulmonary fibrosis, Aged, Aged, 80 and over, Disease Progression, Double-Blind Method, Female, Humans, Idiopathic Pulmonary Fibrosis, Lung, Middle Aged, Phenylpropionates, Prospective Studies, Pyridazines, Treatment Outcome, Internal medicine, 80 and over, Internal Medicine, medicine, Clinical endpoint, Prospective cohort study, business.industry, Hazard ratio, General Medicine, medicine.disease, Interim analysis, Pulmonary hypertension, Surgery, business, medicine.drug
Abstract

BACKGROUND Idiopathic pulmonary fibrosis (IPF) is characterized by formation and proliferation of fibroblast foci. Endothelin-1 induces lung fibroblast proliferation and contractile activity via the endothelin A (ETA) receptor. OBJECTIVE To determine whether ambrisentan, an ETA receptor-selective antagonist, reduces the rate of IPF progression. DESIGN Randomized, double-blind, placebo-controlled, event-driven trial. (ClinicalTrials.gov: NCT00768300). SETTING Academic and private hospitals. PARTICIPANTS Patients with IPF aged 40 to 80 years with minimal or no honeycombing on high-resolution computed tomography scans. INTERVENTION Ambrisentan, 10 mg/d, or placebo. MEASUREMENTS Time to disease progression, defined as death, respiratory hospitalization, or a categorical decrease in lung function. RESULTS The study was terminated after enrollment of 492 patients (75% of intended enrollment; mean duration of exposure to study medication, 34.7 weeks) because an interim analysis indicated a low likelihood of showing efficacy for the end point by the scheduled end of the study. Ambrisentan-treated patients were more likely to meet the prespecified criteria for disease progression (90 [27.4%] vs. 28 [17.2%] patients; P = 0.010; hazard ratio, 1.74 [95% CI, 1.14 to 2.66]). Lung function decline was seen in 55 (16.7%) ambrisentan-treated patients and 19 (11.7%) placebo-treated patients (P = 0.109). Respiratory hospitalizations were seen in 44 (13.4%) and 9 (5.5%) patients in the ambrisentan and placebo groups, respectively (P = 0.007). Twenty-six (7.9%) patients who received ambrisentan and 6 (3.7%) who received placebo died (P = 0.100). Thirty-two (10%) ambrisentan-treated patients and 16 (10%) placebo-treated patients had pulmonary hypertension at baseline, and analysis stratified by the presence of pulmonary hypertension revealed similar results for the primary end point. LIMITATION The study was terminated early. CONCLUSION Ambrisentan was not effective in treating IPF and may be associated with an increased risk for disease progression and respiratory hospitalizations. PRIMARY FUNDING SOURCE Gilead Sciences.

Published
2013

29. Treatment of Idiopathic Pulmonary Fibrosis With Ambrisentan

Author

Raghu, G, Behr, J, Brown, Kk, Egan, Jj, Kawut, Sm, Flaherty, Kr, Martinez, Fj, Nathan, Sd, Wells, Au, Collard, Hr, Costabel, U, Richeldi, L, de Andrade, J, Khalil, N, Morrison, Ld, Lederer, Dj, Shao, L, Li, X, Pedersen, Ps, Montgomery, Ab, Chien, Jw, O'Riordan, Tg, ARTEMIS IPF Investigators: Amin, D, Baker, A, Baratz, D, Baughman, R, Cagino, A, Chan, A, Chapman, J, Cordova, F, Edelman, J, Enelow, R, Ettinger, N, Glassberg, M, Golden, J, Ilowite, J, Kreider, M, Kureishy, S, Lancaster, L, Lederer, D, Limper, A, Morrison, L, Nathan, S, Strek, M, Padilla, M, Fisher, M, Riley, D, Mohabir, P, Safdar, Z, Sahn, S, Schaumberg, T, Scholand, Mb, Smith, C, Sussman, R, Yung, G, Saggar, R, Geffen, D, Zibrak, J, Alvarez, J, Chan, K, Ruzi, J, Mcconnell, J, Mehta, J, Verghese, G, Talwar, A, Haddad, T, Sood, N, Goldberg, H, Sundar, K, Ziedalski, T, Gibson, K, Chan, C, Lien, D, Fell, C, Fox, G, Poirier, C, Provencher, S, Wilcox, P, Vilayi Weiler, Z, Kramer, M, Yigla, M, Baloira, A, Parakova, Z, Kra, H, Schwarz, Y, Martinez, C, Ben Dov, I, Kahler, C, Xaubet, A, Skrickova, J, Kolek, V, Parfrey, H, Echave Sustaeta, J, Wuyts, W, Geiser, T, Muller Quernheim, J, Whyte, M, Pfeifer, M, Grohe, C, Bourdin, A, Olschewski, H, Sibille, Y, Snizek, T, Vytiska, J, Pesek, M, Crestani, B, Wallaert, B, Chanez, P, Biet, Di, Pompidou, G, Dromer, C, Gläser, S, Wagner, U, Witt, C, Herth, F, Hoeffken, G, Coswig, F, Egan, J, Breuer, R, Kerem, E, Adir, Y, Agostini, Carlo, Cremona, G, Vitulo, P, Poletti, V, Rottoli, P, Rybacki, C, Piotrowski, W, Morera, J, Hattotuwa, K, Warburton, C, Corris, P, Leonard, C, Booth, H, Britton, M, Marchand Adam, S, Marquette, Ch, Tamm, M, Lazor, R, Chalmers, Gw, Hirani, N, De Vuyst, P, Saltini, C, Harari, Sa, Maher, T, Campos, F, Ramirez, A, Wehbe, L, Altieri, H, Fuchigami, Am, Salinas, Cc, Mattos, W, Posadas, R, Fiss, E, Diaz Castanon, J, Munoz, S, Ramirez, Ln, Chercoff, J, Fritscher, Cc, Cardoso, A, Moreira, Ma, Steidle, L, Arakaki, J, Florenzano, M, Leon, Lp, Bernardini, Su, Gilberto, A, Duque, Ca, Awad, C, Severiche, D, Lucro, De, Grimaldos, Fb, Rubin, A, Barrera, Ci, Ore, Dj, Heredia, C, Mazzei, J, Matiz, C, Glanville, A, Hopkins, P, Smallwood, D, Veitch, E, Musk, M, Glaspole, I, Wood Baker, R, and Veale, A.

Published
2013

30. Macitentan for the treatment of idiopathic pulmonary fibrosis: the randomised controlled MUSIC trial

Author

Raghu, G, Million Rousseau, R, Morganti, A, Perchenet, L, Behr, J, Goh, N, Glanville, A, Musk, M, Hopkins, P, Lien, D, Chan, C, Rolf, J, Wilcox, P, Cox, P, Manganas, H, Cottin, V, Valeyre, D, Walleart, B, Andreas, S, Neurohr, C, Guenther, A, Schonfeld, N, Koch, A, Kramer, M, Breuer, R, Ben Dov, I, Fink, G, Schwarz, Y, Albera, C, Confalonieri, M, Saltini, C, Harari, S, Flezar, M, Greenblatt, M, Ras, G, Morell, F, Alvarez Sala, J, Xaubet, A, Sueiro, A, Linares, M, Sko, M, Kayacan, O, Mogulkoc, N, Chan, A, Chapman, J, Parambil, J, Ettinger, N, Meyer, K, Swigris, J, Yung, G, Antin Ozerkis, D, Mohabir, P, Wesselius, L, de Andrade, J, Cordova, F, Safdar, Z, Wencel, M, O'Connor, C, Nashan, B, Demets, D, Gray, A, Raghu, G, Million-Rousseau, R, Morganti, A, Perchenet, L, Behr, J, Goh, N, Glanville, A, Musk, M, Hopkins, P, Lien, Dc, Chan, C, Rolf, Jd, Wilcox, P, Cox, Pg, Manganas, H, Cottin, V, Valeyre, D, Wallear, B, Andreas, S, Neurohr, C, Guenther, A, Schönfeld, N, Koch, A, Kramer, M, Breuer, R, Ben-Dov, I, Fink, G, Schwarz, Y, Albera, C, Confalonieri, M, Et, Al, and Ege Üniversitesi

Subjects
Endothelin Receptor Antagonists, Male, Vital capacity, Settore MED/10 - Malattie dell'Apparato Respiratorio, Vital Capacity, Gastroenterology, Pulmonary function testing, law.invention, chemistry.chemical_compound, Idiopathic pulmonary fibrosis, Randomized controlled trial, Usual interstitial pneumonia, law, Forced Expiratory Volume, Prospective Studies, Aged, 80 and over, Sulfonamides, Alanine Transaminase, Middle Aged, ComputingMilieux_MANAGEMENTOFCOMPUTINGANDINFORMATIONSYSTEMS, Treatment Outcome, Liver, Female, InformationSystems_MISCELLANEOUS, Adult, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Placebo, Double-Blind Method, Internal medicine, medicine, Humans, controlled study, Aspartate Aminotransferases, Aged, Macitentan, idiopathic pulmonary fibrosis, macicentan, idiopathic pulmonary fibrosi, Endothelin receptor antagonist, business.industry, ComputerSystemsOrganization_COMPUTER-COMMUNICATIONNETWORKS, medicine.disease, Idiopathic Pulmonary Fibrosis, Surgery, ComputingMethodologies_PATTERNRECOGNITION, Dyspnea, Pyrimidines, chemistry, business
Abstract

PubMed ID: 23682110, Idiopathic pulmonary fibrosis is a progressive, fatal disease. This prospective, randomised, double-blind, multicentre, parallel-group, placebo-controlled phase II trial (NCT00903331) investigated the efficacy and safety of the endothelin receptor antagonist macitentan in idiopathic pulmonary fibrosis. Eligible subjects were adults with idiopathic pulmonary fibrosis of, Actelion Pharmaceuticals Ltd.

Published
2013

31. An official American Thoracic Society clinical practice guideline: the clinical utility of bronchoalveolar lavage cellular analysis in interstitial lung disease

Author

Meyer, K. C., Raghu, G., Baughman, R. P., Brown, K. K., Costabel, Ulrich, du Bois, R. M., Drent, M., Haslam, P. L., Kim, D. S., Nagai, S., Rottoli, P., Saltini, C., Selman, M., Strange, C., Wood, B., and American Thoracic Society Committee on BAL in Interstitial Lung Disease

Subjects
Pulmonary and Respiratory Medicine, Adult, Adult, Bronchoalveolar Lavage Fluid, cytology, Bronchoalveolar Lavage, methods/standards, Cell Count, methods/standards, Diagnosis, Differential, Flow Cytometry, methods/standards, Humans, Lung Diseases, Interstitial, diagnosis/radiography, Specimen Handling, methods/standards, Tomography, X-Ray Computed, medicine.medical_specialty, bronchoscopy, Settore MED/10 - Malattie dell'Apparato Respiratorio, MEDLINE, Medizin, Cell analysis, Cell Count, diagnosis/radiography, Critical Care and Intensive Care Medicine, Bronchoalveolar Lavage, Specimen Handling, Diagnosis, Differential, Bronchoscopy, Diagnosis, medicine, Humans, cell differential count, Intensive care medicine, Tomography, lung diseases, interstitial lung disease, medicine.diagnostic_test, business.industry, Interstitial lung disease, Guideline, respiratory system, medicine.disease, Flow Cytometry, respiratory tract diseases, Clinical Practice, Bronchoalveolar lavage, bronchoscopy, bronchoalveolar lavage, lung diseases, interstitial lung disease, cell differential count, Differential, cytology, methods/standards, Differential diagnosis, business, Lung Diseases, Interstitial, Tomography, X-Ray Computed, Bronchoalveolar Lavage Fluid
Abstract

The clinical utility of bronchoalveolar lavage fluid (BAL) cell analysis for the diagnosis and management of patients with interstitial lung disease (ILD) has been a subject of debate and controversy. The American Thoracic Society (ATS) sponsored a committee of international experts to examine all relevant literature on BAL in ILD and provide recommendations concerning the use of BAL in the diagnosis and management of patients with suspected ILD.To provide recommendations for (1) the performance and processing of BAL and (2) the interpretation of BAL nucleated immune cell patterns and other BAL characteristics in patients with suspected ILD.A pragmatic systematic review was performed to identify unique citations related to BAL in patients with ILD that were published between 1970 and 2006. The search was updated during the guideline development process to include published literature through March 2011. This is the evidence upon which the committee's conclusions and recommendations are based.Recommendations for the performance and processing of BAL, as well as the interpretation of BAL findings, were formulated by the committee.When used in conjunction with comprehensive clinical information and adequate thoracic imaging such as high-resolution computed tomography of the thorax, BAL cell patterns and other characteristics frequently provide useful information for the diagnostic evaluation of patients with suspected ILD.

Published
2012

32. Hot of the breath: mortality as a primary end-point in IPF treatment trials: the best is the enemy of the good

Author

Wells, Au, Behr, J, Costabel, U, Cottin, V, Poletti, V, Richeldi, L, Albera, C, Ancochea, J, Antoniou, Km, Bonella, F, Bonniaud, P, Bouros, D, Bresser, P, Cordier, Jf, Crestani, B, Domagala Kulawik, J, Drent, M, Egan, Jj, Geiser, T, Grunewald, J, Grutters, J, Gudmundsson, G, Guenther, A, Harai, S, Harrison, Nk, Hirani, N, Hodgson, U, Kahler, Cm, Keane, Mp, Kiter, G, Kneussl, M, Maher, Tm, Mogulkoc, N, Muller Quernheim, J, Neurohr, C, Nunes, H, Parfrey, H, Peros Golubicic, T, Polychronopoulos, V, Prevot, G, Renzoni, Er, Robalo Cordeiro, C, Saltini, C, Skold, M, Spagnolo, P, Thomeer, M, Tomasseti, S, Valeyre, D, Vancheri, Carlo, Wallaert, B, Wuyts, W, and Xaubet, A.

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, Pathology, Statement (logic), Endpoint Determination, Settore MED/10 - Malattie dell'Apparato Respiratorio, Alternative medicine, Food and drug administration, Clinical endpoint, medicine, Maxim, Humans, Clinical Trials, Clinical Trials as Topic, Clinical Trials, Phase III as Topic, Disease Progression, Idiopathic Pulmonary Fibrosis, Research Design, Treatment Outcome, Set (psychology), Idiopathic pulmonary fibrosis, end-point in clinical trials, business.industry, respiratory system, Adversary, humanities, respiratory tract diseases, Phase III as Topic, Family medicine, Form of the Good, business
Abstract

The problem of the selection of accurate primary end-points for treatment studies in idiopathic pulmonary fibrosis (IPF) has recently been aired in a controversial paper from the USA.1 The limitations of current end-points are discussed and the authors conclude that all-cause mortality and all-cause nonelective hospitalisation best meet clinically meaningful end-point criteria. Much of the article is well argued and there is no quarrel with the view that current primary end-points are flawed. We also agree that all-cause mortality would, indeed, be the most clinically meaningful primary end-point and, therefore, the preferred primary end-point, were it not impractical, as discussed below. However, readers of the statement should reflect on the wise maxim that ‘the best may be the enemy of the good’. The purpose of our document is to provide a perspective on all-cause mortality as a primary end-point, endorsed by 52 European clinicians Including the authors (with one abstention), exploring the implications of the statement by Raghu and colleagues. We believe strongly that the adoption of the views of these authors by licensing bodies—with, by implication, a statistically significant mortality benefit a pre-requisite for drug registration—would set back progress in the treatment of IPF by a decade or more. It should be acknowledged at the outset that the statement of Raghu and colleagues does not make explicit recommendations with regard to drug licensing. Indeed, the authors declare that it is not their aim to make such recommendations and their intentions in this regard should not be questioned. However, if the statement has, indeed, been widely ‘misread’, the reasons for this are clear enough. Representatives of the US Food and Drug Administration (FDA) were active participants in a forum in Bethesda, Maryland (July 2011) which gave rise to the document as a proceedings statement.1 It is widely known …

Published
2012

33. Surveillance of anti-tuberculosis drug resistance: Results of the 1998/1999 proficiency testing in Italy

Author

Migliori GB, Ambrosetti M, Fattorini L, Penati V, Vaccarino P, Besozzi G, Ortona L, Saltini C, Orefici G, Moro ML, Iona E, Cassone A, De Santis A, Giorgio V, Vinciguerra P, Angarano G, Petrozzi L, Costa D, Gozzellino F, Perboni A, Marchetti D, Pascali A, Falcone F, Mariano V, Rizza F, Pretto P, Turano A, Matteelli A, Carosi GP, Tedoldi S, Pinsi G, Farris AG, Ligia GP, Orani G, Farris B, Foschi C, Trucco G, Aiolfi S, Ceruti T, Parpanesi M, Calabro S, Felisatti G, Tortoli E, Nutini S, Montini G, Fiorentini F, D'Ambrosio V, Ceraminiello A, Bernorio S, Buono L, Montesano P, Vinci E, Sabato E, Gamba S, Crepaldi P, Bertoli G, Rupianesi F, Losi M, Richeldi L, Ferrara G, Muccio E, Napolitano G, Molinari GL, Saini L, Garzone A, Vertuccio C, Marcias, Menozzi, Marone P, Peona, Nascimbene, Pasi, Cascina, Casali, Monaco, Penza, Pasticci, M.B., Bistoni, Sposini, Colorizio, Confalonieri M, Bottrighi P, Orsi, Schiavi, Macor, Moretti, Fatigante, Barbaro, Agati, Zacarra, Viola, Le Donne, Farinelli, Mancini, Ermeti, Migliori, Gb, Ambrosetti, M, Fattorini, L, Penati, V, Vaccarino, P, Besozzi, G, Ortona, L, Saltini, C, Orefici, G, Moro, Ml, Iona, E, Cassone, A, De Santis, A, Giorgio, V, Vinciguerra, P, Angarano, G, Petrozzi, L, Costa, D, Gozzellino, F, Perboni, A, Marchetti, D, Pascali, A, Falcone, F, Mariano, V, Rizza, F, Pretto, P, Turano, A, Matteelli, A, Carosi, Gp, Tedoldi, S, Pinsi, G, Farris, Ag, Ligia, Gp, Orani, G, Farris, B, Foschi, C, Trucco, G, Aiolfi, S, Ceruti, T, Parpanesi, M, Calabro, S, Felisatti, G, Tortoli, E, Nutini, S, Montini, G, Fiorentini, F, D'Ambrosio, V, Ceraminiello, A, Bernorio, S, Buono, L, Montesano, P, Vinci, E, Sabato, E, Gamba, S, Crepaldi, P, Bertoli, G, Rupianesi, F, Losi, M, Richeldi, L, Ferrara, G, Muccio, E, Napolitano, G, Molinari, Gl, Saini, L, Garzone, A, Vertuccio, C, Marcias, Menozzi, Marone, P, Peona, Nascimbene, Pasi, Cascina, Casali, Monaco, Penza, Pasticci, M., B., Bistoni, Sposini, Colorizio, Confalonieri, M, Bottrighi, P, Orsi, Schiavi, Macor, Moretti, Fatigante, Barbaro, Agati, Zacarra, Viola, Le, Donne, Farinelli, Mancini, and Ermeti

Subjects
Tuberculosi, Drug susceptibility testing, Proficiency testing
Published
2000

37. Effect of interferon gamma-1b on survival in patients with idiopathic pulmonary fibrosis (INSPIRE): a multicentre, randomised, placebo-controlled trial

Author

King TE Jr, Albera, C, Bradford, Wz, Costabel, U, Hormel, P, Lancaster, L, Noble, Pw, Sahn, Sa, Szwarcberg, J, Thomeer, M, Valeyre, D, du Bois RM, INSPIRE Study Group, Agostini, Carlo, Allen, J, Anzueto, A, Behr, J, Bonnet, R, Buhl, R, Burge, S, Chan, A, Chan, C, Chanez, P, Chapman, J, Cordier, J, Covelli, H, Crimi, N, de Andrade, J, Delaval, P, Dromer, C, Egan, J, Enelow, R, Ettinger, N, Flaherty, K, Floreani, A, Frankel, S, Frost, A, Gibson, K, Glassberg, M, Gottfried, M, Harari, S, Helmersen, D, Hollingsworth, H, Horton, M, Jennings, J, Kallay, M, Lasky, J, Lee, A, Leonard, C, Lorch, D, Lynch, J, Mageto, Y, Mette, S, Millar, A, Morell Brotad, F, Müller Quernheim, J, Nathan, S, Noth, I, Padilla, M, Poletti, V, Raghu, G, Richeldi, L, Robbins, M, Rolf, J, Roman, J, Rosen, G, Rottoli, P, Saltini, C, Schaberg, T, Schaumberg, T, Scholand, M, Schönfeld, N, Sharma, S, Simonelli, P, Steele, M, Sussman, R, Tino, G, Vogelmeier, C, Wallaert, B, Wells, A, Wencel, M, Wesselius, L, Whelan, T, Wilcox, P, Wolters, P, Xaubet, A, and Zisman, D.

Subjects
Male, medicine.medical_specialty, Settore MED/10 - Malattie dell'Apparato Respiratorio, Injections, Subcutaneous, Vital Capacity, Placebo-controlled study, Kaplan-Meier Estimate, Placebo, Severity of Illness Index, Drug Administration Schedule, Pulmonary function testing, Injections, Idiopathic pulmonary fibrosis, Interferon-gamma, Double-Blind Method, Internal medicine, Pulmonary fibrosis, medicine, Humans, Aged, Analysis of Variance, Disease Progression, Europe, Exercise Test, Female, Idiopathic Pulmonary Fibrosis, North America, Proportional Hazards Models, Pulmonary Diffusing Capacity, Recombinant Proteins, Survival Rate, Treatment Failure, Medicine (all), Survival rate, business.industry, Subcutaneous, Hazard ratio, General Medicine, Interim analysis, medicine.disease, Surgery, business
Abstract

Summary Background Idiopathic pulmonary fibrosis is a fatal disease for which no effective treatment exists. We assessed whether treatment with interferon gamma-1b improved survival compared with placebo in patients with idiopathic pulmonary fibrosis and mild-to-moderate impairment of pulmonary function. Methods 826 patients with idiopathic pulmonary fibrosis were enrolled from 81 centres in seven European countries, the USA, and Canada. Patients were randomly assigned (double-blind) in a 2:1 ratio to receive 200 μg interferon gamma-1b (n=551) or equivalent placebo (n=275) subcutaneously, three times per week. Eligible patients were aged 40–79 years, had been diagnosed in the past 48 months, had a forced vital capacity of 55–90% of the predicted value, and a haemoglobin-corrected carbon monoxide diffusing capacity of 35–90% of the predicted value. The primary endpoint was overall survival time from randomisation measured at the second interim analysis, when the proportion of deaths had reached 75% of those expected by the study conclusion. This study is registered with ClinicalTrials.gov, number NCT00075998. Findings At the second interim analysis, the hazard ratio for mortality in patients on interferon gamma-1b showed absence of minimum benefit compared with placebo (1·15, 95% CI 0·77–1·71, p=0·497), and indicated that the study should be stopped. After a median duration of 64 weeks (IQR 41–84) on treatment, 80 (15%) patients on interferon gamma-1b and 35 (13%) on placebo had died. Almost all patients reported at least one adverse event, and more patients on interferon gamma-1b group had constitutional signs and symptoms (influenza-like illness, fatigue, fever, and chills) than did those on placebo. Occurrence of serious adverse events (eg, pneumonia, respiratory failure) was similar for both treatment groups. Treatment adherence was good and few patients discontinued treatment prematurely in either group. Interpretation We cannot recommend treatment with interferon gamma-1b since the drug did not improve survival for patients with idiopathic pulmonary fibrosis, which refutes previous findings from subgroup analyses of survival in studies of patients with mild-to-moderate physiological impairment of pulmonary function. Funding InterMune.

Published
2009

38. Serum CA 15-3 is increased in pulmonary fibrosis

Author

Ricci, A., Mariotta, S., Bronzetti, E., Bruno, P., Vismara, L., Dominicis, C., Laganà, B., Paone, G., Mura, M., Rogliani, P., Mastrangelo, M., Salvatore Sciacchitano, and Saltini, C.

Subjects
Adult, Male, Scleroderma, Systemic, Sarcoidosis, Biopsy, Settore MED/10 - Malattie dell'Apparato Respiratorio, Mucin-1, Enzyme-Linked Immunosorbent Assay, Fibroblasts, Middle Aged, Prognosis, Immunohistochemistry, Severity of Illness Index, Idiopathic Pulmonary Fibrosis, Cell Line, Respiratory Function Tests, Up-Regulation, Predictive Value of Tests, Case-Control Studies, Humans, Female, Tomography, X-Ray Computed, Lung, Biomarkers, Aged
Abstract

Carbohydrate antigen CA 15-3 is a glycoprotein whose expression, aberrant intracellular localization and changes in glycosylation have been associated with a wide range of cancers. Pulmonary fibrosis represents the final evolution of a chronic inflammation and is defined by the overgrowth of fibroblasts and exaggerated extracellular matrix deposition. The aim of the present study was to evaluate the possible diagnostic role of CA 15-3 in fibrosis in different idiopathic interstitial pneumonias.CA 15-3 was measured in serum samples from healthy subjects (n=25) and patients affected with idiopathic pulmonary fibrosis (IPF/UIP) (n=20), sarcoidosis (n=22) at different stages (I, II, and III) and systemic sclerosis (n=25). CA 15-3 protein expression was also evaluated by immunohistochemistry in 21 lung biopsies and in 6 primary lung fibroblasts cell lines.The CA 15-3 serum levels were significantly higher in patients with IPF/UIP and with clinically advanced sarcoidosis (stage III). Serum CA 15-3 levels were slightly increased in patients with systemic sclerosis. No difference was observed between serum CA 15-3 levels in patients with sarcoidosis at stages I and II compared with control subjects. In IPF/UIP and in sarcoidosis at stage III elevated CA 15-3 serum levels significantly correlated with decreased total lung capacity, decreased diffusing capacity of carbon monoxide and high resolution computed tomography findings. Immunohistochemical analysis showed an intense specific CA 15-3 staining in fibroblasts within fibroblastic foci, surrounding sarcoid granulomas and in all cell cultures of lung fibroblasts from IPF/UIP lungs.Our results indicate that increased CA 15-3 levels are associated with pulmonary interstitial damage, fibroblast activity and progression to fibrosis of the lung. Therefore, CA-15-3 may be considered a sensitive marker useful in the identification of patients with advanced fibrosis and more severe prognosis.

Published
2009

39. Molecular diagnosis of fatal Nocardia farcinica pneumonia in an HIV-negative patient

Author

Bocchino, M, Paglia, Mg, Marruchella, A, Contini, S, Festa, A, Saltini, C, Bocchino, Marialuisa, M. G., Paglia, A., Marruchella, S., Contini, A., Festa, and C., Saltini

Subjects
heat shock protein 65, gene amplification, Nocardia farcinica, polymerase chain reaction, Settore MED/10 - Malattie dell'Apparato Respiratorio, DNA sequence, Nocardia Infections, cotrimoxazole, imipenem, prednisone, aged, anamnesis, article, case report, clinical examination, clinical feature, computer assisted tomography, diagnostic procedure, DNA extraction, female, hospital admission, human, Human immunodeficiency virus, human tissue, immunocompromised patient, laboratory test, lung auscultation, lung nocardiosis, nocardiosis, nucleotide sequence, pneumonia, priority journal, respiratory distress, sputum cytodiagnosis, thorax radiography, vasculitis, Aged, Fatal Outcome, Female, Heat-Shock Proteins, HIV Seronegativity, Humans, Immunocompromised Host, Nocardia, Pneumonia, Bacterial, Polymerase Chain Reaction, Sequence Analysis, DNA, Molecular diagnosis, Pneumonia, Bacterial, DNA, Sequence Analysis
Published
2008

40. Tubercolosi e Micobatteriosi

Author

Casali, Lucio and Saltini, C.

Subjects
terapia antimicobatterica, micobatteriosi, tubercolosi
Published
2008

41. M. avium binding to HLA-DR expressed alleles in silico: A model of phenotypic susceptibility to sarcoidosis

Author

Saltini, C., Pallante, M., Puxeddu, E., Contini, S., Voorter, C. E., Drent, M., Massimo Amicosante, Pulmonologie, and RS: NUTRIM - R3 - Chronic inflammatory disease and wasting

Subjects
phenotype, Settore MED/10 - Malattie dell'Apparato Respiratorio, atypical mycobacteriosis, HLA DR antigen, lofgren syndrome, bacterial genome, granulomatous inflammation, Tuberculosis, antigen binding, controlled study, human, sarcoidosis, epitope, nonhuman, Chronic sarcoidosis, Epitope prediction, HLA-DR, Löfgren's syndrome, Susceptibility, T-cell response, pathogenesis, allele, article, bioinformatics, lung tuberculosis, Mycobacterium tuberculosis, major clinical study, priority journal, gene expression, chronic disease, computer model, genetic susceptibility, Mycobacterium avium
Abstract

Sarcoidosis is a systemic granulomatosis disease of unknown origin where a number of microbes, in particular M. tuberculosis and non-tuberculous mycobacteria, have been hypothesized to play a role in disease pathogenesis, possibly through bacterial antigen-driven hypersensitivity. To test this concept, we used bioinformatic tools allowing the identification of antigenic peptides in whole microbial genomes to analyze the interaction between the expressed HLA-DR gene allelic variants and the HLA-DR immunome of all pathogenic bacteria in a population of 149 sarcoidosis affected subjects and 447 controls, all HLA-typed at high resolution. We show here that patients with the Lofgren's syndrome, express HLA-DR alleles that recognize in silico a significantly higher number of bacterial antigen epitopes compared to the control population (18,496+9,114 vs 17,954+8,742; p

Published
2008

42. CYTOFLUORIMETRIC ANALYSIS OF CYTOKINE-PRODUCING LYMPHOCYTES IN BAL FROM TB PATIENTS

Author

MAZZARELLA, Gennaro, SALTINI C, PEMA F, PETILLO O, MARGARUCCI S, CALABRESE, Cecilia, D’AURIA D, MARSICO SA, Mazzarella, Gennaro, Saltini, C, Pema, F, Petillo, O, Margarucci, S, Calabrese, Cecilia, D’Auria, D, and Marsico, Sa

Abstract

9 TB patients, 4 without (Group I) and with (Group II) chest X-ray evidence of cavitary disease were evaluated at admission for the frequencies of TH1 and TH2 CD4 T-cells in the BAL fluid using intracellular immunofluorescence with anti INF-y (TH1) and anti-IL-4 (TH2) antibodies and flow-cytometric analysis and for the release in 24 h. culture supematants of IFNy. TH1 CD4+ cells dominated (93 ± 2%) the alveolar lymphocytes while TH2 CD4+ T-cells were absent in Group I patients; on the other hand, both TH1 (66 ± 4%) and TH2 CD4+ T-cells (28 ± 5%) were present in Group II patients. Also, BAL cells from Group I patients release high levels of IFNy (144 ±13 pg/ml) with minimal levels of IL-4 (

Published
1997

48. Predictive valdue of BAL cellular analysis in differentiating pulmonary tuberculosis and sarcoidosis (multiple letters) [3]

Author

Greco, S, Marruchella, A, Massari, M, Saltini, C, and Welker, L

Subjects
probability, Settore MED/10 - Malattie dell'Apparato Respiratorio, letter, CD8 antigen, lung tuberculosis, major clinical study, lung lavage, lung sarcoidosis, priority journal, statistical analysis, diagnostic test, sensitivity and specificity, validation process, differential diagnosis, controlled study, diagnostic accuracy, diagnostic value, human, CD4 antigen, reproducibility, statistical significance
Published
2005

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