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6. Epidemiology

Author

Fixa, B., Komárková, O., Krejsek, K., Bures, J., Nozicka, Z., Giorcelli, W., Rodi, M., Camisasca, G., Martinotti, R. G., Mendall, M. A., Goggin, P. M., Molineaux, Nicola, Levy, Joanne, Toosy, T., Strachan, D., Northfield, T. C., Vorobjova, T., Vassiljev, V., Kisand, K., Wadström, T., Uibo, R., Zotz, R. B., Xu, S. G., Recklinghausen, G. von, Meusers, P., Goebell, H., Rhee, K. H, Youn, H. S., Paik, S. K., Lee, W. K., Cho, M. J., Park, C. K., Li, Yuyuan, Hu, Pinjin, Du, Guoguang, Wong, Zhijin, Hazell, Stuart L., Mitchell, Hazel M., Korwin, J. D. de, Remot, P., Hartemann, Ph, Catelle, A., Conroy, M. C., Schmitt, J., Stolte, M., Wellens, E., Bethke, B., Ritter, M., Eidt, H., Zanten, S. Veldhuyzen van, Best, L., Bezanson, G., Marrie, T., Poniewierka, E., Gosciniak, G., Matysiak-Budnik, T., Quatrini, M., Boni, F., Baldassarri, A. R., Vecchi, A. De, Castelnovo, C., Viganò, E., Tenconi, L., Bianchi, P. A., Carlucci, A., Ferrini, G., Bianco, I, Larcinese, G., Sciascio, A. Di, Fly, G. F., Hauge, T., Persson, J., Coelho, L. G. V., Teixeira, M. M., Passos, M. C. F., Givisiez, C. B., Santos, C. M. F. R., Rodrigues, C. J. S., Chausson, Y., Castro, L. P., Hyvärinen, Hannu, Seppälä, Kari, Kivilaakso, Eero, Kosunen, Timo, Gormse, Martin, Pilotto, A., Vianello, F., Tornaboni, D., Dotto, P., Battaglia, G., Binda, F., Mario, F. Di, Donisi, P. M., Pasini, M., Benve-nuti, M. E., Stracca-Pansa, V., Pasquino, M., Jablonowski, H., Szelényi, H., Hengels, K. J., Strohmeyer, G., Banatvala, N., Mayo, K., Megraud, F., Jennings, R., Deeks, J. J., Feldman, R. A., Bulighin, G., Ederie, A., Pilati, S., Franzin, G., Zamboni, G., Maran, M., Musola, R., Tobin, A., Hackman, R. C., McDonald, G. B., Fatela, N., Cristino, J. Melo, Monteiro, L., Ramalho, F., Saragoça, A., Salgado, M. J., Moura, M. Cameiro de, Pretolani, S., Gasbarrini, G., Bonvicini, F., Baraldini, M., Tonelli, E., Gatto, M. R. A., Ghironzi, G. C., égraud, F. M, Bouchard, S., Lubcvzumiska-Kowalska, W., Knapik, Z., Meenan, J., Goggins, M., Shahi, C., Keeling, P. W. N., Keane, C., Weir, D. G., Vaira, D., Miglioli, M., Mulè, P., Holten, J., Menegati, M., Biasco, G., Vergura, M., Nannetti, A., Barbara, L., Boschini, A., Begnini, M., Menegatti, M., Ghira, C., D’Errico, A., Evans, D. G., Asnicar, M. A., Evans, D. J., Graham, D. Y., Lee, C. H., Coschieri, M., Fosse, T., Paul, M. C. St., Michiels, J. R., Delmont, J. P., Péroux, J. L., Pradier, C., Rampai, P., Pazzi, P., Merighi, A., Gamberini, S., Scarliarini, R., Bicochi, R., Libanore, M., Bisi, G., and Gulllini, S.

Published
1992
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7. Abstract form for the Irish Journal of Medical Science v workshop on gastroduodenal pathology and Helicobacter pylori July 5th — 7th 1992 — Dublin, Ireland

Author

Logan, R. P. H., Gummett, P. A., Walker, M. M., Karim, Q. N., Baron, J. H., Misiewicz, J. J., Trieber, G., Walker, S., Klotz, U., Lozniewski, A., Weber, M., de Korwin, J. D., Floquet, J., Conroy, M. C., Burdin, J. C., Mannes, G. A., Bayerdörffer, E., Höchter, W., Weingart, J., Heldwein, W., Sommer, A., Müller-Lissner, S., Bomschein, W., Miehlke, S., Weinzierl, M., Ruckdeschel, G., von Wulffen, H., Köpcke, W., Stolte, M., Rune, S. J., Justesen, T., Hansen, J. M., Jensen, T. G., Eriksen, J., Thomsen, O. ø., Scheibel, J., Bonnevie, O., Bremmelgaard, A., Vilien, M., Knuhtsen, S., Elsborg, L., Hansen, J., Lauritsen, K., Wulff, H. R., Boixeda, D., Ballestero, S., Cantón, R., De Rafael, L., Martinm de Argila, C., Pozuelo, M. J., Sampedro, J., Baquero, F., Grigoriev, P. Ya., Isakov, V. A., Iakovenko, E. P., Hirschl, A. M., Brandstätter, G., Dragosics, B., Hentschel, E., Kundi, M., Rotter, M. L., Schütze, K., Taufer, M., Neri M, Susi D, Bovani I, Pindo R, Cuccurullo F., Coelho, L. G. V., Passos, M. C. F., Chausson, Y., Vieira, W. L. S., Castro, F. J., Franco, J. M. M., Fernandes, M. L. M., Castro, L. P., Jonas, C., De Koster, E., Van Gossum, M., Depierreux, M., Cheval, M., Deltenre, M., Schütz, E., Bethke, B., Lee, A., Hegedus, E., O’Rourke, J., Larsson, H., Sjöstedt, S., Veress, B., Nord, C. E., Sobala, G. M., George, R., Tompkins, D., Finlay, J., Manning, A., Sant, S., Xia, H. X., Daw, M., Gilvarry, J., Keane, C. T., O’Morain, C., Rubio, M. A., Hegarty, B., Blum, A. L., Sulser, E., Stadelmann, O., Munoz, N., Buiatti, E., Vivas, J., Oliver, W., Cano, E., Peraza, S., Castro, D., Sanchez, V., Andrade, O., Benz, M., Mendz, G. L., Hazell, S. L., Salmela, K. S., Roire, R. P., Hook-Nikanne, J., Kosunen, T. U., Salaspur, M., Luke, C. J., Reynolds, D. D. J., Penn, C. W., Bode, G., Mauch, F., Ditschuneit, H., Malfertheiner, P., Ferrero, Richard L., Agnes Labigne, Eaton, K. A., Krakowka, S., Mobley, H. L. T., Hu, Li-Tai, Foxall, P. A., Moran, A. P., Helander, I. M., Altman, C., Sobhani, I., Vissugaire, C., Migrant, M., Etienne, J. P., Sommi, P., Ricci, V., Fiocca, R., Cova, E., Figura, N., Romano, M., Ivey, K. J., Solcia, E., Ventura, U., Nilius, M., Schieffer, S., Hengels, K. J., Jablonowski, H., Strohmeyer, G., Cabrai, M. D., Barbosa, A. J. A., Lima Hr., G. F., Oliveira, C. A., Polak, J. M., Oderda, G., Villani, L., Altare, F., Morra, I., Miserendino, L., Ansaldi, N., Dixon, M. F., Wyatt, J. I., Axon, A. T. R., Beattie, S., Hamilton, H., Shabib, S., Cutz, E., Drumm, B., Sherman, P., Noach, L. A., Rolf, T., Bosma, N. B., Schwartz, M. P., Oosting, J., Rauws, E. A. J., Tytgat, G. N. J., Andrew, A., Nardone, G., d’Ormiento, F., Pontillo, M., Lobo, A. J., Uff, J. S., McNulty, C. N. M., Wilkinson, S. P., Suriani, R., Pallante, C., Ravizza, M., Galliano, D., Sallio, D., Malandrino, M., Oneglio, R., Colozza, M., Mazzucco, D., Gaia, E., Eidt, S., Vincent, P., Gottrand, F., Turck, D., Lecomte-Houcke, M., Leclerc, H., Bonvicini, F., Pretolani, S., Baraldini, M., Cilla, D., Baldinelli, S., Bazocchi, E., Acampora, P., Careddu, N., Brocchi, E., Gasbarrini, G., Joubert, M., Bazin, N., Thiaucourt, D., Protte, E., Gissler, C., Duprez, A., Merlin, P., Forestier, S., Labenz, J., Gyenes, E., Rühl, G. H., Börsch, G., Daskalopoulos, G., Carrick, J., Lian, R., Wagner, S., Bleck, J., Gebel, M., Bär, W., Manns, M., Lamouliatte, H., Bernard, P. H., Cayla, R., Vialette, G., Quinton, A., Mégraud, F., Lemaire, M., Quinten, A., De Mascarel, A., Webb, P., Forman, D., Knight, T., Wilson, A., Graves, S., Newell, D., Elder, J., Tonelli, E., Gatte, M. R. A., Ghironzi, G. C., Giulianelli, G., Bamford, K. B., Collins, J. S. A., Bickley, J., Johnston, B. T., Potts, S., Boston, V., Owen, R. J., Sloan, J., Basso, L., Lawlor, S., Clune, J., Szelényi, H., Stohmeyer, G., Macedo, G., Iglésias, I., Chaves, A. P., Loureiro, A., Katelaris, P. H., Seow, F., Lin, B., Napoli, J., Hones, D. B., Ngu, M. C., Akopyantz, Natalia S., Bukanov, Nikolay O., Westblom, T. Ulf, Berg, Douglas E., Nyst, J. F., Denis, P., Buset, M., De Reuck, M., Nielsen, H., Andersen, L. P., Birkholz, Sabine, Knipp, Ulrich, Nietzki, Claudia, Opferkuch, Wolfgang, Crabtree, J. E., Peichl, P., Lindly, I. J. D., Deusch, K., Seifirth, C., Funk, A., Dahie, I., Reut, K., Classen, M., Gionchetti, P., Vaira, D., Campieri, M., Bertinelli, E., Menegatti, M., Belluzzi, A., Briognola, C., Miglioli, M., Barbara, L., Tommaso, A. Di, Magistris, M. T. De, Bugnoli, M., Petracca, R., Covacci, A., Censini, S., Rappuoli, R., Abrignani, S., Territo, M. C., Smela, K. L., Reeve, J. R., Lee, T. D., Walsh, J. H., Armellini, D., Crabtree, J. E., Xiang, Z. Y., Mitchell, H. M., Hu, P. J., Li, Y. Y., Wang, Z. J., Zhao, S. M., Liu, Q., Chen, M., Du, G. G., Filipe, M. I., Reed, P. I., Craanen, M. E., Blok, P., Dekker, W., Colombo, E., Redaelli, D., Santangelo, M., Spinelli, M., Farinati, F., Valiante, F., Delia Libera, G., Germanà, B., Baffa, R., Rugge, M., Vianelo, F., Di Mario, F., Sipponen, Pentti, Rokkas, T., Popotheodorou, G., Kaldgeropoulos, N., Deprez, C., Galand, P., Fox, J. G., Wishnok, P., Murphy, J. C., Tannenbaum, S., Correa, P., Parsonnet, Julie, Macor, C., Da Broi, G. L., Avellinio, C., Reifen, R., Rasooly, I., Millson, M. E., Murphy, K., Thomas, J. E., Eastham, E. J., Malorgio, E., Dell’Olio, D., Kemmer, T. P., Dominguez-Munoz, J. E., Klingel, H., Gatto, M. R. A., Olivieri, R., Bayeli, R. F., Abate, L., De Gregorio, L., Aziz, J., Esposito, E., Basagni, C., Guilluy, R., Rousseau-Tsangaris, M., Brazier, J. L., Wadstiöm, Torkel, Tyszkiewicz, Tadeusz, Bergenzaun, Per, Olsson, Karin, Birac, C., Tall, F., Albenque, M., Labigne, A., Megraud, F., Feldman, R. A., Deeks, J., Glupczynski, Y., Burette, A., Goossens, H., Van den Boore, C., Butzler, J. P., Veldhuyzen van Zanten, S., Best, L., Benzanson, G., Haldane, D., Hazell, S., Mapstone, N. P., Lynch, D. A. F., Quirke, P., Taylor, D. E., Chang, N., Eaton, M., Stockdale, E., Salama, S. M., Thompson, L., Cockayne, A., Spiller, R. C., Leen, E., Sweeney, E., Klann, H., Hatz, R., Bornschein, W., Simon, T., Eimiller, A., Bolle, F., Schweikert, C., Köpeke, W., Moss, S. F., Bishop, A. E., Calam, J., Cahill, R. J., Xia, H., Solnick, J., and Tompkins, L.

Published
1992
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9. Development of a chemoluminescent enzyme immunoassay for urinary 1--hydroxypyrene

Author

RODA A., SIMONI P., PIAZZA F., MIRASOLI M., BARALDINI M., VIOLANTE FS, RODA A., SIMONI P., PIAZZA F., MIRASOLI M., BARALDINI M., and VIOLANTE FS

Subjects
urinary 1--hydroxypyrene, chemoluminescent enzyme immunoassay
Abstract

A chemiluminescent enzyme-immunoassay for urinary 1-hydroxypyrene has been developed and optimized. The enzymatic activity of horseradish peroxidase-labeled tracer was measured with an enhanced chemiluminescent system and the results were compared with those from conventional colorimetric detection. The method fulfilled all the requirements of accuracy and precision and the detection limit was 0.001 pmol/well, which enabled analysis in less than 1 microL urine. Subjects working in the center of Bologna who were exposed daily to vehicular exhaust gas were studied. Their urinary 1-hydroxypyrene concentrations were compared with the levels of benzo( a)pyrene in air particulate matter. Urinary 1-hydroxypyrene, which ranged from 0.5 to 10 nmol L(-1), correlated poorly with the concentration of benzo( a)pyrene in air particulate matter, which ranged from 5 to 140 ng m(-3). No significant effect of vehicle exhaust gas exposure was observed among the different groups of subjects working in different areas of the town. Thus, at a relatively low level of exposure 1-hydroxypyrene does not seem to be a sensitive biomarker of exposure to polycyclic aromatic hydrocarbons.

Published
2002

10. A comparison of the analytical performance of sodium dodecyl sulfate-polyacrylamide gel electrophoresis, electrospray and matrix-assisted laser desorption/ionization mass spectrometry in the study of the protein extract from bothrops jararaca snake venom

Author

Roda A., Gioacchini A. M., Seraglia R., Montagnani M., Baraldini M., Pedrazzini S., Puricelli M., Traldi P., Roda A., Gioacchini A.M., Seraglia R., Montagnani M., Baraldini M., Pedrazzini S., Puricelli M., and Traldi P.

Subjects
polyacrylamide gel electrophoresis, mass spectrometry, protein extract, bothrops jararaca, snake venom
Abstract

Bothrops jararaca Snake venom extract has been analysed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) electrospray mass spectrometry (ESI-MS) and matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) in order to obtain a rapid and accurate characterization. By the SDS-PAGE and MALDI-MS techniques about fourteen components are evidenced; with the latter technique, faster analysis and a more accurate molecular weight determination have been achieved. By ESI-MS the data obtained strongly depend on the operating conditions employed.

Published
1997

29. Mechanism of compensation in pre-ascitic cirrhosis

Author

Bernardi, M., primary, Trevisani, F., additional, Di Mareo, C., additional, Andreone, P., additional, Cursaro, C., additional, Baraldini, M., additional, De Collibus, C., additional, Zacà, F., additional, and Gasbarrini, G., additional

Published
1990
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31. Antibodies against human liver-specific protein (LSP) in acute and chronic viral hepatitis types A, B and non-A, non-B.

Author

Meliconi, R., Baraldini, M., Stefanini, G. F., Facchini, A., Miglio, F., Bortolotti, Flavia, Alberti, A., Realdi, G., and Amoroso, P.

Subjects
*HEPATITIS C, *LIVER diseases, *HEPATITIS, *IMMUNOGLOBULINS, *VIRAL hepatitis, *PATIENTS
Abstract

Sera from 42 patients with acute viral hepatitis (AVH), 97 patients with chronic active liver disease (CALD) and 89 controls were tested by radinimmunoprecipitation for the presence of antibodies against human liver-specific protein (LSP). Anti-LSP were found in all but one patient with AVH type A (93%) and in a smaller percentage of AVH type B (55%). In non-A, non-B cases, anti-LSP were found in low percentages: 27% in acute cases, 10% in chronic cases. Furthermore, in CALD, a significant difference was found between HBsAg-positive CAH and `autoimmune' CAH, both in anti-LSP prevalence (21%, 67%; P < 0.005) and in anti-LSP titre (1: 154 ± 170, 1:316 ± 186; P < 0.005). In HBsAg-negative/anti-HBc-positive CAH, three of 15 patients were anti-LSP positive. Anti-LSP were found only in three of 57 patients with various non-hepatic diseases with autoimmune features. None of the 12 healthy HBsAg carriers was positive. Hence there is evidence for a considerable heterogeneity in anti-LSP response in acute and in chronic inflammatory HBsAg-negative liver diseases. These data suggest that anti-LSP antibodies do not play a prominent role in the process of transition to chronicity of acute viral hepatitis particularly in non-A, non-B cases, whereas these antibodies may be important in the mechanism of ongoing liver cell injury in patients with `autoimmune' CAH, and can represent a useful diagnostic marker of this type of hepatitis. [ABSTRACT FROM AUTHOR]

Published
1981

34. Renal function impairment induced by change in posture in patients with cirrhosis and ascites.

Author

Bernardi, M, Santini, C, Trevisani, F, Baraldini, M, Ligabue, A, and Gasbarrini, G

Abstract

The assumption of upright posture by patients with liver cirrhosis leads to striking activation of adrenergic and renin-angiotensin systems. The tilting-induced modifications in renal function of eight healthy controls and 14 untreated patients with liver cirrhosis and ascites were related to plasma concentrations of noradrenaline, renin activity and aldosterone. All patients had preserved renal blood perfusion. All parameters were evaluated during bed rest for two hours and in the sitting posture for one hour. Basal plasma renin activity (0.1 greater than p greater than 0.05), aldosterone and noradrenaline concentrations (p less than or equal to 0.01) were raised in cirrhotics. The renal function tests (creatinine clearance, filtered sodium, tubular rejection fraction, urinary sodium excretion) were significantly reduced in cirrhosis. Under basal conditions, in cirrhotic patients tubular rejection fraction and urinary sodium excretion were inversely related to both noradrenaline and aldosterone concentrations. After tilting, the noradrenaline and aldosterone integrated outputs (sigma delta) were significantly greater in cirrhosis. All renal function tests significantly decreased in cirrhotics, whereas creatinine clearance only significantly decreased in controls. Patient's tubular rejection fraction of sodium and sodium excretion were related to sigma delta aldosteronaemia (r = -0.72; p less than 0.01), but no longer to sigma delta plasma noradrenaline. [ABSTRACT FROM PUBLISHER]

Published
1985

35. Lymphocytotoxicity against autologous hepatocytes and membrane-bound IgG in viral and autoimmune chronic active hepatitis.

Author

Stefanini, G. F., Meliconi, R., Miglio, F., Mazzetti, Maura, Baraldini, M., Facchini, A., and Gasbarrini, G.

Abstract

ABSTRACT- Membrane-bound IgG and lymphocytotoxic activity of total, T-enriched and T-depleted lymphocytes, using autologous hepatocytes have been evaluated in: (a) 31 patients with chronic active hepatitis (CAH) (six autoimmune and 25 hepatitis B virus - HBV-related); (b) five patients with inactive alcoholic cirrhosis; and (c) nine subjects with normal hepatic histology. Lymphocytotoxicity was positive in 83% of autoimmune CAH and 68% of HBV-related cases; it was confined to the T-depleted subpopulation in the first group, while it was present in both the T-enriched and T-depleted subpopulations in 81% of HBV-related cases. Membrane-bound IgG was present in 58% of group (a) and in none of the other groups. A linear pattern was found in four out of five autoimmune CAH patients with positive lymphocytotoxic activity. The autoimmune patient with lymphocytotoxic activity within the normal range did not show any membrane fluorescence. Among HBV-related CAH patients, 13 presented a granular pattern, two an associated granular and linear pattern and ten were negative. These data suggest that different lymphocytotoxic mechanisms are involved in the two forms of CAH studied. [ABSTRACT FROM AUTHOR]

Published
1983
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36. Occurrence and significance of IgG liver membrane autoantibodies (LMA) in chronic liver diseases of different aetiology.

Author

Meliconi, R., Stancari, M. Valeria, Garagnani, M., Baraldini, M., Stefanini, G. F., Miglio, F., and Gasbarrini III, G.

Subjects
LIVER diseases, LIVER cells, BLOOD plasma, AUTOANTIBODIES, IMMUNOFLUORESCENCE, IMMUNOCYTOCHEMISTRY
Abstract

The prevalence of liver cell membrane antibodies (LMA) was evaluated in the sera of 124 untreated patients with various chronic liver diseases. in 17 acute hepatitis patients and in 40 normal controls by indirect immunofluorescence on rabbit hepatocytes. isolated by non-enzymatic method. The presence of LMA was compared with the presence of HBs Ag. anti-HBc and non-organ specific autoantibodies (anti-nuclear antibody. ANA; smooth muscle antibody, SMA: anti-mitochondrial antibody. A MA: liver kidney microsomal antibody. L K M), LMA was found in 83% of autoimmune chronic active liver disease (CALD), in 47% of cryptogenic CALD and in 42%, of primary biliary cirrhosis (PBC). LMA prevalence both in HBsAg positive and HBsAg negative/anti-H Be positive CALD was 11% significantly lower than in the other three groups. In the cryptogenic group the prevalence of non-organ specific autoantihodies was significantly lower than LMA prevalence. The 35 LMA positive sent were titred to end point dilution. Autoimmune cases presented litres higher than those of all the other groups. Adsorption experiments showed that in autoimmune cases LMA fluorescence is not blocked by pre-incubation with liver antigens LSP and LP2, while a mild blocking effect was observed in some H BsAg positive cases or PBC sera. No cross-reaction with mitochondrial antigens was observed in PBC sera. LMA can still be considered a marker of autoimmune CALD only when present at high tint and without cross-reactivity with other liver antigens. [ABSTRACT FROM AUTHOR]

Published
1983

37. Alterations in Helper-Specific Circulating T Lymphocytes and in the Autologous Mixed Lymphocyte Reaction in Chronic Hepatitis B.

Author

Mazzetti, M., Stefanini, G. F., Mazzeo, V., Baraldini, M., Canonica, G. W., Marini, E., Miglio, F., Gasbarrini, G., and Lee, W. M.

Subjects
T cells, LYMPHOCYTE transformation, HEPATITIS B, MONOCLONAL antibodies, VIRAL replication
Abstract

Defects in T lymphocyte subpopulations and in the functional characteristics of such cells have been thought to play a role in the evolution of chronic hepatitis B, but the precise nature of the alterations and their significance remains unresolved. We studied lymphocyte subsets in 27 patients with chronic hepatitis B utilizing standard monoclonal antibodies including 1,2a,3a,7 and D1/12 (against the common determinant of the Dr molecule), as well as a newly described monoclonal antibody, "5/9," which is thought to characterize a unique subpopulation of T4 cells with specific helper/inducer function. These results were compared with those obtained using the autologous mixed lymphocyte reaction assay for the same patients in order to further delineate the lymphocyte alterations in chronic hepatitis B. A significant reduction in the mean number of Leu 3a (T4) positive cells was observed as well as a reduction in the number of 5/9 positive cells. These changes were most evident in those positive for HBeAg in serum. Reduction in Leu 3a cells was associated with a reduced autologous mixed lympbocyte reaction assay response, and was most marked in the HBeAg-positive individuals. These findings suggest that HBeAg-positive patients in whom active viral replication is occurring have a defect in T lymphocyte number and function, which may be due in part to reduced 5/9 positive cells. These alterations may be related to the persistence of virus in chronic active hepatitis B patients. [ABSTRACT FROM AUTHOR]

Published
1987

38. Chronobiological study of factors affecting plasma aldosterone concentration in cirrhosis

Author

Bernardi, M., de Palma, Rossana, Trevisani, F., Santini, Costanza, Capani, F., Baraldini, M., and Gasbarrini, G.

Abstract

We studied the mechanisms leading to derangement of aldosterone secretion in cirrhosis. The circadian patterns of plasma renin activity (PRA), aldosterone, cortisol, sodium, and potassium were studied in 16 nonazotemic cirrhotics (group 1 without ascites, 7 cases; group 2 with ascites, 9 cases) and 7 healthy controls. Group 1 did not differ from controls in aldosterone, sodium, and potassium mean daily levels (mesors), but had reduced PRA mesor (p < 0.05). Moreover, minor derangements in circadian patterns of PRA, aldosterone, and potassium were also found. Group 2 not only showed an increased mesor of PRA (p < 0.05), aldosterone (p < 0.001), and reduced sodium (p < 0.005), but also achronia in daily fluctuations of PRA, aldosterone, and potassium. In all groups the mesors of PRA and aldosterone were correlated (r ≥ 0.82; p < 0.01 or less), but the regression line slopes of patients were steeper than those of controls (group 1, p < 0.05; group 2, p < 0.01). Moreover, although in controls and some group 1 patients aldosterone paralleled cortisol rhythmicity, most group 2 patients had aldosterone daily patterns correlated with those of PRA. Finally, no relationships between plasma potassium and aldosterone concentrations were found in patients, whereas they were strictly related in controls. These results suggest that the reninangiotensin system is the prevalent determinant of aldosterone secretion in cirrhosis.

Published
1986
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39. Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis

Author

Bernardi, M., De Palma, Rossana, Trevisani, F., Malatesta, R., Baraldini, M., Cursaro, Carmela, and Gasbarrini, G.

Abstract

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.

Published
1988
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40. Liver-Specific Autoantibodies in Chronic Hepatitis B Virus Infection

Author

Meliconi, R., Facchini, A., Miglio, F., Trevisan, A., Alberti, A., Realdi, G., Baraldini, M., and Gasbarrini, G.

Abstract

1. Anti-liver-specific protein (LSP) antibody and liver membrane autoantibody (LMA) have been evaluated in 88 patients with hepatitis B virus (HBV)-induced chronic liver disease by means of radioimmunoprecipitation and immunofluorescence. Among our patients, 38 presented circulating HBe antigen while 43 had HBe antibody and seven were negative for both. 2. Anti-LSP was mainly found in HBeAg positive chronic active hepatitis (CAH), anti-HBe in positive CAH and in anti-HBe positive chronic persistent hepatitis (CPH). 3. Similar prevalences of LMA (range 13-33%) were detected in the various groups studied. 4. Taking into account the histological diagnosis of disease activity (periportal inflammation and piecemeal necrosis) no significant differences were found between active and inactive patients. 5. Taking into account the HBeAg/anti-HBe status, no significant differences were found between the patients positive for ‘e’ antigen or ‘e’ antibody. 6. Humoral autoimmune reactions may also play a role in HBV-induced chronic (active) liver disease irrespective of HBeAg/anti-HBe status and hence of the viral replication activity of the patients.

Published
1985
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42. Circadian variation in renal sodium and potassium handling in cirrhosis

Author

Trevisani, F., Bernardi, M., De Palma, Rossana, Pancione, L., Capani, F., Baraldini, M., Ligabue, A., and Gasbarrini, G.

Abstract

Renal sodium and potassium handling, plasma aldosterone and cortisol concentrations, and urine free norepinephrine excretion were determined every 4 h for 24 h in 15 cirrhotics (7 without ascites, group 1; 8 with ascites, group 2) and 7 healthy controls during controlled salt intake and recumbency. Renal sodium excretion was significantly reduced in group 2, whereas it exceeded threefold the salt intake in group 1. Its circadian rhythm was disrupted in both groups of patients. Significant inverse correlations with plasma aldosterone were found erratically in controls, never in group 1, and at every 4-h interval in group 2. In the latter, the indexes of tubular activity and effectiveness of aldosterone were also significantly increased. Urine norepinephrine excretion was never related to sodium excretion in either controls or patients; in group 2 it was directly correlated with glomerular filtration rate in many instances. The cortisol-related circadian rhythm of kaliuresis was retained only in group 1. The 24-h renal potassium excretion of controls and patients was comparable, in spite of the striking hyperaldosteronism, and the more than doubled contribution of aldosterone to kaliuresis shown in group 2. The influence of aldosterone on potassium excretion was also witnessed by the direct correlation between these variables found in group 1 and, when kaliuresis was corrected by the distal sodium delivery, group 2. Renal sodium handling in cirrhosis is altered even before ascites formation and compensated patients can undergo “spontaneous natriuresis.” Aldosterone is the main cause of sodium retention in nonazotemic ascitic patients, while Sympathoadrenergic hyperactivity may contribute to preserve renal perfusion. The influence of aldosterone on kaliuresis is enhanced, but renal potassium wasting in patients with ascites and hyperaldosteronism is prevented by reduced distal tubular availability of sodium.

Published
1989
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43. Chronobiological evaluation of sympathoadrenergic function in cirrhosis

Author

Bernardi, M., Trevisani, F., De Palma, Rossana, Ligabue, A., Capani, F., Baraldini, M., and Gasbarrini, G.

Abstract

Intraday activity of the adrenergic system was investigated in 7 healthy controls and in cirrhotic patients without ascites (group 1, 7 cases) and with ascites (group 2, 9 cases) by determining the urinary norepinephrine and vanillylmandelic acid excretions at 4-h intervals for 24 h. Mean arterial pressure and heart rate were also recorded. In controls, the statistical evaluation by the cosinor method showed a circadian rhythm of such variables, with zenith in the morning and nadir at night. Intraday changes of urinary excretion of norepinephrine were closely related to arterial pressure and heart rate in most subjects. The most important change in cirrhotic patients was the achronia [no detection of a statistically significant (p > 0.05) rhythm] in urinary excretion of norepinephrine and arterial pressure. This occurred not only in group 2 patients, who had lower arterial pressure and higher NE mesors than controls (p < 0.05), but also in group 1 patients, whose mesors were comparable to controls. The statistical significance of heart rate rhythmicity was preserved in patients, but its zenith was progressively displaced toward evening (group 1) and night hours (group 2, whose mesor was increased). Changes in urinary excretion of vanillylmandelic acid roughly paralleled those of norepinephrine both in controls and patients, but they did not significantly increase even in the group with ascites. In both groups of cirrhotic patients, the correlation between urinary excretion of norepinephrine, arterial pressure, and heart rate within the same subject was lost in most cases. This chronobiological study showed that the sympathoadrenergic activity can be deranged also in the early stages of cirrhosis, and suggested that an altered control of cardiovascular homeostasis is present even under steady state conditions. This alteration might blunt adrenergic responses to stress conditions.

Published
1987
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46. Prostanoids in peritoneal fluid of infertile women with pelvic endometriosis and PID

Author

Pungetti D, Lenzi M, Travisani D, Cantiero D, Maurizio G, Sarti G, Zanardi E, PIETRO ANDREONE, Baraldini M, and Gasbarrini G

Subjects
Thromboxane B2, Prostaglandins E, Prostaglandins F, Endometriosis, Ascitic Fluid, Humans, Female, Infertility, Female, Leukotriene B4, Pelvic Inflammatory Disease
Abstract

Peritoneal fluid collected at celioscopy in infertile subjects was assayed for steroids and several prostanoids (PGE2, PGF2, TXB2, LTB4) as part of a study into pathophysiology of the female reproductive tract. Prostaglandins, produced massively in the pelvis, might interfere with fertility through various mechanisms (alterations in the egg implantation, follicle genesis, luteinization as well as tubal disorders). Our study of 54 patients showed a marked increase only of TXB2 out of the prostanoids assayed in overall endometriosis. In pelvic flogosis peritoneal LTB4 (and TXB2) were considerably increased if related to controls. This would suggest their role in the ethiopathogenesis of unexplained infertility (in relation to these pathologic patterns).

Published
1987

47. Influence of cimetidine in low doses (less than ED50) on prostanoid production by human gastric mucosa in vitro

Author

PIETRO ANDREONE, Baraldini M, Micaletti E, Cursaro C, Saggioro A, Della Monica A, Bortoluzzi F, Miglio F, and Gasbarrini G

Subjects
Adult, Male, Adolescent, Proteins, 6-Ketoprostaglandin F1 alpha, In Vitro Techniques, Dinoprost, Dinoprostone, Thromboxane B2, Gastric Mucosa, Prostaglandins, Humans, Female, Cimetidine
Abstract

Cimetidine has been defined as a cytoprotective agent and numerous studies have reported that it is able to influence prostaglandin production as well as mechanisms which protect the surface epithelium of the gastric mucosa. However, results have been contradictory and high drug concentrations contrasting the cytoprotection concept have been utilized. The present study tried to evaluate whether low concentrations (less than ED50) of cimetidine in vitro are able to modify prostanoids produced by gastric mucosa fragments. Thirteen patients without histological lesions were examined. Five mucosal biopsy specimens were obtained from the antrum in seven patients and from the body in another six patients. One biopsy was utilized for histological examination, while the remaining four specimens were incubated in the absence or in the presence of 5, 50 and 500 ng/ml of cimetidine, respectively. Concentrations of PGE2, 6-oxo-PGF1 alpha, PGF2 alpha and TXB2 in the incubate were determined by radioimmunoassay. Cimetidine at 50 ng/ml increased PGE2 production at the antrum level while 500 ng/ml of cimetidine increased PGF 2 alpha and TXB2 production at the body level. Furthermore, the drug dose was directly related to PGE2 production (at the antrum level) and TXB2 (at the body level). The differences in prostanoid production between the antrum and body could be due to the different cell composition of the two anatomical areas, and suggest that the effects of cimetidine are mediated through binding to H2-receptors. The authors conclude that cimetidine in low doses stimulates the net production of some but not all prostanoids, the observed effects varying with anatomical site.

Published
1989

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