Helicobacter Pylori' Gastritis Must Be Classified As A Disease [gastrite Por 'helicobacter Pylori' Deve Ser Classificada Como Doenca]

Helicobacter pylori gastritis is considered a disease by the authors, and is excluded from the diagnosis of functional dyspepsia. They emphasize that, although not associated to specific clinical features, this gastritis type has an etiologic agent and defined hisotpathological alterations. These characteristics are similar to those of other infectious diseases, such as chronic B and C virus hepatitis.16624724

Hepatic Osteodystrophy [osteodistrofia Hepática]

Hepatic osteodystrophy is a disorder of bone mineralization associated to liver disease, clinically manifested by osteoporosis and more rarely osteomalacia. Although seldomly diagnosed and varying greatly in literature, most of the time, it presents asymptomatically and, when it is not recognized, it enhances considerably the risk of fracture and permanent sequelae. Indeed it requires a high grade of suspicion and it is confirmed by means of bone densitometry evaluation in clinical practice. Presenting with a multifactorial physiopathology, it involves factors, such as genetical, environmental, and patient clinical-nutritional status. A greater attention must be spent on patients with liver disease, especially those malnourished, with advanced cirrhosis, chronic cholestatic disease, and transplanted, because of a higher risk of bone demineralization. In this data, it will be reviewed the bone synthesis metabolism and the physiopathology of bone mineralization disorder - since fisiopatogenic mechanisms in chronic liver disease, diagnosis and recent therapeutic review employed.3025261Leslie, W.D., A Patient With Autoimmune Liver Disease on Steroids: Screening and Treatment of Bone Disease (2006) Clinical Gastroenterology and Hepatology, 4 (12), pp. 1440-1444. , DOI 10.1016/j.cgh.2006.09.022, PII S1542356506009505Collier, J., Bone disorders in chronic liver disease (2007) Hepatology, 46 (4), pp. 1271-1278. , DOI 10.1002/hep.21852Lewiecki, E.M., Gordon, C.M., Baim, S., Leonard, M.B., Bishop, N.J., Bianchi, M.L., International Society for Clinical Densitometry 2007 Adult and Pediatric Official Positions (2008) Bone, 43, pp. 1115-1121Lérias, C., Portela, F., Da Silva, A.P., Osteoporose na Doença Inflamatória Intestinal (2000) GE - J Portug Gastrenterol, 7, pp. 203-214Labio, E.D., Del, R.D.B., Strasser, S.I., McCaughan, G.W., Crawford, B.A., Effect of Ascites on Bone Density Measurement in Cirrhosis (2007) Journal of Clinical Densitometry, 10 (4), pp. 391-394. , DOI 10.1016/j.jocd.2007.07.001, PII S1094695007001813George, J., Ganesh, H.K., Acharya, S., Bandgar, T.R., Shivane, V., Karvat, A., Bone mineral density and disorders of mineral metabolism in chronic liver disease (2009) World J Gastroenterol, 15, pp. 3516-3522Daniel, D.B., Vitamin, D., Insufficiency/Deficiency in Gastrointestinal Disorders (2007) J Bone Miner Res, 22, pp. V50-V54PcDuarte, M., Farias, M.L.F., Coelho, H.S.M., McMendonca, L., MdStabnov, L., Oliveira, M.D.C.D., Lamy, R.A., Oliveira, D.S., Calcium-parathyroid hormone-vitamin D axis and metabolic bone disease in chronic viral liver disease (2001) Journal of Gastroenterology and Hepatology, 16 (9), pp. 1022-1027. , DOI 10.1046/j.1440-1746.2001.02561.xPares, A., Guanabens, N., Treatment of bone disorders in liver disease (2006) Journal of Hepatology, 45 (3), pp. 445-453. , DOI 10.1016/j.jhep.2006.06.007, PII S0168827806003394Maerevoet, M., Martin, C., Duck, L., Osteonecrosis of the jaw and biphosphanates (2005) N Engl J Med, 353, pp. 99-102Beuers, U., Boberg, K.M., Chapman, R.W., Chazouillères, O., Invernizzi, P., Jones, D.E., EASL Clinical Practice Guidelines: Management of cholestatic liver diseases (2009) J Hepatol, 51, pp. 237-267. , European Association for the Study of the LiverPares, A., Guanabens, N., Osteoporosis in Primary Biliary Cirrhosis: Pathogenesis and Treatment (2008) Clinics in Liver Disease, 12 (2), pp. 407-424. , DOI 10.1016/j.cld.2008.02.005, PII S1089326108000226Wariaghli, G., Mounach, A., Achemlal, L., Benbaghdadi, I., Aouragh, A., Bezza, A., Osteoporosis in chronic liver disease: A case-control study (2010) Rheumatol Int, 30, pp. 893-899Peter, R.E., Approach to the Patient with Transplantation-Related Bone Loss (2009) J Clin Endocrinol Metab, 94, pp. 1483-1490. , MayNinkovic, M., Love, S., Tom, B.D.M., Bearcroft, P.W.P., Alexander, G.J.M., Compston, J.E., Lack of effect of intravenous pamidronate on fracture incidence and bone mineral density after orthotopic liver transplantation (2002) Journal of Hepatology, 37 (1), pp. 93-100. , DOI 10.1016/S0168-8278(02)00100-9, PII S0168827802001009Pennisi, P., Trombetti, A., Giostra, E., Mentha, G., Rizzoli, R., Fiore, C.E., Pamidronate and osteoporosis prevention in liver transplant recipients (2007) Rheumatology International, 27 (3), pp. 251-256. , DOI 10.1007/s00296-006-0196-2Hommann, M., Abendroth, K., Lehmann, G., Patzer, N., Kornberg, A., Voigt, R., Seifert, S., Scheele, J., Effect of transplantation on bone: Osteoporosis after liver and multivisceral transplantation (2002) Transplantation Proceedings, 34 (6), pp. 2296-2298. , DOI 10.1016/S0041-1345(02)03242-6, PII S0041134502032426Crawford, B.A.L., Kam, C., Pavlovic, J., Byth, K., Handelsman, D.J., Angus, P.W., McCaughan, G.W., Zoledronic acid prevents bone loss after liver transplantation: A randomized, double-blind, placebo-controlled trial (2006) Annals of Internal Medicine, 144 (4), pp. 239-248Hay, J.E., Guichelaar, M.M.J., Evaluation and management of osteoporosis in liver disease (2005) Clinics in Liver Disease, 9 (4), pp. 747-766. , DOI 10.1016/j.cld.2005.07.003, PII S1089326105000644, Recent Advances in the Treatment of Liver DisordersCarey, E.J., Balan, V., Kremers, W.K., Hay, J.E., Osteopenia and osteoporosis in patients with end-stage liver disease caused by hepatitis C and alcoholic liver disease: Not just a cholestatic problem (2003) Liver Transplantation, 9 (11), pp. 1166-1173. , DOI 10.1053/jlts.2003.50242Newton, J., Francis, R., Prince, M., James, O., Bassendine, M., Rawlings, D., Jones, D., Osteoporosis in primary biliary cirrhosis revisited (2001) Gut, 49 (2), pp. 282-287. , DOI 10.1136/gut.49.2.282Kaneki, M., Hosoi, T., Ouchi, Y., Orimo, H., Pleiotropic actions of vitamin K: protector of bone health and beyond? (2006) Nutrition, 22 (7-8), pp. 845-852. , DOI 10.1016/j.nut.2006.05.003, PII S089990070600222XMoschen, A.R., Kaser, A., Stadlmann, S., Millonig, G., Kaser, S., Muhllechner, P., Habior, A., Tilg, H., The RANKL/OPG system and bone mineral density in patients with chronic liver disease (2005) Journal of Hepatology, 43 (6), pp. 973-983. , DOI 10.1016/j.jhep.2005.05.034, PII S0168827805004198Hofmann, W.P., Kronenberger, B., Bojunga, J., Stamm, B., Herrmann, E., Bücker, A., Prospective study of bone mineral density and metabolism in patients with chronic hepatitis C during pegylated interferon a and ribavirin therapy (2008) Journal of Viral Hepatitis, 15, pp. 790-796Leslie, W.D., Bernstein, C.N., Leboff, M.S., AGA Technical Review on Osteoporosis in Hepatic Disorders (2003) Gastroenterology, 125, pp. 941-966. , American Gastroenterological Association Clinical Practice CommiteeCollier, J.D., Ninkovic, M., Compston, J.E., Guidelines on the management of osteoporosis associated with chronic liver disease (2002) Gut, 50 (SUPPL. 1), pp. i1-i

Gastric Polyps: A Retrospective Analysis Of 26,000 Digestive Endoscopies

Background - Gastric polyps are small gastric lesions, asymptomatic in most cases and are generally discovered inadvertently during upper digestive endoscopy. Aim - To retrospectively review the characteristics and frequency of gastric polyps, derived from the gastric mucosal epithelium in a large series of endoscopies. Methods - One hundred and fifty three patients in a series of 26,000 consecutive upper digestive endoscopies done over a 5-year period, being that each patient had only one examination were analyzed and their histological and Yamada classification, as well as their location, size, histopathological findings and treatment studied. All patients had at least one gastric polyp, as confirmed by histological examination. Results - The polyps were classified as hyperplastic, adenomatous and fundic gland polyps. The most of them measure less than 1 cm (hyperplastic polyps - 60,5%; adenomatous polyps - 73,6%; fundic gland polyps - 72%). Hyperplastic polyps were the most frequent and accounted for 71.3% of the cases, whereas fundic gland polyps accounted for 16.3% and adenomatous polyps for 12.4%. Hyperplastic and adenomatous polyps were primarily single, whereas fundic gland polyps tended to be multiple. A carcinoma was detected in one hyperplastic polyp (0.9%) and in two adenomatous polyps (10.5%). High grade dysplastic foci were found in four adenomatous polyps (21%). Conclusions - The digestive endoscopy is the safest and efficient method for the diagnosis of the gastric polyps, that in most of the patients does not show characteristic symptoms. The histopathological definition is not possible to the endoscopic glance being needed the pathologist's aid, once the conduct to be adopted will depend on the result of the biopsy.4411417Burt, R.W., Gastric fundic gland polyps (2003) Gastroenterology, 125, pp. 1462-1469Daibo, M., Itabashi, M., Hirota, T., Malignant transformation of gastric hyperplastic polyp (1987) Am J Gastroenterol, 82, pp. 1016-1025Deppish, L.M., Rona, V.T., Gastric epithelial polyps: A 10-year study (1989) J Clin Gastroenterol, 11, pp. 10-15Di Giulio, E., Lahner, E., Micheletti, A., Milione, M., D'Ambra, G., Bordi, C., Delle Fave, G., Annibale, B., Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-up (2005) Aliment Pharmacol Ther, 21, pp. 567-567Ginsberg, G.G., Firas, H.A.K., Fleischer, D.E., Reilly, H.F., Benjamin, S.B., Gastric polyps: Relationship of size and histology to cancer risk (1995) Am J Gastroenterol, 91, pp. 714-717Hattori, T., Morphological range of hyperplastic polyps of the stomach (1985) J Clin Pathol, 38, pp. 622-630Hnizdil, L., Piskac, P., Dvorak, M., Endoscopic gastric polypectomy - personal experience (2002) Rozhl Chir, 81, pp. 324-326Hughes, R., Gastric polyps and polypectomy: Rational, technique and complications (1984) Gastrointest Endosc, 30, pp. 101-102Macenlle-Garcia, R., Bassante-Flores, L.A., Fernandez-Seara, J., Gastric epithelial polyps. A retrospectrive study 1995-2000 (2003) Rev Clin Esp, 203, pp. 368-372Ming, S.C., Malignant potential of epithelial polyps of stomach (1984) Precursors of gastric cancer, p. 219. , Ming SC, editor, New York: Praeger;Muehldorfer, S.M., Stolte, M., Martus, P., Hahn, E.G., Ell, C., Diagnostic accuracy of forceps biopsy versus polypectomy for gastric polyps: A prospective multicentre study (2002) Gut, 50, pp. 465-470Nakamura, T., Nakano, G., Histopathological classification and malignant chance in gastric polyps (1985) J Clin Pathol, 38, pp. 754-764Oota K. Histological typing of gastric and oesophageal tumors. In: WHO, editor. International classification of tumors, 18. Genève: WHO1977. p.37Palacios-Salas, F., Frisancho-Velarde, O., Palomino-Portilla, E., Gastric polyps and histological changes in surrounding mucosa (2003) Rev Gastroenterol Peru, 23, pp. 245-253Randall, G.M., Endoscopic diagnosis of gastric neoplasm (1992) Gastrointest Endosc Clin North Am, 2, pp. 469-493Robbins, S.L., Tumors of the stomach (1995) Pathological basis of disease, p. 161. , Robbins SL, editor, Boston: W.B. Saunders;Seifert, E., Gail, K., Weismuller, J., Gastric polypectomy (1985) Endoscopy, 15, pp. 8-11Sivelli, R., Del Rio, P., Bonati, L., Sianesi, M., Gastric polyps: A clinical contribution (2002) Chir Ital, 54, pp. 37-40Snover, D., Benign epithelial polyps of the stomach (1985) Pathol Ann, 20 (PART I), pp. 303-329Yamada, T., Ichikawa, H., X-ray diagnosis of elevated lesions of the stomach (1974) Radiology, 110, pp. 79-8

Eosinophilic Esophagitis In Adults [esofagite Eosinofílica Em Adultos]

Eosinophilic esophagitis is a primary inflammatory chronic disease, with eosinophilic infiltration into the esophagus mucosa. It has undefined pathogenesis, but there is an important association with allergic disorders and family history. The main features are dysphagia, food impaction and heartburn may occur. The diagnosis is made by endoscopy and histologic analysis of the esophagus mucosa. The most effective treatment has been topic corticosteroid, with good clinical and histological outcomes. © Copyright Moreira Jr. Editora.659273278Straumann, A., Simon, H.U., The physiological and pathophysiological roles of eosinophils in the gastrointestinal tract (2004) Allergy, 59, pp. 15-25Barak, N., Hart, J., Sitrin, M.D., Enalapril-induced eosinophilic gastroenteritis (2001) J Clin Gastroenterol, 33, pp. 157-158Dhawan, A., Seemayer, T.A., Pinsinski, C., Posttransplant eosinophilic gastroenteritis in children (1997) Liver Transpl, 3, pp. 591-593Egesten, A., Andersson, P., Persson, T., Eosinophils in gastrointestinal inflammation: From innocent bystanders to offenders (2002) Scan J Gastroenterol, 37, pp. 1117-1125Straumann, M.D., Beglinger, C., Eosinophilic esophagitis: The endoscopist's enigma (2006) Gastrointest Endosc, 63 (1), pp. 13-14Furuta, G.T., Liacouras, C.A., Collins, M.H., Eosinophilic Esophagitis in Children and Adults: A Systematic Review and Consensus Recommendations for Diagnosis and Treatment (2007) Gastroenterology, 133, pp. 1342-1363Landres, R.T., Kuster, G.G., Strum, W.B., Eosinophilic esophagitis in a patient with vigorous achalasia (1978) Gastroenterology, 74, pp. 1298-1301Pasha, S.F., DiBaise, J.K., Kim, H.J., Patient characteristics, clinical, endoscopic and histologic findings in adult eosinophilic esophagitis: A case series and systematic review of the medical literature (2007) Dis Esophagus, 20, pp. 311-319Noel, R.J., Putman, P.E., Rothenburg, M.E., Eosinophilic esophagitis (2004) N Engl J Med, 351, pp. 940-941Desai, T.K., Stecevic, V., Chang, C.-H., Goldstein, N.S., Badizadegan, K., Furuta, G.T., Association of eosinophilic inflammation with esophageal food impaction in adults (2005) Gastrointest Endosc, 61, pp. 785-801Straumann, A., Simon, H.U., Eosinophilic esophagitis: Escalating epidemiology? (2005) J Allergy Clin Immunol, 115, pp. 418-419Straumann, A., Spichtin, H.P., Grize, L., Bucher, K.A., Beglinger, C., Simon, H.U., Natural history of primary eosinophilic esophagitis: A follow up of 30 adults patients for up to 11.5 years (2003) Gastroenterology, 125, pp. 1660-1669Dellon, E.S., Aderoju, A., Woosley, J.T., Sandler, R.S., Shaheen, N.J., Variability in Diagnostic Criteria for Eosinophilic Esophagitis: A Systematic Review (2007) Am J Gastroenterol, 102, pp. 1-14Croese, J., Fairley, S.K., Masson, J.W., Clinical and Endoscopic Features of Eosinophilic Esophagitis in Adults (2005) Gastrointest Endosc, 58, pp. 516-522Orenstein, S.R., Shalaby, T.H., DiLorenzo, C., Putan, P.E., Sigurdsson, L., Kocoshis, S.A., The spectrum of pediatric eosinophilic esophagitis beyond infancy: A clinical series of 30 children (2000) Am J Gastroenterol, 95, pp. 1422-1430Teitelbaum, J.E., Fox, V.L., Twarog, F.J., Eosinophilic esophagitis in children: Immunopathological analysis and response to fluticasone propionate (2002) Gastroenterology, 122, pp. 116-125Remedios, M., Campbell, C., Jones, D.M., Kerlin, P., Eosinophilic esophagitis in adults: Clinical, endoscopic, histologic findings and response to treatment with fluticasone propionate (2006) Gastrointest Endosc, 63, pp. 3-12Quaglietta, L., Coccorullo, P., Miele, E., Pascarella, F., Troncone, R., Straiano, A., Eosinophilic esophagitis and celiac disease: Is there an association? (2007) Aliment Pharmacol Ther, 26, pp. 487-493Khan S, Orenstein SR. - Eosinophilic Disorders of the Gastrointestinal Tract. In: Feldman M, Friedman LS, Brandt LJ. Gastrointestinal and Liver Disease, Philadelphia, Saunders Elsevier, 8th ed, I, 2006. P543-56Winterkamp, S., Raithel, M., Hahn, E.G., Secretion and tissue content of eosinophil cationic protein in Crohn's disease (2000) J Clin Gastroenterol, 30, pp. 170-175Fogg, M.I., Ruchelli, E., Spergel, J.M., Pollen and eosinophilic esophagitis (2003) J Allergy Clin Immunol, 112, pp. 796-797Mishra, A., Hogan, S.P., Brandt, E.B., Rothenberg, M.E., An etiological role for aeroallergens and eosinophils in experimental esophagitis (2001) J Clin Invest, 107, pp. 83-87Konikoff, M.R., Blanchard, C., Kirby, C., Potential of blood eosinophils, eosinophil-derived neurotoxin and eotaxin-3 as biomarkers of eosinophilic esophagitis (2006) Clin Gastroenterol Hepatol, 4, pp. 1328-1336Zimmerman, S.L., Levine, M.S., Rubesin, S.E., Idiopatic eosinophilic esophagitis in adults: The ringed esophagus (2005) Radiology, 236, pp. 159-165Kaplan, M., Mutlu, E.A., Jakate, S., Endoscopy in eosinophilic esophagitis: "feline" esophagus and perforation risk (2003) Clin Gastroenterol Hepatol, 1, pp. 433-437Potter JW, Saeian K, Staff D, et al. - Eosinophilic esophagitis in adults: am emerging problem with unique esophageal features. Gastrointest Endosc 200459:355-61Baxi, S., Gupta, S.K., Swigonski, N., Clinical presentation of patients with eosinophilic inflammation of the esophagus (2006) Gastrointest Endosc, 64, pp. 473-478Castell, D.O., Mainie, I., Tutuian, R., Non-acid gastroesophageal reflux: Documenting its relationship to symptoms using multichannel intraluminal impedance (MII) (2005) Trans Am Clin Climatol Assoc, 116, pp. 321-333Fox, V.L., Nurko, S., Teitelbaum, J.E., Badizadegan, K., Furuta, G.T., High-resolution EUS in children with eosinophilic "allergic" esophagitis (2003) Gastrointest Endosc, 57, pp. 30-36Attwood, S.E., Smyrk, T.C., Demeester, T.R., Esophageal eosinophilia with disphagia. A distinct clinicopathologic syndrome (1993) Dig Dis Sci, 38, pp. 109-116Lee, R.G., Marked eosinophilia in esophageal mucosal biopsies (1985) Am J Surg Pathol, 9, pp. 475-479Ronkainen, J., Talley, N.J., Aro, P., Prevalence of esophageal eosinophilis and eosinophilic esophagitis in adults: The population-based Kalixanda study (2007) Gut, 56, pp. 615-620Straumann, A., Rossi, L., Simon, H.U., Heer, P., Spichtin, H.P., Beglinger, C., Fragility of the esophageal mucosa: A pathognomonic endoscopic sign of primary eosinophilic esophagitis? (2003) Gastrointest Endosc, 57, pp. 407-412Straumann, A., Spichtin, H.P., Bucher, K.A., Eosinophilic esophagitis: Red on microscopy, white on endoscopy (2004) Digestion, 70, pp. 109-116Gonsalves, N., Policarpio-Nicolas, M., Zhang, Q., Rao, M.S., Hirano, I., Histophatologic variability and endoscopic correlates in adults with eosinophilic esophagitis (2006) Gastrointest Endosc, 64, pp. 313-319Parfitt, J.R., Gregor, J.C., Suskin, N.G., Eosinophilic esophagitis in adults: Distinguishing features from gastroesophageal reflux disease: a study of 41 patients (2006) Mod Pathol, 19, pp. 90-96Walsh, S., Antonioli, D., Goldman, H., Allergic esophagitis in children- a clinicopathological entity (1999) Am J Surg Pathol, 23, pp. 390-396Noel, R.J., Putnam, P.E., Collins, M.H., Clinical and immunopathologic effects of swallowed fluticasone for eosinophilic esophagitis (2004) Clin Gastroenterol Hepatol, 2, pp. 568-575Gupta, S.K., Fitzgerald, J.F., Chong, S.K.F., Croffie, J.M., Collins, M.H., Vertical lines in distal esophageal mucosa (VLEM): A true endoscopic manifestation of esophagitis in children? (1997) Gastrointest Endosc, 45, pp. 485-489Untersmayr, E., Scholl, I., Swoboda, L., Antacid medication inhibits digestion of dietary proteins and causes food allergy: A fish allergy model in BALB/c mice (2003) J Allergy Clin Immunol, 112, pp. 616-623Untersmayr, E., Bakos, N., Scholl, I., Anti-ulcer drugs promote IgE formation toward dietary antigens in adult patients (2005) FASEB J, 19, pp. 656-658Steiner, S.J., Gupta, S.K., Croffie, J.M., Fitzgerald, J.F., Correlation between number of eosinophils and reflux index on same day esophageal biopsy and 24 hour esophageal pH monitoring (2004) Am J Gastroenterol, 99, pp. 801-805Sant'Anna, A.M., Rolland, S., Fournet, J.C., Yazbeck, S., Drouin, E., Eosinophilic esophagitis in children: Symptoms, histology, and pH probe results (2004) J Pediatr Gastroenterol Nutr, 39, pp. 373-377Liacouras, C.A., Spergel, J.M., Ruchelli, E., Eosinophilic esophagitis: A 10-year experience in 381 children (2005) Clin Gastroenterol Hepatol, 3, pp. 1198-1206Kelly, K.J., Lazenby, A.J., Rowe, P.C., Yardley, J.H., Perman, J.A., Sampson, H.A., Eosinophilic esophagitis attributed to gastroesophageal reflux: Improvement with an amino acid-based formula (1995) Gastroenterology, 109, pp. 1503-1512Markowitz, J.E., Spergel, J.M., Ruchelli, E., Liacouras, C.A., Elemental diet is an effective treatment for eosinophilic esophagitis in children and adolescents (2003) Am J Gastroenterol, 98, pp. 777-782Spergel, J.M., Andrews, T., Brown-Whitehorn, T.F., Beausoleil, J.L., Liacouras, C.A., Treatment of eosinophilic esophagitis with specific food elimination diet directed by a combination of skin prick and patch tests (2005) Ann Allergy Asthma Immunol, 95, pp. 336-343Kagalwalla, A.F., Sentongo, T.A., Ritz, S., Effect of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis (2006) Clin Gastroenterol Hepatol, 4, pp. 1097-1102Attwood, S.E., Lewis, C.J., Bronder, C.S., Morris, C.D., Armstrong, G.R., Whittam, J., Eosinophilic oesophagitis: A novel treatment using Montelukast (2003) Gut, 52, pp. 181-185Gupta, S.K., Peters-Golden, M., Fitzgerald, J.F., Cysteinyl leukotriene levels in esophageal mucosal biopsies of children with eosinophilic inflammation: Are they all the same? (2006) Am J Gastroenterol, 101, pp. 1125-1128Simon, D., Braathen, L.R., Simon, H.U., Anti-interleukin-5 antibody therapy in eosinophilic diseases (2005) Pathobiology, 72, pp. 287-292Garrett, J.K., Jameson, S.C., Thomson, B., Antiinterleukin-5 (mepolizumab) therapy for hypereosinophilic syndromes (2004) J Allergy Clin Immunol, 113, pp. 115-119Nurko, S., Teitelbaum, J.E., Husain, K., Association of Schatzki ring with eosinophilic esophagitis in children (2004) J Pediatr Gastroenterol Nutr, 38, pp. 436-441Langdon, D.E., Primary eosinophilic esophagitis (2004) Gastroenterology, 127, pp. 364-365Sanjeevi, A., Ashwat, G., Komorowski, R., Massey, B., Shaker, R., Hogan, W., Early recognition and specific medical treatment affects the frequency of esophageal dilatations in patients with eosinophilic esophagitis (2006) Gastrointest Endosc, 64, pp. 128-13

Peptic Ulcer [Úlcera Péptica]

Peptic ulcer is a common disease. The Helicobacter pylori infection and the use of anti-inflammatory drugs are the main risk factors. There is no characteristic clinical finding and some patients have no symptom. Epigastric pain is a common finding and is associated with food. The diagnosis is done by upper gastrointestinal endoscopy and endoscopic biopsies can identificate H.pylori. Eradication of the organism is the therapy of choice in infected patients. Drugs that inhibit acid gastric secretion can promote ulcer healing in almost all patients. The protom pump inhibitors are the most effective. They can be used in prevention of ulcer in high risk patients that use anti-inflammatory, as in elderly, patients with severe comorbid conditions and patients taking corticosteroids or anticoagulants.60SPEC. ISS.2532Kurata, J.H., Epidemiology of peptic ulcer disease (1984) Clin Gastroenterol, 13, p. 289Munnangi, S., Time trends of physician visits and treatment patterns of peptic ulcer disease in the United States (1997) Arch Intern Med, 157, pp. 1489-1494Higham, J., Kang, J.Y., Majeed, A., Recent trends in admissions and mortality due to peptic ulcer in England: Increasing frequency of haemorrhage among older subjects (2002) Gut, 50, pp. 460-464Marshall, B.J., Warren, J.R., Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulcerations (1984) Lancet, 1, pp. 1311-1315Cohen, H., Peptic ulcer and Helicobacter pylori (2000) Gastroenterol Clin North Am, 29, p. 775El-Omar, E.M., Penman, I.D., Ardill, J.E., Chittajallu, R.S., Howie, C., McColl, K.E., Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease (1995) Gastroenterology, 109, pp. 681-691Beales, I., Calam, J., Post, L., Effect of transforming growth factor alpha and interleukin 8 on somatostatin release from canine fundic D cells (1997) Gastroenterology, 112, pp. 136-143Hogan, D.L., Rapier, R.C., Dreilinger, A., Duodenal bicarbonate secretion: Eradication of Helicobacter pylori and duodenal structure and function in humans (1996) Gastroenterology, 110, pp. 705-716Segal, E.D., Cha, J., Lo, J., Falkow, S., Tompkins, L.S., Altered states: Involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori (1999) Proc Natl Acad Sci USA, 96, pp. 14559-14564Uemura, N., Okamoto, S., Yamamoto, S., Helicobacter infection and the development of gastric cancer (2001) N Engl J Med, 345, pp. 784-789Wolfe, M.M., Lichtenstein, D.R., Singh, G., Gastrointestinal toxicity of non-steroidal anti-inflammatory drugs (1999) N Engl J Med, 340, p. 1888Wallace, J.L., Keenan, C.M., Granger, D.N., Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil-dependent process (1990) Am J Physiol, 259, pp. 462-467Silverstein, F.E., Faich, G., Goldstein, J.L., Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflamamatory drugs for osteoarthritis and rheumatoid arthritis (2000) JAMA, 284, pp. 1247-1255Wallace, J.L., McKnight, W., Reuter, B.K., Vergnolle, N., NSAID-induced gastric damage in rats: Requirement for inhibition of both cyclooxygenase 1 and 2 (2000) Gastroenterology, 119, pp. 706-714Huang, J.Q., Sridhar, S., Hunt, R.H., Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: A meta-analysis (2002) Lancet, 359, pp. 14-22Zeitune, J.M.R., Monici, L.T., Nishimura, N.F., Diagnóstico da infecção pelo Helicobacter pylori (2000) Gastroenterologia III/Farid Nader, , Pelotas: Editora UniversitáriaBorody, T.J., Cole, P., Noonan, S., Recurrence of duodenal ulcer and Campylobacter pylori infection after eradication (1989) Med J Aust, 151, pp. 431-435Porro, G.B., Parente, F., Antacids for duodenal ulcer: Current role (1990) Scand J Gastroenterol, 25, p. 48Deakin, M., Williams, J.G., Histamine H2-receptor antagonists in peptic ulcer disease. Efficacy in healing peptic ulcers (1992) Drugs, 44, p. 709Lee, F.I., Collin-Jones, D.G., Golding, P.L., Double-blind comparative study of omeprazole and ranitidine in patients with duodenal or gastric ulcer: A multicentre trial (1991) Gut, 26, p. 137Malfertheiner, P., Megraud, F., O'Morain, C., Current concepts in the management of Helicobacter pylori infection: The Maastricht 2-2000 Consensus Report (2002) Aliment Pharmacol Ther, 16, pp. 167-180Vaira, D., Vakil, N., Menegatti, M., The stool antigen test for detection of Helicobacter pylori after eradication therapy (2002) Ann Intern Med, 136, pp. 280-287Yeomans, N.D., Tulassay, Z., Juhasz, L., Omeprazole compared with ranitidine for ulcers associated with nonsteroidal antiinflamatory drugs (1998) N Engl J Med, 338, pp. 719-726Rich, M., Scheiman, J., Nonsteroidal anti-inflammatory drug gastropathy at the new millennium: Mechanisms and prevention (2000) Sem Arthritis Rheum, 30, p. 167Norton, J., Surgery to cure Zollinger-Ellison syndrome (1999) N Engl J Med, 341, p. 63

Esophageal Lesion During Endoscopic Variceal Ligation [lesao Esofagica Durante Ligadura Elastica De Varizes]

The authors present a case of cervical esophageal laceration after endoscopic variceal band ligation caused by overtube. Complications of band ligation are not frequently described, but can be serious. This case had a good evolution with clinical treatment. The authors discuss the case and present a review of the literature about complications of band ligations.16310310

Inflammatory bowel disease in an underdeveloped region of northeastern Brazil

AIM: To evaluate the demographic characteristics and clinical phenotypes of inflammatory bowel disease (IBD) in a geographic area in Northeastern Brazil. METHODS: This retrospective study was conducted at the Hospital of the Federal University of Piauí in Northeastern Brazil. Demographic characteristics and clinical phenotypes of IBD were analyzed in relation to the time of diagnostic confirmation, which was defined as the date of disease onset. Data were collected between January 2011 and December 2012 and included all census patients 18 years of age or older during that period for whom there was diagnostic confirmation of Crohn's disease (CD), ulcerative colitis (UC), or unclassified colitis according to the Montreal criteria. We also analyzed the period of time between the onset of clinical manifestations and the diagnosis of IBD (delay in the diagnosis). Statistical analyses included means and standard deviations for numeric variables and the Pearson Χ 2 adherence test for nominal variables. The annual index occurrence and overall prevalence of IBD at our institution were also calculated, with P values < 0.05 indicating statistical significance. This study was approved by the Institutional Ethics and Research Committee. RESULTS: A total of 252 patients with IBD were included, including 152 (60.3%) UC patients and 100 (39.7%) CD patients. The clinical and demographic characteristics of all patients with IBD showed a female to male ratio of 1.3:1.0 and a mean age of 35.2 (SD=14.5) years. In addition, the majority of patients were miscegenated (171, 67.9%), had received higher education (157, 62.4%), lived in urban areas (217, 86.1%), and were under the age of 40 years (97, 62.5%). For patients with CD, according to the Montreal classification, the predominant features present from the onset of disease were an age between 17 and 40 years (A2); colonic disease location (L2); and nonstricturing, nonfistulizing disease behavior (B1). However, approximately one-quarter of all CD patients demonstrated perineal involvement. We also observed considerable delay in the diagnosis of IBD throughout the entire study period (mean=35.5 mo). In addition, the annual index occurrence rose from 0.08 to 1.53 cases/105 inhabitants/year during the study period, and the prevalence rate was 12.8 cases/105 inhabitants in 2012. Over the last two decades, there was a noted increase in the frequency of IBD in the study area. CONCLUSION: In this study, there was a predominance of patients with UC, young people under 40 years of age, individuals with racial miscegenation, and low annual incomes.To evaluate the demographic characteristics and clinical phenotypes of inflammatory bowel disease (IBD) in a geographic area in Northeastern Brazil. METHODS: This retrospective study was conducted at the Hospital of the Federal University of Piauí in Northeastern Brazil. Demographic characteristics and clinical phenotypes of IBD were analyzed in relation to the time of diagnostic confirmation, which was defined as the date of disease onset. Data were collected between January 2011 and December 2012 and included all census patients 18 years of age or older during that period for whom there was diagnostic confirmation of Crohn's disease (CD), ulcerative colitis (UC), or unclassified colitis according to the Montreal criteria. We also analyzed the period of time between the onset of clinical manifestations and the diagnosis of IBD (delay in the diagnosis). Statistical analyses included means and standard deviations for numeric variables and the Pearson Χ 2 adherence test for nominal variables. The annual index occurrence and overall prevalence of IBD at our institution were also calculated, with P values < 0.05 indicating statistical significance. This study was approved by the Institutional Ethics and Research Committee. RESULTS: A total of 252 patients with IBD were included, including 152 (60.3%) UC patients and 100 (39.7%) CD patients. The clinical and demographic characteristics of all patients with IBD showed a female to male ratio of 1.3:1.0 and a mean age of 35.2 (SD=14.5) years. In addition, the majority of patients were miscegenated (171, 67.9%), had received higher education (157, 62.4%), lived in urban areas (217, 86.1%), and were under the age of 40 years (97, 62.5%). For patients with CD, according to the Montreal classification, the predominant features present from the onset of disease were an age between 17 and 40 years (A2); colonic disease location (L2); and nonstricturing, nonfistulizing disease behavior (B1). However, approximately one-quarter of all CD patients demonstrated perineal involvement. We also observed considerable delay in the diagnosis of IBD throughout the entire study period (mean=35.5 mo). In addition, the annual index occurrence rose from 0.08 to 1.53 cases/105 inhabitants/year during the study period, and the prevalence rate was 12.8 cases/105 inhabitants in 2012. Over the last two decades, there was a noted increase in the frequency of IBD in the study area. CONCLUSION: In this study, there was a predominance of patients with UC, young people under 40 years of age, individuals with racial miscegenation, and low annual incomes2141197120