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13 results on '"Laudanna, Antonio Atilio"'

5. The impact of Helicobacter pylori resistance on the efficacy of a short course pantoprazole based triple therapy

Author

Eisig, Jaime Natan, André, Suraia Boaventura, Silva, Fernando Marcuz, Hashimoto, Cláudio, Moraes-Filho, Joaquim Prado Pinto, and Laudanna, Antonio Atilio

Subjects
Peptic ulcer, Infecções por helicobacter, Helicobacter pylori, Sulfoxides, Úlcera péptica, Benzimidazoles, Benzimidazóis, Sulfóxidos, Anti-ulcer agents, Antiulcerosos, Helicobacter infections
Abstract

BACKGROUND: Many of the currently used Helicobacter pylori eradication regimens fail to cure the infection due to either antimicrobial resistance or poor patient compliance. Those patients will remain at risk of developing potentially severe complications of peptic ulcer disease. AIM: We studied the impact of the antimicrobial resistance on the efficacy of a short course pantoprazole based triple therapy in a single-center pilot study. METHODS: Forty previously untreated adult patients (age range 20 to 75 years, 14 males) infected with Helicobacter pylori and with inactive or healing duodenal ulcer disease were assigned in this open cohort study to 1 week twice daily treatment with pantoprazole 40 mg, plus clarithromycin 250 mg and metronidazole 400 mg. Helicobacter pylori was assessed at entry and 50 ± 3 days after the end of treatment by rapid urease test, culture and histology of gastric biopsies. The criteria for eradication was a negative result in the tests. Susceptibility of Helicobacter pylori to clarithromycin and metronidazole was determined before treatment with the disk diffusion test. RESULTS: One week treatment and follow up were complete in all patients. Eradication of Helicobacter pylori was achieved in 35/40 patients (87.5%) and was higher in patients with nitroimidazole-susceptible strains [susceptible: 20/20 (100%), resistant: 10/15 (67%)]. There were six (15%) mild adverse events reports. CONCLUSIONS: A short course of pantoprazole-based triple therapy is well tolerated and effective in eradicating Helicobacter pylori. The baseline metronidazole resistance may be a significant limiting factor in treatment success. OBJETIVO: Vários esquemas utilizados na erradicação do Helicobacter pylori falham por resistência ao antibiótico ou por pouca aderência ao tratamento pelo paciente. Esses pacientes permanecerão com alto risco de desenvolver complicações decorrentes da úlcera péptica. Assim, estudou-se o impacto da resistência antimicrobiana na eficácia de esquema tríplice em um único centro. MÉTODOS: Quarenta pacientes, virgens de tratamento para erradicação da bactéria (idade entre 20 e 75 anos, 14 homens) infectados pelo Helicobacter pylori e com úlcera duodenal ativa ou em cicatrização foram avaliados em um estudo aberto durante 1 semana com esquema de tratamento constituído por pantoprazol 40 mg, claritromicina 250 mg e metronidazol 400 mg, todos administrados duas vezes ao dia. A presença do Helicobacter pylori foi analisada no início e entre 50 ± 3 dias após o final do tratamento, pelo teste rápido da urease, cultura e histologia, obtidos através de biopsias gástricas. O critério de erradicação foi o resultado negativo em todos os testes. A susceptibilidade da claritromicina e metronidazol foi determinada antes do tratamento pelo teste de disco difusão em agar. RESULTADOS: O tratamento e o seguimento foi completo em todos os pacientes. A erradicação do Helicobacter pylori foi verificada em 35/40 pacientes (87,5%) e foi maior nos pacientes com cepas susceptíveis ao nitroimidazólico (susceptíveis 20/20 (100%), resistentes 10/15 (67%)). Seis pacientes (15%) referiram sintomas adversos leves. CONCLUSÕES: O esquema tríplice a curto prazo com pantoprazol é bem tolerado e efetivo na erradicação do Helicobacter pylori. A resistência ao metronidazol pode ser fator limitante significativo no sucesso terapêutico.

Published
2003

6. Prevalence of immune disturbances and chronic liver disease in family members of patients with primary biliary cirrhosis

Author

BITTENCOURT, PAULO LISBOA, primary, FARIAS, ALBERTO QUEIROZ, additional, ABRANTES-LEMOS, CLARICE PIRES, additional, GONCALVES, LUCIANA LOFEGO, additional, GONCALVES, PATRICIA LOFEGO, additional, MAGALHAES, EMILIA PEREIRA, additional, CARRILHO, FLAIR JOSE, additional, LAUDANNA, ANTONIO ATILIO, additional, and CANCADO, EDUARDO LUIZ RACHID, additional

Published
2004
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9. Celiac Disease in Brazilian Adults

Author

de Freitas, Isabella Nicácio, primary, Sipahi, Aytan Miranda, additional, Damião, Adérson O.M.C., additional, de Brito, Thales, additional, Cançado, Eduardo Luiz Rachid, additional, Leser, Paulo Guilherme, additional, and Laudanna, Antonio Atilio, additional

Published
2002
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11. Celiac Disease in Brazilian Adults

Author

Freitas, Isabella Nicácio de, Sipahi, Aytan Miranda, Damião, Adérson O.M.C., de Brito, Thales, Cançado, Eduardo Luiz Rachid, Leser, Paulo Guilherme, and Laudanna, Antonio Atilio

Abstract

Forty-eight adult patients with celiac disease between 15 and 68 years of age (mean, 41 years) were studied. Sixty-seven percent were female and 33 were male patients. Most of the patients were white (98). The main clinical features were diarrhea (90), weight loss (70), and abdominal pain (56). On physical examination, the main findings were pallor (40), aphthous stomatitis (31), and arthralgia (23). Associated disorders included diabetes mellitus type I, osteoporosis, and atopy (6 each); dermatitis herpetiformis and depression (4 each); and hypothyroidism, hyperthyroidism, duodenal carcinoma, and Gilbert syndrome (2 each). The histologic results according to Marsh criteria (modified by Rostami) are as follows type I, 10; type II, 21; type IIIa, 19; type IIIb, 17; and type IIIc, 33. The sensitivity and specificity for the antiendomysium antibody–immunoglobulin A test were 92 and 100, respectively, when considering the whole group of patients; however, the sensitivity (but not the specificity) decreased to 86 when taking into account only the group of patients with mild histologic alterations (Marsh type I, II, and IIIa).

Published
2002

13. CFTR, PRSS1 and SPINK1 mutations in the development of pancreatitis in Brazilian patients.

Author

Bernardino AL, Guarita DR, Mott CB, Pedroso MR, Machado MC, Laudanna AA, Tani CM, Almeida FL, and Zatz M

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Brazil epidemiology, Child, Chronic Disease, Cystic Fibrosis genetics, DNA Mutational Analysis methods, Female, Genetic Testing methods, Humans, Male, Middle Aged, Pancreatitis epidemiology, Pancreatitis, Alcoholic genetics, Serine Proteinase Inhibitors genetics, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Genetic Predisposition to Disease genetics, Mutation genetics, Pancreatitis enzymology, Pancreatitis genetics, Trypsin, Trypsinogen genetics
Abstract

Context: Mutations in cystic fibrosis transmembrane conductance regulator (CFTR), in cationic trypsinogen (PRSS1) and in serine protease inhibitor Kazal type 1 (SPINK1) genes have been associated with chronic pancreatitis (alcohol related, idiopathic and hereditary). However, the inheritance pattern is still not clear., Patients: Eighty-two unrelated Brazilian patients with chronic pancreatitis (alcohol-related disease in 64, idiopathic disease in 16, and hereditary disease in 2). Two hundred unrelated individuals with an ethnic distribution comparable to the patients were studied as controls., Main Outcome Measure: Detection of mutations in CFTR, PRSS1, and SPINK1 genes., Results: Mutations in the CFTR gene were found in 8 patients (9.8%) with chronic pancreatitis, 5 of them with idiopathic disease. Interestingly, the only clinical symptom in a male patient in the alcoholic group, who was a compound heterozygote (DeltaF508/R170C) for two CFTR mutations, was pancreatitis without infertility or pulmonary involvement. In the PRSS1 gene, the E79K change in exon 3 was found in one patient (1.2%) with alcohol-related chronic pancreatitis. Four different alterations were identified in the SPINK1 gene., Conclusions: Mutations in the CFTR gene represent the major cause of idiopathic chronic pancreatitis in Brazilian patients. No mutation was found in the PRSS1 gene among our patients suggesting further genetic heterogeneity for hereditary and idiopathic chronic pancreatitis. Interestingly, the most frequent SPINK1 N34S mutation was not present in patients or controls. Moreover, the -253C allele for the SPINK1 gene was significantly more frequent in patients than controls (P=0.004), suggesting that it might represent a risk factor for the development of pancreatitis in our population.

Published
2003

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