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1.
Vnitr Lek ; 58(1): 18-23, 2012 Jan.
Artigo em Tcheco | MEDLINE | ID: mdl-22448696

RESUMO

UNLABELLED: INTRODUCTION, STUDY AIM: Colorectal carcinoma is one of the most frequent malignancies. Most frequently, neoplasms, including malignant precursors, are in the form of polyps, although these might be of a non-tumour origin. The aim of this prospective multicentre study was to provide an overview of coloscopic identification and biological nature of polyps. RESULTS: 3,400 consecutive coloscopies performed between 2009 and 2010 were analyzed. At different centres, the top of the cecum was reached in 89% to 93% and terminal ileum in 73% to 87% of cases. In the above 40 age group, 26.6% were screening coloscopies. The mean age of the above 40 patients was 56 years. The incidence of potential neoplastic lesions (polyps, carcinomas), advanced adenomas and carcinomas were: 7.8 %, 0.8 % and 0.16 %, respectively, in the above 40 age group, 41.5 %, 9.8 % and 1.6 %, respectively, in the 40-50 years age group and 70.5 %, 31.3 % and 6.8 %, respectively, in the above 50 age group. The incidence of tubular adenoma and hyperplastic polyps was 23.9% and 66.2%, respectively, in the below 40 age group and 53.1% and 26.1% in the above 50 age group. 57.8% of advances neoplasms were located in the rectosigmoid a descendent colon. The incidence ratio for adenomas and hyperplastic polyps was 76.6% and 14%, respectively, for rectosigmoid colon, 63.6 and 17.4 %, respectively, for descendent colon, 63.6 and 11.4 % for traverse colon and 63,4 a 17,9 %, respectively, for cecum and ascendant colon. The incidence of tubulovillous adenomas and hyperplastic polyps in pedunculated polyps larger than 1 cm was 19.4 % and 20.4 %, respectively, and 34.2 % and 13.1 %, respectively, in other polyps. The incidence of potential lesions (polyps and carcinomas), advanced adenomas, carcinomas and advanced neoplasms was 66.7 %, 23.1 %, 5.8 % and 28.9 %, respectively, in women and 63.1 %, 30.0 %, 5.7 % and 34.7 %, respectively, in men. CONCLUSION: The top of the cecum was reached in a higher proportion of cases than required, although this was lower than in the majority of other recent studies. Terminal ileum was reached in high number of cases. The incidence of polyps and neoplasms rose sharply from 40 years of age. Therefore, the screening threshold should be extended to the below 50 age group. Hyperplastic polyps predominated in younger age and adenomas in the above 40 age group. Histological profile was similar and did not suggest importantly different pathogenesis with respect to localization. There were relatively fewer adenomas and more hyperplastic polyps in pedunculated polyps and vice verse in other types of polyps, suggesting a higher risk associated with non-pedunculated lesions. Both sexes differed less than suggested based on epidemiological statistics.


Assuntos
Pólipos do Colo/diagnóstico , Colonoscopia , Neoplasias Colorretais/diagnóstico , Adenoma/diagnóstico , Adolescente , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem
2.
Endoscopy ; 40(9): 711-6, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18698534

RESUMO

BACKGROUND AND STUDY AIMS: Barrett's esophagus is a premalignant condition. The risk of developing high grade intraepithelial neoplasia (HGIN) or adenocarcinoma is currently a matter of debate. Due to several shortcomings, previous studies have probably overestimated the risk. The main aim of our study was to investigate the incidence of HGD and adenocarcinoma in a cohort of patients with Barrett's esophagus. PATIENTS AND METHODS: In a prospective, cohort study, all patients had intestinal metaplasia and macroscopic evidence of short- or long-segment (< 3 cm or > or = 3 cm) Barrett's esophagus. All patients underwent a standard protocol including regular endoscopies with biopsies and were treated with a proton pump inhibitor or antireflux surgery. RESULTS: A total of 135 patients underwent 623 endoscopies during 700 patient-years (mean follow-up 5.2 +/- 2.3 years). Simultaneous HGIN and adenocarcinoma were detected in two patients with long-segment Barrett's esophagus (1.5%; 2 and 6 years after the index endoscopy). Low grade intraepithelial neoplasia (LGIN) was detected in 25 patients (18.5%); in 11 of these patients (44%), LGIN was not confirmed in later biopsies. Our study shows an incidence of HGIN/adenocarcinoma of 1/350 patient-years. Endoscopic regression of Barrett's esophagus was seen in 20.7% of patients. CONCLUSION: The incidence of HGIN/adenocarcinoma is low in patients with adequately treated Barrett's esophagus. The annual risk of developing HGIN/adenocarcinoma is 0.21% (1.6% in long-segment Barrett's esophagus).


Assuntos
Adenocarcinoma/epidemiologia , Esôfago de Barrett/epidemiologia , Carcinoma in Situ/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Comorbidade , Endoscopia , Feminino , Infecções por Helicobacter/epidemiologia , Helicobacter pylori , Hérnia Hiatal/epidemiologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Medição de Risco
3.
World J Gastroenterol ; 13(27): 3714-20, 2007 Jul 21.
Artigo em Inglês | MEDLINE | ID: mdl-17659731

RESUMO

AIM: To establish an optimum combination of molecular markers resulting in best overall diagnostic sensitivity and specificity for evaluation of suspicious pancreatic mass. METHODS: Endoscopic ultrasound (EUS)-guided fine needle aspiration cytology (FNA) was performed on 101 consecutive patients (63 males, 38 females, 60 +/- 12 years; 81 with subsequently diagnosed pancreatic cancer, 20 with chronic pancreatitis) with focal pancreatic mass. Samples were evaluated on-site by an experienced cytopathologist. DNA was extracted from Giemsa stained cells selected by laser microdissection and the presence of K-ras, p53 and p16 somatic mutations was tested by cycling-gradient capillary electrophoresis (CGCE) and single-strand conformation polymorphism (SSCP) techniques. In addition, allelic losses of tumor suppressor genes p16 (INK4, CDKN2A) and DPC4 (MADH4, SMAD4) were detected by monitoring the loss of heterozygosity (LOH) at 9p and 18q, respectively. RESULTS: Sensitivity and specificity of EUS-guided FNA were 75% and 85%, positive and negative predictive value reached 100%. The remaining 26% samples were assigned as inconclusive. Testing of molecular markers revealed sensitivity and specificity of 70% and 100% for K-ras mutations (P < 0.001), 24% and 90% for p53 mutations (NS), 13% and 100% for p16 mutations (NS), 85% and 64% for allelic losses at 9p (P < 0.001) and 78% and 57% for allelic losses at 18q (P < 0.05). When tests for different molecular markers were combined, the best results were obtained with K-ras + LOH at 9p (92% and 64%, P < 0.001), K-ras + LOH at 18q (92% and 57%, P < 0.001), and K-ras + LOH 9q + LOH 18q (96% and 43%, P < 0.001). When the molecular markers were used as complements to FNA cytology to evaluate inconclusive samples only, the overall sensitivity of cancer detection was 100% in all patients enrolled in the study. CONCLUSION: EUS-guided FNA cytology combined with screening of K-ras mutations and allelic losses of tumor suppressors p16 and DPC4 represents a very sensitive approach in screening for pancreatic malignancy. Molecular markers may find its use particularly in cases where FNA cytology has been inconclusive.


Assuntos
Biomarcadores Tumorais/genética , Biópsia por Agulha Fina/métodos , Cromossomos Humanos Par 18 , Cromossomos Humanos Par 9 , Endossonografia , Técnicas de Diagnóstico Molecular , Neoplasias Pancreáticas/diagnóstico , Pancreatite Crônica/diagnóstico , Adulto , Idoso , Idoso de 80 Anos ou mais , Inibidor p16 de Quinase Dependente de Ciclina/genética , Eletroforese Capilar , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Perda de Heterozigosidade , Masculino , Pessoa de Meia-Idade , Mutação , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patologia , Pancreatite Crônica/genética , Pancreatite Crônica/patologia , Polimorfismo Conformacional de Fita Simples , Valor Preditivo dos Testes , Proteínas Proto-Oncogênicas p21(ras)/genética , Sensibilidade e Especificidade , Proteína Smad4/genética , Proteína Supressora de Tumor p53/genética
6.
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