The role of high sensitive C-reactive protein and histopathological evaluation in chronic gastritis patients with or without Helicobacter pylori infection

Abstract Purpose: To evaluate serum levels of high-sensitivity C-reactive protein (hs-CRP) in chronic gastritis patients to predict Helicobacter pylori (HP) infection, inflammatory activity, and precancerous lesions. Methods: A total of 811 patients with upper gastrointestinal symptoms and histopathological diagnosis of chronic gastritis were enrolled in the study. On endoscopy, five gastric biopsies were taken according to Modified Sydney protocol, which were stained with hematoxylin & eosin and Giemsa Results: HP infection was found in 28.6% of patients, being significantly more common in specimens with acute and chronic inflammatory activity. Mucosal atrophy, intestinal metaplasia, and dysplasia were found in 20.2%, 18.8% and 2.7% of biopsy specimens. Mean hs-CRP was 1.9±1.6 mg/dl for males and 2.2±1.9 mg/dl for females. hs-CRP average were significantly higher in patients with severe acute inflammation (p:0.049), in patients with severe chronic inflammation (p:0.015) and in those with HP (p: 0.001) . The severity of HP infection increased significantly with the increased degree of acute inflammation, chronic inflammation and hs-CRP level (p=0.001 for both). Conclusion: Serum hs-CRP level increases in patients with chronic gastritis, it could be an indicator of severity of acute or chronic mucosal inflammation, and presence of HP infection. Therefore, hs-CRP may aid the diagnosis of chronic gastritis, but it is not associated with pre-cancerous lesions.

Short segment Barrett's esophagus and distal gastric intestinal metaplasia / Esôfago de Barrett de segmento curto e metaplasia intestinal gástrica distal

BACKGROUND: Short segment Barrett's esophagus is defined by the presence of <3 cm of columnar-appearing mucosa in the distal esophagus with intestinal metaplasia on histophatological examination. Barrett's esophagus is a risk factor to develop adenocarcinoma of the esophagus. While Barrett's esophagus develops as a result of chronic gastroesophageal reflux disease, intestinal metaplasia in the gastric cardia is a consequence of chronic Helicobacter pylori infection and is associated with distal gastric intestinal metaplasia. It can be difficult to determine whether short-segment columnar epithelium with intestinal metaplasia are lining the esophagus (a condition called short segment Barrett's esophagus) or the proximal stomach (a condition called intestinal metaplasia of the gastric cardia). AIMS: To study the association of short segment Barrett's esophagus (length <3 cm) with gastric intestinal metaplasia (antrum or body) and infection by H. pylori. PATIENTS AND METHODS: Eight-nine patients with short segment columnar-appearing mucosa in the esophagus, length <3 cm, were studied. Symptoms of gastroesophageal reflux disease were recorded. Biopsies were obtained immediately below the squamous-columnar lining, from gastric antrum and gastric corpus for investigation of intestinal metaplasia and H. pylori. RESULTS: Forty-two from 89 (47.2 percent) patients were diagnosed with esophageal intestinal metaplasia by histopathology. The mean-age was significantly higher in the group with esophageal intestinal metaplasia. The two groups were similar in terms of gender (male: female), gastroesophageal reflux disease symptoms and H. pylori infection. Gastric intestinal metaplasia (antrum or body) was diagnosed in 21 from 42 (50.0 percent) patients in the group with esophageal intestinal metaplasia and 7 from 47 (14.9 percent) patients in the group with esophageal columnar appearing mucosa but without intestinal metaplasia. CONCLUSION: Intestinal metaplasia is a frequent finding in patients with <3 cm of columnar-appearing mucosa in the distal esophagus. In the present study, short segment intestinal metaplasia in the esophagus is associated with distal gastric intestinal metaplasia. Gastroesophageal reflux disease symptoms and H. pylori infection did not differ among the two groups studied.

RACIONAL: Esôfago de Barrett de segmento curto é definido pela presença de mucosa semelhante à gástrica no esôfago distal, extensão <3 cm, com metaplasia intestinal na histopatologia. Esôfago de Barrett é fator de risco ao adenocarcinoma do esôfago. Enquanto esôfago de Barrett se desenvolve como resultado do refluxo gastroesofágico crônico, metaplasia intestinal da cárdia é conseqüência da infecção crônica pelo Helicobacter pylori e está associada à metaplasia gástrica distal. Epitélio colunar com metaplasia intestinal localizada no esôfago distal, extensão <3 cm (condição denominada de esôfago de Barrett de segmento curto) ou a mesma entidade localizada no estômago proximal (condição denominada de metaplasia intestinal da cárdia) por ser muitas vezes confundida. OBJETIVO: Estudar a associação de esôfago de Barrett segmento curto (extensão <3 cm) com metaplasia intestinal gástrica (corpo e antro) e infecção pelo Helicobacter pylori. PACIENTES E MÉTODOS: Participaram do estudo 89 pacientes com mucosa do esôfago distal semelhante à gástrica, extensão <3 cm. Os pacientes foram questionados sobre sintomas de doença do refluxo gastroesofágico. Biopsias foram obtidas imediatamente abaixo da transição escamocolunar e do corpo e antro gástrico para investigação de metaplasia intestinal e pesquisa de Helicobacter pylori. RESULTADOS: Quarenta e dois dos 89 (47,2 por cento) pacientes foram diagnosticados com metaplasia intestinal esofágica na histopatologia. A idade média foi significativamente mais alta no grupo com metaplasia intestinal esofágica. Nos dois grupos estudados (com e sem metaplasia intestinal de esôfago distal), a relação masculino/feminino, sintomas de doença do refluxo gastroesofágico e infecção pelo Helicobacter pylori foi semelhante. Metaplasia intestinal gástrica (corpo e antro) foi diagnosticada em 21 de 42 (50,0 por cento) dos pacientes com metaplasia intestinal esofágica e 7 de 47 (14,9 por cento) do grupo com mucosa colunar esofágica, mas sem evidência de metaplasia intestinal. CONCLUSÃO: Metaplasia intestinal é achado freqüente em pacientes com mucosa semelhante à gástrica no esôfago distal, extensão <3 cm. No presente estudo, metaplasia intestinal de segmento curto no esôfago está associada à metaplasia gástrica distal. A freqüência de sintomas de refluxo gastroesofágico e infecção pelo Helicobacter pylori não mostrou diferenças significativas nos dois grupos estudados.

Alteraciones genéticas en gastritis crónica: Estudio de inestabilidad microsatelital y pérdida de la heterocigocidad / Genetic changes in chronic gastritis: study of microsatellite instability and loss of heterozygosity

Background: Multifocal chronic gastritis, associated to intestinal metaplasia, is considered a preneoplastic lesion, closely associated to intestinal type gastric cancer. Aim: To study the frequency of microsatellite instability (MSI) and loss of heterozygosity (LOH) in areas of chronic gastritis and intestinal metaplasia in gastric biopsies of patients without cancer. Material and methods: Gastric biopsy samples from 34 patients without cancer (22 with multifocal atrophic gastritis and 12 with diffuse antral gastritis), were studied. Glands from areas of chonic gastritis and intestinal metaplasia and lymphocytes, were collected using laser microdissection of paraffin embedded samples. The analysis of 15 mono and dinucleotide microsatellites was used to assess LOH and MSI. Results: LOH and MSI were found in some of the markers in 55% (12/22) and 59% (13/22) of cases with intestinal metaplasia, respectively. Only one of 12 areas with diffuse atrophic gastritis had MSI and a different area had LOH (p <0.05 or less, when compared with areas of multifocal atrophic gastritis). Three areas of normal epithelium in patients with multifocal atrophic gastritis, also had alterations. Most of these alterations were concordant with adjacent areas with intestinal metaplasia. Conclusions: LOH and MSI was found in areas of intestinal metaplasia in more than half of the studied cases and in few areas of atrophic gastritis without intestinal metaplasia. These findings suggest that genotypic alterations may precede phenotypic modifications and that intestinal metaplasia is a preneoplastic lesion (Rev Méd Chile 2003; 131: 1365-74).

Neoplasias y displasias de vesícula biliar y su relación con litiasis. Estudio clinicopatológico de casos y controles / Neoplasm and dysplasia of the gallbladder and their relation with lithiasis. A case-control clinical-pathological study

Antecedentes. la litiasis es uno de los mayores factores de riesgo para cambios inflamatorios, metaplásicos, displásicos y neoplásicos de vesícula biliar, con frecuencia variable en diferenes poblaciones. Objetivo. determinar la frecuencia de asociación de los principales procesos patológicos y datos clínicos con litiasis vesicular. Material y métodos. estudio transveral, descriptivo de 1,367 piezas de colecistectomía, con (1,096) y sin (271) litiasis fue la siguiente: metaplasia psudopilórica 50 por ciento y 25 por ciento; metaplasia intestinal 16 por ciento y 2 por ciento; displasia de bajo grado 40 por ciento y 17 por ciento; displasia de alto grado 16 por ciento y 2 por ciento; carcinoma in situ 1.5 por ciento y 0 por ciento y carcinoma invasor 2.6 por ciento y 0 por ciento. El 80 por ciento de los casos con litiasis, el 65 por ciento de los casos de carcinoma in situ y el 90 por ciento de los casos de carcinoma invasor correspondieron a mujeres. La edad media de los pacientes con displasia de bajo y alto grado, carcinoma in situ y carcinoma invasor fue de 42, 48, 53 y 61 años, en ese orden. Conclusiones. la frecuencia de procesos inflamatorios agudos, colecititis crónica xantogranulomatosa, adenomiomatosis, metaplasia pseudopilórica e intestinal, pólipos hiperplásicos, displasia de bajo y alto grado, adenomas tubulares, carcinoma in situ y carcinoma invasor fue mayor en vesículas con litiasis que en vesículas sin litiasis (p<.05)

Incidência da doença fibrocística em 516 mamoplastias reparadoras / Incidence of fibrocystic disease in 516 repairing mamaplasties

Os autores descrevem a incidência da doença fibrocística em 516 mamoplastias reparadoras em pacientes sem história prévia de doença de mama. A idade das pacientes variou de 14 a 91 anos com um pico ao redor da terceira e quarta décadas de vida. Em 347 pacientes (67,25 por cento) havia evidências de alteraçoes fibrocísticas nao proliferativas como fibrose estromal, cistos, inflamaçao crônica, metaplasia apócrina e alteraçoes fibroadenomatóides. Porém, em 13,26 por cento dos casos havia alteraçoes proliferativas como hiperplasia epitelial típica (n=34), adenose esclerosante (n=6) e hiperplasia epitelial atípica (n=6). Um caso de carcinoma ductal in situ também foi precocemente diagnosticado pela análise deste material. As pacientes com história familiar de câncer de mama e doença fibrocística com alteraçoes proliferativas podem ter risco de desenvolvimento de carcinoma até dez vezes maior que a populaçao em geral. Nossos achados enfatizam que todos os espécimes provenientes de mamoplastias devem ser submetidos a exame histopatológico para que as pacientes do grupo de risco de desenvolvimento de carcinoma sejam diagnosticadas e observadas clinicamente.