Concordant and Discordant Exudates and Their Effect on the Accuracy of Light's Criteria to Diagnose Exudative Pleural Effusions.

INTRODUCTION: To describe the incidence of discordant exudate (DE) effusions, their underlying etiologies and their effect on the accuracy of the Light's criteria to diagnose exudate effusions. METHODS: A retrospective review of pleural fluid analysis (PFA) from a cohort of patients with pleural effusion (PE) who underwent thoracentesis. PEs were defined as exudative based on the Light's criteria. The effusions were further classified in concordant or DE. RESULTS: From 847 PE samples, 611 (72.1%) were diagnosed as an exudate and 236 (27.9%) as a transudate. In 10.3% of cases (n = 87), there was discordancy between the final pleural fluid diagnosis and the PFA defined by Light's criteria. 281 (33.2%) of the 632 effusions classified as an exudate by Light's criteria were DE (52 transudates and 229 exudates). 182 (65%) of the 281 DE were found to be protein discordant (37 transudates and 145 exudates), and 99 (35.2%) were lactate dehydrogenase discordant (15 transudates and 84 exudates). The positive predictive value and positive likelihood ratio of Light's criteria for the diagnosis of an exudate effusion decreased from 99.4% and 67.4%, respectively, when the exudates were concordant to 81.5% and 1.7, respectively, if they were discordant. CONCLUSIONS: In a significant percentage of patients, there is discordancy between the results of the PFA and the final clinical diagnosis. DE decreased the accuracy of Light's criteria to identify exudate PE, increasing the risk of misclassifying a transudate as an exudate. Concordant exudates almost universally established the presence of an exudative PE.

[Latin American contribution to the study of Helicobacter pylori]. / Contribución de Latinoamérica al estudio del Helicobacter pylori.

UNLABELLED: We have reviewed Lilacs, PubMed and Google searching for original articles related to Helicobacter pylori published by Latin American investigators from 2003 to 2008. Contributions in the following fields by countries are: Molecular biology: Brasil, Chile, Colombia, Peru y Venezuela. EPIDEMIOLOGY: Argentina, Brasil, Colombia, Cuba, Peru y Venezuela. DIAGNOSTIC METHODS: Argentina, Bolivia, Brasil, Chile, Costa Rica, Colombia, Mexico, Peru y Venezuela. Helicobacter pylori and gastroduodenal diseases: Brasil, Cuba, Peru y Venezuela. Helicobacter pylori and extra digestive diseases: Brasil, Colombia and Venezuela. Pediatrics: Brasil, Cuba y Venezuela. TREATMENT: Argentina, Brasil, Chile, Colombia, Costa Rica, Mexico, Peru y Venezuela.

[Helicobacter pylori 25 years after (1983 -2008): epidemiology, microbiology, pathogenics, diagnostics and treatment]. / Helicobacter pylori 25 años después (1983 -2008): epidemiología, microbiología, patogenia, diagnóstico y tratamiento.

EPIDEMIOLOGY: People have been infected by this bacteria 58,000 years ago. Prevalence of infection varies in different nation. In developing countries infection is acquired in early childhood. The forms of infection are/fecal-oral, oral-oral an gastro oral. In Perú we found same prevalence in the coast, jungle and sierra and described that water is one of the ways of infection.MICROBIOLOGY: Three strains predominant in Spanish, Asiatic and people from India have been identified. DNA has 1.65 million bases. Different factors of virulence, enzymes and toxins have also been described. PATHOGENESIS: Inflamatory response; neutrophiles, lymphocytes T and B, plasma cells, macrophages.METHODS OF DIAGNOSIS: Invasive and non invasive procedures. THERAPY: Different treatment schemes are described: 1st, 2nd, 3rd lines, rescue therapies. Secondary reactions, alternative schemes, recurrence, reinfection and experience in Perú are also described.

Helicobacter Pylori 25 años después (1983 -2008): epidemiología, microbiología, patogenia, diagnóstico y tratamiento / Helicobacter Pylori 25 years after (1983 -2008): epidemiology, microbiology, pathogenics, diagnóstics and treatment

EPIDEMIOLOGÍA: Los seres humanos han estado infectados por esta bacteria hace 58,000 años. La prevalencia de la infección varía en diferentes naciones. En países en vías de desarrollo se adquiere en edades más tempranas. Las vías de contagio son la fecal-oral, oral-oral y gastro-oral. En el Perú se ha encontrado iguales tasas de prevalencia en la costa, sierra y selva y el agua como uno de los factores de infección. MICROBIOLOGÍA: Se han identificado 3 cepas bacterianas que predominan en hispanos, asiáticos e hindúes. El ADN de esta bacteria consta de 1.65 millones de pares, identificándose diferentes factores de virulencia, de enzimas y toxinas bacterianas. PATOGENIA: La respuesta inflamatoria se da a través de neutrófilos, linfocitos T y B, células plasmáticas, macrófagos. MÉTODOS DE DIAGNÓSTICO: Se han establecido diferentes métodos: Invasivos y no invasivos. TRATAMIENTO: Se dispone de terapias de 1ª, 2ª y 3ª línea o de rescate, esquemas alternativos, analizándose la recurrencia, reinfección y la experiencia en el Perú.

EPIDEMIOLOGY: People have been infected by this bacteria 58,000 years ago. Prevalence of infection varies in different nation. In developing countries infection is acquired in early childhood. The forms of infection are/fecal-oral, oral-oral an gastro oral. In Perú we found same prevalence in the coast, jungle and sierra and described that water is one of the ways of infection. MICROBIOLOGY: Three strains predominant in Spanish, Asiatic and people from India han been identified. ADN has 1.65 million of basis. Different factors of virulence, enzymes and toxins have also been described. PATHOGENESIS: Inflamatory response; neutrophiles, lifocites T and B, plasma cells, macrophages. METHODS OF DIAGNOSIS: Invasive and non invasive procedures. THERAPY: Different treatment schemes are discrebed: 1st, 2nd, 3rd lines, rescue therapies. Secondary reactions, alternative schemes, recurrence, reinfection and experience in Perú are also described.

[Helicobacter pylori and gastric cancer]. / Helicobacter pylori y cáncer gástrico.

Since its discovery and identification in gastric tissue by Marshall and Warren in 1983, our knowledge about the effects of Helicobacter pylori infection has grown considerably. Its role in the multifactorial pathology of peptic ulcer disease (gastrodudodenal ulcer disease), gastric adenocarcinoma, and MALT lymphoma is now widely accepted while its involvement in extraintestinal disease is still controversial.The correlation between the colonization of the stomach by H. pylori and gastric lymphoma has been demonstrated in multiple studies. Between 65 and 80% of distal gastric adenocarcinomas are attributed to H. pylori infection. However, gastric carcinogenesis cannot be explained by H. pylori infection alone. Among those individuals infected by this bacteria, only a small percentage (2-5%) ever develops gastric cancer, the majority exhibit benign lesions. There is a wide individual variation in the outcome of this infection in patients. This individual and population specific variation is due to the intricate relationship between genetics, the environment, bacterial virulence, diet, and socio-economic status and it explains the multiple outcomes of this infection. In this article, we conduct a review of the widely accepted theories regarding gastric cancer, Helicobacter pylori, the correlations and enigmas between them, the reported geographical variations, and the various proposed hypotheses on the carcinogenic mechanism of Helicobacter pylori.

Helicobacter Pylori y cáncer gástrico: [revisión] / Helicobacter pylori and gastric cancer: [revision]

Desde el hallazgo e identificación del Helicobacter pylori en material de tejido gástrico por Marshall y Warrent en 1983, nuestro conocimiento sobre esta infección ha evolucionado notablemente. Se acepta al momento actual, su rol su rol dentro de la multifactoriedad de la patología ulcero péptica gastroduodenal y el adenocarcinoma y MALTomagástrico, permaneciendo aun controversial su relación con algunas enfermedades extraintestinales. Múltiples estudios han demostrado una asociación entre la infección del estómago por el H. pylori y el Maltoma gástrico. Aproximadamente 65 a 80% de casos de adenocarcinoma del estómago distal son atribuidos a la infección por H. pylori. Sin embargo, carcinogenesis gástrica no puede ser solo explicada por la infección por el H. pylori. De los infectados por esta bacteria solo un mínimo porcentaje desarrolla adenocarcinoma gástrico (2-5%). La mayoría presentan lesiones benignas. Existe pues una marcada variación individual del resultado de esta infección en los pacientes. Esta variación individual y poblacional sedebería a la compleja interacción de factores genéticos, del medio ambiente, bacterianos, alimentarios y nivel socio económico que explican los diferentes resultados a los que se llega con la infección. En este artículo hacemos una revisión de los conceptos aceptados en relación al cáncer gástrico, al H. pylori, las correlaciones y enigmas descritos entre ambos, las variaciones geográficas reportadas y las diversas hipótesis sobre el mecanismo carcinogénico del Helicobacter pylori.

Since its discovery and identification in gastric tissue by Marshall and Warren in 1983, our knowledge about the effects of Helicobacter pylori infection has grown considerably. Its role in the multifactorial pathology of peptic ulcer disease (gastrodudodenal ulcer disease), gastric adenocarcinoma, and MALT lymphoma is now widely accepted while its involvement in extraintestinal disease is still controversial. The correlation between the colonization of the stomach by H. pylori and gastric lymphoma has been demonstrated in multiple studies. Between 65 and 80% of distal gastric adenocarcinomas are attributed to H. pylori infection. However, gastric carcinogenesiscannot be explained by H. pylori infection alone. Among those individuals infected by this bacteria, only a small percentage (2-5%) ever develops gastric cancer, the majority exhibit benign lesions. There is a wide individual variation in the outcome of this infection in patients. This individual and population specific variation is due to the intricate relationship between genetics, the environment, bacterial virulence, diet, and socio-economic status and it explains the multiple outcomes of this infection. In this article, we conduct a review of the widely accepted theories regarding gastriccancer, Helicobacter pylori, the correlations and enigmas between them, the reported geographical variations, and the various proposed hypotheses on the carcinogenic mechanism of Helicobacter pylori.

Tratamiento conservador en cáncer de mama: experiencia en el Servicio de Oncología Ginecológica del Hospital Nacional Edgardo Rebagliati Marins / Conservative treatment in breast cancer experience of Ginecologic Oncology Service, Edgardo Rebagliati Martins PSSI National Hospital

Varios estudios han demostrado que con la cirugía de conservación y la radioterapia se logran índices de control local y regional y supervivencias semejantes a la mastectomía radical. El presente estudio se realiza en el Servicio de Oncología Ginecológica del Hospital Nacional "Edgardo Rebagliati Martins" del IPSS. Comprende el estudio de 40 casos de cáncer de mama en etapas clínicas T1-2. Toda paciente es sometida en un primer tiempo a tumorectomía y disección radical de axila, luego recige cobalto en toda la mama: 5000 cGy, seguida de un refuerzo en el sitio del tumor, hasta completar 6000 cGy. Se analizan diferentes aspectos: edad, estadio clínico, estado ganglionar, tipo de cirugía, resultado cosmético, tipo histológico, recurrencia, sobrevida y complicaciones. Nuestros resultados a 5 años, al 100 por ciento han demostrado que este tipo de tratamiento está plena y ampliamente justificado, alcanzamos una sobrevida de 97.5 por ciento y una recurrencia local de 5 por ciento. A nivel nacional no encontramos referencia de trabajos similares