Objetivo: estudiar la frecuencia de positividad de las pruebas serológicas en pacientes con biopsias compatible con enfermedad celiaca. Material y métodos: estudio transversal. Se incluyeron pacientes con biopsia duodenal histológicamente compatible con enfermedad celiaca y determinación de anticuerpos antigliadina, antiendomisio y antitransglutaminasa IgA. Definimos como caso de enfermedad celiaca a quienes tuvieran biopsia positiva y anticuerpos antiendomisio y/o antitransglutaminasa positivos. Resultados: 31 pacientes fueron incluidos de los cuales 6 fueron antiendomisio positivo, 5 fueron antitransglutaminasa positivo y antigliadina fue positivo en 14. Por lo tanto de 31 pacientes con cambios histológicos compatibles con enfermedad celiaca sólo 10 tuvieron serología diagnóstica. Sólo uno de los pacientes tuvo positividad tanto para antitransglutaminasa como para antiendomisio. Conclusiones: a) encontramos que la mayoría de biopsias de duodeno con un cuadro histológico sugerente de enfermedad celiaca no se corresponden con serología diagnóstica de esta enfermedad; b) encontramos baja coincidencia en la positividad serológica entre antiendomisio y antitransglutaminasa. / Objective: to study the frequency of positive serology for celiac disease (CD) in patients with duodenal biopsies suggestive of this disease. Material and methods: cross sectional study. We included patients with duodenal biopsies histologically compatible with CD and antigliadin, antiendomysial and IgA antitransglutaminase antibodies. We defined a “case” of CD if there was a positive biopsy and either antiendomisial or antitransglutaminase positive antibodies. Results: thirty one patients were included in our study. Six were antiendomysial positive and 5 antitransglutaminase positive while the antigliadin was positive in 14 cases. Therefore, out of 31 patients only 10 had a serology compatible with CD and only one had positive both antibodies, antiendomysial and antitransglutaminase. Conclusions: a) we have found that most of the duodenal biopsies compatible with CD are not diagnosed with positive serology; and b) we found a low correlation between serological diagnostic tests.

Objectives: The study aim was to analyse the kinetics of stem and transit cells in the crypts of jejunal mucosa infected with HIV and Microsporidia. Design: The size of villi, depth of crypts and proliferative activity of transit and stem cells in jejunal mucosa were measured using morphometric techniques. Methods: The surface area/volume ratio (S/V) of jejunal biopsies was estimated under light microscopy using a Weibel graticule. Crypt length was measured by counting enterocytes along the crypt side from the base to the villus junction, and the mean crypt length was calculated. The S/V and crypt lengths of the jejunal mucosa of 21 HIV and Microsporidia-infected test cases were compared with 14 control cases. The labelling index in relation to the crypt cell position of 10 of the test cases was analysed compared with 13 control cases. Results: Differences were found in the S/V and crypt length, and there was a negative correlation between S/V and crypt length in test and control cases combined. Cell labelling indices fell into low and high proliferation groups. There were significant differences in labelling indices between low proliferation test cases and controls, between high proliferation test cases and controls, and between high and low proliferation test cases. Conclusion: Villous atrophy induced by HIV and Microsporidia is attributed to crypt cell hyperplasia and the encroachment of crypt cells onto villi. These infections induce crypt hypertrophy by stimulating cell mitosis predominantly in transit cells but also in stem cells. Increased stem cell proliferation occurs only in high proliferation cases.

Coeliac disease (CD) is a clinically heterogeneous autoimmune disease with variable presentation and progression triggered by gluten intake. Molecular or genetic factors contribute to disease heterogeneity, but the reasons for different outcomes are poorly understood. Transcriptome studies of tissue biopsies from CD patients are scarce. Here, we present a high-resolution analysis of the transcriptomes extracted from duodenal biopsies of 24 children and adolescents with active CD and 21 individuals without CD but with intestinal afflictions as controls. The transcriptomes of CD patients divide into three groups—a mixed group presenting the control cases, and CD-low and CD-high groups referring to lower and higher levels of CD severity. Persistence of symptoms was weakly associated with subgroup, but the highest marsh stages were present in subgroup CD-high, together with the highest cell cycle rates as an indicator of virtually complete villous atrophy. Considerable variation in inflammation-level between subgroups was further deciphered into immune cell types using cell type de-convolution. Self-organizing maps portrayal was applied to provide high-resolution landscapes of the CD-transcriptome. We find asymmetric patterns of miRNA and long non-coding RNA and discuss the effect of epigenetic regulation. Expression of genes involved in interferon gamma signaling represent suitable markers to distinguish CD from non-CD cases. Multiple pathways overlay in CD biopsies in different ways, giving rise to heterogeneous transcriptional patterns, which potentially provide information about etiology and the course of the disease.