Benoît Martin

Comparison of clinical and post-mortem findings in intensive care unit patients

The autopsy has long been regarded as an important tool for clinical confrontation, education and quality assurance. The aims of this study were to examine the correlation between the clinical diagnosis and autopsy findings in adult patients who died in an intensive care unit (ICU) and to identify the types of errors in diagnosis to improve quality of care. Autopsies from 289 patients who died in the ICU during a 2-year period were studied. Post-mortem examination revealed unexpected findings in 61 patients (21%) including malignancy, pulmonary embolism, aspergillosis, myocardial or mesenteric infarction and unsuspected bacterial, viral or fungal infection. These unexpected findings were classified as Goldman class I errors in 17 (6%), class II in 38 (13%) and class III in six (2%) cases. Although the incidence of unexpected findings with clinical significance was low, post-mortem examination remains a valuable source of pertinent information that may improve the management of ICU patients.

The galectin family and digestive disease

The soluble‐type lectins or galectins constitute a family of proteins defined by shared consensus amino acid sequence and affinity for beta‐galactose‐containing oligosaccharides. These molecules are widely distributed in the animal kingdom; to date, 15 mammalian galectins have been described but more are likely to be discovered. These proteins are involved in many biological processes including cell–cell and cell–matrix adhesion, growth regulation, signaling, and cytokine secretion. Over the last decade, a vast amount of reports has shown the importance of several galectins in the development and progression of malignancies in the digestive tract, mainly colorectal cancers. More recent data indicate that some of these molecules are also involved in inflammatory bowel diseases. This review focuses on the current knowledge of galectin expression and putative functions in the oesophagus, stomach, small intestine, and colon. It also highlights that the rapid accumulation of research data promises future scenarios in which individual members of the galectin family and/or their ligands will be used as diagnostic and therapeutic modalities for neoplastic as well as inflammatory disorders. However, the concretization of these potential modalities requires substantial improvements in terms of standardization of galectin expression evaluation together with prospective validation of the present data. Copyright

Endothelial hyperplasia and endothelial galectin-3 expression are prognostic factors in primary central nervous system lymphomas

Recently, considerable attention has been focused on the identification of clinically relevant prognostic markers for primary central nervous system lymphomas (PCNSL). The present study investigated whether three morphological features, i.e. necrosis, reactive perivascular T‐cell infiltrate and endothelial hyperplasia, and galectin‐1 and galectin‐3 immunohistochemical expression have prognostic roles in a series of 58 PCNSL samples from 44 immunocompetent and 14 immunocompromised patients. The presence of endothelial hyperplasia (identified in 21% of the assessable cases) was identified as a bad prognostic factor for immunocompetent PCNSL patients, whereas the other morphological features were not associated with any prognostic value. Lymphomatous cells of eight PCNSL cases expressed galectin‐3 without any prognostic value, and lymphomatous cells did not express galectin‐1. In contrast, endothelial expression of galectin‐3 was identified (by means of uni‐ and multi‐variate analyses) as a bad prognostic factor for immunocompetent PCNSL patients. In addition, a combination of endothelial hyperplasia and/or endothelial galectin‐3 expression was shown to be an independent prognostic factor for immunocompetent PCNSL patients treated with methotrexate‐based chemotherapy. In summary, this study suggests that endothelial‐related markers can identify risk groups of PCNSL patients and indicates that galectin‐3 could be involved in PCNSL angiogenesis.