Thrombotic Microangiopathy After Long-Lasting Treatment by Gemcitabine: Description, Evolution and Treatment of a Rare Case.

Thrombotic microangiopathy (TMA) is an uncommon but severe complication that may occur in cancer patients under gemcitabine chemotherapy. Gemcitabine-induced thrombotic microangiopathy (G-TMA) can clinically and biologically present as atypical hemolytic uremic syndrome, with activation of the complement pathway asking the question of the use of eculizumab. We describe here the case of a patient suffering from metastatic cholangiocarcinoma treated by gemcitabine for 4 years leading to the remission of the underlying neoplasia.

Genetic predisposition to porto-sinusoidal vascular disorder.

Porto-sinusoidal vascular disorder (PSVD) is a rare liver disease. The pathophysiological mechanisms underlying the development of PSVD are unknown. Isolated cases of PSVD associated with gene mutations have been reported, but no overview is available.

Brief Report of Anti-Programmed Cell Death Protein-1 in Human Immunodeficiency Virus Setting: Relevant and Breaking Results in First-Line NSCLC Therapy.

In the recent past, we observed an increased risk of cancer in the population with human immunodeficiency virus (HIV) owing to the development of antiretroviral therapies that decreased mortality caused by HIV-specific infections. This particularly fragile population is frequently excluded from clinical trials, and up-to-date recommendations for these patients are lacking. Only few cases of patients with HIV suffering from cancer and undergoing first-line immunotherapy have been reported so far.

Diffuse alveolar hemorrhage after gadolinium injection during a MRI.

Gadolinium is a frequently used contrast product for MRI exam. It is well known to be less immuno-reactive than iodine used in tomodensitometry but is safety is not completely exempt of secondary effect. Here we report one case of acute interstitial pulmonary toxicity due to gadolinium.

IGF-1R Reduction Triggers Neuroprotective Signaling Pathways in Spinal Muscular Atrophy Mice.

Unlabelled: Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by the selective loss of spinal motor neurons due to the depletion of the survival of motor neuron (SMN) protein. No therapy is currently available for SMA, which represents the leading genetic cause of death in childhood. In the present study, we report that insulin-like growth factor-1 receptor (Igf-1r) gene expression is enhanced in the spinal cords of SMA-like mice.

The Black cells phenotype is caused by a point mutation in the Drosophila pro-phenoloxidase 1 gene that triggers melanization and hematopoietic defects.

Melanization contributes to arthropod-specific innate immunity through deposition of melanin at wound sites or around parasites, with concomitant release of microbicidal reactive oxygen species. Melanization requires sequential activation of proteolytic enzymes in the hemolymph, including the final enzyme pro-phenoloxidase. Black cells (Bc) is a mutation causing spontaneous melanization of Drosophila crystal cells, a hemocyte cell type producing phenoloxidases.