Wait!!! No Steroids for this Asthma

Strongyloides stercoralis (SS) is a parasite seen in certain parts of the USA and in people from other endemic areas. In these patients steroids might precipitate or exacerbate asthma. Apart from worsening of asthma, serious complications like hyperinfection syndrome and even death can occur in these patients if treated with steroids. Treatment is either ivermectin or albendazole based on severity of the disease. Clinicians have to be very careful when prescribing steroids in patients presenting with an exacerbation of asthma from areas endemic for Strongyloides stercoralis. A young woman with history of asthma presented with complaints of nausea, vomiting, abdominal pain, wheezing, and dry cough. Physical examination revealed diffuse expiratory wheezing and mild diffuse abdominal pain without rebound or guarding. Laboratory results showed leukocytosis with eosinophilia. Stool studies showed Strongyloides stercoralis. Imaging revealed ground-glass opacities in the right upper and lower lobe along with an infiltrate in the lingular lobe on the left side. Bronchoscopy showed Strongyloides stercoralis. The patient was diagnosed with hyperinfection syndrome due to Strongyloides stercoralis most probably exacerbated by prednisone given for her asthma. Steroids were then discontinued and the patient was started on ivermectin. The patient improved with treatment. Repeat stool examination was negative for Strongyloides stercoralis. Clinicians have to be very careful when prescribing steroids in patients presenting with an exacerbation of asthma who are from areas endemic for Strongyloides stercoralis and should test for it (preferably with serology test) before starting treatment

Cell-penetrating, antioxidant SELENOT mimetic protects dopaminergic neurons and ameliorates motor dysfunction in Parkinson's disease animal models

International audienceParkinson's disease (PD) is a neurodegenerative disorder characterized by motor dysfunction for which there is an unmet need for better treatment options. Although oxidative stress is a common feature of neurodegenerative diseases, notably PD, there is currently no efficient therapeutic strategy able to tackle this multi-target pathophysiological process. Based on our previous observations of the potent antioxidant and neuroprotective activity of SELENOT, a vital thioredoxin-like selenoprotein, we designed the small peptide PSELT from its redox active site to evaluate its antioxidant properties in vivo, and its potential polyfunctional activity in PD models. PSELT protects neurotoxin-treated dopaminergic neurons against oxidative stress and cell death, and their fibers against neurotoxic degeneration. PSELT is cell-permeable and acts in multiple subcellular compartments of dopaminergic neurons that are vulnerable to oxidative stress. In rodent models of PD, this protective activity prevented neurodegeneration, restored phosphorylated tyrosine hydroxylase levels, and led to improved motor skills. Transcriptomic analysis revealed that gene regulation by PSELT after MPP+ treatment negatively correlates with that occurring in PD, and positively correlates with that occurring after resveratrol treatment. Mechanistically, a major impact of PSELT is via nuclear stimulation of the transcription factor EZH2, leading to neuroprotection. Overall, these findings demonstrate the potential of PSELT as a therapeutic candidate for treatment of PD, targeting oxidative stress at multiple intracellular levels