ABSTRACT
Abatacept is a biological agent that modulates T-cell costimulation by blocking CD28 signalling. This cytotoxic T-lymphocyte-associated antigen-4-Ig fusion protein was approved for treatment of rheumatoid arthritis (RA). However, a few case reports have revealed respiratory failure after abatacept treatment. In this report, we present a patient with RA who developed severe acute respiratory distress syndrome (ARDS) and who passed away 2 months after starting abatacept. A comprehensive analysis including radiology, blood examinations, infectious panel and flow cytometry lymphocyte analysis was done to determine the cause of respiratory failure. Since no infection was detected in this patient, an association between ARDS and abatacept is a strong possibility due to significant adverse reactions to the biological agent. Considering the rapid progression of respiratory failure after abatacept treatment in this report, we suggest that pulmonary function testing and lung structure evaluation be regarded throughout the early stage of treatment of patients with RA.
Subject(s)
Abatacept/adverse effects , Antirheumatic Agents/adverse effects , Arthritis, Rheumatoid/drug therapy , Respiratory Distress Syndrome/chemically induced , Abatacept/therapeutic use , Aged , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/complications , Diagnosis, Differential , Fatal Outcome , Female , Humans , Respiratory Distress Syndrome/diagnostic imaging , Tomography, X-Ray Computed/methodsABSTRACT
Obstructive sleep apnea syndrome (OSAS) is a prevalent condition caused by dynamic upper airway collapse during sleep. The pathological impact and consequences are due to chronic intermittent hypoxia (CIH). Hypoxia increases the expression of several inflammatory stress markers and endothelial dysfunction. Recent studies suggest that patients with a similar AHI but with severe nocturnal hypoxia using oximetric parameters, such as the lowest saturation of oxygen during the night (min SaO2), percentage of total sleep time with oxygen saturation < 90% (T90) or the oxygen desaturation index (ODI-3%), commonly reported during the sleep study, are indicative of the increased expression of inflammatory markers due to severe nocturnal hypoxia and CIH during the night compared to subjects with moderate-severe OSAS without severe nocturnal hypoxia. The aim of this review is to describe physiological pathways involved in OSAS and their clinical consequences, focused in CIH and oximetric parameters showed in sleep study and their potential utility as inflammatory markers.
