Association of anti-triosephosphate isomerase antibodies with aseptic meningitis in patients with neuropsychiatric systemic lupus erythematosus

Abstract

Autoantibodies to triosephosphate isomerase (TPI), which is an important glycolytic enzyme in red blood cells and neuronal cells, have been reported to be associated with neuropsychiatric systemic lupus erythematosus (NPSLE) pathogenesis. However, the clinical features regarding anti-TPI antibody (anti-TPI)-positive NPSLE are not yet known. The aim of this study is to investigate the clinical features of anti-TPI-positive NPSLE patients using anti-TPI index values determined by enzyme-linked immunosorbent assay (ELISA). Thirty-one NPSLE patients treated in our department were included in this study. Serum samples were collected, and serum anti-TPI titers were measured by ELISA. The anti-TPI index values were defined as follows: (OD of samples - OD of negative control)/(OD of positive control - OD of negative control) × 100. Anti-TPI index values greater than 2 standard deviations above the mean of healthy controls were regarded as positive. The clinical features of anti-TPI-positive and anti-TPI-negative NPSLE were compared. Ten of the 31 NPSLE patients had anti-TPI positivity (32.3%). The clinical features of anti-TPI-positive NPSLE were comparable with those of anti-TPI-negative NPSLE, except for a higher frequency of aseptic meningitis (p = 0.027) and a lower frequency of acute confusional state (P = 0.026). Laboratory data in patients with anti-TPI-positive NPSLE showed significantly higher serum IgG levels. Furthermore, anti-TPI index values positively correlated with serum IgG levels. Our study indicates that serum anti-TPI increases in the presence of elevated IgG levels and can be associated with the pathogenesis of aseptic meningitis in NPSLE.

Triosephosphate isomerase, carbonic anhydrase, and creatinine kinase‐brain isoform are possible antigen targets in patients with achalasia

“…Autoantibodies anti‐TPI in cerebrospinal fluid is associated with neuropsychiatric lupus and MRL/MpJ‐Fas lpr mouse . Recent studies have shown to the association of anti‐TPI antibodies and neurological lupus, as well as a possible mechanism through the formation and deposition of immune complexes in regions near the ventricles, and the hippocampus choroid plexus that could contribute to brain damage and behavioral deficit . In the present study, we show that the antibodies of achalasia patients recognized TPI.…”

“…Studies showed that the inhibition of TPI activity influences microtubule stabilization and induces neuronal death in cultured murine cortical cells . Autoantibodies anti‐TPI in cerebrospinal fluid is associated with neuropsychiatric lupus and MRL/MpJ‐Fas lpr mouse . Recent studies have shown to the association of anti‐TPI antibodies and neurological lupus, as well as a possible mechanism through the formation and deposition of immune complexes in regions near the ventricles, and the hippocampus choroid plexus that could contribute to brain damage and behavioral deficit .…”

Anti-GAPDH Autoantibody Is Associated with Increased Disease Activity and Intracranial Pressure in Systemic Lupus Erythematosus

“…The recent studies reported that the prevalence of NPSLE manifestations was up to 56% in patients with SLE and the neuropsychiatric damage negatively affected the overall 5-year survival [3, 4]. The manifestations of NPSLE vary from patient to patient and lead to poor prognosis because of clinical heterogeneity and inefficient diagnosis [5]. To date, because of lack of specific diagnostic biomarkers, NPSLE is still diagnosed based on a comprehensive conception of clinical observations, laboratory tests, and imaging techniques [6].…”

Neuropsychiatric Immune-related Adverse Events Induced by Pembrolizumab in a Patient with Lung Adenocarcinoma and Systemic Lupus Erythematosus

“…NPSLE refers to neuropsychiatric involvement in SLE, which affects the central nervous system, peripheral nervous system, or both (10). NPSLE is clinically heterogeneous and therefore difficult to diagnose (11). The precise pathophysiology of NPSLE is not clearly understood.…”