The purpose of this study was to obtain electrophysiological documentation of possible involvement of central and peripheral nervous system (CNS and PNS) in systemic lupus erythematosus (SLE) patients even in the absence of neurological manifestations. The study included 30 consecutive patients with SLE and 25 age- and sex-matched volunteers as a control group. They were subjected to neurological and rheumatological tests and an extensive battery of neurophysiological tests, besides Wechsler adult intelligence scale. Overt neurological manifestations were observed in 14 patients (46.7%). Neurophysiological data revealed that 25 patients (83%) had at least 2 abnormal tests; 11 (68.8%) patients of the asymptomatic group and 14 patients (100%) of the symptomatic group with no significant differences between them. Seventeen patients (56.7%) had evidence of PNS dysfunction either in nerves (46.7%) or muscles (10%); 7 of them in the asymptomatic group. Twenty-four patients (80%) had evidence of CNS dysfunction. Twenty-two patients (73%) had abnormalities recorded on electroencephalography; 9 patients in the asymptomatic group and 13 patients in the symptomatic group. Eleven patients (37%) had abnormal values of P100 of visual evoked potential; 5 patients in the asymptomatic group and 6 in the symptomatic group. Eight patients (26.7%) had abnormal latency of wave I of brain stem response; 3 of them in the asymptomatic group. Abnormal prolongation of the P300 component of event-related potentials was recorded in 2 patients (12.5%) of the asymptomatic group, while low IQ was observed in 8 patients of each group. Neurophysiological abnormalities are fairly common in SLE patients whether symptomatic or asymptomatic. The use of such tests favors a true incidence of nervous system involvement, more accurate diagnosis, and may lead to better clinical care before the development of debilitating CNS and PNS changes.

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ObjectiveTo evaluate peripheral nerve involvement in patients with SLE with neuromuscular ultrasonography (NMUS) and understand its role in investigating SLE-related peripheral neuropathy.MethodsThis is an observational cross-sectional study on patients with SLE and healthy controls. Five nerves in each patient were examined bilaterally with NMUS, and the cross-sectional area (CSA) of each nerve at certain sites was estimated. The mean CSA at each site, for each nerve, in each group was statistically analysed and compared between groups.Results370 nerves were evaluated in 37 patients. By nerve conduction study (NCS), 36 patients had polyneuropathy (80.6% mixed type, 19.4% sensory). Significant mean CSA enlargement was present among the ulnar nerve at the Guyon’s canal and mid-humerus (both p=0.001); tibial nerve at the distal leg and proximal to the tarsal tunnel (p=0.003 and p=0.001, respectively); and peroneal nerve at the popliteal fossa (p=0.042). The mean CSA showed high specificity compared with NCS.ConclusionOur study shows that CSA could be a complementary tool to NCS for studying peripheral neuropathy in SLE. Furthermore, NMUS provides data on the different pathophysiological aspects of nerve involvement in SLE. Future studies using more than one sonographic parameter in combination with NCS and nerve histopathology are recommended to further investigate SLE-related neuropathy.Trial registration numberNCT04527172.

Background A decrease in bone mass has been described in a high percentage with increased risk of osteoporosis in JIA subtypes. The pathogenesis of bone loss in active JIA is complex, and results in reduced bone mineral density. Recent data have indicated an overlapping pathway between bone biology and biology of inflammation giving impression that inflammation may have a role in pathology of osteoporosis. Understanding the role of OPG/RANK/RANKL modulation in pathogenesis of bone loss among JIA subtypes will hold the key for identification of patients at risk and for management of osteoporosis. Objectives To evaluate the role of receptor activation of nuclear factor kB (RANK)/receptor activator of nuclear factor kB ligand (RANKL)/osteoprotegerin (OPG) modulation in juvenile idiopathic arthritis (JIA) subtypes with and without bone erosions. Methods Seventy children presenting JIA subtypes were recruited for the study and were chosen according to ILAR, 2001 criteria. They were compared with thirty healthy controls of matched age, sex, and ethnicity. Both groups had the average dietary intake of calcium products and sun exposure. Clinical presentations, laboratory investigations, and treatments used especially corticosteroids were recorded. JIA subtypes were oligo articular, polyarticular RF negative, RF positive, systemic onset JIA (SOJIA), enthesitis related arthritis (ERA) and psoriatic (PsA). All involved articulations were assessed by plain radiography for juxtaarticular osteoporosis and bone erosions. Disease activity was measured by Juvenile Arthritis Disease Activity Score (JADAS-27). Serum levels of OPG, RANK and RANKL were measured with estimation of OPG/RANKL ratio, using an enzyme-linked immunosorbent assay (ELISA). Results A significant low serum concentration of OPG was found in all JIA subgroups. There was a significant increase in serum level of RANKL, and a significant decrease of OPG/RANKL ratio. OPG/RANKL ratio was significantly lower in SOJIA, active polyarticular JIA and ERA than other groups within the subtypes. A significant low OPG/RANKL ratio was found in patients with prolonged steroid use and those with erosions. To our knowledge, this research is the first one studied these biomarkers in JIA subtypes, including ERA. Conclusions OPG/RANKL ratio can be an early predictor of increased bone resorption, and may be a valuable biomarker for bone damage in JIA subtypes. Systemic onset juvenile idiopathic arthritis, active polyarticular juvenile idiopathic arthritis and enthesitis related arthritis are at higher risk for osteoporosis. Disclosure of Interest None Declared

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