Aim This study was carried out to determine the effects of interleukin (IL)-10 gene polymorphism 1082A/G on clinical diversity and activity of systemic lupus erythematosus (SLE), as it was shown to be associated with E26 transcription factor binding site, and to assess IL-10 concentration in SLE patients. Patients and methods Blood was drawn from 54 SLE patients and 27 healthy controls for DNA extraction. The single nucleotide polymorphism was identified using the PCR-restriction fragment length polymorphism, and serum sample was collected to assay IL-10 concentration. Results There was an increase in IL-10 concentration in SLE total patients (mean 49.5 pg/ml). Mutant allele A (76.9%) was found more frequently in SLE patients compared with allele G (23.1%). Genotype AA (66.7%) was found more frequently, followed by AG (20.4%) and GG (12.9%). Conclusion IL-10 concentration was elevated in SLE patients and was shown to be associated with disease activity. IL-10 gene polymorphism is not a strong indicator to show susceptibility of the disease.

Introduction Systemic lupus erythematosus (SLE) is an autoimmune disorder that has multiorgan involvement. The continuation of inflammation in lupus could be attributed to failure of the resolution process because of deficiency of potent endogenous proresolution-inducing molecules such as lipoxin A4 (LXA4), leading to progression and flares of lupus and lupus nephritis. Objective The aim of this study was to assess the levels of urinary LXA4 in SLE patients and in healthy controls, and to correlate them with various clinical and laboratory data as well as renal biopsy and disease activity indices (DAIs). Patients and methods A total of 40 adult female SLE patients were included in this study. Forty healthy women age-matched with SLE patients served as the control group. All patients were subjected to a full assessment of history, clinical examination, assessment of DAIs (SLEDAI and renal SLEDAI), and laboratory investigations including the urinary LXA4/creatinine ratio assessed by enzyme linked immunosorbent assay. Results Urinary LXA4/creatinine ratio levels were found to be significantly higher in all SLE patients compared with the healthy controls (P = 0.037). The median level of the urinary LXA4/creatinine ratio was lower in SLE patients with nephritis than in patients without nephritis (0.1 and 0.3 ng/ml, respectively), but with no statistical significance (P = 0.11). The urinary LXA4/creatinine ratio levels were found to be significantly lower in SLE patients with cardiovascular manifestations as well as those with neuropsychiatric manifestations (P = 0.009, 0.04 respectively). Conclusion This was a novel study that was carried out to assess the levels of urinary LXA4 in SLE patients. It showed that the urinary LXA4/creatinine ratio levels were significantly lower in SLE patients with cardiovascular and neuropsychiatric manifestations and nonsignificantly lower in patients with nephritis, suggesting that insufficiency of LXA4 in the human body may be responsible for major organ involvement in SLE patients. Accordingly, LXA4 is suggested to be an inflammatory biomarker not only for lupus nephritis but also for other systemic manifestations in SLE.

Background Early diagnosis and treatment of rheumatoid arthritis (RA) leads to better control and prevents irreversible joint damage. Antimutated citrullinated vimentin (anti-MCV) is one of the members of the anticitrullinated antibody family that can function as a serological marker in the early diagnosis of RA. Aim of the work This study aimed to measure serum levels of anti-MCV antibodies and study their relationship using clinical, laboratory, and radiological findings in RA patients. Patients and methods We measured anti-MCV in the serum of 60 RA patients, in 20 patients with psoriatic arthritis, and in 20 healthy controls. In RA patients, the disease activity score (DAS28) and the Health Assessment Questionnaire score were used. The immunoglobulin-M rheumatoid factor titer, anticyclic citrullinated peptide antibody (anti-CCP) titer, and C-reactive protein levels were also measured. The hands of RA patients were radiologically scored using the Larsen method. Results In RA patients the mean anti-MCV antibody serum level was 150.83 ± 125.95 U/ml, which was significantly higher (P < 0.001) compared with the mean serum level in psoriatic arthritis patients and healthy controls (17.4 ± 10.039 and 17.2 ± 10.63 U/ml, respectively). Serum levels of anti-MCV antibodies significantly correlated with DAS28 (r = 0.79, P < 0.05), Health Assessment Questionnaire scores (r = 0.53, P < 0.05), rheumatoid factor titer (r = 0.74, P < 0.05), anti-CCP antibody titer (r = 0.83, P < 0.05), and Larsen's score (r = 0.76, P < 0.05). Conclusion The significantly elevated anti-MCV antibody levels that are well correlated with RA disease activity and severity markers are highly suggestive of their potential role in the pathogenesis of RA. The considerable correlation of anti-MCV antibodies with other autoantibodies would imply their consistent diagnostic and prognostic role.

Introduction Systemic lupus erythematous (SLE) is a systemic, multifaceted inflammatory disease with clinical manifestations is protean and follows a relapsing and remitting course. Lupus Nephritis (LN) is one of the most frequent and serious manifestation. Endothelial protein C receptor (EPCR) is a transmembrane receptor that is shed into soluble form (sEPCR) in inflammatory status. It is demonstrated as a part of the pathobiology of the SLE disease. Aim of the work To assess correlation of sEPCR level in SLE patients to the disease activity in these patients and to relate sEPCR to LN. Patients and methods Serum level of sEPCR using enzyme-linked immunosorbent assay (ELISA), chemical and immunological markers of SLE were measured in 30 SLE patients and 30 age and sex matched apparently healthy controls. SLE patients were subgrouped into 20 patients without LN and 10 with LN. Disease activity was assessed using SLE Disease Activity Index (SLEDAI). Results A significantly higher sEPCR level was found on comparing SLE patients to controls with statistically highly significant difference (z = 4.8, P < 0.001). Moreover, there was a significantly higher sEPCR level on comparing SLE patients with LN to those without LN with statistically highly significant difference (z = 3.9, P < 0.001). Serum sEPCR had a highly significant positive correlation with SLEDAI in SLE patients (r = 0.66, P < 0.01). Conclusion sEPCR has a possible role in the pathogenesis of SLE and particularly LN diseases, reflecting disease activity in SLE patients.

Purpose The aim of our study was to assess, electrophysiologically, the possibility of associated subclinical trigeminal neuropathy in sickle cell anemia (SCA) patients and correlate the results with disease severity and findings of computerized tomography. Materials and methods Fifty patients with SCA were included; 20 of these patients had clinical unilateral trigeminal neuropathy (group II), whereas the others were asymptomatic (group I). Forty matched healthy individuals served as a control group. Trigeminal evoked potential (TEP) and inferior alveolar nerve (IAN) conduction studies were carried out for all patients and controls. Findings were correlated with the frequency of vaso-occlusive crisis, mental foramen (MF), and mandibular canal (MC) dimensions as measured by computerized tomography. Results There were highly significantly longer N13, 19, and 20 latencies and reduced N13-P19 amplitude in patient groups in comparison with the controls (P<0.001). There were delayed P19 latency, IAN latency, reduced IAN amplitude (P<0.05), and conduction velocity (P<0.001) in SCA patients with trigeminal neuropathy versus those without trigeminal neuropathy, and also in asymptomatic patients versus controls. The vaso-occlusive crisis frequency in group II was correlated positively with all TEP waves' latencies and IAN latency and correlated negatively with IAN amplitude, conduction velocity, and N13/P19 amplitude. MF and MC dimensions were significantly reduced in group II in comparison with the controls (P<0.05). MF height and MC diameter were correlated negatively with ipsilateral P19 latency. Conclusion Subclinical trigeminal neuropathy may be associated with SCA. The trigeminal nerve could be affected along its peripheral or the central pathway. Central affection may occur as a result of lesions in its nuclei or at the somatosensory cortex. Electrophysiological assessment is recommended in SCA patients to diagnose trigeminal neuropathy and detect the level of its affection. This will provide new insights into its prevention and treatment.

Introduction The majority of the fibromyalgia syndrome (FMS) patients do not exercise regularly and their physical fitness is low. Physical inactivity accelerates bone loss. This suggests that FMS patients are at risk in terms of osteoporosis. The aim of this study was to measure serum C-telopeptide of type I collagen (CTX-1) as a marker of bone resorption in premenopausal women with FMS. Patients and methods A total of 100 premenopausal female patients with FMS diagnosed according to the American College of Rheumatology (ACR) criteria 1990 and 50 healthy women were chosen to serve as the control group. Serum CTX-1 levels were measured using beta-CrossLaps Roche Elecsys. Results The serum CTX-1 level was significantly higher in patients with FMS compared with the control group. The mean serum CTX-1 in FMS patients was 340.2 ± 112.6 pg/ml compared with 283.6 ± 113.1 pg/ml in controls (P = 0.004). The serum CTX-1 level was positively correlated with the visual analogue scale(VAS) of pain (P = 0.028), the VAS of fatigue (P = 0.031), the VAS of global severity (P = 0.016), the VAS of anxiety (P = 0.013), the Health Assessment Questionnaire score (P = 0.022), the Fibromyalgia Impact Questionnaire (P = 0.010), the Beck Depression Inventory (P = 0.007), the tender points count (P = 0.003), the tender points score (P = 0.004), and the Pittsburg Sleep Quality Index (P = 0.021). The mean serum CTX-1 level was also significantly higher in FMS patients with postexertion pain (P = 0.010), confusion (P = 0.025), dizziness (P = 0.012), depression (P = 0.029), mood disturbance (P = 0.018), anxiety (P = 0.030), short memory difficulties (P = 0.017), and sleep disturbance (P = 0.028) than in those without these symptoms. Conclusion We found a significant increase in serum CTX-1 in FMS patients compared with controls, and this was correlated with the disease severity. Increased CTX-1 may lead to the early development of osteoporosis. More comprehensive and detailed studies are needed to determine the exact role of CTX-1 in FMS.

Background Systemic lupus erythematosus (SLE) is an autoimmune, multiorgan disease that affects connective tissues of many organs or systems, including the nervous system, where it affects the autonomic, the peripheral, and the central nervous system. Objective The aim of this study was to investigate the association of subclinical autonomic and peripheral neuropathy with SLE and to correlate neurophysiological parameters with clinical and laboratory data. Patients and methods Fifty-six SLE patients were included in this study. In addition, thirty age-matched and sex-matched healthy participants served as a control group. Exclusion criteria included patients having symptoms or signs indicating autonomic dysfunction or peripheral neuropathy. Also, endocrinal, toxic, compression, and traumatic neuropathies were excluded. Patients were assessed clinically and by laboratory investigations. Neurophysiological assessment included sympathetic skin response of the median nerve including latency and amplitude. In addition, nerve conduction study of both median and ulnar nerves was performed including motor distal latency, amplitude, nerve conduction velocity, and distal sensory latency. Results Pure sensory abnormality was detected in one patient, whereas pure motor neuropathy was found in 19 patients. Mixed sensory-motor abnormalities were detected in two patients. Sympathetic skin response was not elicited in 13 patients, whereas latency and amplitude abnormalities were detected in 11/43 and 9/43 patients, respectively. Sympathetic and axonal neuropathy was not correlated with the disease duration or the disease activity. Conclusion The pattern of neuropathy in SLE is mainly axonal. Also, the sympathetic nervous system is affected in lupus patients with a rate of up to 40% of the cases.

Introduction Somatosensory-evoked blink reflex (SBR) is an eye blink response obtained from electrical stimulation of peripheral nerves or the skin area of the body away from the face. Aim The aim of this study was to investigate the presence of SBR in peripheral facial palsy (PFP) and its relation with clinical and electrophysiological changes occurring in PFP as compared with postfacial syndrome (PFS). Setting and design This was a single-center, public hospital-based electromyography laboratory study. It was designed as a cross-sectional examination of consecutive patients with PFP and PFS and apparently healthy volunteers. Patients and methods The study included 25 patients with PFP, 25 patients with PFS, and 31 healthy volunteers. Facial nerve motor conduction, trigeminal blink reflex, and SBR were studied. Statistical analysis Quantitative data were compared using the Mann-Whitney test and the Kruskal-Wallis test. Qualitative data were analyzed using Pearson's Chi-square test. Results SBR was elicited in 67.7% of controls, in 68% of PFS patients, and in 32% of PFP patients. In the PFP group, SBR was found on the nonparalytic side in 28% of patients with paralyzed side stimulation and in 24% of patients with healthy side stimulation. For the PFS group, SBR was found on the nonparalytic side in 48%. Bilateral SBR elicitability was higher than its unilateral elicitability. Conclusion SBR occurs in patients with PFP and PFS and in healthy individuals. It has no relation with the clinical and electrophysiological changes occurring in PFP and PFS. Increased brainstem interneurons excitability is not essential to generate SBR. The hypothetical sensory-motor gating mechanism could be responsible for SBR generation.

Polymyalgia rheumatica (PMR) is a connective tissue disorder of unknown aetiology. It is hypothesized that, in a genetically predisposed person, its pathogenesis is triggered by an environmental factor, possibly a hitherto unknown infectious agent. We present the case of a 68-year-old woman who is being treated for PMR. She developed tubercular lymphadenitis and erythema nodosum and improved with antitubercular treatment. We hypothesize that the trigger for pathogenesis of PMR in this lady was antigen of Mycobacterium tuberculosis.