Morbidity In Systemic Lupus Erythematosus Research Articles

Effect of Vitamin D Supplementation on Regulatory T Cells of Systemic Lupus Erythematosus: A Systematic Review

Background. Systemic lupus erythematosus (SLE) is associated with a global reduction in regulatory T cells (Tregs). Vitamin D supplementation that is efficacious, safe, and reasonably priced has the potential to reduce morbidity in SLE. This study was aimed to systematically assess the efficacy of vitamin D supplementation in enhancing Tregs concentration or Tregs-related marker.
 Methods. A systematic review of the literature for clinical studies was performed on Pubmed, Proquest, and Google Scholar. Studies were assessed for risk of bias using Newcastle Ottawa Scale. All clinical studies that investigated the effects of vitamin D supplementation on Tregs in SLE patients were included. Key evidence was analyzed and qualitatively synthesized.
 Results. Three relevant studies were included. All studies were of high-quality. Vitamin D supplementation consistently increased Tregs concentration across all included studies.
 Conclusion. The current study supports the evidence that vitamin D supplementation enhanced Tregs concentration in SLE patients.

Updating medications and treatment strategy for systemic lupus erythematosus: A narrative review

Systemic lupus erythematosus (SLE) is one of the most heterogeneous systemic autoimmune diseases physicians manage. Despite therapeutic advances, the morbidity of SLE has remained considerable. All hopes for the future in this regard are pinned on targeting the interferon pathways, drugs that block B-cell function or T-cell function, Janus kinase inhibitors, also known as JAK inhibitors, and approaches involving stem cells or mesenchymal cells. New treatment recommendations clarifying anti-inflammatory and immuno-modulatory drugs emphasized the treat-to-target medical strategy, which combines low disease activity and low glucocorticoid (GC) exposure. Researchers support GCs at the lowest dose. The SLE patients need to take hydroxychloroquine. Biological medicines, including belimumab and anifrolumab, are prescribed based on disease stage and severity. To proceed with personalized therapy choices, we need a deeper understanding of biological pathways and specific disease-perpetuating components. New information from ongoing therapeutic studies and real-world data will assist in further clarifying the underlying multidimensional interrelations, bringing in a new era of precision medicine in lupus erythematosus that will benefit both patients and physicians. In order to determine the most effective therapy plan for lupus nephritis, rheumatologists and nephrologists should engage in close interdisciplinary communication. This review study will examine the most recent steps to deal with and treat this disease and future plans to help SLE patients.

Evaluating the Construct of Damage in Systemic Lupus Erythematosus.

The Systemic Lupus International Collaborating Clinics (SLICC), American College of Rheumatology (ACR), and the Lupus Foundation of America are developing a revised systemic lupus erythematosus (SLE) damage index (the SLICC/ACR Damage Index [SDI]). Shifts in the concept of damage in SLE have occurred with new insights into disease manifestations, diagnostics, and therapy. We evaluated contemporary constructs in SLE damage to inform development of the revised SDI. We conducted a 3-part qualitative study of international SLE experts. Facilitated small groups evaluated the construct underlying the concept of damage in SLE. A consensus meeting using nominal group technique was conducted to achieve agreement on aspects of the conceptual framework and scope of the revised damage index. The framework was finally reviewed and agreed upon by the entire group. Fifty participants from 13 countries were included. The 8 thematic clusters underlying the construct of SLE damage were purpose, items, weighting, reversibility, impact, time frame, attribution, and perspective. The revised SDI will be a discriminative index to measure morbidity in SLE, independent of activity or impact on the patient, and should be related to mortality. The SDI is primarily intended for research purposes and should take a life-course approach. Damage can occur before a diagnosis of SLE but should be attributable to SLE. Damage to an organ is irreversible, but the functional consequences on that organ may improve over time through physiological adaptation or treatment. We identified shifts in the paradigm of SLE damage and developed a unifying conceptual framework. These data form the groundwork for the next phases of SDI development.

A Clinical Approach of Lupus Nephritis Associated with Catastrophic Antiphospholipid - Antibody Syndrome - Review and Case Report

Abstract Glomerulonephritis is a major cause of morbidity in systemic lupus erythematosus (SLE). In fact, immune complex formation and deposition in the kidney results in intraglomerular inflammation with recruitment of leukocytes and activation and proliferation of resident renal cells. Intense injury may destroy resident renal cells by necrosis or apoptosis resulting in fibrinoid necrosis. When injury is less intense, endocapillary cells respond by proliferating and production of extracellular matrix (proliferative lesions). Renal biopsy, examination of urine sediment and measurement of C3 levels (and to less anti-DNA titers) are essential for the management of lupus nephritis. Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thrombotic episodes in the arterial or venous circulation, in the presence of antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), anticardiolipin antibodies, and anti-β2glycoprotein-I antibodies (anti-β2GPI). Catastrophic APS (CAPS) is a very rare (---lt---1%) and extremely severe variant of APS. It is characterized by multiple systems and thrombotic organ involvement that occurs in a very short period (days to weeks). Renal involvement is a common feature in CAPS, the most frequent finding is thrombotic microangiopathy (TMA), but other chronic lesions of APSN can also be found.

Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?

Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE. This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA. miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters. Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.

A Clinical Approach of Lupus Nephritis Associated with Catastrophic Antiphospholipid-Antibody Syndrome Review and Case Report

Glomerulonephritis is a major cause of morbidity in systemic lupus erythematosus (SLE). In fact, immune complex formation and deposition in the kidney results in intraglomerular inflammation with recruitment of leukocytes, and activation and proliferation of resident renal cells. Intense injury may destroy resident renal cells by necrosis or apoptosis resulting in fibrinoid necrosis. When injury is less intense, endocapillary cells respond by proliferating and production of extracellular matrix (proliferative lesions). Renal biopsy, examination of urine sediment and measurement of C3 levels (and to less anti-DNA titers) are essential for the management of lupus nephritis. Treatment depends on the severity of the lupus nephritis. Disease severity depends on the presence or absence of high-risk factors. These include demographic (male gender, black race), clinical (failure to achieve response or marked delay in response, multiple relapses, pregnancy), laboratory (impaired renal function, severe anemia with hematocrit less than 26%) and histologic features (mixed membrane- proliferative or proliferative nephritis; cellular crescents and/or fibrinoid necrosis; cellular crescent and/or fibrinoid necrosis; and moderate to high degrees of interstitial fibrosis and/or tubular atrophy).

Placental damage in pregnancies with systemic lupus erythematosus: A narrative review.

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease of unknown cause, which mainly affects women of childbearing age, especially between 15 and 55 years of age. During pregnancy, SLE is associated with a high risk of perinatal morbidity and mortality. Among the most frequent complications are spontaneous abortion, fetal death, prematurity, intrauterine Fetal growth restriction (FGR), and preeclampsia (PE). The pathophysiology underlying obstetric mortality and morbidity in SLE is still under investigation, but several studies in recent years have suggested that placental dysfunction may play a crucial role. Understanding this association will contribute to developing therapeutic options and improving patient management thus reducing the occurrence of adverse pregnancy outcomes in this group of women. In this review, we will focus on the relationship between SLE and placental insufficiency leading to adverse pregnancy outcomes.

A prospective study on the prevalence of neurally mediated hypotension in systemic lupus erythematosus

<p class="abstract"><strong>Background:</strong> Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease which affects skin and organ systems. Cardiovascular manifestations are one of the important cause for mortality and morbidity in SLE. Neurally mediated hypotension (NMH) caused by autonomic neuropathy is found to be associated with fibromyalgia responsible for chronic fatigue syndrome in SLE. Our study aims to find the prevalence of NMH in SLE.</p><p class="abstract"><strong>Methods:</strong> This is a prospective study conducted in the Department of Dermatology, Chengalpattu Medical College from May 2017 to December 2018. All SLE patients who attended the Dermatology OPD were included in the study. The diagnosis of SLE was made based on the ARA criteria. After obtaining informed consent, baseline blood pressure of all patients included in the study were recorded. In patients with low blood pressure other causes of hypotension were ruled out. Patients with no discernible cause of hypotension were subjected to the two stage tilt table test. A drop in systolic BP of >20 mm of Hg or diastolic BP of >10 mm of Hg is considered to be positive.<strong></strong></p><p class="abstract"><strong>Results:</strong> A total of 20 patients were included in the study, of which 19 were female and one male. The mean age was 31.7 years. 70% of the SLE patients included in our study were found to have NMH.</p><p><strong>Conclusions:</strong> Neurally Mediated Hypotension was found to be highly prevalent in SLE.</p>

Atherosclerotic Vascular Events in Systemic Lupus Erythematosus: An Evolving Story

Atherosclerotic vascular events (AVE) are a major cause of mortality and morbidity in systemic lupus erythematosus (SLE). We aimed to determine the effect of early recognition and therapy for both classic risk factors for AVE and for SLE, on the burden of AVE in SLE in recent decades. Inception patients who entered the University of Toronto Lupus Clinic between 1975 and 1987 followed to 1992 (Cohort 1), and between 1999 and 2011 followed to 2016 (Cohort 2) were studied. AVE attributed to atherosclerosis and occurring during the 17 years were identified. SLE disease activity and therapy as well as hypertension, hypercholesterolemia, hyperglycemia, and smoking were assessed. Analysis included descriptive statistics on baseline characteristics, traditional risk factors over the followup, outcome rates by each 100 person-years (PY), Kaplan-Meier cumulative AVE curves, as well as competing risk Cox models adjusted by inverse probability weights. Of the 234 patients in Cohort 1, 26 patients (11%) had an AVE compared with 10 of 262 patients (3.8%) in Cohort 2. The rate per 100 PY of followup was 1.8 in Cohort 1 and 0.44 in Cohort 2 (p < 0.0001). Better control of all risk factors and disease activity was achieved in Cohort 2. There was a reduction of 60% in the risk for AVE in Cohort 2. The incidence of AVE in SLE in the modern era has declined in large part owing to more effective management of classic coronary artery risk factors and of SLE.

The spectrum of neuropsychiatric lupus in a Black Caribbean population: a report of the Barbados National Lupus Registry.

Objective The objective of this study was to examine neuropsychiatric lupus in a Black Caribbean population. Methods We reviewed Barbados National Lupus Registry patients with ≥4 American College of Rheumatology criteria and a diagnosis of neuropsychiatric lupus using the American College of Rheumatology 19 case definitions. Results From 366 patients with four or more American College of Rheumatology criteria for systemic lupus erythematosus, 55 (15%) had evidence of neuropsychiatric lupus. There were 51 females and four males (F:M = 13:1) with a median age of 31 years. A total of 76.4% had a single neuropsychiatric lupus complication and 23.6% had two or three complications occurring sequentially or concurrently. The top three complications were psychosis - 49.1% (95% CI 35.8, 62.5); ischaemic stroke - 32.7% (21.4, 46.5); and generalized tonic-clonic seizures - 12.7% (6.0, 24.8). Twelve of the American College of Rheumatology 19 neuropsychiatric syndromes were represented: 91.2% central; 8.8% peripheral. There were 521 observation years, and for 32 patients (58%) neuropsychiatric lupus was a presenting feature. For the remaining 23 (42%) the first neuropsychiatric lupus event came after systemic lupus erythematosus diagnosis - median time of two years. Of the 22 deaths, systemic lupus erythematosus nephritis caused almost half (45.5%) at a median age of 32. The prevalence of nephritis was lower in the neuropsychiatric lupus subgroup (25.5%) compared with the Barbados National Lupus Registry data (47%) ( P = 0.01). Ischaemic stroke caused 22.7% of deaths at a median age of 46 and was the main cause of chronic neurologic deficits amongst survivors. Conclusion Neuropsychiatric lupus was an early cause of morbidity in systemic lupus erythematosus with predominantly singular central nervous system complications, the most common of which was psychosis. Most deaths occurred at a young age, principally from systemic lupus erythematosus nephritis. Ischaemic stroke was the main neurologic cause of death and disability.

A potential link between immune response to a periodontal bacterium, Aggregatibacter actinomycetemcomintans and Systemic Lupus Erythematosus

Abstract Infections are a significant cause of morbidity in Systemic Lupus Erythematosus (SLE). Although oral health is considerably compromised in SLE patients, the role of oral pathogens in influencing lupus pathogenesis is not known. In the present study, antibody responses to a periodontogenic, facultative anaerobic bacterium, Aggregatibacter actinomycetemcomitans (Aa), (which serve as an indicator of past or ongoing infection with Aa), were measured in SLE patients (n=587) and healthy controls (n=75). The associations between anti-Aa antibody titers and clinical measures of SLE were evaluated. The effect of Aa infection on development of lupus was investigated in the NZM2328 mice. The ability of Aa to induce neutrophil extracellular traps (NETs) was studied in vitro. Both SLE patients and controls showed the presence of anti-Aa. In SLE patients, the anti-Aa titers correlated strongly with anti-dsDNA, anti-chromatin, anti-RNP, and anti-Sm; but not with anti-Ro52, anti-Ro60, and anti-La antibodies. NZM2328 mice developed a robust immune response to Aa, and the Aa infection caused an accelerated onset of autoantibody and renal disease. In addition, Aa readily induced NETosis in NZM2328 neutrophils. Our data suggest for the first time that SLE patients are exposed to oral pathogen Aa, and this exposure significantly influences immune responses against a subset of lupus-associated autoantigens, possibly through NETosis. Furthermore, our studies suggest that management of oral health in SLE patients might prove to be beneficial for controlling lupus.

Smoking and Its Association With Morbidity in Systemic Lupus Erythematosus Evaluated by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index: Preliminary Data and Systematic Review.

Due to the increased availability of effective treatments, patients with systemic lupus erythematosus (SLE) now have longer survival times, and factors involved in cumulative chronic damage in SLE need to be better understood. This study was undertaken to evaluate the relationship between smoking and cumulative chronic damage in SLE patients. A cross-sectional study of SLE patients was performed to investigate the possible association between smoking exposure (ever [previous or current, active or secondhand smokers] or never) and cumulative chronic damage as measured by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI). A systematic review of the literature was conducted by cross-searching Medline for the terms lupus and smoking. We enrolled 105 patients with SLE (96% female), with a mean ± SD age of 40.7 ± 11.4 years and a mean followup time of 8.98 years. Of the 105 patients, 74 had an SDI score of 1-10, and 31 had an SDI score of 0. The difference between smoking exposure and no smoking exposure was significant (P = 0.02 by chi-square test in contingency table analysis), and SLE patients who were never exposed to smoking had 0.78 times the risk of progressing toward a cumulative damage status (SDI score of > 0) (95% confidence interval 0.16-0.98) throughout the followup period compared to those who were ever exposed. In the systematic review of the literature, we found only a small number of articles that addressed some aspects of the relationship between smoking exposure and cumulative damage in SLE patients. Our findings indicate that smoking exposure is associated with cumulative chronic damage, as determined by the SDI score, in patients with SLE. Smoking exposure may have deleterious effects on lupus morbidity, and more detailed studies of this association are needed.

Prevalence of vascular disease in systemic lupus erythematosus compared with type-1 diabetes mellitus: a cross-sectional study of two cohorts.

Systemic lupus erythematosus (SLE) is associated with considerable cardiovascular morbidity that has not yet been directly compared with other diseases with known cardiovascular risk. Two hundred and forty-one patients of the multicentre Swiss SLE cohort study (SSCS) were cross-sectionally assessed for coronary heart disease (CHD), cerebrovascular disease (CVD) and peripheral artery disease (PAD). SLE patients were compared with a cohort of 193 patients with type-1 diabetes mellitus being followed at the University Hospital Basel. A subgroup analysis of 50 age- and sex-matched patients from the University Hospital Basel was performed. Of patients within the SSCS 13.3% had one or more vascular events: 8.3% CHD, 5% CVD and 1.2% PAD. In type-1 diabetes mellitus patients, 15% had vascular events: 9.3% CHD, 3.1% CVD and 5.6% PAD. In the matched subgroup, 26% of SLE patients had vascular events (14% CHD) compared with 12% in type-1 DM patients (2% CHD). Cardiovascular risk factors were similar in both groups. Vascular events in SLE patients were associated with age, longer disease duration, dyslipidaemia, and hypertension. Cardiovascular morbidity in SLE is at least as frequent as in age- and sex-matched type-1 diabetes mellitus patients. Therefore, aggressive screening and management of cardiovascular risk factors should be performed.

Challenges for lupus management in emerging countries

In emerging countries, systemic lupus erythematosus (SLE) has been associated with several unfavorable outcomes including disease activity, damage accrual, work disability and mortality. Poor socioeconomic status (SES) and lack of access to healthcare, especially in medically underserved communities, may be responsible for many of the observed disparities. Diagnostic delay of SLE or for severe organ damages (renal involvement) have a negative impact on those adverse outcomes in lupus patients who either belong to minority groups or live in emerging countries. Longitudinal and observational prospective studies and registries may help to identify the factors that influence poor SLE outcomes in emerging countries. Infection is an important cause of mortality and morbidity in SLE, particularly in low SES patients and tuberculosis appears to be frequent in SLE patients living in endemic areas (mainly emerging countries). Thus, tuberculosis screening should be systematically performed and prophylaxis discussed for patients from these areas. SLE treatment in the developing world is restricted by the availability and cost of some immunosuppressive drugs. Moreover, poor adherence has been associated to bad outcomes in lupus patients with a higher risk of flares, morbidity, hospitalization, and poor renal prognosis. Low education and the lack of money are identified as the main barrier to improve lupus prognosis. Newer therapeutic agents and new protocols had contributed to improve survival in SLE. The use of corticoid-sparing agents (hydroxychloroquine, methotrexate, azathioprine and mycophenolate mofetif) is one of the most useful strategy; availability of inexpensive generics may help to optimize access to these medications.

SIRT1 promoter polymorphisms as clinical modifiers on systemic lupus erythematosus

Silent mating type Information Regulator 2 homolog 1 (SIRT1) is a deacetylase protein that participates in several physiological processes with importance in transcriptional silencing, apoptosis, immune system regulation and inflammation. Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease in which upregulated expression of SIRT1 on CD4+ T lymphocytes of active patients has been reported. Also, global hypoacetylation of histones H3 and H4, with H3 hypoacetylation was correlated with a higher disease activity index. SIRT1 promoter rs12778366 and rs3758391 may account for differential expression of this molecule and the role of these variants was investigated in SLE susceptibility and morbidity. Genomic DNA was extracted from peripheral blood of 367 SLE patients and 290 healthy controls of a Southern Brazilian population. SIRT1 rs12778366 and rs3758391 were amplified through PCR and genotyped through sequencing. No statistically significant differences were observed between patients and controls for allelic, genotypic or haplotypic frequencies. Nevertheless, SIRT1 rs3758391 was not in Hardy-Weinberg equilibrium, presenting a paucity of CT heterozygous both in patients and controls. SLE patients with TT and CT genotypes displayed a higher chance of developing lupus nephritis (Pc = 0.012, OR = 2.04 95 % CI 1.32-3.14) and presented a higher disease activity index (Mean rank 170.95 vs 137.26, Pc = 0.006) when compared with CC homozygous patients. Our results suggest that SIRT1 rs3758391 modifies SLE morbidity, with rs3758391 T allele being a risk factor for nephritis and a higher SLEDAI. Nevertheless, it remains to be elucidated how SIRT1 rs3758391 functionally influences SLE severity.

Dysregulated CD4+ T cells from SLE-susceptible mice are sufficient to accelerate atherosclerosis in LDLr−/− mice

ObjectiveAccelerated atherosclerosis is a major source of morbidity in systemic lupus erythematosus (SLE). However, the cause of SLE-accelerated atherosclerosis remains unclear.MethodsCD4+ T cells from C57/Bl/6 (B6) or SLE-susceptible B6.Sle1.2.3 (B6.SLE)...

THU0509 Chronic Kidney Disease Independently Predicts Cardiovascular Morbidities among Hospitalized Patients with Systemic Lupus Erythematosus: Findings from a United States National Study

BackgroundGlomerulonephritis leading to chronic kidney disease (CKD) is a major cause of morbidity in systemic lupus erythematosus (SLE). Accelerated atherosclerosis has been recognized as the major underlying factor of the...

Renal transplantation in lupus nephritis: a Brazilian cohort

To determine the epidemiological profile and outcome of patients with lupus nephritis (LN) undergoing renal transplantation. The archival records of 50 patients with LN and end-stage renal disease (ESRD) treated by kidney transplantation from March 1992 to December 2010 were reviewed. All patients met the American College of Rheumatology criteria for systemic lupus erythematosus (SLE). Fourteen patients were included in the study. The majority were women (85.7%) and non-Caucasian (85.7%); the mean age at diagnosis of SLE and LN was 24 ± 8 and 25 ± 8 years, respectively. Renal biopsy was performed in 12 patients, with 75% of them showing proliferative lesions (class III and IV according to the World Health Organization and International Society of Nephrology/Renal Pathology Society classification). Thirteen patients (93%) underwent intermittent hemodialysis or peritoneal dialysis before transplantation. The median time between the start of dialysis and transplantation was 30 months (range 3-103 months); 67% of the procedures involved deceased donors and 33% involved living-related donors. The graft survival rates were 93.3%, 90.9%, and 85.7% at 1, 5 and 10 years, respectively. Post-transplant immunosuppressive agents were mycophenolate mofetil (84%), azathioprine (17%), tacrolimus (25%), sirolimus (58%) and cyclosporine (8%). Eight episodes of acute rejection were noted in six patients. There was a graft loss due to renal vein thrombosis in the one patient with secondary antiphospholipid syndrome. The mean SLICC by the time of kidney transplantation was 5 ± 2. In total, 13 patients (92.8%) developed at least one infectious event during the follow-up, with one dying in the immediate post-transplant period because of sepsis. Two patients (14%) had a lupus flare. There was no clinical or histological evidence of LN recurrence. LN is the major cause of morbidity in SLE, with progression to ESRD in 10-22% of cases. Despite concerns about LN recurrence after renal transplantation, the data obtained in our sample indicate this procedure as a safe alternative therapy for ESRD in this population.

Influence of chronic inflammation and autoimmunity on coronary calcifications and myocardial perfusion defects in systemic lupus erythematosus patients

ObjectiveConventional risk factors for coronary artery disease fail to explain the increased frequency or cardiovascular morbidity in systemic lupus erythematosus (SLE) patients. This study was conducted to determine the possible influence of autoimmune and inflammatory phenomena markers on coronary artery calcifications and myocardial perfusion abnormalities in SLE patients.Materials and methodsMulti-detector computed tomography (MDCT)-based coronary calcium scoring and single photon emission computerized tomography (SPECT) studies (Tc-99m sestamibi) were performed in 60 SLE patients in stable clinical condition, without a prior history of coronary artery disease. Laboratory evaluation included serum C-reactive protein (CRP), complement C3c and C4 components and antiphospholipid antibodies (aPL). The latter included anticardiolipin (aCL) and anti-β2-glycoprotein I (aβ2GPI) antibodies, of both IgG and IgM classes, and lupus anticoagulant (LA) in plasma.ResultsSPECT revealed persistent perfusion defects in 22 (36.7%) patients and exercise-induced defects in eight (13.3%), while MDCT revealed coronary calcifications in 15 (25%). Calcium scores ranged from 1 to 843.2 (mean 113.5 ± 259.7). No association was found between conventional coronary artery disease risk factors (obesity, hypertension, tobacco use, hyperlipidaemia, diabetes) nor CRP, C3c or C4 levels and coronary calcifications or myocardial perfusion defects. On the contrary, in patients with these pathologies, augmented autoimmunization was found, reflected by increased aCL IgG and antiβ2GPI IgG levels. In patients with aCL IgG >20 RU/ml or antiβ2GPI IgG >3 RU/ml, the relative risk of coronary calcification formation was 4.1 compared to patients with normal values. Accordingly, in LA-positive patients the relative risk of coronary calcification formation was 4.4 compared to LA-negative patients.ConclusionsConventional risk factors for coronary artery disease as well as markers of an ongoing inflammation did not show any association with perfusion defects and/or coronary artery calcifications in SLE patients. On the contrary, calcified atherosclerotic plaques and myocardial perfusion defects were observed mainly in patients with elevated levels of anticardiolipin and aβ2GPI antibodies of the IgG class. It might be speculated that coronary artery calcifications and perfusion defects are a result of antiphospholipid antibodies-induced coronary artery microthrombosis.

Clinical expression and morbidity of systemic lupus erythematosus during a post-diagnostic 5-year follow-up: a male:female comparison

The aim of this study was to analyse the prevalence of the most relevant clinical features of the diagnosis of systemic lupus erythematosus (SLE) in a sample of male patients with lupus as well as the incidence of the main causes of morbidity in a 5-year period after the diagnosis. A further aim of this study was to investigate the impact of gender on expression and morbidity of SLE. Data were collected from the medical records of 59 male and 535 female patients with SLE who were diagnosed at the hospitals in the region of Thessaloniki. Several differences in the expression and morbidity of the disease were found in relation to the gender of the patient. Male patients had a higher prevalence of thromboses, nephropathy, strokes, gastrointestinal tract symptoms and antiphospholipid syndrome when compared with female patients, but tended to present less often with arthralgia, hair loss, Raynaud's phenomenon and photosensitivity as the initial clinical manifestations. During the 5-year follow-up, positive associations have been found between male gender and the incidence of tendonitis, myositis, nephropathy and infections, particularly of the respiratory tract. In conclusion, this study has provided information regarding the features of clinical expression and morbidity in male patients, and has shown that gender is a possible factor that can influence the clinical expression of SLE.