Uptake of Best Medical Therapy: Secondary Prevention of Cardiovascular Disease in Vascular Surgical Patients in Western Australia.

Best medical therapy (BMT) for peripheral arterial disease (PAD), carotid artery stenosis (CAS) and abdominal aortic aneurysm (AAA) involving concomitant use of antiplatelets, lipid-lowering agents, and blood pressure control, improves patient survival and prevents clinical cardiovascular disease (CVD). We performed a single-center cross-sectional study, over a 4-year period, describing BMT use in Western Australian patients with symptomatic PAD, CAS and AAA in the community. Overall, 45.3% of our cohort (n = 1689) were on appropriate BMT (CAS, 58.1%; PAD, 43.1%; AAA, 41.1%). There was highest uptake of blood pressure control at 93.0% (lipid-lowering agents, 65.3%; antithrombotics 63.5%). PAD was associated with highest uptake of blood pressure control (PAD 93.9%; CAS, 91.4%; AAA, 91.1%, P = .092) whilst CAS had highest uptake of antithrombotics (CAS 76.3%; PAD, 61.0%; AAA 60.4%, P < .001) and lipid-lowering agents (CAS 78.7%; PAD, 63.1%; AAA, 60.4%, P < .001). Our study indicates suboptimal use of BMT in patients with vascular disease in the community. The risk of CVD in CAS is likely misperceived as higher than PAD and AAA.

Cancer development in patients hospitalized with systemic lupus erythematosus: A population-level data linkage study.

AIM: To explore the association between systemic lupus erythematosus (SLE) with the risk of cancer development and subsequent 5-year mortality in Western Australia (WA). METHODS: Population-level, data linkage study of SLE patients (n = 2111) and general population comparators (n = 21 110) hospitalized between 1980 and 2014. SLE patients (identified by ICD-9-CM: 695.4, 710.0, and ICD-10-AM: L93.0, M32.0) were nearest matched (10:1) for age, sex, Aboriginality, and temporality. Follow up was from time zero (index SLE hospitalization) to cancer development, death or 31 December 2014. We assessed the risk of cancer development and subsequent 5-year mortality between SLE patients and comparators with univariate and multivariate-adjusted Cox proportional hazards regression models. RESULTS: SLE patients had similar multivariate-adjusted risk (adjusted hazard ratio [aHR] 1.03, 95% confidence interval [CI] 0.93-1.15; p = .583) of cancer development. Cancer development risk was higher in SLE patients <40 years old (aHR 1.58, 95% CI 1.29-1.94; p < .001), and from 1980 to 1999 (aHR 1.16, 95% CI 1.02-1.31; p < .001). SLE patients had higher risk of developing cancer of the oropharynx (aHR 2.13, 95% CI 1.30-3.50), vulvo-vagina (aHR 3.22, 95% CI 1.34-7.75), skin (aHR 1.20, 95% CI 1.01-1.43), musculoskeletal tissues (aHR 2.26, 95% CI 1.16-4.40), and hematological tissues (aHR 1.78 95% CI 1.25-2.53), all p < .05. After cancer development, SLE patients had increased risk of 5-year mortality (aHR 1.31, 95% CI 1.06-1.61); highest in patients <50 years old (aHR 2.03, 95% CI 1.03-4.00), and in those with reproductive system and skin cancers. CONCLUSIONS: Hospitalized SLE patients had increased risk of multiple cancer sub-types. Following cancer development, SLE patients had increased risk of 5-year mortality. There is scope to improve cancer prevention and surveillance in SLE patients. TRIAL REGISTRATION: Not applicable. This low-risk risk study used de-identified administrative linked health data.

The relationship between clinical phenotype and kallikrein-kinin bioregulation in different forms of arthritis.

OBJECTIVE: Patients with rheumatoid arthritis (RA) have shown increased levels of neutrophils generating kallikrein-kinin peptides in blood which are potent mediators of inflammation. This study investigated the association between the bioregulation of kinin-mediated inflammation with the clinical, quality of life, and imaging characteristics (e.g. ultrasonography) of different arthritides. METHODS: Patients with osteoarthritis (OA, n = 29), gout (n = 10) and RA (n = 8) were recruited and screened for clinical symptoms, quality of life, and ultrasonographical assessment of arthritis. Blood neutrophils were assessed for the expression of bradykinin receptors (B1R and B2R), kininogens and kallikreins by immunocytochemistry with visualization by bright field microscopy. Levels of plasma biomarkers were measured by ELISA and cytometric bead array. RESULTS: Quality of life (SF-36 domains and summary scores; including pain; and, HAQ) was similar across OA, gout and RA patients; with the exception of worse physical functioning scores between OA and gout patients. Synovial hypertrophy (on ultrasound) differed between groups (p = 0.001), and the dichotomised Power Doppler (PD) score of greater than or equal to 2 (PD-GE2) was marginally significant (p = 0.09). Plasma IL-8 were highest in patients with gout followed by RA and OA (both, P < 0.05). Patients with RA had higher plasma levels of sTNFR1, IL-1ß, IL-12p70, TNF and IL-6, compared to OA and gout patients (all, P < 0.05). Patients with OA had higher expression of K1B and KLK1 on blood neutrophils followed by RA and gout patients (both, P < 0.05). Bodily pain correlated with B1R expression on blood neutrophils (r = 0.334, p = 0.05), and inversely with plasma levels of CRP (r = -0.55), sTNFR1 (r = -0.352) and IL-6 (r = -0.422), all P < 0.05. Expression of B1R on blood neutrophils also correlated with Knee PD (r = 0.403) and PD-GE2 (r = 0.480), both P < 0.05. CONCLUSIONS: Pain levels and quality of life were similar between patients with OA, RA and gout with knee arthritis. Plasma inflammatory biomarkers and B1R expression on blood neutrophils correlated with pain. Targeting B1R to modulate the kinin-kallikrein system may pose as a new therapeutic target in the treatment of arthritis.

Mortality Rates in Patients With Ankylosing Spondylitis With and Without Extraarticular Manifestations and Comorbidities: A Retrospective Cohort Study.

OBJECTIVE: To examine mortality rates in hospitalized patients with ankylosing spondylitis (AS) and the association of extraarticular manifestations (EAMs) and comorbidities with mortality rates. METHODS: This study was a retrospective, population-based cohort study using linked administrative data from patients with AS who were hospitalized (n = 1791) and patients in a matched comparison group (n = 8955). Mortality data for patients were obtained from the Western Australia Death Register. The presence of EAMs and comorbidities was identified from hospital records. Mortality rates were compared between the 2 groups using Cox proportional hazard models overall and stratified by a history of EAMs, comorbidities, and smoking status. RESULTS: Crude mortality rates were significantly higher among patients with AS than among patients in the comparison group (hazard ratio [HR] 1.85, 95% CI 1.62-2.12), with excess mortality in the AS group associated with cardiovascular disease (CVD; HR 5.32, 95% CI 3.84-7.35), cancer (HR 1.68, 95% CI 1.27-2.23), external causes (HR 3.92, 95% CI 2.28-6.77), and infectious diseases (HR 25.92, 95% CI 7.50-89.56). When patients were stratified by history of EAMs, CVD, and smoking, the risk of mortality was elevated in patients both with and without each risk factor. Among patients with AS, histories of CVD (HR 6.33, 95% CI 4.79-8.38), diabetes (HR 2.81, 95% CI 1.99-3.95), smoking (HR 1.49, 95% CI 1.18-1.89), and EAMs (HR 1.62, 95% CI 1.24-2.11) were associated with an increased risk of mortality. CONCLUSION: The presence of comorbidities, EAMs, and smoking contributes to an increased risk of all-cause mortality among patients with AS who are hospitalized compared to patients in the comparison group. These results support the need to prevent or reduce the occurrence of comorbidities and smoking in patients with AS.

Mortality and cause of death in patients with ANCA-associated vasculitis and polyarteritis nodosa in Australia-a population-based study.

OBJECTIVES: We compared survival and causes of death in Western Australian (WA) ANCA-associated vasculitis (AAV) and PAN patients with controls and the WA population. METHODS: In this data linkage study, we identified patients with incident AAV/PAN and age, sex and temporally matched controls 1980-2014 from the WA Rheumatic Disease Epidemiological Registry. Survival analyses and time-varying analyses were performed. RESULTS: Six hundred and fourteen patients with incident AAV/PAN were compared with 6672 controls; 229 AAV/PAN patients died over 5277 person-years of follow-up and 1009 controls died over 73835 person-years. Survival was reduced in patients with AAV/PAN compared with matched controls [hazard ratio (HR) 3.5 (95% CI: 3.1, 4.1)], and matched WA population rates [standardized mortality ratio 3.3 (95% CI: 2.9, 3.8)]. Greatest excess mortality in AAV/PAN patients was observed in the first year after diagnosis and remained higher than controls throughout follow-up. Greater excess mortality was observed in patients >60 years at diagnosis. In cause-specific analyses, mortality HR for vasculitis, infection and non-infective respiratory disease were greatest early after diagnosis and remained persistently elevated. The HRs for malignancy and cerebrovascular disease related deaths increased during follow-up, and were constant for ischaemic heart disease related deaths. CONCLUSION: Mortality was increased in AAV/PAN patients compared with controls, with patients older at diagnosis at greater risk. These findings provide mortality risk for AAV/PAN in an Australian population, highlighting key contributors to mortality at different time periods over follow-up and potential areas of focus for reducing mortality.

Cancer in Anti-Neutrophil Cytoplasm Antibody-Associated Vasculitis and Polyarteritis Nodosa in Australia: A Population-Based Study.

OBJECTIVE: The study objective was to compare incident cancer rates among patients with anti-neutrophil cytoplasm antibody-associated vasculitis (AAV) and polyarteritis nodosa (PAN) in Western Australia (WA) with the general population and perform time-varying analyses to identify periods with greatest excess cancers. METHODS: Administrative health data from patients hospitalized with incident AAV/PAN from 1980 to 2014 were linked to the WA cancer registry, which holds compulsorily reported cancer data (excluding skin squamous cell and basal cell carcinomas). Incident cancer rates in patients with AAV/PAN were compared with age-, sex-, and calendar-year-matched WA population rates. RESULTS: Patients with AAV/PAN had higher overall rates of incident cancer compared with the matched population (standardized incidence ratio [SIR], 1.74; 95% confidence interval [CI], 1.42-2.10). In subgroup analyses, incident cancer rates in patients with granulomatosis with polyangiitis/eosinophilic granulomatosis with polyangiitis were approximately double the general population (SIR, 2.21; 95% CI, 1.73-2.78) but similar to the general population in patients with microscopic polyangiitis/PAN (SIR, 1.21; 95% CI, 0.85-1.68). Patients with AAV/PAN had higher rates of genitourinary, skin, hematological, and lung cancers. Excess rates of hematological and lung cancers peaked early after diagnosis, whereas excess skin and genitourinary cancer rates peaked at 5 and 10 years, respectively. CONCLUSION: This study highlights the importance of long-term cancer surveillance in patients with AAV/PAN and defines time frames of excess risk for specific cancers, which may help inform guidance on cancer screening. Furthermore, it indicates the need for skin surveillance for melanoma in addition to nonmelanoma skin cancers in patients who have greater environmental ultraviolet exposure, such as in Australia.

Smoking associates with increased BAFF and decreased interferon-γ levels in patients with systemic lupus erythematosus.

OBJECTIVE: In SLE, smoking increases the burden of cutaneous disease and organ damage, and leads to premature mortality. However, the effect of smoking on disease manifestations and cytokine levels of patients with SLE is unclear. This study compared characteristics of patients with SLE across smoking status, and determined the association of smoking with serum cytokine levels. METHOD: A cross-sectional study of patients with SLE (n=99) during a research visit in which smoking status was ascertained. Smoking status was compared across classification criteria (American College of Rheumatology Classification Criteria for SLE (ACR97)), disease activity (SLE Disease Activity Index), autoantibody levels, accrued damage (Systemic Lupus International Collaborating Clinics/ACR Damage Index), and circulating concentrations of serum interferon-gamma (IFN-γ), interleukin (IL)-1ß, IL-4, IL-6, IL-10, IL-12, IL-17, B cell-activating factor (BAFF), tumour necrosis factor-alpha, transforming growth factor beta 1 (TGF-ß1), macrophage inflammatory protein 1 alpha (MIP-1α), MIP-1ß and monocyte chemoattractant protein 1. Linear regression models determined the association between smoking and cytokine levels, adjusting for age and sex, clinical characteristics (model 1), and anti-inflammatory (IL-4, IL-10 and TGF- ß1) and regulatory (IL-1ß) cytokines (model 2). RESULTS: Among patients with SLE (97.9% ANA+; mean 48.48 years old; 86.9% female; mean 10 years of disease duration), 35.4% (n=35 of 99) were smoking (an average of 7 cigarettes/day for 24 years). Smokers had increased odds of prevalent ACR97 malar rash (OR 3.40, 95% CI 1.23 to 9.34) and mucosal ulcers (OR 3.31, 95% CI 1.36 to 8.05). Smokers had more arthritis (OR 3.19, 95% CI 1.19 to 8.60), migraine (OR 2.82, 95% CI 1.07 to 7.44), Raynaud's phenomenon (OR 5.15, 95% CI 1.95 to 13.56) and increased non-steroidal anti-inflammatory drug use (OR 6.88, 95% CI 1.99 to 23.72). Smoking associated with 27% increased BAFF levels (95% CI 6% to 48%) and 42% decreased IFN-γ levels (95% CI -79% to -5%) in model 2. CONCLUSION: In patients with SLE, smoking independently associated with increased BAFF and decreased IFN-γ levels, and an increased frequency of arthritis, migraine and Raynaud's phenomenon. Smoking cessation is advisable to reduce systemic inflammation, reduce disease activity and improve host defence.

Cancer diagnosis and mortality in patients with ankylosing spondylitis: A Western Australian retrospective cohort study.

AIM: Ankylosing spondylitis (AS) has been associated with a modest increase in the risk of cancer. However, little is known as to how AS influences risk of mortality following cancer diagnosis. This study compared the risk of cancer and subsequent mortality in patients with AS compared with a non-AS population group. METHODS: Patients diagnosed with AS in Western Australia (WA) between 1980 and 2014 were identified from the WA Rheumatic Disease Epidemiological Register (N = 2152; 31 099 patient-years). A non-AS comparison group (N = 10 760; 165 609 patient-years) was selected from hospital records, matched 1:5 on age, Aboriginality, and gender. Data on cancer diagnosis, comorbidities and mortality were extracted from state cancer, hospital, and mortality registers. The relative risk of cancer (overall and by type) and mortality following cancer diagnosis between AS and non-AS comparators was compared using Cox proportional hazard models, adjusting for risk factors and comorbidities. RESULTS: Ankylosing spondylitis patients had a 15% increase in the crude risk of cancer (hazard ratio [HR]: 1.15, 95% CI: 1.02-1.30). However, this association was attenuated following adjustment for smoking and common comorbidities (adjusted HR: 1.08, 95% CI: 0.95-1.22). Following a cancer diagnosis, patients with AS had an increased risk of 5-year mortality in the unadjusted (HR: 1.24, 95% CI: 1.03-1.49) and the adjusted models (adjusted HR: 1.37, 95% CI: 1.13-1.66). CONCLUSION: Ankylosing spondylitis was not associated with an increased risk of cancer diagnosis. Following a cancer diagnosis, AS was associated with an increased risk of 5-year mortality.

The Effect of Adiposity on Anti-Tumor Necrosis Factor-Alpha Levels and Loss of Response in Crohn's Disease Patients.

INTRODUCTION: A high body mass index is known to adversely affect antitumor necrosis factor-alpha trough levels and secondary loss of response (SLOR) in patients with Crohn's disease. We hypothesize that high levels of adiposity negatively affect these outcomes and aimed to determine if this relationship exists. METHODS: We performed a retrospective cross-sectional study of 69 patients with Crohn's disease from two tertiary inflammatory bowel disease centers between February 1, 2015, and June 30, 2018. Primary responders to infliximab (IFX) or adalimumab (ADA) who had a trough level performed within 6 months of CT or MRI scan and at least 12 months of clinical follow-up were eligible for inclusion. Body composition as measured on CT/MRI scans were correlated with trough concentration and time SLOR. Multivariate adjustments were made for established risk factors known to affect trough levels and SLOR. RESULTS: Of 69 included patients, 44 (63.8%) and 25 (36.2%) patients received IFX and ADA, respectively. Multivariate analysis revealed that IFX trough concentrations were inversely correlated with visceral fat area (-0.02 [-0.04, -0.003], P = 0.03), visceral fat index (-0.07 [-0.12, -0.01], P = 0.02) and visceral fat: skeletal muscle area ratio (-3.81 [-7.13, -0.50], P = 0.03), but not body mass index (-0.23 [-0.52, 0.06], P = 0.11). No predictive factors were found for ADA. Increased total adipose area was associated with an increased risk of SLOR in ADA-treated patients, but not IFX-treated patients (hazard ratio = 1.01 [1.002, 1.016], P = 0.011). DISCUSSION: Visceral adiposity is an important predictor of IFX trough levels, and high total adiposity predicts for SLOR to ADA.

Serum Midkine, estimated glomerular filtration rate and chronic kidney disease-related events in elderly women: Perth Longitudinal Study of Aging Women.

Midkine (MDK), a heparin-binding growth factor cytokine, is involved in the pathogenesis of kidney diseases by augmenting leukocyte trafficking and activation. Animal models and small case control studies have implicated MDK as a pathological biomarker in chronic kidney diseases (CKD), however this is yet to be confirmed in prospective human studies. In a prospective study of 499 elderly, predominantly Caucasian women aged over 70 years the association between serum MDK collected in 1998, and renal function change and the risk of CKD-related hospitalisations and deaths at 5 and 14.5 years, respectively, was examined. Baseline serum MDK was not associated with 5-year change in estimated glomerular filtration rate using the CKD Epidemiology Collaboration creatinine and cystatin C equation (Standardised ß = - 0.09, 95% confidence interval - 3.76-0.48, p = 0.129), 5-year rapid decline in renal function (odds ratio = 0.97, 95% confidence interval 0.46-2.02, p = 0.927) or the risk of 14.5-year CKD-related hospitalisations and deaths (hazard ratio = 1.27, 95% confidence interval .66-2.46, p = 0.470) before or after adjusting for major risk factors. In conclusion, in this cohort of elderly women with normal or mildly impaired renal function, serum MDK was not associated with renal function change or future CKD-related hospitalisations and deaths, suggesting that MDK may not be an early biomarker for progression of CKD.

The Risk and Consequences of Vertebral Fracture in Patients with Ankylosing Spondylitis: A Population-based Data Linkage Study.

OBJECTIVE: To compare the long-term prevalence, incidence, and outcomes of vertebral fracture (VF) between ankylosing spondylitis (AS) patients and matched controls, including the role of extraarticular manifestations (EAM) and osteoporosis. METHODS: This was a statewide observational study using linked health data for 2321 patients with AS and 22,976 controls presenting to hospital from 1980 to 2015. Data were analyzed using incidence rates (per 1000 person-yrs) and ratios (IRR), multivariable Cox proportional hazards regression, and Kaplan-Meier survival curves. RESULTS: Over a median 13.92 (interquartile range 7.58-21.67) years of follow-up, patients with AS had a greater VF prevalence and greater incidence of developing a new VF compared to controls (9.3% vs 2.5%, 6.8% vs 1.9%, respectively, all P < 0.001). Patients with AS had an increased risk of developing a VF after adjustments for age, sex, and osteoporosis (HR 2.55, 95% CI 2.11-3.09) compared to controls; this risk remained throughout the study period. Patients with AS were 5 years younger at time of first VF (P = 0.008) and had a greater likelihood of a recurrent VF (IRR 4.64; 95% CI 4.54-4.75) compared to respective controls. Mortality overall was comparable between patients with AS and controls after adjustment for age, sex, osteoporosis, and VF status (HR 0.90; 95% CI 0.80-1.01). CONCLUSION: The significantly increased risk of VF in patients with AS has not altered following the introduction of tumor necrosis factor inhibitor treatment. Although patients with AS experience a first VF at a younger age than controls, this does not lead to an increased risk of death.

The importance of tubuloreticular inclusions in lupus nephritis.

Tubuloreticular inclusions (TRI) are distinctive cytoplasmic structures of unknown origin that typically associate with autoimmune and viral diseases. We investigated the clinical and prognostic relevance of TRI detection in patients with lupus nephritis (LN). We conducted a single centre study of patients (n=84) with biopsy evidence of LN. Clinical variables included demographics, SLEDAI score, and autoantibody profiling; while histological evaluation included TRI presence, International Society of Nephrology/Renal Pathology Society (ISN/RPS) classification with NIH activity and chronicity indices, immunofluorescence, and other EM findings. Patients with and without TRI were compared by non-parametric statistical methods and survival analysis for the endpoints of death and renal failure. TRI were detected in 37 patients (44%) that were younger (28.4 vs 34.3 years, p=0.02) and more often from Asian background (37.8% vs 19.1%, p=0.04) compared to patients without TRI. SLEDAI score (11 vs 12 units, p=0.36) and amount of proteinuria (370 vs 340 mg/mmol, p=0.71) were similar in both groups; however, TRI positive patients had increased frequency of anti-SSB antibodies (16% vs 2%, p=0.02), 'full house' immune complex deposition (85% vs 58%, p=0.04) and subendothelial electron dense deposits (83% vs 65%, p=0.07), but were less often anti-dsDNA Ab positive (62% vs 85%, p=0.02). Patient and renal survival were not influenced by TRI status. TRI were observed in nearly half of all LN patients and TRI positive patients more often carried anti-SSB antibodies. However, TRI had little bearing on disease presentation or outcome in LN.

The Impact of Cytokines on the Health-Related Quality of Life in Patients with Systemic Lupus Erythematosus.

INTRODUCTION: Systemic lupus erythematosus (SLE) reduces the health-related quality of life (HRQoL), even during periods of disease quiescence. We investigated whether subclinical inflammation as reflected by cytokine levels is linked with reduced HRQoL. METHODS: A cross-sectional study of SLE patients (n = 52, mean age 47.3, 86.5% female) who completed a Short Form Health Survey-36 (SF-36) questionnaire. The clinical and demographic data, scores for the disease activity (SLEDAI-2K), organ damage (SDI), and laboratory data were collected simultaneously. The autoantibody and cytokine levels (IFN-γ, IL-1ß, IL-4, IL-6, IL-10, IL-12, IL-17, BAFF, TNF-α, TGF-ß1, MIP-1α, MIP-1ß and MCP-1 (levels in pg/mL) were quantified by sandwich ELISA. The comparisons and associations were assessed non-parametrically, and a multiple regression determined the effect sizes (ES) of the variables on the SF-36 domain and summary scores. RESULTS: The SF-36 summary and domain scores for SLE patients were significantly (20-40%) lower than in a comparable control group, with the exception of the Mental Health scores (p = 0.06). SLE patients had a normal body mass index (BMI) (median, 24.2 kg/m2), a high rate of smoking (69.2%), and usage of social security benefits (90.4%). TGF-ß1 (ES 0.06), IL-12 (ES -0.11), IFN-γ (ES 0.07) and MCP-1 (ES 0.06) influenced the SF-36 domain scores; and MCP-1 (ES 0.04) influenced the Mental Health Summary Score (MCS). Obvious manifestations, including patient visual analogue scale (VAS) (ES -2.84 to -6.29), alopecia (ES -14.89), malar rash (ES -14.26), and analgesic requirement (ES -19.38), independently influenced the SF-36 items; however, the SF-36 scores were not reflected by the physician VAS or disease activity (SLEDAI-2K). CONCLUSIONS: Cytokines had a minimal impact on HRQoL in SLE patients, especially compared to visible skin manifestations, central nervous system (CNS) damage, and pain. Better tools are needed to capture HRQoL in measures of disease activity.

IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role.

OBJECTIVE: The interleukin 17 (IL-17) cytokine family is involved in a number of chronic inflammatory diseases. In spite of contradictory findings and a lack of causality in clinical studies, IL-17 inhibition for systemic lupus erythematosus (SLE) has regained attention as a potential therapeutic pathway, after demonstrating disease-modifying capabilities in ankylosing spondylitis. We investigated the clinical associations of interleukin 17 A (IL-17A) in patients with SLE. MATERIAL AND METHODS: A cross-sectional study was performed involving SLE patients (n=102; age: 49 years; 86% female) recruited from a regional registry. IL-17A levels were determined by immunoassay, disease activity by Systemic Lupus Erythematosus Disease Activity Index-2K (SLEDAI-2K), and cumulative damage by Systemic Lupus International Collaborative Clinics Damage Index (SDI) scores. Non-parametric techniques were used to examine the association between IL-17A and disease activity and autoantibody profiles were compared with healthy controls (n=31): principal component analysis (PCA) was used to determine the interplay of immune cells across disease states and damage development in SLE patients. RESULTS: SLE patients had higher IgG levels, lower T-cell and B-cell counts, but median IL-17A levels did not differ from the controls (28.4 vs. 28.4 pg/mL, p=0.9). In SLE patients, IL-17A did not correlate with SLEDAI-2K or SDI, but was inversely related with age (correlation coefficients, Rs.=-0.29, p<0.05), systolic blood pressure (Rs.=-0.31, p<0.05), years of smoking (Rs.=-0.43, p<0.05), cumulative heart (Rs.=-0.22, p<0.05), and malignancy damage (Rs.=-0.18, p<0.05). Serological correlations for IL-17A existed with immunoglobulin G (IgG) levels (Rs.=0.21, p<0.05), high sensitivity C-reactive protein (hs-CRP) levels (Rs.=0.28, p<0.05), proteinuria (Rs.=0.64, p<0.05), and pre-albumin (Rs.=-0.22, p<0.05). Longitudinal data showed only modest fluctuation in IL-17A levels, independent of SLEDAI-2K. CONCLUSION: These results suggest that IL-17A, while participating in inflammation, may also serve a protective purpose in SLE patients.