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.

Neuropathic foot ulcers in the tallest patients with acromegalic gigantism: a common and significant problem. Historical overview.

PURPOSE: We present a historical overview on neuropathic ulcers in patients with acromegalic gigantism. MATERIALS AND METHODS: The case histories of 6 famous patients with acromegalic gigantism and living in the twentieth century were analyzed. The combined final height and maximum weight of these giants were: 272 cm. & 215.9 kg., 218.4 cm. & 125 kg., 242 cm. & 165 kg., 220.5 cm. & 135 kg., 235 cm. & 136 kg. and 224.8 cm. & 174 kg. CONCLUSIONS: Neuropathic foot ulcers leading to hospital admissions and surgical and medical interventions were reported in 6 patients with acromegalic gigantism. These ulcers significantly impaired the daily activities of these individuals. Neuropathies of the sural nerve in patients with acromegalic gigantism can lead to hypoesthesia and hypoalgesia of the lower legs and feet. Potential contributing factors for the development of neuropathic ulcers of the feet in patients with acromegalic gigantism and neuropathy might be leg and foot deformities, muscle weakness and poor quality footwear. Diabetes mellitus, or impaired glucose intolerance does not necessarily seem to play a role.

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.

Risk of Major Adverse Cardiovascular Event Following Incident Hospitalization for Acute Gout: A Western Australian Population-Level Linked Data Study.

BACKGROUND: Cardiovascular disease is the most common cause of death in people with gout. Acute inflammation, which is a characteristic of gout, may have a mechanistic role in major adverse cardiovascular events (MACEs). We aimed to examine the relationship between admissions to a hospital with acute gout and MACEs in a large population-based data set. METHODS: We extracted data from the Hospital Morbidity Data Collection and Death Registrations of the Western Australian Rheumatic Disease Epidemiology Registry. We identified patients admitted to hospital with incident acute gout and who had admissions or a death record because of MACEs. We compared the risk of MACEs during the postdischarge period (1-30 days after acute gout admission) and control period (365 days prior to admission and 365 days after the postdischarge period) using a self-controlled case-series (SCCS) design, which is a within-person design that controls for time-invariant patient-specific confounding. We performed conditional fixed-effects Poisson regression to obtain rate ratios (RRs). RESULTS: We identified 941 patients (average age: 76.4 years; SD: 12.6; 66.7% male) with an incident acute gout admission and documented MACEs during the control and/or postdischarge periods. Of the 941 patients, 898 (95%) experienced MACEs during the combined control period (730-day period) and 112 (12%) during the postdischarge period (30-day period). The rates of MACEs during the total control and postdischarge periods were 0.84 and 1.45 events per person-year, respectively. Regression analysis confirmed increased rate during the postdischarge period (RR: 1.67; 95% CI: 1.38-2.03) compared with the control period. Sensitivity analyses indicated that our results were robust in relation to known limitations of the SCCS design. CONCLUSION: We report an increased risk of MACEs in the first 30 days after an incident hospital admission with acute gout, suggesting a temporal association between acute inflammation and subsequent MACEs in patients with gout.

Adult-onset Still's disease in Western Australia: Epidemiology, comorbidity and long-term outcome.

AIM: Adult-onset Still's disease (ASD) is a rare, potentially life-threatening autoinflammatory condition. As reported prevalence shows regional variation and long-term outcome data are scarce, we investigated epidemiology and long-term health outcomes of ASD in Western Australia (WA). METHODS: Population-based cohort study using longitudinally linked administrative health data from all WA hospitals between 1999 and 2013 for ASD patients (ICD-10-AM M06.1) and controls matched for age, gender, and index year. Rate ratios and odds ratios (RR/OR) with 95% confidence intervals (CI) compared ASD patients with controls. RESULTS: The average ASD incidence (n = 52) was 0.22/100 000 with 2.4/100 000 point-prevalence as of December 31, 2013. ASD patients (median age 41.5 years, 59.6% female) had higher odds of previous liver disease (OR 2.67, 95% CI 1.31-5.45), fever (OR 54.10, 95% CI 6.60-433.0), rash (OR 15.70, 95% CI 4.08-60.80), and serious infections (OR 4.36, 95% CI 2.11-22.80) than controls. Despite biological disease-modifying antirheumatic drugs in 27% of patients, ASD patients had higher odds for joint replacement (n = 7, 13.5%) (OR 45.5, 95% CI 4.57-93.70), osteoporosis (OR 31.3, 95% CI 3.43-97), and serious infections (RR 5.68; 95% CI 6.61-8.74) during follow up. However, crude mortality (11.5% vs 7.5%; P = 0.34), survival at 1 and 5 years (P= 0.78), and last modified Charlson Comorbidity score (median 2 vs 2) were similar between groups. CONCLUSION: The epidemiology and demographics of ASD in Western Australia fall within the internationally reported range. ASD patients present increased rates of liver disease, rash, and serious infections before disease onset. Mortality following ASD was not increased for 5 years despite high rates of chronic arthritis requiring joint replacement, serious infections, and osteoporosis.

Fracture liaison service utilising an emergency department information system to identify patients effectively reduce re-fracture rate is cost-effective and cost saving in Western Australia.

OBJECTIVES: To assess the benefits of the Emergency Department Information System (EDIS)-linked fracture liaison service (FLS). METHODS: Patients identified through EDIS were invited to attend an FLS at the intervention hospital, the Sir Charles Gairdner Hospital (SCGS-FLS). The intervention group was compared to usual care. Retrospective control (RC) at this hospital determined historical fracture risk (SCGH-RC). Prospective control (PC) was from a comparator, Fremantle Hospital (FH-PC). The main outcome measures were cost-effectiveness from a health system perspective and quality of life by EuroQOL (EQ-5D). Bottom-up cost of medical care, against the cost of managing recurrent fracture (weighted basket), was determined from the literature and 2013/14 Australian Refined Diagnosis Related Groups (AR-DRG) prices. Mean incremental cost-effectiveness ratios were simulated from 5000 bootstrap iterations. Cost-effectiveness acceptability curves were generated. RESULTS: The SCGH-FLS program reduced absolute re-fracture rates versus control cohorts (9.2-10.2%), producing an estimated cost saving of AUD$750,168-AUD$810,400 per 1000 patient-years in the first year. Between-groups QALYs differed with worse outcomes in both control groups (p < 0.001). The SCGH-FLS compared with SCGH-RC and FH-PC had a mean incremental cost of $8721 (95% CI -$1218, $35,044) and $8974 (95% CI -$26,701, $69,929), respectively, per 1% reduction in 12-month recurrent fracture risk. The SCGH-FLS compared with SCGH-RC and FH-PC had a mean incremental cost of $292 (95% CI -$3588, $3380) and -$261 (95% CI -$1521, $471) per EQ-5D QALY gained at 12 months respectively. With societal willingness to pay of $16,000, recurrent fracture is reduced by 1% in >80% of patients. CONCLUSIONS: This simple and easy model of identification and intervention demonstrated efficacy in reducing rates of recurrent fracture and was cost-effective and potentially cost saving.

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.

Septic arthritis due to Neisseria gonorrhoea in Western Australia.

BACKGROUND: A high prevalence of gonococcal infections has been reported from remote parts of Western Australia, but the occurrence of disseminated infection leading to arthritis has not been studied. AIMS: To investigate the frequency, risk factors and long-term outcome of gonococcal arthritis (GA) in Western Australia (WA). METHODS: A population-based data linkage study of patients with a hospital-based diagnosis of GA in WA between 1990 and 2014. Demographics, standardised incidence rates per million and comorbidity accrued before (lookback 186 months, interquartile range (IQR) 86-267) and after the index hospital contact for GA (follow up 100 months, IQR 60-209) are presented as frequency (%), median (IQR) or rates /1000 months. RESULTS: In total, 98 patients were diagnosed with GA. The annual incidence of GA increased from 1.35 to 2.10 per million between 1990 and 2014, but the rate of GA complicating all gonococcal infections was stable around 0.25%. Female patients with GA (54%; n = 53/98) were younger (24 vs 38 years) and more frequently identified as indigenous (88% vs 49%) than male patients (46%; n = 45/98; P = 0.002). Female patients had higher rates of prior infections (15.5 vs 8.1 per 1000 months; P = 0.002) and diabetes mellitus (15.9% vs 2.5%; P = 0.03) and a longer hospital stay (10 vs 8 days; P = 0.02). GA recurrence rate during follow up was low (2%), but a broad range of comorbidities developed contributing to a 14% crude death rate. CONCLUSIONS: GA stably complicates 0.25% of gonococcal infections in WA with young indigenous females and middle-aged non-indigenous males most affected. Prior infectious disease and diabetes mellitus are potential risk factors for GA in females. GA recurs rarely, but its development reflects a high risk of morbidity and mortality over the following 10 years.

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.

Abdominal aortic calcification, cardiac troponin I and atherosclerotic vascular disease mortality in older women.

OBJECTIVE: Examine if two inexpensive measures of atherosclerotic vascular diseases (ASVD), abdominal aortic calcification (AAC) and high-sensitivity cardiac troponin I (hs-cTnI) provide complementary information for 10-year ASVD mortality and all-cause mortality risk in older women. METHODS: 908 community-dwelling women without prevalent ASVD (≥75 years) were followed-up between 2003 and 2013. AAC and plasma hs-cTnI measures were obtained in 2003. AAC was assessed on lateral spine images using a semiquantitative method (AAC24). Linked health records were used for mortality outcomes. RESULTS: Mean±SD age was 79.9±2.6 years. 276 (30.4%) women died during follow-up, including 138 (15.2%) ASVD-related deaths. AAC24 and hs-cTnI were independently associated with ASVD and all-cause mortality (p<0.001). The cohort was dichotomised into four groups: (1) low AAC24 (AAC24: 0 or 1) and 1) and

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.

Hospitalisation for systemic lupus erythematosus associates with an increased risk of mortality in Australian patients from 1980 to 2014: a longitudinal, population-level, data linkage, cohort study.

OBJECTIVE: Mortality rates for patients with SLE have not been reported in Australia. This study determined the association between a hospitalisation for SLE with mortality. METHODS: Population-level cohort study of patients with SLE (n=2112; 25 710 person-years) and general population comparators (controls) (n=21, 120; 280 637 person-years) identified from hospital records contained within the WA Rheumatic Disease Epidemiological Registry from 1980 to 2013. SLE was identified by ICD-9-CM: 695.4, 710.0, ICD-10-AM: L93.0, M32.0. Controls were nearest matched (10:1) for age, sex, Aboriginality and temporality. Using longitudinal linked health data, we assessed the association between a hospitalisation for SLE mortality and mortality with univariate and multivariate Cox proportional hazards and competing risks regression models. RESULTS: At timezero, patients with SLE were similar in age (43.96 years), with higher representation of females (85.1% vs 83.4%, p=0.038), Aboriginal Australians (7.8% vs 6.0%) and smokers (20.5% vs 13.2%). Before study entry, patients with SLE (mean lookback 9 years) had higher comorbidity accrual (Charlson Comorbidity Index ≥1 item (42.0% vs 20.5%)), especially cardiovascular disease (CVD) (44.7% vs 21.0%) and nephritis (16.4% vs 0.5%), all p<0.001. During follow-up (mean 12.5 years), 548 (26.0%) patients with SLE and 2450 (11.6%) comparators died. A hospitalisation for SLE increased the unadjusted (HR 2.42, 95% CI 2.20 to 2.65) and multivariate-adjusted risk of mortality (aHR 2.03, 95% CI 1.84 to 2.23), which reduced from 1980 to 1999 (aHR 1.42) to 2000-2014 (aHR 1.27). Females (aHR 2.11), Aboriginal Australians (aHR 3.32), socioeconomically disadvantaged (aHR 2.49), and those <40 years old (aHR 7.46) were most vulnerable. At death, patients with SLE had a higher burden of infection (aHR 4.38), CVD (aHR 2.09) and renal disease (aHR 3.43), all p<0.001. CONCLUSIONS: A hospitalisation for SLE associated with an increased risk of mortality over the 1980-2014 period compared with the general population. The risk was especially high in younger (<40 years old), socioeconomically disadvantaged and Aboriginal Australians.

Non-gonococcal septic arthritis of native joints in Western Australia. A longitudinal population-based study of frequency, risk factors and outcome.

OBJECTIVE: To describe the incidence and long-term outcome of non-gonococcal septic arthritis (SA) in Western Australia (WA). METHODS: Newman criteria were applied to define culture-positive SA and suspected SA cases in the state-wide West Australian Rheumatic Diseases Epidemiological Registry with longitudinally linked health data for patients >16 years with a first diagnostic code of pyogenic arthritis (711.xx [ICD-9-CM] and M00.xx [ICD-10-AM]) between 1990-2010. Annual incidence rates/100 000 (AIR) and standardized (against WA population) mortality rates/1000 person-years (SMR) and outcomes during 10.1 years follow-up are reported. RESULTS: Among 2633 SA patients (68.6% male, age 47.4 years), 1146 (43.5%) had culture-positive SA. The overall AIR for culture-positive (1.6-6.3) and total SA cases (4.3-12.9) increased between 1990 and 2010 as did age at onset (39.5-54 years) and proportion of females (23-35.6%). Knees (33.6.%) were most frequently affected and 37.1% of cultures showed microorganisms other than Gram-positive cocci. Thirty-day rates for readmission and mortality were 25.4% and 3.2.%. During follow-up rates for serious infections (56.4%), osteoarthrosis (5.2%) and osteomyelitis (2.7%) were higher in culture-positive SA. SMR was increased for all SA patients but especially in those 17-40 years of age with culture-positive SA (24.2; 95% CI 2.3-261). CONCLUSIONS: The incidence of SA in WA has risen steeply over 20 years. SA now occurs at higher age, affects females more often with over a third of cases caused by Gram-negative microorganisms. Not only culture-positive, but also suspected SA led to increased bone/joint complications, in-hospital and late mortality.

Muscle shear wave elastography, conventional B mode and power doppler ultrasonography in healthy adults and patients with autoimmune inflammatory myopathies: a pilot cross-sectional study.

BACKGROUND: Before the role of shear wave elastography (SWE) and B mode ultrasound (US) in the diagnosis of different forms of idiopathic inflammatory myopathies (IIM) can be investigated, normative data is required. This study aimed to describe and then compare normative SWE and B mode ultrasound metrics of muscles in healthy controls and patients with IIM. METHODS: Twenty nine healthy adult controls and 10 IIM patients (5 with inclusion body myositis and 5 with necrotising autoimmune myopathy) underwent a full clinical examination, laboratory investigations, SWE and US measurements of selected proximal and distal limb muscles. Shear wave speed (SWS) and multiple US domains [echogenicity, fascial thickness, muscle bulk and power Doppler (PD)] were measured in both groups. RESULTS: In healthy controls (n = 29; mean age 46.60 ± 16.10; 44.8 % female), age was inversely correlated with SWS at the deltoid (stretch) (Rs. -0.40, p = 0.030) and PD score at the deltoid (rest) (Rs. -0.40, P = 0.032). Those ≥ 50 years old had a lower SWS at the deltoid (stretch) compared to the < 50 year group (2.92 m/s vs. 2.40 m/s, P = 0.032). Age correlated with increased echogenicity in the flexor digitorum profundus (Rs. 0.38, P = 0.045). Females had a smaller muscle bulk in the deltoid (P = 0.022). Body mass index (BMI) was inversely associated with SWS in the deltoid (stretch) (Rs - 0.45, P = 0.026), and positively correlated with echogenicity in the deltoid (Rs. 0.69, P = 0.026). In patients ≥50 years of age, patients with IIM (mean age 61.00 ± 8.18; females 20.0 %) had a higher proportion of abnormal echogenicity scores at the flexor digitorum profundus (FDP) (40.00 % vs. 14.30 %, P = 0.022) and tibialis anterior (TA) (80.00 % vs. 28.60 %, P = 0.004). Fascial thickness was lower in the FDP (0.63mm vs. 0.50mm, p = 0.012) and TA (0.58mm vs. 0.45mm, P = 0.001). CONCLUSIONS: Our findings suggest there is scope for US techniques to be useful for diagnostic screening of affected muscles in patients with IIM, especially in those with suspected inclusion body myositis or necrotising autoimmune myopathy. We provide normative data for future studies into SWE and US techniques in skeletal muscle. The differences between IIM patients and controls warrant further study in a broader IIM patient cohort.

Septic Arthritis in Children: A Longitudinal Population-Based Study in Western Australia.

OBJECTIVE: To describe the incidence, risk factors and long-term outcomes in children hospitalised with septic arthritis (SA) in Western Australia (WA). METHODS: We extracted state-wide longitudinally linked administrative health data for patients aged < 16 years with a first diagnostic code of 711.X (ICD9-CM) and M00.X (ICD10-AM) in WA in the period 1990-2010. Annual incidence rates (AIR) per 100,000 with 95% confidence intervals (CIs), prior conditions during a median lookback period of 63.2 [interquartile range (IQR) 19.8-117.1] months and outcomes, including standardised mortality rates (SMR), during a median follow-up of 10 years are reported. RESULTS: A total of 891 patients [62% male, median age 6.4 (IQR 1.9-10.6) years with 34% aged < 3 years] were admitted for SA during the observation period. The overall AIR (per 100,000) was 9.85 (95% CI 4.79-14.41), and was higher in Indigenous Australians [34.9 vs. 5.5 (non-Indigenous), p < 0.001] and in males [11.9 vs. 7 (females), p < 0.01]; AIR showed no temporal or seasonal variation. Knees (43.9%), hips (34.6%) and ankles (13.3%) were most frequently affected, with Staphylococci predominant (49%) in patients with positive cultures (41.5%). Prior infection(s) (40.4%) and respiratory disease (7%) were the main pre-existing morbidities. Median hospital stay was 4.0 (IQR 2-8) days, with 1.9% requiring admission to the intensive care unit and 10.4% requiring readmission within 30 days. During follow-up, 26 patients (3.1%) developed osteomyelitis, nine patients were diagnosed with osteoarthrosis (1.1%) and five patients (0.6%) underwent joint replacement. Female patients developed other serious infections more often than male patients (40.5 vs. 27.1%, p < 0.01), as well as other comorbidities (Charlson Comorbidity Index > 0: 34.6 vs. 27.2%, p = 0.02), including diabetes (4.2 vs. 0%; p = 0.001), cardiovascular events (4.2 vs 1.4%, p = 0.002) and chronic arthritis (1 vs. 0%, p = 0.05). The crude mortality rate was low (0.3%), with 99.4% survival at 180 months and no increase in the SMR. CONCLUSIONS: The incidence of SA in children in WA did not change over the 20-year observation period. SA did not lead to excess mortality, but bone and joint complications developed in 5% of patients. The high propensity to comorbid conditions in this young cohort suggests an underlying role of comorbidity in SA development.

As more children are living with complex and chronic conditions, we investigated whether children in Western Australia (WA) have become more prone to joint infections. During a 20-year observation period we collected health data for all children admitted to any hospital in the state with an infected joint and recorded their health outcomes. We found that joint infection occurs in nearly ten out of 100,000 children each year, but we saw no change in the frequency over time. We did observe higher rates in Indigenous children (35/100,000) than in non-indigenous children (6/100,000) but found no noticeable influence of the seasons on the frequency of joint infections. Knees, hips and ankles were most often affected, and 15% had additional bone infection. Children needed to be treated in hospital for 4­5 days, and only a small minority (1.2%) were so ill they needed intensive care. Joint infections led to chronic, long-term complications in about 5% of patients, but we found no evidence that joint infections increased the risk of death compared to children in the general population.

Morbidity and mortality in adult-onset IgA vasculitis: a long-term population-based cohort study.

OBJECTIVES: With sparse data available, we investigated mortality and risk factors in adults with IgA vasculitis (IgAV). METHODS: This was an observational population-based cohort study using state-wide linked longitudinal health data for hospitalized adults with IgAV (n = 267) and matched comparators (n = 1080) between 1980 and 2015. Charlson comorbidity index (CCI) and serious infections (SIs) were recorded over an extensive lookback period prior to diagnosis. Date and causes of death were extracted from the Western Australia Death Registry. Mortality rate (deaths/1000 person-years) ratios (MRRs) and hazard ratio (HR) for survival were assessed. RESULTS: During 9.9 (9.8) years lookback patients with IgAV accrued higher CCI scores (2.60 vs 1.50, P < 0.001) and had higher risk of SI (OR = 8.4, P < 0.001), not fully explained by CCI scores. During 19 years' follow-up, the rate of death in patients with IgAV (n = 137) was higher than in comparators (n = 397) (MRR = 2.06, 95% CI: 1.70-2.50; P < 0.01) and the general population (standardized mortality rate ratio = 5.64, 95% CI: 4.25, 7.53; P < 0.001). Survival in IgAV was reduced at 5 (72.7 vs 89.7%) and 20 years (45.2% vs 65.6%) (both P < 0.05). CCI (HR = 1.88, 95% CI: 1.25, 2.73; P = 0.001), renal failure (HR = 1.48, 95% CI: 1.04, 2.22; P = 0.03) and prior SI (HR = 1.48, 95% CI: 1.01, 2.16; P = 0.04) were independent risk factors. Death from infections (5.8 vs 1.8%, P = 0.02) was significantly more frequent in patients with IgAV. CONCLUSION: Premorbid comorbidity accrual appears increased in hospitalized patients with IgAV and predicts premature death. As comorbidity does not fully explain the increased risk of premorbid infections or the increased mortality due to infections in IgAV, prospective studies are needed.

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.

Outcomes in buried versus non-buried peritoneal dialysis catheters: A retrospective cohort study.

AIMS: To compare the rates of infections (peritonitis and exit site infections) in patients undergoing non-buried versus buried peritoneal dialysis catheterisation for end-stage renal failure. METHODS: A retrospective review of all patients who underwent peritoneal dialysis catheter placement by one primary surgeon between January 2008 and August 2019. Information collected included, catheter characteristics, immediate post-operative complications, date of catheter exteriorisation, date of peritoneal dialysis commencement, rate of successful catheter function at initiation of peritoneal dialysis and rates of catheter-related complications (i.e. infection, revision status and obstruction). RESULTS: 110 peritoneal dialysis catheters were inserted (43 non-buried and 67 buried peritoneal dialysis catheters). The non-buried group was associated with a higher proportion acquiring an infection than the buried group (15% vs 30%, p = 0.054). Patients with buried catheters also had a 72% and 65% decreased likelihood of experiencing a catheter-related infection and peritonitis, respectively, over time compared to patients with non-buried catheters in the unadjusted (crude incidence rate ratio 0.28, 95% confidence interval 0.11, 0.70; P = 0.003). The proportion of catheter function at first use was 85% in the non-buried group and 78% in the buried group. Patients with non-buried versus buried catheters had similar proportions of complications, including: obstructions (25.6% vs 20.9%, p = 0.770), herniation (7.0% vs 4.0%, p = 0.327) and leaks (7.0% vs 1.5%, p = 0.134). CONCLUSION: The use of the buried peritoneal dialysis catheter technique as compared to the standard technique has revealed fewer overall catheter-related infections, particularly episodes of peritonitis and similar rates of mechanical complications in our series. In addition to that, the other benefits of buried peritoneal dialysis catheters such as lower healthcare cost, patient convenience and a viable option for patients in remote communities should prompt physicians to continue assessing suitable candidates for buried peritoneal dialysis catheters.