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BACKGROUND Therapeutic drug monitoring of anti-tumour necrosis factor (TNF) drugs and anti-drug antibodies (ADA) is now recommended in the treatment of inflammatory bowel disease. However, assay types and drug concentration thresholds are still debated. AIM To correlate inflammatory bowel disease activity in a New Zealand cohort with trough concentrations of infliximab and adalimumab, and ADA using locally developed competitive-binding enzyme-linked immunosorbent assays (ELISA) to establish threshold concentrations. METHODS Patients with ulcerative colitis (UC) and Crohn disease (CD) from Christchurch and Dunedin on anti-TNF drugs >12 weeks were enrolled. Trough blood samples were assayed for drug and ADA concentrations. Other data included quality of life, blood count, C-reactive protein, albumin, renal function and disease activity indices. RESULTS Of 103 patients, 53 were on infliximab (36 CD, 15 UC and 2 unclassified) and 50 adalimumab (48 CD and 2 UC). Median (range) infliximab and adalimumab concentrations were 10.5 (0-41) and 9.61 mg/L (0-30). CD remission, Crohn Disease Activity Index

Objective To determine the incidence of ANCA Associated Vasculitis (AAV) during the 3-year period before (period 1), and the 3 years following (period 2), the earthquake that occurred on 22 February 2011 in Christchurch, New Zealand. Methods All ANCA tests performed in the Canterbury region for 3 years before the earthquake (period one, 2007-2010), and for 3 years after the earthquake (period two, 2011-2014) were examined. AAV was defined according to The European Medicines Agency classification algorithm. Medical records were reviewed and cases were included if they were newly diagnosed within the study period. Incidence was calculated using population data from the 2013 New Zealand census. Results 52 new cases of AAV were identified. The incidence in period one was 1.87/100,000/annum (95% C.I. 1.23 - 2.72), and for period two was 1.73/100,000/annum (95% C.I. 1.12 - 2.55). There was no statistically significant difference in incidence between the two study periods. There was no difference when analyzing by MPO or PR3 status, or restricting the analyses to those residing in an urban environment. The mean age at diagnosis for MPO AAV was significantly younger in period two than period one (61 years vs 71 years, p = 0.05). There were no other clinically important differences between the two groups. Conclusion This study does not support the hypothesis that an environmental agent, caused by dust pollution related to earthquake damage, has a causative role in the pathogenesis of AAV.

Background Benzbromarone is a potent uricosuric, but is not widely available due to concerns about hepatotoxicity. In Aotearoa New Zealand benzbromarone has been available since April 2013, subject to funding restrictions, for patients with inadequate urate-lowering response or intolerance to allopurinol and probenecid. Aim The aim of this study was to assess the safety and efficacy of benzbromarone in a real-life setting. Methods All patients who received funding for benzbromarone from 1/4/2013 to 30/9/2014 were identified. Prescribers were sent a questionnaire for each individual. Information on demographics, efficacy of previous urate-lowering drugs and reasons for discontinuation were collected. Specific information about the dose, effect on serum urate, adverse effects and liver function tests after commencing benzbromarone was recorded. Results Completed questionnaires were returned for 123/164 (75%) patients. Mean (SD) serum urate prior to benzbromarone was 0.57 (0.12) mmol/l and estimated glomerular filtration rate (eGFR) 50.3 (22.8) ml/min/1.73 m2. The median dose of benzbromarone was 100 mg/day (25-200 mg/day). Six months after commencing benzbromarone, mean (SD) serum urate was 0.35 (0.12) mmol/l. Benzbromarone related adverse events included rash (n = 4), diarrhoea (n = 9), nausea (n = 6), and urate stones (n = 3). Liver function tests abnormalities were uncommon and tended to be mild. There were 14 patient deaths; none were considered related to benzbromarone. Allopurinol had been prescribed prior to benzbromarone in 117/123 patients; median maximum allopurinol dose was 200 mg/day (range 25-600 mg/day), and 19% patients received allopurinol >300 mg/day. Conclusions Benzbromarone provides useful urate-lowering efficacy and does not appear unsafe in patients with gout. Urate-lowering therapy prescribing requires further optimisation.

BACKGROUND The management of gout in chronic kidney disease and end-stage renal disease is challenging and remains controversial. There are limited data on the use of urate-lowering therapy in people receiving dialysis. AIM To estimate the point prevalence of gout, gout treatment and achievement of target serum urate (SU) among adults treated with long-term dialysis. METHODS Three secular cohorts of adults receiving dialysis for at least 90 days on 1 February 2017, 1 January 2016 and 1 January 2015 were identified. Medical records were reviewed for SU concentrations. Results were compared between haemodialysis (HD) and peritoneal dialysis (PD), and participants prescribed and not prescribed urate-lowering therapy. The percentage reduction in SU 24- and 48-h post-HD was estimated based on data from a previous study. SU concentrations were then used to estimate the percentage time the SU was

Background There are few current data on the prevalence of hyperuricaemia and gout in New Zealand, particularly among the indigenous Māori population. Aims To determine the prevalence of gout and hyperuricaemia in rural and urban Māori and non-Māori community samples and describe the treatment and comorbidities of participants with gout. Methods Participants aged 20–64 years were recruited by random selection from the electoral roll. Māori samples were selected from among those identified as being of Māori descent on the roll and who self-identified as being of Māori ethnicity at interview. Personal medical history, blood pressure, anthropometrics, fasting lipids, glucose, HbA1c and urate were recorded. Results There were 751 participants. Mean serum urate (SU) was 0.30 mmol/L (0.06–0.69 mmol/L). Māori had a significantly higher prevalence of hyperuricaemia (SU > 0.40 mmol/L) compared with non-Māori (17.0% vs 7.5%, P = 0.0003). A total of 57 participants had a history of gout, with a higher prevalence in Māori compared with non-Māori (10.3% vs 2.3%, P 0.36 mmol/L. Participants with gout were more likely to have metabolic syndrome, diabetes, cardiac disease or hypertension. Conclusions Gout and hyperuricaemia were more prevalent in Māori, and participants with gout were more likely to have comorbidities. There was not a higher overall adjusted cardiovascular disease risk in Māori participants with gout. Despite the high prevalence of gout, management remains suboptimal.

Our aim was to describe the treatment and survival characteristics of Wegener's granulomatosis (WG) in Canterbury, New Zealand. The medical records of 48 patients diagnosed between 1 July 1997 and 31 December 2008 and fulfilling validated classification criteria for WG were reviewed to characterise survivorship in the province of Canterbury, New Zealand. The age at diagnosis was 61 years (range 20 to 83 years) with an equal number of males and females. Using Kaplan-Meier product-limit analysis, the probability of survival at 1 and 10 years was 91% and 62% respectively. Of the 12 deaths in the cohort, four occurred within 12 months of diagnosis: two from pulmonary haemorrhage and two from renal failure. Beyond 12 months, two patients died of renal failure, two of myocardial infarction and one from cardiac arrhythmia, one from cerebrovascular disease and two from colorectal carcinoma. The median time to relapse was 6.75 years, and the probability of relapse within 10 years was 67%. Survivorship, treatment response rate and the rate of relapse from WG in a cohort of patients from this high-prevalence southern hemisphere region were similar to that reported for northern hemisphere cohorts with a similar prevalence.

Aims: It has been suggested that elevated mean red cell volume (MCV) may be a predictor of haematological toxicity in rheumatoid arthritis (RA) patients receiving methotrexate (MTX). We wished to identify whether there was an association between MCV, red cell folate and haematological toxicity in patients on MTX monotherapy for the long-term management of RA. Methods: Evidence of haematological toxicity was sought by note review of patients recruited in a cross-sectional study of MTX monotherapy in RA. Retrospective data included MCVs from before MTX initiation and after 3 and 6 months of treatment. Data were collected prospectively every 6 months for up to 2 years after enrolment. Any record of cytopenia or the development of haematological malignancy was recorded from commencement of MTX until the present day. Red cell folate concentrations were tested on enrolment to the study. Results: A total of 165 patients was included, 74.5% female, median disease duration 7 years (range 3 months–57 years). The median duration of MTX treatment was 74.9 months (range 10–241 months) giving 1030.2 patient-years of MTX exposure. Twenty-four patients (14.5%) had a MCV > 98 fL on study entry. Evidence of haematological abnormality was found in six patients (3.6%); chronic lymphocytic leukaemia (1), persistent lymphocytosis (1), persistent monocytosis (1) and neutropenia (3). There was no association between red cell folate or MCV and haematological toxicity. Conclusion: Neutropenia and pancytopenia are rare side-effects of MTX therapy in this cohort. Elevated MCV or low mean red cell folate does not appear to be associated with haematological malignancy or toxicity in this cohort of patients on long-term MTX therapy.

Gout is a common chronic arthritis that can lead to significant disability. Gout is one of the few rheumatological conditions that can be diagnosed with certainty, has a known cause and can be cured with appropriate therapy. Hypouricaemic agents reduce uric acid concentrations through inhibiting uric acid production (allopurinol) or enhancing uric acid excretion (probenecid, benzbromarone). Allopurinol is the most commonly used hypouricaemic agent but at recommended doses often fails to reduce adequately uric acid concentrations and prevent acute attacks of gout. The use of probenecid is limited by lack of efficacy in renal impairment. In the last few years, new agents in the management of hyperuricaemia and gout have become available. Febuxostat, a new xanthine oxidase inhibitor, is an effective hypouricaemic agent although further data are required for patients with renal impairment and other significant medical conditions. Rasburicase, a recombinant uricase (which catalyses the conversion of uric acid to the more readily excreted allantoin) is available for prevention of tumour lysis syndrome. However, its repeated use, as would be required in chronic gout, is limited by antigenicity. A less antigenic PEGylated uricase can rapidly reduce serum uric acid concentrations and promote resorption of tophi. However, further information with regard to the long-term risks and benefits of these agents is required. These agents may ultimately be used in the short term to rapidly deplete urate stores (induction therapy) followed by long-term therapy with an alternative hypouricaemic agent to prevent subsequent accumulation of uric acid (maintenance therapy).

Aim: The aim of the study was to review all cases of Pneumocystis carinii pneumonia (PCP) in patients seen by the Christchurch Hospital Rheumatology service over a 5-year period and to determine the annual incidence of PCP. Methods: The Canterbury Health Laboratory database was searched for rheumatology patients testing positive for PCP from 31 December 2000 to 31 December 2005. The rheumatology database was then searched to identify patients receiving the same immunosuppressant medication as those who developed PCP to determine the annual incidence of PCP in this group. Results: Four rheumatology patients were diagnosed with PCP during the 5-year period. Two were receiving oral methotrexate (MTX) for rheumatoid arthritis and two were receiving cyclophosphamide (CYC), one each for Wegener’s granulomatosis and dermatomyositis. None of the four cases was receiving PCP chemoprophylaxis. Five hundred and forty-seven patients commenced MTX over the same 5-year period and 47 commenced CYC. Only 14 of 47 (29.7%) CYC-treated patients received PCP prophylaxis. The annual incidence of PCP was 0.17% (95% confidence interval (CI) 0.02–0.63) and 5.33% (95%CI 0.65–19.24) in patients prescribed MTX and CYC, respectively. For the 33 patients receiving CYC without concomitant PCP prophylaxis the annual incidence was 9.50% (95%CI 1.15–34.33). Conclusion: In our study the annual incidence of PCP in patients taking MTX was low and would not support the use of routine PCP chemoprophylaxis. In patients receiving CYC without concomitant PCP chemoprophylaxis the annual incidence of PCP was higher although the number of cases was small. Given the high morbidity and mortality in this group, PCP chemoprophylaxis should be considered.

Background: The aim of the study was to determine whether there was evidence for a geographic gradient in the incidence of Wegener’s granulomatosis (WG) and WG-like disease in New Zealand (NZ). Methods: The National Minimum Dataset of the Ministry of Health, NZ was searched for individual patient discharges coded by the International Classification of Diseases 10th Revision, Australian Modification as either M301 (polyarteritis with lung involvement, including Churg Strauss and allergic granulomatous angiitis) or M313 (WG, necrotizing respiratory granulomatosis) for the period 1 January 1999 to 31 December 2003. Data were standardized using the 2001 NZ census. Results: One hundred and ninety-five patients (95 men) were given a first-time discharge code of either M301 (40 patients) or M313 (155 patients). No gender bias was seen. The rate among Europeans was twice that of NZ Maoris or Asians. The rate of disease peaked in the age band 70–79 years and during winter months. A significant positive north–south geographic gradient was present for M313. No difference in the rate of readmission or time to relapse between geographic regions was found for M313. Conclusion: A north–south gradient in the rate of patient discharges given a diagnostic code of M313 (WG, necrotizing respiratory granulomatosis) was present in NZ. This finding supports the hypothesis that there is a latitude-dependent risk factor(s) for WG possibly common to both global hemispheres.