Publications by authors named "Peter J Gow"

Urate is a frequently measured blood test in people with gout and those at risk of gout. Although gout is potentially curable with long-term urate lowering therapy, confusion about the details of urate measurement has contributed to suboptimal care. In this article, we provide recommendations regarding urate testing in gout, focusing on the use of this test in clinical practice.

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Objectives: Weight loss leads to reduced serum urate (SU) in people with obesity. However, the clinical relevance of such reductions in SU is unknown. This study examined the impact of non-surgical weight loss and bariatric surgery on SU targets in people with morbid obesity and diabetes.

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Aims: To estimate incidence, review clinical characteristics and management of newly diagnosed patients with idiopathic inflammatory myositis in Counties Manukau and to compare the findings with other reported series in New Zealand and overseas.

Methods: A case note study of computer generated data of patients having a diagnosis of inflammatory myopathy from January 2004 to December 2008 were included in this retrospective review.

Results: Twelve patients were newly diagnosed in the 5-year period.

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Aim: The aims of this study were to identify the impact of a new podiatric rheumatology service on reducing foot pain, impairment and disability in patients with foot problems associated with rheumatic disease, and to report on patient satisfaction with the service.

Method: A retrospective study of 245 patients with rheumatic disease at Counties Manukau DHB was conducted. Foot pain, impairment and disability were measured using a self-reporting patient outcome measure, the Foot Function Index.

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Objective: Probenecid is recommended as urate-lowering therapy (ULT) in patients with gout where xanthine oxidase inhibitors are ineffective, not tolerated, or contraindicated. The aim of our study was to determine the efficacy of probenecid to achieve serum urate (SU) targets (< 0.36 mmol/l) in clinical practice.

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Objective: To estimate the degree of undercount of people diagnosed with gout in administrative datasets using capture-recapture methods.

Methods: Hospitalization and drug dispensing claims (allopurinol or colchicine) data for all Aotearoa New Zealand were used to estimate the prevalence of gout in 2009 (n = 4 295 296). As a comparison, we calculated gout prevalence using a large primary care dataset using general practitioner diagnosis and prescribing records (n = 555 313).

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Introduction: Two major gout-causing genes have been identified, the urate transport genes SLC2A9 and ABCG2. Variation within the SLC17A1 locus, which encodes sodium-dependent phosphate transporter 1, a renal transporter of uric acid, has also been associated with serum urate concentration. However, evidence for association with gout is equivocal.

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Objective: Previous small studies in Aotearoa New Zealand have indicated a high prevalence of gout. This study sought to determine the prevalence of gout in the entire Aotearoa New Zealand population using national-level health data sets.

Methods: We used hospitalization and drug dispensing claims for allopurinol and colchicine for the entire Aotearoa New Zealand population from the Aotearoa New Zealand Health Tracker (ANZHT) to estimate the prevalence of gout in 2009, stratified by age, gender, ethnicity and socio-economic status (n = 4 295 296).

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Introduction: The C allele of the nonsynonymous Arg265His (rs3733591) variant of SLC2A9 confers risk for gout in Han Chinese, Solomon Island and Japanese samples, with a stronger role in tophaceous gout. There is no evidence for an association with gout in Caucasian populations. In the present study, we tested rs3733591 for association with gout in New Zealand (NZ) Māori, Pacific Island and Caucasian samples.

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Aims: The role of CYP pharmacogenetics in the bioactivation of cyclophosphamide is still controversial. Recent clinical studies have suggested a role for either CYP2C19 or CYP2B6. The aim of this study was to clarify the role of these pharmacogenes.

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Objectives: The Trp(620) allotype of PTPN22 confers susceptibility to rheumatoid arthritis (RA) and certain other classical autoimmune diseases. There has been a report of other variants within the PTPN22 locus that alter risk of RA; protective haplotype '5', haplotype group '6-10' and susceptibility haplotype '4', suggesting the possibility of other PTPN22 variants involved in the pathogenesis of RA independent of R620W (rs2476601). Our aim was to further investigate this possibility.

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Background: Azathioprine (AZA) is a commonly used drug for the management of various rheumatologic disorders. Due to individual variation of the metabolism of AZA, related to genetic polymorphism of the thiopurine methyl transferase (TPMT), serious toxic effects can result if inappropriate dose is administered. AZA dosing according to patients TPMT status can reduce drug-induced morbidity and can be cost effective.

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Genetic variation in ABCG2 (rs2231142, Q141K), encoding a uric acid transporter, is associated with gout in diverse populations. The aim of this study was to examine a role for ABCG2 in gout susceptibility in New Zealand Māori, Pacific Island and Caucasian samples. Patients (n = 185, 173 and 214, for Māori, Pacific Island and Caucasian, respectively) satisfied the American College of Rheumatology gout classification criteria.

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Introduction: The single nucleotide polymorphism (SNP) rs6822844 within the KIAA1109-TENR-IL2-IL21 gene cluster has been associated with rheumatoid arthritis (RA). Other variants within this cluster, including rs17388568 that is not in linkage disequilibrium (LD) with rs6822844, and rs907715 that is in moderate LD with rs6822844 and rs17388568, have been associated with a number of autoimmune phenotypes, including type 1 diabetes (T1D). Here we aimed to: one, confirm at a genome-wide level of significance association of rs6822844 with RA and, two, evaluate whether or not there were effects independent of rs6822844 on RA at the KIAA1109-TENR-IL2-IL21 locus.

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Objective: There is increasing evidence that variation in gene copy number (CN) influences clinical phenotype. The low-affinity Fcgamma receptor 3B (FCGR3B) located in the FCGR gene cluster is a CN polymorphic gene involved in the recruitment to sites of inflammation and activation of polymorphonuclear neutrophils (PMNs). Given recent evidence that low FCGR3B CN is a risk factor for systemic but not organ-specific autoimmune disease and the potential importance of PMN in the pathophysiology of rheumatoid arthritis (RA), the authors hypothesised that FCGR3B gene dosage influences susceptibility to RA.

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Objective: To examine the role of genetic variation in the renal urate transporter SLC2A9 in gout in New Zealand sample sets of Māori, Pacific Island, and Caucasian ancestry and to determine if the Māori and Pacific Island samples could be useful for fine-mapping.

Methods: Patients (n= 56 Māori, 69 Pacific Island, and 131 Caucasian) were recruited from rheumatology outpatient clinics and satisfied the American College of Rheumatology criteria for gout. The control samples comprised 125 Māori subjects, 41 Pacific Island subjects, and 568 Caucasian subjects without arthritis.

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Background: At diagnosis, 16% of rheumatoid arthritis (RA) patients may have foot joint involvement, increasing to 90% as disease duration increases. This can lead to joint instability, difficulties in walking and limitation in functional ability that restricts activities of daily living. The podiatrist plays an important role in the multidisciplinary team approach to the management of foot problems.

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The product of the deleted in colorectal carcinoma (DCC) gene has a role in apoptosis and is a positional candidate for IDDM6, the putative chromosome 18q12-q23 autoimmune disease locus. We hypothesised that a nonconservative substitution (DCC 201 R --> G; nucleotide (nt) 601 C --> G), located in an extracellular immunoglobulin-like domain of DCC, is an aetiological determinant of autoimmunity. We tested this hypothesis by genetically testing the nt 601 C --> G polymorphism for association with three autoimmune phenotypes in a large population-based case-control study.

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