Objectives(1) To investigate the demographic and clinical characteristics contributing to the delay from symptom onset to the first visit to a rheumatologist; (2) to compare clinical, radiographic and patient-reported outcome measures of those who saw a rheumatologist early in their disease course with those who were diagnosed later.MethodsAll psoriatic arthritis (PsA) patients, fulfilling CASPAR criteria, with an average disease duration of >10 years were invited for detailed clinical evaluation. The total lag time from symptom onset to their first rheumatological encounter was studied. The data were extracted from the referral letters and medical records. Patients were classified as early consulters or late consulters depending on whether they were seen by a rheumatologist within or beyond 6 months of symptom onset.Results283 PsA patients were studied. Median lag time from the disease onset to the first rheumatological assessment of the cohort was 1.00 years (IQR 0.5–2). 30% (n=86), 53% (n=149) and 71% (n=202) of the cohort were seen by a rheumatologist within 6 months, 1 and 2 years of symptom onset, respectively. PsA patients with low education status (OR 2.09, p=0.02) and Body Mass Index (OR 0.92, p=0.01) were significantly more likely to have a diagnostic delay of >2 years. On multiple stepwise regression analysis, the model predicted significant association of late consulters with the development of peripheral joint erosions (OR 4.25, p=0.001) and worse Health Assessment Questionnaire scores (OR 2.2, p=0.004).ConclusionsEven a 6-month delay from symptom onset to the first visit with a rheumatologist contributes to the development of peripheral joint erosions and worse long-term physical function.

29% of Ps patients attending dermatology clinics had undiagnosed PsA. Psoriasis severity was associated with a new diagnosis of PsA. Poor sensitivities for the screening questionnaires were noted due to inadequate detection of patterns of arthritis other than polyarticular disease.

Among patients with PsA, MetS and IR are highly prevalent, and are independently associated with the severity of underlying PsA.

This review focuses on the genetic features of psoriatic arthritis (PsA) and their relationship to phenotypic heterogeneity in the disease, and addresses three questions: what do the recent studies on human leukocyte antigen (HLA) tell us about the genetic relationship between cutaneous psoriasis (PsO) and PsA – that is, is PsO a unitary phenotype; is PsA a genetically heterogeneous or homogeneous entity; and do the genetic factors implicated in determining susceptibility to PsA predict clinical phenotype? We first discuss the results from comparing the HLA typing of two PsO cohorts: one cohort providing the dermatologic perspective, consisting of patients with PsO without evidence of arthritic disease; and the second cohort providing the rheumatologic perspective, consisting of patients with PsA. We show that these two cohorts differ considerably in their predominant HLA alleles, indicating the heterogeneity of the overall PsO phenotype. Moreover, the genotype of patients in the PsA cohort was shown to be heterogeneous with significant elevations in the frequency of haplotypes containing HLA-B*08, HLA-C*06:02, HLA-B*27, HLA-B*38 and HLA-B*39. Because different genetic susceptibility genes imply different disease mechanisms, and possibly different clinical courses and therapeutic responses, we then review the evidence for a phenotypic difference among patients with PsA who have inherited different HLA alleles. We provide evidence that different alleles and, more importantly, different haplotypes implicated in determining PsA susceptibility are associated with different phenotypic characteristics that appear to be subphenotypes. The implication of these findings for the overall pathophysiologic mechanisms involved in PsA is discussed with specific reference to their bearing on the discussion of whether PsA is conceptualised as an autoimmune process or one that is based on entheseal responses.

Approximately 40% of patients presenting with idiopathic AAU have undiagnosed SpA. A simple to apply algorithm is described with excellent sensitivity and specificity.

Different HLA susceptibility genes were associated with particular features that defined the PsA phenotype of a given patient. Additive interactions between different susceptibility HLA alleles defined the propensity for a more severe or milder musculoskeletal phenotype.

Patients with inflammatory arthritis are more prone to have CKD. This could have serious implications, as the majority of rheumatology patients use non-steroidal anti-inflammatory drugs and different immunosuppressives, such as methotrexate. No association of kidney dysfunction was noted with inflammatory disease-specific characteristics; rather it appears to have a positive independent association with cardiovascular diseases.

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