Aim Fatigue is commonly associated with psoriatic arthritis (PsA). However, information about its prevalence and associated factors is sparse. The primary objective here was to find the prevalence and magnitude of PsA fatigue. The secondary objective was to explore its associated risk factors, particularly emphasis on the effect of disease activity control. Methods PsA patients who fulfilled Classification Criteria For Psoriatic Arthritis were consecutively recruited from local rheumatology clinics. Fatigue was assessed by a 13‐item self‐administered questionnaire (Functional Assessment of Chronic Illness Therapy – Fatigue [FACIT‐F]) (0‐52). Data collected and analyzed included: demographic data, disease activity data, comorbidities and medications use. Results There were 231 eligible PsA patients recruited. The mean FACIT‐F score was 37.5 ± 9.1. Severe fatigue, defined as FACIT‐F score < 30, was found in 49 (22.1%) of them. The univariate model identified these associated factors of fatigue: tender and swollen joint count, dactylitis count, Psoriasis Area and Severity Index (PASI) score, pain and general health perception, Disease Activity in Psoriatic Arthritis (DAPSA) score, Health Assessment Questionnaire, the use of cyclosporine, sulphasalazine and biologic agents. The final regression model identified DAPSA and PASI were closely associated with severe fatigue (P = .003 and P = .04 respectively). No associations with fatigue were found between age, gender, disease duration, comorbidities and medication use. However, there were weak correlations between the magnitude of FACIT‐F score, DAPSA and PASI with r = −.3 and r = −.26 respectively. Conclusion Severe fatigue was common in PsA patients, and its magnitude was closely correlated with DAPSA and PASI score, indicating its multifactorial nature. Achieving DAPSA and PASI remission could significantly alleviate the fatigue intensity to a certain extent. However, treatment for PsA‐related fatigue should adopt a multidisciplinary approach in addition to disease activity control.

Aim Psychological distress commonly occurs in patients with psoriatic arthritis (PsA). The primary objective of this study was to determine the prevalence of depression in PsA. The secondary objective was to explore its associated factors, including socio‐demographics, disease activity data and comorbidities. Methods Patients with PsA fulfilling the Classification Criteria for Psoriatic Arthritis were consecutively recruited from local rheumatology clinics. Depression was assessed by a self‐administered Chinese‐Cantonese version of the Hospital Anxiety and Depression Scale (HADS). Results Two hundred and eight eligible patients with PsA were recruited, with 82 females and 126 males. Depression was found in 62 (29.8%) of them. The univariate model identified these associated factors: (1) Psoriasis Area and Severity Index score; (2) disease activity measurement, that is tender and swollen joint count, erythrocyte sedimentation rate, C‐reactive protein, Disease Activity in Psoriatic Arthritis (DAPSA) score, Leeds Enthesitis Index and tender dactylitis count; (3) quality of life measurement, that is Health Assessment Questionnaire ‐ Disability Index (HAQ‐DI), pain and general health perception; (4) PsA duration; and (5) body mass index. The final regression model identified DAPSA and HAQ‐DI were closely associated with depression, P = .007 and P = .02 respectively. Moderate and strong correlations with HADS score were found with DAPSA (Kendall's tau‐b coefficient [τb] = 0.25) and HAQ‐DI (τb = 0.4) respectively. No associations with depression were found between age, living and employment status, gender, demographics, inflammatory markers, disease duration, skin involvement and comorbidities, in term of Charlson's Comorbidity Index. Conclusion Depression was prevalent among PsA patients and it was closely correlated with disease activity and physical function impairment. Achieving low disease activity and maintaining physical function in patients with PsA may mitigate the psychological burden. The present study also highlighted the unmet needs of strategies to identify this common phenomenon.

Majority of rheumatic diseases are complex and multifactorial in etiology. Emerging studies has suggested that the change of human microbiota, especially in the gut, play a pivotal role in its pathogenesis. Dysequilibrium of the gut microbiota triggers the imbalance between pro- and anti- inflammatory immune responses and results in different rheumatic manifestations, such as rheumatoid arthritis (RA) and spondyloarthritis (SpA). In this article, current and future role of the human gut microbiota in rheumatic diseases are discussed.

Human parvovirus B19 infections are well reported to be associated with different autoimmune disorders. They can either mimic or trigger autoimmune diseases, such as systemic lupus erythematous (SLE), rheumatoid arthritis (RA), and vasculitis. A lack of awareness about this infection can result in delays in diagnosis and poor care. In this review, the basic biology and clinical aspects of the parvovirus, human immune response, and the pathogenesis in the rheumatic diseases are discussed.

A 51-year-old man, a non-smoker and non-drinker, with history of pulmonary tuberculosis (TB), hypertension, hyperlipidemia and gout, was admitted for rash over his bilateral lower limbs for a few days (Figure 1). The rash was neither itchy nor tender. His complete blood picture including eosinophilic count, renal and function tests were grossly normal, but both ESR and CRP were elevated with 63mm/h (<20mm/h) and 30.9mg/L (<=8.2mg/L) respectively. Anti-nuclear Antibody (ANA) was negative and C3 and C4 level were normal. Anti-myeloperoxidase anti-neutrophilic cytoplasmic antibody (Anti-MPO ANCA) was positive with a level of 53 unit (<= 20 units). Urine protein creatinine ratio was 29 (<= 11mg/mmol Cr) and there was no dysmorphic red blood cell detected. His Chest X-ray (CXR) was completely clear. Skin biopsy showed that the small vessels were infiltrated by neutrophils with fibrinoid necrosis, nuclear dusts and extravasated red blood cells. Scanty eosinophils were also seen. The larger vessels were not involved. Immunofluorescence studies with IgA, IgG, IgM, C3 and fibrinogen were all negative with no deposits in the vessels wall. The overall feature was compatible with leukocytoclastic vasculitis. A low dose of oral prednisolone 15 mg daily was started for the cutaneous small vessel vasculitis. However, he had mild bloodstained sputum 3 days later. He was given Augmentin and intravenous hydrocortisone empirically. His serial CXR remained clear (Figure 2). However, he developed respiratory failure 3 days later and his new CXR reviewed extensive infiltrates bilaterally (Figure 3). He was intubated and transferred to the intensive care unit. Urgent computed tomography (CT) scan of the thorax showed diffuse airspace consolidations in both the lungs with batwings distribution (Figure 4). His hemoglobin level was dropped from 10.6 to 7.5 g/dL (13.5-17.3g/dL) at that time.