Interstitial lung disease (ILD) is a common extra-articular manifestation of rheumatoid arthritis (RA) and a significant cause of morbidity and mortality. Usual interstitial pneumonia and nonspecific interstitial pneumonia seem to be the most frequent patterns in RA patients with ILD, although the proportion of patients with usual interstitial pneumonia is higher than among patients with other systemic rheumatic autoimmune diseases. RA patients with ILD most frequently present with chronic symptoms of cough and dyspnea when climbing stairs or walking uphill. A physical examination may reveal inhalatory crackles and a pulmonary function test demonstrates restrictive physiology, often with reduced diffusing capacity. High-resolution computed tomography is generally sufficient to confirm a diagnosis of ILD, although a minority of cases may require a surgical lung biopsy. Conventional disease-modifying antirheumatic drugs such as methotrexate (MTX) or leflunomide (LEF) and biological agents such as TNF-blocking agents or rituximab may trigger or aggravate ILD in RA patients, and infections may contribute to increased mortality in such patients. LEF should not be used in patients with a history of MTX pneumonitis. The prevalence of interstitial pneumonia among RA patients treated with anti-TNF agents ranges from 0.5 to 3%; however, as the evidence that anti-TNF increases or decreases the risk of ILD is controversial, it is not clear whether this indicates more severe RA requiring biological therapy or the effect of exposure to potentially toxic drugs such as MTX or LEF. The development of treatment-related ILD is a paradoxical adverse event, and patients should be warned about this rare but serious complication of biological or disease-modifying antirheumatic drug therapy.

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Fibromyalgia (FM) is a chronic pain syndrome that affects at least 2% of the adult population. It is characterised by widespread pain, fatigue, sleep alterations and distress, and emerging evidence suggests a central nervous system (CNS) malfunction that increases pain transmission and perception. FM is often associated with other diseases that act as confounding and aggravating factors, such as rheumatoid arthritis (RA), spondyloarthritides (SpA), osteoarthritis (OA) and thyroid disease. Mechanism-based FM management should consider both peripheral and central pain, including effects due to cerebral input and that come from the descending inhibitory pathways. Rheumatologists should be able to distinguish primary and secondary FM, and need new guidelines and instruments to avoid making mistakes, bearing in mind that the diffuse pain of arthritides compromises the patients' quality of life.

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Background Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease that usually develops in women aged 18-50 years. It is known that age at onset modifies the clinical manifestations of SLE, and so the elderly may form a specific patient subgroup. It is now well established that the serum levels of the cytokines interleukin (IL) 6 and IL10 are increased in patients with SLE (1). Objectives The primary aim was to compare the type of clinical involvement and autoantibodies in patients with late-onset (LO) or early-onset (EO) SLE. The second aim was to compare IL6 levels in the two patient groups and their possible correlations with clinical and immunological manifestations. Methods Fifty-five patients meeting the American College of Rheumatology (ACR) criteria for the classification of SLE (47 F, 8 M) were consecutively enrolled. They were evaluated for the presence and intensity of clinical manifestations and laboratory abnormalities, and divided into two subgroups on the basis of the age of onset of SLE symptoms. The patients who developed SLE at or after the age of 65 years were considered LO-SLE cases. Antinuclear antibodies (ANA) and anti-double-stranded DNA (dsDNA) were detected by means of indirect immunofluorescence respectively using HEp-2 cells and Crithidiae luciliae as a substrate. Anti-extractable nuclear antigen (anti-ENA) antibodies (anti-Sm, anti-Ro/SSA and anti-La/SSB) were tested by means of counter-immunoelectrophoresis using control sera provided by the Center for Disease Control (Atlanta, USA). Serum IL6 levels were measured using the Quantikine high sensitivity human IL6 immunoassay (R & D Systems Europe, Abingdon, Oxon., UK). Results Twenty-five patients hadLO-SLE and 30 EO-SLE. The female to male ratio was similar in the two goups (9:1 vs. 8:1). The LO-SLE patients were more likely to have arthritis (88% vs 82%; p =0.813) and serositis (28% vs 13%; p=0.34). The prevalence of the other SLE manifestations was lower in the LO-SLE patients: malar rash (60% vs 82%; p =0.176), nephropathy (3% vs 10%; p =0.245), photosensitivity (35% vs 82%; p=0.176), alopecia (15% vs 82%; p= 0.0001) and Raynaud’s phenomenon (32% vs 70%; p=0.001). The LO-SLE patients had a higher prevalence of anti-SSA (52% vs 33%; p= 0.162), ANA antibodies (30% vs 27%; p=0.295) and were more frequently affected by secondary Sjogren syndrome (SS) (44% vs 16%; p= 0.001). Thee prevalence of other antinuclear antibodies was lower in LO-SLE than in EO-SLE (anti-dsDNA: 74,3% vs. 78,8%, anti-Sm 17,1% vs. 20%; all p=n.s; anti-SSB (24% vs 66%, p=0.002).IL6 levels were significantly higher (p=0.005) in the patients with LO-SLE, and there was a correlation between IL6 levels and secondary SS (p = 0.002, r =20.26). Conclusions Patients with LO-SLE tend to have a less severe clinical picture than those with EO-SLE; however, they frequently suffer from secondary SS. The increased IL6 levels in the patients with EO-SLE may influence the development of secondary SS. These findings are in line with those of increasing number of s...