| 1. |
- Baecklund, Eva, et al.
(författare)
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Rheumatoid arthritis and malignant lymphomas
- 2004
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Ingår i: Current Opinion in Rheumatology. - : Ovid Technologies (Wolters Kluwer Health). - 1040-8711 .- 1531-6963. ; 16:3, s. 254-261
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW:The reason for the increased lymphoma risk in patients with rheumatoid arthritis (RA) has remained unclear. Reports of lymphomas in patients treated with TNF-blockers have brought renewed interest in this issue. This review summarizes data on possible associations between RA and lymphomas, including different treatments and RA disease related risk factors.RECENT FINDINGS:Some recent studies reported increased lymphoma risks linked to RA disease activity. The hypothesis that disease-modifying drugs, and in particular methotrexate, would increase the lymphoma risk receives little support. Observation times for the TNF-blocking therapies are still short, but so far no clear increased risk for lymphoma has been observed. Presence of Epstein-Barr virus, as analyzed with EBER in situ hybridization, appears to be uncommon in RA related lymphomas. Hypothetically, an increased proliferative drive caused by self or non-self antigens may play a role in lymphoma development in RA patients, but this has to be further studied.SUMMARY:Rheumatologists need to be aware of the increased lymphoma risk in their RA patients. The reason for the increased lymphoma risk in RA patients is still unclear, but available studies rather support the hypothesis of a link between RA disease severity and the risk of lymphoma than increased risks associated with specific treatment regimens. To facilitate the future evaluation of lymphoma risks in connection with treatment, we suggest that patients treated with new drugs should be subject to structured surveillance. Collected information should include data about RA disease activity and severity.
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| 2. |
- Danielsson, Olof, et al.
(författare)
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Skeletal muscle immunohistochemistry of acquired and hereditary myopathies
- 2021
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Ingår i: Current Opinion in Rheumatology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1040-8711 .- 1531-6963. ; 33:6, s. 529-536
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review The continued development in the field of immunohistochemistry (IHC) has improved the ability to diagnose muscle diseases. Many hereditary diseases are diagnosed by the absence or abnormal localization of proteins. Detection of secondary pathological protein expression is also used in diagnostics, and to study disease processes. We relate and discuss recent reports, where IHC has been an important tool in the investigation of muscle diseases. Recent findings In idiopathic inflammatory myopathies, IHC has extended its role to diagnose subgroups. This is most evident concerning immune-mediated necrotizing myopathy and antisynthetase syndrome. The availability of new antibodies has increased the sensitivity of a muscle biopsy to diagnose several hereditary myopathies. The introduction of protein restoration therapies in muscular dystrophies also comes with the need to detect and measure protein levels. For the study of disease processes at the protein level, in both acquired and hereditary myopathies IHC, often combined with gene studies, PCR-based methods, western blotting and electron microscopy, continues to bring forth interesting results. IHC is an integrated tool in muscle pathology, where recent studies contribute to improved diagnostic skills and increased insights into disease processes.
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| 3. |
- Klareskog, Lars, et al.
(författare)
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Antibodies to citrullinated proteins in arthritis : pathology and promise
- 2008
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Ingår i: Current Opinion in Rheumatology. - 1040-8711 .- 1531-6963. ; 20:3, s. 300-305
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: The purpose of this review is to describe how the current knowledge of antibodies to citrullinated protein antigens in rheumatoid arthritis and related conditions emerged; to discuss the diagnostic and prognostic value associated with antibodies to citrullinated protein antigens as a biomarker; and most importantly for this review, to discuss the potential pathogenetic significance of these antibodies. RECENT FINDINGS: Antibodies to citrullinated protein antigens have evolved from being mainly a diagnostic marker, to being recognized as something that can help us understand fundamental etiologic and pathogenetic features of rheumatoid arthritis. Fundamental in this context is the finding that rheumatoid arthritis can be divided into two distinct subsets by means of presence or absence of antibodies to citrullinated protein antigens. Thus, several genetic as well as environmental risk factors differ between these two variants of rheumatoid arthritis. From analysis of these genetic and environmental risk factors, new testable hypotheses have been produced concerning triggering of antibodies to citrullinated protein antigens, and potential pathogenicity of antibodies to citrullinated protein antigens and accompanying immune reactions. SUMMARY: The implications of the findings are that antibodies to citrullinated protein antigens can be used for early and precise diagnosis of a subset of rheumatoid arthritis with worse prognosis than other polyarthritides, and that a new basis is formed for etiologic and pathogenetic studies of antibodies to citrullinated protein antigens-positive rheumatoid arthritis.
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| 4. |
- Lindblom, Julius, et al.
(författare)
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Diagnostic, predictive and prognostic biomarkers in systemic lupus erythematosus : current insights
- 2022
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Ingår i: Current Opinion in Rheumatology. - : Lippincott Williams & Wilkins. - 1040-8711 .- 1531-6963. ; 34:2, s. 139-149
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: Biomarkers for diagnosis, monitoring and prognosis still constitute an unmet need for systemic lupus erythematosus (SLE). Focusing on recent findings, this review summarises the current landscape of biomarkers in lupus.RECENT FINDINGS: Urine activated leukocyte cell adhesion molecule (ALCAM) exhibited good diagnostic ability in SLE and lupus nephritis (LN) whereas cerebrospinal fluid neutrophil gelatinase-associated lipocalin (NGAL) showed promise in neuropsychiatric SLE. Urine ALCAM, CD163 and vascular cell adhesion molecule 1 (VCAM-1) may be useful in surveillance of LN. Urine monocyte chemoattractant protein 1 was found to predict treatment response in SLE, and urine CD163 and NGAL treatment response in LN. Serum complement component 3 (C3) and urinary VCAM-1 have been reported to portend long-term renal prognosis in LN.SUMMARY: NGAL holds promise as a versatile biomarker in SLE whereas urine ALCAM, CD163 and VCAM-1 displayed good performance as biomarkers in LN. The overall lack of concerted corroboration of leading candidates across multiple cohorts and diverse populations leaves the current biomarker landscape in SLE in an urgent need for further survey and systematic validation.
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| 5. |
- Lorentzon, Mattias, 1970, et al.
(författare)
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Osteoporosis epidemiology using international cohorts
- 2022
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Ingår i: Current Opinion in Rheumatology. - : Ovid Technologies (Wolters Kluwer Health). - 1040-8711 .- 1531-6963. ; 34:5, s. 280-288
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Tidskriftsartikel (refereegranskat)abstract
- Purpose of review To provide an update on the most important new cohort studies within osteoporosis and their bearing on clinical management and directions for future research. Recent findings We identified a collection of new observational cohort studies - including new reports from already established large cohorts - and intervention studies providing new insights into osteoporosis pathophysiology, risk finding, intervention, and treatment barriers. Recent cohort studies in osteoporosis highlight the importance of timely identification and treatment of people who are at high risk of suffering osteoporotic fractures. Physical performance is a strong indicator of fracture risk and one that is tightly linked to a number of chronic conditions, not least inflammatory conditions like rheumatoid arthritis. Advances in case finding may involve opportunistic screening for low bone mineral density and vertebral fractures of radiology images obtained for other purposes, polygenic risk scores, and routinely collected medication and comorbidity information.
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| 6. |
- Lundberg, IE, et al.
(författare)
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Registries in idiopathic inflammatory myopathies
- 2013
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Ingår i: Current opinion in rheumatology. - : Ovid Technologies (Wolters Kluwer Health). - 1531-6963 .- 1040-8711. ; 25:6, s. 729-734
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Rantapää-Dahlqvist, Solbritt, 1947-
(författare)
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What happens before the onset of rheumatoid arthritis?
- 2009
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Ingår i: Current Opinion in Rheumatology. - : Lippincott Williams & Wilkins, Inc. - 1040-8711 .- 1531-6963. ; 21:3, s. 272-278
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: To give an overview of publications on presence of autoantibodies, rheumatoid factor and anticitrullinated protein/peptide antibodies (ACPAs) and their relationships to genetic markers and soluble factors as indicators of immune activation and identified predating the onset of symptoms of rheumatoid arthritis (RA). RECENT FINDINGS: The development during recent years concerning autoantibodies with high specificity for RA, ACPAs, has confirmed previous findings of presence of autoantibodies, such as rheumatoid factors and antikeratin antibodies, years before disease onset. Particularly, ACPAs in combination with human leukocyte antigen-shared epitope alleles and PTPN22 1858T carriage increased the relative risks of developing RA compared with not having these factors. Both shared epitope alleles and 1858T variant seemed to contribute to development of ACPAs rather than independently contribute to RA. Soluble factors such as hypersensitive C-reactive protein, cytokines, cytokine receptors and chemokines are upregulated before disease onset, though, not as long antedating time as ACPAs and rheumatoid factors. SUMMARY: Presence of ACPAs and rheumatoid factors are present several years before disease onset suggesting a gradual process leading to the development of RA. Genetic markers such as shared epitope alleles and PTPN22 1858T variant increase the relative risk for disease development. Soluble immunological markers are also increased closer to the onset of symptoms indicating activation of the immune system.
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| 8. |
- Rönnblom, Lars, et al.
(författare)
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The interferon signature in autoimmune diseases
- 2013
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Ingår i: Current Opinion in Rheumatology. - 1040-8711 .- 1531-6963. ; 25:2, s. 248-253
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW:An increased expression of type I interferon (IFN) regulated genes (an IFN signature) has been reported in blood and tissue cells from patients with SLE and other autoimmune diseases. We review the possible mechanisms behind the IFN signature as well as clinical and therapeutic consequences of this observation.RECENT FINDINGS:Autoantigens from dying cells trigger plasmacytoid dendritic cells to a continuous synthesis of type I IFN, which is promoted by natural killer (NK) cells and B cells. A growing number of genes connected to type I IFN production and response associates with an increased susceptibility to autoimmunity. Besides type I IFN, type III IFN (IFN-λ) may contribute to the IFN signature. In SLE and primary Sjögren's syndrome, a prominent IFN signature is connected to an active disease, whereas in rheumatoid arthritis the IFN signature defines a disease subset with poor clinical outcome and treatment failure to B-cell depleting therapy. Several therapies aiming to inhibit the IFN signature are in clinical trials and early data suggest clinical benefits without major safety problems.SUMMARY:The observed IFN signature in several autoimmune diseases is a biomarker of active disease and is investigated as a tool when selecting treatment for individual patients.
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| 9. |
- Rönnblom, Lars, et al.
(författare)
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Type I interferon and lupus
- 2009
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Ingår i: Current Opinion in Rheumatology. - 1040-8711 .- 1531-6963. ; 21:5, s. 471-477
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: Patients with lupus have signs of an ongoing production of type I interferons (IFNs) that are of importance both for the etiopathogenesis and the clinical manifestations. In this review, we summarize the latest information concerning the type I IFN system in lupus. RECENT FINDINGS: Activated plasmacytoid dendritic cells are responsible for the IFNalpha production in lupus and can be found in target organs such as glomeruli. The plasmacytoid dendritic cells are triggered by interferogenic immune complexes, and produced IFNalpha activates the immune system and impairs T-regulatory cell function. Autoantibodies, which can form interferogenic immune complexes, are not only present in serum of lupus patients but also in the cerebrospinal fluid of patients with neuropsychiatric manifestations. There is a strong association between risk to develop lupus and gene variants connected to the production and effects of type I IFN. Risk variants can not only cause either increased serum IFNalpha activity or sensitivity but also a more severe disease phenotype. Administration of monoclonal anti-IFNalpha antibodies to lupus patients downregulates several proinflammatory pathways and reduces disease activity. SUMMARY: Increasing evidence indicates that the activated type I IFN system in lupus is critical in the etiopathogenesis of the disease and is an important therapeutic target.
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| 10. |
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| 11. |
- Söderberg, Daniel, et al.
(författare)
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Neutrophil extracellular traps in vasculitis, friend or foe?
- 2018
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Ingår i: Current Opinion in Rheumatology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1040-8711 .- 1531-6963. ; 30:1, s. 16-23
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review Neutrophil extracellular traps (NETs) can be found at the sites of vascular lesions and in the circulation of patients with active small vessel vasculitis. Neutrophils from vasculitis patients release more NETs in vitro, and NETs have properties that can harm the vasculature both directly and indirectly. There are several ways to interfere with NET formation, which open for new therapeutic options. However, there are several types of NETs and different mechanisms of NET formation, and these might have different effects on inflammation. Here we review recent findings regarding the pathogenesis and therapeutic potentials of NETs in vasculitis. Recent findings Experimental mouse models support a role for NETs in promoting vascular damage, where histones and mitochondrial DNA appear to be driving forces. Impaired formation of NETs, however, in an SLE-like mouse model leads to more severe disease, suggesting that NETs can be important in limiting inflammation. Studies on drug-induced vasculitis reveal that levamisole can induce NETosis via muscarinic receptors, predisposing for the generation of autoantibodies, including antineutrophil cytoplasmic autoantibodies (ANCA). This supports the notion that NETs can bridge the innate and adaptive immune systems. Summary NETs can participate in the pathogenesis of vasculitis, but in some models there also seem to be protective effects of NETs. This complexity needs further evaluation with experimental models that are as specific as possible for human primary vasculitis.
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| 12. |
- Thorlacius, Gudny Ella, et al.
(författare)
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An update on the role of type I interferons in systemic lupus erythematosus and Sjogren's syndrome
- 2018
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Ingår i: Current Opinion in Rheumatology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1040-8711 .- 1531-6963. ; 30:5, s. 471-481
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review Systemic lupus erythematosus (SLE) and primary Sjogren's syndrome (pSS) share several clinical and laboratory features, including an overexpression of type I interferon (IFN) regulated genes. The genetic background to this IFN signature and the role of the type I IFN system in the disease process have been partly clarified. Here, we summarize the latest information concerning the type I IFN system in both diseases. Recent findings A number of gene variants in the type I IFN signalling pathways associate with an increased risk for both SLE and pSS in several ethnicities. The function of some risk gene variants has been elucidated, as well as the importance of epigenetic changes in type I IFN regulated genes. MicroRNA-451 and miR-302d have been shown to target IFN regulatory factor 8 and 9, suggesting that noncoding RNAs can control the IFN system. A prominent type I IFN activation is related to several disease manifestations, and in SLE to a more severe disease phenotype. Phase II studies in SLE suggest beneficial effects of blocking the type I IFN receptor. Summary The activated type I IFN system in SLE and pSS has a strong genetic component, is important in the disease etiopathogenesis and can be targeted.
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| 20. |
- Chard, Jiri, et al.
(författare)
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Osteoarthritis
- 2002
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Ingår i: Clinical evidence. - 1462-3846. ; 14:5, s. 571-572
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Tidskriftsartikel (refereegranskat)
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| 39. |
- Nordborg, Elisabeth, 1948, et al.
(författare)
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Giant cell arteritis: strategies in diagnosis and treatment.
- 2004
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Ingår i: Current opinion in rheumatology. - 1040-8711. ; 16:1, s. 25-30
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: This review summarizes current diagnostic assessments and therapeutic strategies in giant cell arteritis. Giant cell arteritis or temporal arteritis is a chronic vasculitis of large and medium-size vessels. Concurrent symptoms of proximal muscular ache and morning stiffness, polymyalgia rheumatica, are commonly seen. Recent investigations support the contention that polymyalgia rheumatica and temporal arteritis are two different expressions of the same underlying vasculitic disorder. RECENT FINDINGS: The symptomatology of giant cell arteritis is quite varying. Recently a frequent occurrence of audiovestibular manifestations was demonstrated, which should be actively searched for in the clinical investigation. Although color Doppler ultrasound, MRI, and positron emission tomography have illustrated the widespread nature of giant cell arteritis, none of these techniques may currently replace temporal artery biopsy. Biopsy of the superficial temporal artery is a safe and simple procedure, and remains the gold standard for the diagnosis of giant cell arteritis. The importance of long biopsies and meticulous histologic examination using sub-serial sectioning is emphasized. Numerous recent publications confirm the low diagnostic yield of a second, contralateral biopsy. Corticosteroids remain the cornerstone in the treatment of giant cell arteritis. Although steroid treatment promptly eliminates symptoms of systemic inflammation, its effect on inflammatory morphology is delayed. Consequently, there is a need for new therapeutic strategies. The potential role of aspirin has recently been implicated.
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| 40. |
- Ohlsson, Claes, 1965, et al.
(författare)
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Effects of growth hormone and insulinlike growth factor-I on body growth and adult bone metabolism.
- 2000
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Ingår i: Current opinion in rheumatology. - 1040-8711. ; 12:4, s. 346-8
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Tidskriftsartikel (refereegranskat)abstract
- The anabolic action of growth hormone (GH) on bone is well demonstrated by the short stature and delayed bone maturation in children with GH deficiency and in acromegalic patients with increased cortical bone mass. The body growth is regulated by growth hormone and insulin-like growth factor-I (IGF-I). The classic somatomedin hypothesis of this regulation is that most IGF-I in the blood originates in the liver and that body growth is controlled by the concentration of IGF-I in the blood. We have recently abolished IGF-I production in the livers of mice by using the Cre/loxP recombination system. The mice, in which IGF-I production had been inactivated in the liver, displayed a more than 80% reduction in serum IGF-I. In contrast, they demonstrated a normal postnatal growth, indicating that extrahepatic, autocrine/paracrine-acting IGF-I is the main determinant of postnatal growth. GH is also important for normal adult bone remodeling. Adults with GH deficiency have reduced bone mass, and GH treatment increases bone mass in GH-deficient adults. Future clinical studies will determine whether some patients with decreased bone mass for other reasons will benefit from treatment with GH alone or in combination with other treatments.
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| 45. |
- Segelmark, Mårten, et al.
(författare)
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The challenge of managing patients with polyarteritis nodosa.
- 2007
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Ingår i: Current Opinion in Rheumatology. - 1531-6963. ; 19:1, s. 33-38
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review In this short review we focus on the problems faced by clinicians caused by the changing definitions of polyarteritis nodosa. Recent findings the term polyarteritis nodosa has been used for more than 100 years as a diagnostic term for patients with systemic vasculitis, however, specific vasculitides have been singled out like branches being chopped off a tree. Now, so little is left of the trunk of that tree that it is questionable to what extent we can trust older literature with respect to clinical features, natural history and response to treatment. Many authors of case reports, as well as authors of reviews and book chapters, claim they adhere to the Chapel Hill Consensus Conference definition of polyartentis nodosa yet still cite almost exclusively studies using older definitions without highlighting this dilemma. In the past year, two proposals affecting classification have been published: one stating that cutaneous polyarteritis nodosa and hepatitis associated polyarteritis nodosa, and one providing an algorithm to separate microscopic polyangiitis from classical polyarteritis nodosa. Summary There is hope that a wide acceptance of the new classification principles will lead to a more uniform way to diagnose classical polyarteritis nodosa, which will facilitate clinical studies and eventually improve management.
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| 46. |
- Strömbeck, Britta, et al.
(författare)
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The role of exercise in the rehabilitation of patients with systemic lupus erythematosus and patients with primary Sjögren's syndrome.
- 2007
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Ingår i: Current Opinion in Rheumatology. - 1531-6963. ; 19:2, s. 197-203
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review: The purpose of this review is to present an update on the evidence-based effects of exercise in systemic lupus erythematosus and in primary Sjögren's syndrome. Recent findings: Physical capacity is reduced in both systemic lupus erythematosus and primary Sjögren's syndrome and fatigue is a dominating and disabling symptom in both conditions. The documentation on the effect of exercise on the rehabilitation of patients with systemic lupus erythematosus and primary Sjögren's syndrome is sparse; the studies are few and the sample sizes often small. The available studies indicate that patients with systemic lupus erythematosus of mild to moderate disease activity as well as patients with primary Sjögren's syndrome benefit from exercise of moderate to high intensity. Positive effects can be expected with regard to aerobic capacity, fatigue, physical function and depression. Summary: There is reason to believe that exercise should be included in the rehabilitation of patients with mild to moderate systemic lupus erythematosus and patients with primary Sjögren's syndrome. Further research is needed and should aim to evaluate the effect of exercise on groups with varying degree of disease severity and to document the long-term impact on the disease.
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| 47. |
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| 48. |
- Trysberg, Estelle, 1960, et al.
(författare)
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Cerebral inflammation and degeneration in systemic lupus erythematosus
- 2004
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Ingår i: Curr Opin Rheumatol. - 1040-8711. ; 16:5, s. 527-33
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: This review deals with new information related to central nervous system lupus, with special emphasis on mechanisms engaged in inflammation and neurodegeneration. RECENT FINDINGS: We report the very recent findings related to neuropsychiatric lupus in areas of (1) neuroimaging, (2) immunology and genetics, (3) biochemistry, and (4) neuropsychological tests. The relation between treatment of central nervous system lupus and immunologic/biochemical parameters as an outcome variable is also reported. SUMMARY: The recent advances in the field of neuropsychiatric lupus allow better understanding of the pathogenesis of the disease and follow-up of disease activity during immunosuppressive treatment.
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| 49. |
- Turesson, Carl, et al.
(författare)
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Cardiovascular risk factors, fitness and physical activity in rheumatic diseases.
- 2007
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Ingår i: Current Opinion in Rheumatology. - 1531-6963. ; 19:2, s. 190-196
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review There is increased recognition of an excess risk of cardiovascular disease in patients with rheumatic disorders. Physical inactivity is a frequent complication of arthritis, and also common in the general population. In this review, we highlight recent findings on risk factors for cardiovascular disease in patients with rheumatic diseases, and explore the role of physical activity for the prevention of cardiovascular disease. Recent findings Inflammatory mechanisms are clearly involved in cardiovascular disease in patients with systemic lupus erythematosus and rheumatoid arthritis. In rheumatoid arthritis, disability is also a major predictor of cardiovascular disease. A sedentary lifestyle increases the risk of cardiovascular disease in the general population, and high physical activity prevents cardiovascular disease mortality and morbidity. Successful treatment of rheumatic disease with control of inflammation and improved functional capacity may also reduce the risk of cardiovascular disease. Summary As part of the effort to prevent vascular comorbidity, regular exercise should be encouraged in patients with rheumatic diseases, and structured interventions to reduce adverse lifestyle factors scientifically evaluated.
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| 50. |
- Turesson, Carl
(författare)
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Extra-articular rheumatoid arthritis.
- 2013
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Ingår i: Current Opinion in Rheumatology. - 1531-6963. ; 25:3, s. 360-366
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: To discuss recent findings on the epidemiology and pathogenesis of extra-articular manifestations in rheumatoid arthritis (RA), and provide an update on the literature on treatment of patients with extra-articular RA (ExRA) manifestations. RECENT FINDINGS: ExRA is associated with increased comorbidity and mortality. Several surveys suggest that some ExRA manifestations, in particular vasculitis, occur less frequently than previously reported. This is probably due to improved overall control of disease activity. Active RA with high disease activity is associated with increased risk of severe ExRA manifestations. Studies on the impact of treatment with biologics on the occurrence of ExRA are inconclusive. Circulating immune complexes and T cells have been implicated in the pathogenesis of ExRA. The genetic background and related disease mechanisms may be somewhat different in manifestations such as vasculitis and interstitial lung disease. Limited data support a benefit from treatment with cyclophosphamide, TNF-inhibitors or rituximab in patients with severe ExRA. SUMMARY: ExRA remains a major diagnostic and therapeutic challenge in some patients. Further studies of the pathogenesis of systemic involvement and on the effect of treatment on such mechanisms may be helpful for further improvement of the management of RA.
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