Letter to the Editor
Revisiting the association between systemic lupus erythematosus and gout
Revisitando la asociación entre lupus eritematoso sistémico y gota
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Besides age and gender distribution of both diseases, many other factors may play a role in this association.</p><p id="par0010" class="elsevierStylePara elsevierViewall">First, it is known that the inflammatory response in acute gouty arthritis largely arises from the interaction between polymorphonuclear leukocytes and monosodium urate (MSU) crystals. In SLE, it has been demonstrated that these cells have impaired chemotactic activity and phagocytosis, which may hamper the reaction to MSU crystals.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Secondly, it is thought that complement plays an important role in the pathogenesis of gouty arthritis, as MSU crystals activate both classical and alternative pathways of complement in synovial fluid.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> As active SLE is characterized by decreased serum and synovial complement levels, in these situations it is expected that inflammatory response to MSU crystals will be impaired. This view is further supported by the fact that most cases of gout occur when SLE is quiescent, with complement levels in the normal range.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Alterations in the structure of MSU crystals may provide another explanation. It has been demonstrated that Apo B lipoprotein binds to the crystal surface, thereby physically inhibiting particle–cell interaction and subsequent phagocytosis of MSU and membrane activation.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> Apo B lipoprotein levels may be elevated in SLE, by a process that can be related to the disease itself and/or induced by corticosteroids, one of the cornerstone treatments in these patients.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Additionally, it is well known that corticosteroids are powerful suppressors of the inflammatory response, blocking vasodilatation and increased vascular permeability and reducing neutrophils chemotaxis and phagocytosis, and likely impede clinical typical gout attacks.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Furthermore, in clinical practice routine microscopy evaluation of synovial fluid is unfortunately underused, so gout attacks may be misdiagnosed as lupus arthritis flares. Consequently, gout diagnosis is late, with high rates of tophaceous forms.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">More recently, the knowledge about inflammasome contribution to the pathogenesis of certain diseases has progressed. Inflammasome is a term used to describe multimeric cytoplasmic protein complexes that detect pathogen-associated and danger-associated molecular patterns (PAMPS and DAMPs respectively) and mediate the activation of caspase-1, the primary enzyme responsible for activation of the pro-inflammatory cytokines IL-1β and IL-18. Several types of inflammasomes exist, but the best studied is the Nod-like receptor protein 3 (NLRP3) inflammasome.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7,8</span></a> The importance of inflammasome and IL-1 β activation in gout is clearly established, however in SLE it is an emerging concept. It is noteworthy that both uric acid and DNA are DAMPs, and both induce NLRP3 inflammasome, although the exact molecular details of this pathway in both conditions are not entirely known. It has been demonstrated that NLRP3 plays an important role in lupus nephritis animal models.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Moreover, it has been shown that anti-dsDNA antibodies activate NLRP3 inflammasome in monocytes/macrophages by binding to toll-like receptor 4 and inducing the production of mitochondrial reactive oxygen species.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> As gout and SLE share this pathway in their pathogenesis, that appears to be related with SLE activity and nephritis,<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">9,10</span></a> it seems reasonable to think that it could play a role in the interplay between both diseases. As previously stated, gout attacks are less common in active lupus. The authors hypothesize there could be a counterregulatory mechanism in inflammasome pathway. 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| 2022 October | 91 | 30 | 121 |
| 2022 September | 34 | 26 | 60 |
| 2022 August | 43 | 34 | 77 |
| 2022 July | 51 | 31 | 82 |
| 2022 June | 44 | 38 | 82 |
| 2022 May | 49 | 37 | 86 |
| 2022 April | 43 | 33 | 76 |
| 2022 March | 44 | 39 | 83 |
| 2022 February | 54 | 34 | 88 |
| 2022 January | 56 | 33 | 89 |
| 2021 December | 37 | 35 | 72 |
| 2021 November | 32 | 35 | 67 |
| 2021 October | 38 | 49 | 87 |
| 2021 September | 30 | 34 | 64 |
| 2021 August | 21 | 29 | 50 |
| 2021 July | 24 | 32 | 56 |
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