Thrombocytopenia in Systemic Lupus Erythematosus

Jung, Jin Hee; Soh, Moon Seung; Ahn, Young Hwan; Um, Yoo Jin; Jung, Ju‐Yang; Suh, Chang‐Hee; Kim, Hyoun‐Ah

doi:10.1097/md.0000000000002818

Cited by 69 publications

(32 citation statements)

References 26 publications

(40 reference statements)

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“…They revealed that Lgals3 −/− mice naturally developed lupus-like disease by controlling germinal center responses via IFN-γ 17 . In accordance, in the absence of Gal-3, we observed some hematological parameters compatible with SLE, including significant thrombocytopenia 47 . Here, we used a classic model to promote lupus-like disease in mice by pristane 22 .…”

Section: Discussionsupporting

confidence: 86%

Galectin-3 orchestrates the histology of mesentery and protects liver during lupus-like syndrome induced by pristane

Lemos

Pereira

Carvalho

et al. 2019

Sci Rep

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Galectin-3 (Gal-3) controls intercellular and cell-extracellular matrix interactions during immunological responses. In chronic inflammation, Gal-3 is associated with fibrotic events, regulates B cell differentiation and delays lupus progression. Gal-3 deficient mice (Lgals3−/−) have intense germinal center formation and atypical plasma cell generation correlated to high levels IgG, IgE, and IgA. Here, we used pristane (2,6,10,14-tetramethylpentadecane) to induce lupus-like syndrome in Lgals3−/− and Lgals3+/+ BALB/c mice. Mesentery and peritoneal cells were monitored because promptly react to pristane injected in the peritoneal cavity. For the first time, mesenteric tissues have been associated to the pathogenesis of experimental lupus-like syndrome. In Lgals3+/+ pristane-induced mice, mesentery was hallmarked by intense fibrogranulomatous reaction restricted to submesothelial regions and organized niches containing macrophages and B lymphocytes and plasma cells. In contrast, Lgals3−/− pristane-treated mice had diffuse mesenteric fibrosis affecting submesothelium and peripheral tissues, atypical M1/M2 macrophage polarization and significant DLL1+ cells expansion, suggesting possible involvement of Notch/Delta pathways in the disease. Early inflammatory reaction to pristane was characterized by significant disturbances on monocyte recruitment, macrophage differentiation and dendritic cell (DC) responses in the peritoneal cavity of pristane-induced Lgals3−/− mice. A correlative analysis showed that mesenteric damages in the absence of Gal-3 were directly associated with severe portal inflammation and hepatitis. In conclusion, it has suggested that Gal-3 orchestrates histological organization in the mesentery and prevents lupoid hepatitis in experimental lupus-like syndrome by controlling macrophage polarization, Notch signaling pathways and DC differentiation in mesenteric structures.

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Section: Discussionsupporting

confidence: 86%

Galectin-3 orchestrates the histology of mesentery and protects liver during lupus-like syndrome induced by pristane

Lemos

Pereira

Carvalho

et al. 2019

Sci Rep

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“…SLE has many haematological manifestations, including thrombocytopenia. Low platelet count is more frequent in SLE patients than increased platelet number [ 126 ]. It has been associated with other severe symptoms such as kidney injury, haemolytic anaemia, neuropsychiatric manifestations, and a worse course of the disease [ 91 ].…”

Section: Evidence For Platelet Contribution In Autoimmune Disordersmentioning

confidence: 99%

From blood coagulation to innate and adaptive immunity: the role of platelets in the physiology and pathology of autoimmune disorders

2018

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Thrombosis and cardiovascular complications are common manifestations of a variety of pathological conditions, including infections and chronic inflammatory diseases. Hence, there is great interest in determining the hitherto unforeseen immune role of the main blood coagulation executor—the platelet. Platelets store and release a plethora of immunoactive molecules, generate microparticles, and interact with cells classically belonging to the immune system. The observed effects of platelet involvement in immune processes, especially in autoimmune diseases, are conflicting—from inciting inflammation to mediating its resolution. An in-depth understanding of the role of platelets in inflammation and immunity could open new therapeutic pathways for patients with autoimmune disorders. This review aims to summarize the current knowledge on the role of platelets in the patomechanisms of autoimmune disorders and suggests directions for future research.

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“…The association between thrombocytopenia and characteristics of SLE patients has been investigated in several studies. Thrombocytopenia has been shown to be associated with other severe clinical manifestations and poor prognosis in patients with SLE [6–8]. However, multicenter data regarding thrombocytopenia in Chinese SLE patients are limited.…”

Section: Introductionmentioning

confidence: 99%

Chinese SLE Treatment and Research group (CSTAR) registry: Clinical significance of thrombocytopenia in Chinese patients with systemic lupus erythematosus

Jiang

Zhang

et al. 2019

PLoS ONE

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ObjectivesTo investigate the prevalence, clinical characteristics, and prognosis of thrombocytopenia (TP) in Chinese patients with systemic lupus erythematosus (SLE).MethodsThe study was conducted based on the Chinese SLE Treatment and Research group (CSTAR) registry. Thrombocytopenia was defined as the platelet count<100,000/mm3 at enrollment. Severe thrombocytopenia was defined as the platelet count<50,000/mm3. The prevalence of SLE-related TP, the associations of thrombocytopenia with demographic data, organ involvements, laboratory findings, disease activity, damage, and mortality were investigated.ResultsOf 2104 patients with SLE, 342 patients (16.3%) were diagnosed with thrombocytopenia. The prevalence of neuropsychiatric SLE, vasculitis, myositis, nephritis, mucocutaneous lesions, pleuritis, fever, leukocytopenia and hypocomplementemia were significantly higher in patients with thrombocytopenia (p<0.05). SLE disease activity index (SLEDAI) was significantly higher in patients with thrombocytopenia (p<0.05). Multivariate analysis showed that leukocytopenia (OR = 2.644), lupus nephritis (OR = 1.539), hypocomplementemia (OR = 1.497) and elevated SLEDAI (OR = 1.318) were independently associated with thrombocytopenia (p<0.05). Long disease duration (OR = 1.006) was an independent risk factor of severe thrombocytopenia, while anti-rRNP (OR = 0.208) was an independent protective factor of severe thrombocytopenia (p<0.05). Long disease duration was an independent risk factor of mortality in patients with thrombocytopenia (RR = 1.006). The 6-year survival of patients with thrombocytopenia was significantly lower than patients without thrombocytopenia (88.2% vs. 95.5%).ConclusionsThrombocytopenia was a common manifestation of SLE and was associated with leukocytopenia, nephritis and severe disease activity. Severe thrombocytopenia tended to occur in long-term and relatively inactive SLE. Patients with SLE-related thrombocytopenia has a decreased long-term survival rate. Long disease duration was an independent risk factor of mortality in patients with thrombocytopenia.

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Thrombocytopenia in Systemic Lupus Erythematosus

Cited by 69 publications

References 26 publications

Galectin-3 orchestrates the histology of mesentery and protects liver during lupus-like syndrome induced by pristane

Galectin-3 orchestrates the histology of mesentery and protects liver during lupus-like syndrome induced by pristane

From blood coagulation to innate and adaptive immunity: the role of platelets in the physiology and pathology of autoimmune disorders

Chinese SLE Treatment and Research group (CSTAR) registry: Clinical significance of thrombocytopenia in Chinese patients with systemic lupus erythematosus

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