Incidence of infection in systemic lupus erythematosus

Staples, Parker J.; Gerding, Dale N.; Decker, John L.; Gordon, Robert

doi:10.1002/art.1780170102

Cited by 239 publications

(81 citation statements)

References 27 publications

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“…2 Clinically, increased susceptibility to infections is a major cause of morbidity and mortality in patients with SLE. 3,4 In this regard, not only treatment with adrenal glucocorticoids and/or immunosuppressive drugs but also decreased numbers of polymorphonuclear neutrophils (PMNs) is obviously responsible for the increased incidence of infections. [5][6][7][8][9] However, the detailed molecular mechanism of neutropenia in SLE has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

TNF-related apoptosis-inducing ligand is involved in neutropenia of systemic lupus erythematosus

Matsuyama

Yamamoto

Higashimoto

et al. 2004

Blood

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Neutropenia is a common laboratory finding in systemic lupus erythematosus (SLE). However, the molecular mechanism of SLE neutropenia has not been fully explained. In this study, we examined whether TNF-related apoptosisinducing ligand (TRAIL) is involved in the pathogenesis of SLE neutropenia using samples from SLE patients. Serum TRAIL levels in SLE patients with neutropenia were significantly higher than those of SLE patients without neutropenia and healthy volunteers. Serum TRAIL levels showed a significant negative correlation with neutrophil counts in SLE patients. The expression of TRAIL receptor 3 was significantly lower in SLE patients with neutropenia than in patients without neutropenia or in healthy volunteers. Treatment with glucocorticoids negated the decrease of TRAIL receptor 3 expression on neutrophils of SLE patients. TRAIL may accelerate neutrophil apoptosis of neutrophils from SLE patients, and autologous T cells of SLE patients, which express TRAIL on surface, may kill autologous neutrophils. IntroductionNeutropenia in systemic lupus erythematosus (SLE) was first described more than 70 years ago 1 and is found in about 50%-60% of patients with SLE. 2 Clinically, increased susceptibility to infections is a major cause of morbidity and mortality in patients with SLE. 3,4 In this regard, not only treatment with adrenal glucocorticoids and/or immunosuppressive drugs but also decreased numbers of polymorphonuclear neutrophils (PMNs) is obviously responsible for the increased incidence of infections. [5][6][7][8][9] However, the detailed molecular mechanism of neutropenia in SLE has not been fully elucidated.Traditionally, PMNs have been considered to be the first line cell component of the body defense mechanism against bacterial pathogens and were regarded as terminally differentiated cells incapable of protein synthesis and committed to death within 72 hours. [10][11][12] Recently, it was indicated that neutrophils were not only capable of receiving signals from different proinflammatory cytokines and chemokines, but also could synthesize many important proinflammatory cytokines and chemokines to modulate immune responses, such as interferon-gamma (IFN-␥), tumor necrosis factor alpha (TNF-␣), and interleukin-8 (IL-8). 13,14 And these proinflammatory mediators, relevant to the inflamed site in vivo, also act to modulate the constitutive death of neutrophils. 15,16 Regarding neutrophil apoptosis, Fas 17 and TNF-␣ 18 were reported to be able to shorten neutrophil lifespan at early time points. Recently, it was reported that TNF-related apoptosis-inducing ligand (TRAIL) could accelerate neutrophil apoptosis. 19 Also, TRAIL was reported to be involved in the monocyte apoptosis induced by T cells in SLE. 20 However, the role of TRAIL in neutropenia of SLE is still unclear.In this study, we have investigated the TRAIL receptors on neutrophils and TRAIL-induced neutrophil apoptosis using samples from SLE patients. A difference in the expression pattern of TRAIL receptors between SLE patients and healt...

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Section: Introductionmentioning

confidence: 99%

TNF-related apoptosis-inducing ligand is involved in neutropenia of systemic lupus erythematosus

Matsuyama

Yamamoto

Higashimoto

et al. 2004

Blood

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“…Susceptibility to infection, particularly bacterial infection, was increased with steroid use. Staples et al found that the infection rate in hospitalized patients increased from 0.43 to 1.63 per 100 hospital days with an increase in steroid dose from zero to more than 50mg/day [34]. Although infection rarely occurs with a small dose of PSL (2-10 mg/day), the SLE patients treated with PSL of more than 20mg/day have a higher risk of infection due to the higher dose of PSL, especially after 14 days of administration.…”

Section: Adverse Effects and Complications Due To Steroid Treatmentmentioning

confidence: 99%

Glucocorticoid Therapy in Systemic Lupus Erythematosus – Clinical Analysis of 1,125 Patients with SLE

Hashimoto¹

2012

Glucocorticoids - New Recognition of Our Familiar Friend

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“…It must be considered in patients with cirrhosis of the liver and systemic lupus erythematosus, which are common conditions in Saudi Arabia. 3,17 Miliary mottling on the chest radiograph strongly suggests the diagnosis but is often absent for the first six weeks of the illness. Smears taken from the sputum, urine, CSF, bone marrow, material obtained from skin abscesses, lymph nodes, and pleural and peritoneal fluids to test for acid-fast bacilli may sometimes give positive results.…”

Section: Disseminated Tuberculosismentioning

confidence: 99%