Lupus Erythematosus with Nephritis

PEDIATRICS ◽  
1968 ◽  
Vol 42 (2) ◽  
pp. 369-370
Author(s):  
Jerry C. Jacobs

Hagge, Burke, and Stickler in their recent article "Treatment of Systemic Lupus Erythematosus Complicated by Nephritis in Children"1 conclude, "The retrospective analysis showed a definite trend toward prolonged survival among the patients receiving high doses of steroids, compared to those receiving no or low doses." The evidence in their Figure 1, although not statistically significant, appears to support their thesis. The authors do not mention that the broken line low-dose group represents 23 patients seen between 1945 and 1957 and 4 patients seen between 1959 and 1963, while the solid-line plot includes only patients seen since 1959.2

2020 ◽  
Vol 9 (9) ◽  
pp. 2709
Author(s):  
Sabrina Porta ◽  
Alvaro Danza ◽  
Maira Arias Saavedra ◽  
Adriana Carlomagno ◽  
María Cecilia Goizueta ◽  
...  

Since the discovery of glucocorticoids (GCs), their important anti-inflammatory effect, rapid mechanism of action, low cost, and accessibility have made them one of the mainstays of treatment for Systemic lupus erythematosus (SLE). Although their use has allowed controlling the disease and reducing acute mortality in severe conditions, the implementation of a scheme based on high doses for long periods has inevitably been accompanied by an increase in adverse effects and infections, including long-term damage. The objective of this review is to answer some important questions that may arise from its use in daily clinical practice, and to propose a paradigm based on the use of methylprednisolone pulses followed by medium-low doses and a rapid decrease of prednisone.


PEDIATRICS ◽  
1967 ◽  
Vol 40 (5) ◽  
pp. 822-827
Author(s):  
Wolfgang W. Hagge ◽  
Edmund C. Burke ◽  
Gunnar B. Stickler

The clinical course of 41 patients who had systemic lupus erythematosus complicated by nephritis with symptoms beginning before they were 15 years old was reviewed. The retrospective analysis showed a definite trend toward prolonged survival among the patients receiving high doses of steroids, compared to those receiving no or low doses. We conclude that it is no longer justified to withhold high-dose steroid therapy from children with lupus nephritis, but it should be emphasized equally that this does not apply to children with discoid lupus erythematosus, rheumatoid arthritis with a positive LE clot test, or drug-induced lupus erythematosus. Our present plan of management is outlined.


2019 ◽  
Vol 317 (5) ◽  
pp. F1274-F1284 ◽  
Author(s):  
Erin B. Taylor ◽  
Jennifer M. Sasser ◽  
Kenji J. Maeda ◽  
Michael J. Ryan

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder that is characterized by prevalent hypertension, renal injury, and cardiovascular disease. Numerous studies have reported a low prevalence and/or impaired function of regulatory T (TREG) cells in both patients with SLE and murine models of the disease. Evidence suggests that TREG cell dysfunction in SLE results from a deficiency in IL-2. Recent studies have reported that low-dose IL-2 therapy expands TREG cells in mouse models of SLE, but whether expanding TREG cells protects against hypertension and renal injury during SLE is unclear. To examine this question, female SLE (NZBWF1) and control (NZW) mice were injected with vehicle or recombinant mouse IL-2 three times in 24 h followed by single maintenance doses every 5 days for 4 wk. Treatment with IL-2 effectively expanded TREG cell populations in the peripheral blood, spleen, and kidneys. Circulating levels of anti-dsDNA IgG autoantibodies, a marker of SLE disease activity, were higher in SLE mice compared with control mice but were unaffected by IL-2 treatment. As previously reported by our laboratory, mean arterial pressure, measured in conscious mice by a carotid catheter, was higher in SLE mice than in control mice. Mean arterial pressure was significantly lower in IL-2-treated SLE mice compared with vehicle-treated SLE mice, suggesting that expanding TREG cells using low-dose IL-2 attenuates the development of hypertension. While the mechanism for the protection against hypertension is unclear, it does not appear to be related to the delay of SLE disease progression.


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