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Chinese Journal of Integrative Medicine Oct 2021To provide evidence on the efficacy and safety of Chinese herbal medicine (CHM) as interventions for systemic lupus erythematosus (SLE). (Meta-Analysis)
Meta-Analysis
OBJECTIVE
To provide evidence on the efficacy and safety of Chinese herbal medicine (CHM) as interventions for systemic lupus erythematosus (SLE).
METHODS
Seven electronic databases, including the Cochrane Library, Chinese National Knowledge Infrastructure (CNKI), Chinese Scientific Journal Database (VIP), Chinese Biomedical Literature Service System (SinoMed), Wanfang, Embase, and PubMed, were comprehensively searched, from their inception to August 16, 2020, for all randomized controlled trials (RCTs) that focused on CHM used alone or in combination with conventional medicine for SLE. Outcomes were SLE activity index (SLEDAI), traditional Chinese medicine symptom/syndrome score (TCMSS), dosage of glucocorticoids, main serological testing, and incidence of adverse events. Data were extracted and pooled using Review Manager 5.3 software.
RESULTS
A total of 13 RCTs enrolling 856 participants met our inclusion criteria. Meta-analyses showed that, compared to placebo, CHM had statistically significant effect on reducing SLEDAI score (MD=-1.74, 95% CI: -2.29 to -1.18), diminishing TCMSS (SMD=-0.89, 95% CI: -1.16 to -0.62), decreasing dosage of glucocorticoids (MD=-2.41 mg/d, 95% CI: -3.34 to -1.48), lowering erythrocyte sedimentation rate (MD=-4.78 mm/h, 95% CI: -8.86 to -0.71), and increasing serum complement C4 level (MD=0.03 mg/dL, 95% CI: 0.00 to 0.06). No significant difference was found between CHM and placebo on adverse events.
CONCLUSIONS
CHM provided significant beneficial effect on controlling disease activity and reducing dose of glucocorticoids used among SLE patients. Future advanced designed RCTs for CHM treating moderate to severe SLE with multicenter and longer follow-up are urgently needed.
Topics: Drugs, Chinese Herbal; Humans; Lupus Erythematosus, Systemic; Medicine, Chinese Traditional; Multicenter Studies as Topic; Randomized Controlled Trials as Topic
PubMed: 34319503
DOI: 10.1007/s11655-021-3497-0 -
Seminars in Arthritis and Rheumatism Jun 2015Systemic lupus erythematosus (SLE) is an autoimmune disease that may present manifestations that resemble other diseases. Visceral leishmaniasis (VL) is a parasitic... (Review)
Review
OBJECTIVE
Systemic lupus erythematosus (SLE) is an autoimmune disease that may present manifestations that resemble other diseases. Visceral leishmaniasis (VL) is a parasitic infection whose hallmarks may mimic SLE symptoms. Here, we report a case series and evaluate the published, scientific evidence of the relationship between SLE and VL infection.
METHODS
To assess original studies reporting cases of VL-infected patients presenting manifestations that are capable of leading to inappropriate suspicions of SLE or mimicking an SLE flare, we performed an extensive search in several scientific databases (MEDLINE, LILACS, SciELO, and Scopus). Two authors independently screened all citations and abstracts identified by the search strategy to identify eligible studies. Secondary references were additionally obtained from the selected articles.
RESULTS
The literature search identified 53 eligible studies, but only 17 articles met our criteria. Among these, 10 lupus patients with VL mimicking an SLE flare and 18 cases of VL leading to unappropriated suspicions of SLE were described. The most common manifestations in patients infected with VL were intermittent fever, pancytopenia, visceromegaly, and increased serum level of acute phase reactants. The most frequent autoantibodies were antinuclear antibodies, rheumatoid factor, and direct Coombs' test.
CONCLUSION
In endemic areas for VL, the diagnosis of SLE or its exacerbation may be a clinical dilemma. Hepatosplenomegaly or isolated splenomegaly was identified in the majority of the reported cases where VL occurred, leading to unappropriated suspicions of SLE or mimicking an SLE flare. Furthermore, the lack of response to steroids, the normal levels of complement proteins C3 and C4, and the increased level of transaminases suggest a possible infectious origin.
Topics: Adolescent; Adult; Antibodies, Antinuclear; Coombs Test; Diagnosis, Differential; Female; Fever; Humans; Leishmaniasis, Visceral; Lupus Erythematosus, Systemic; Pancytopenia; Rheumatoid Factor
PubMed: 25704907
DOI: 10.1016/j.semarthrit.2014.12.004 -
Clinical Reviews in Allergy & Immunology Dec 2020Diffuse alveolar hemorrhage (DAH) is a rare but potentially deadly manifestation of systemic lupus erythematosus (SLE). The aim of this study was to investigate the... (Meta-Analysis)
Meta-Analysis
Clinical Characteristics and Risk Factors of Diffuse Alveolar Hemorrhage in Systemic Lupus Erythematosus: a Systematic Review and Meta-Analysis Based on Observational Studies.
Diffuse alveolar hemorrhage (DAH) is a rare but potentially deadly manifestation of systemic lupus erythematosus (SLE). The aim of this study was to investigate the clinical characteristics and risk factors of DAH in SLE. A systematic review and meta-analysis of previous observational studies compared the clinical characteristics and risk factors between DAH-SLE and SLE patients without DAH. A total of 5 observational studies were included in this meta-analysis. Compared with the SLE patients without DAH, DAH-SLE patients had a significantly higher incidence of neuropsychiatric events (OR = 4.321, 95% CI (1.686-11.073), P = 0.002, I = 49.2%), nephritis (OR = 3.146, 95% CI (1.663-5.955,), P = 0.000, I = 0.0%), serositis (OR = 6.028, 95% CI (1.418-25.635), P = 0.015, I = 80.3%), dyspnea (OR = 31.241,95% CI (0.202-4833.203), P = 0.181, I = 94.6%), and a significantly lower level of C3 (SMD = - 1.358, 95% CI - 1.685, - 1.031), P = 0.000, I = 98.0%), C4 (SMD = - 1.251, 95% CI (- 1.648, - 0.855), P = 0.000, I = 87.7%), hemoglobin (SMD = - 2.074, 95% CI (- 2.433, - 1.715), P = 0.000, I = 94.2%), and a higher SLEDAI-2K score (SMD = 1.284, 95% CI (0.959, 1.608), P = 0.000, I = 98.2%). However, due to significant heterogeneity, some of these results should be interpreted cautiously. Nevertheless, when the above abnormal indicators are found, especially neuropsychiatric involvement and nephritis, besides the existed diagnostic criteria for DAH in SLE patients, a diagnosis for DAH should be considered and relevant treatment timely initiated. Further prospective multi-center SLE studies with a large cohort of patients and long-term follow-up are needed to clarify further or find out the specific clinical indexes for DAH in SLE patients.
Topics: Biomarkers; Blood Platelets; Complement C3; Complement C4; Diagnosis, Differential; Female; Hemorrhage; Humans; Incidence; Lupus Erythematosus, Systemic; Male; Odds Ratio; Pulmonary Alveoli; Risk Factors; Symptom Assessment
PubMed: 31440948
DOI: 10.1007/s12016-019-08763-8 -
American Journal of Clinical Dermatology Jul 2024Pyoderma gangrenosum (PG) is a rare ulcerative neutrophilic dermatosis that can be associated with primary immunodeficiency. The pathogenesis of PG has not yet been...
BACKGROUND AND OBJECTIVE
Pyoderma gangrenosum (PG) is a rare ulcerative neutrophilic dermatosis that can be associated with primary immunodeficiency. The pathogenesis of PG has not yet been elucidated, although contributions from dysregulation of the immune system in patients with apparent genetic predispositions have been postulated. We conducted a Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)-guided systematic review with the objective of identifying inborn errors of immunity in the presence of PG as well as their clinical characteristics of severity including number of PG lesions and anatomic areas affected, and treatment outcomes.
METHODS
A literature search was performed using PubMed/MEDLINE, Embase, Cochrane Library, and Web of Science through August 24, 2023, for studies published in English using the search terms: "pyoderma gangrenosum," "inborn error of immunity," "immune defect*," and a list of genetic mutations potentially associated with PG.
RESULTS
Seventy-four cases of PG associated with inborn errors of immunity were identified. The results demonstrate an association of PG with a variety of inborn errors of immunity, including genetic mutations not classically associated with the condition. Genetic mutations such as BTK, IL1RN, ITGB2, LPIN2, MEFV, NFkB1, NLRP3, NLRP12, NOD2, PSMB8, PLCG2, PSTPIP1, RAG1, TTC37, and WDR1, as well as complement component 2/complement component 4 (C2/C4) and complement component 7 (C7) deficiencies were identified in the presence of either idiopathic or syndromic PG. Of note, mutations in genes such as PSMB8, NLRP3, and IL1RN were found to be associated with a more severe and atypical course of PG, whereas mutations in RAG1 as well as those causing a C2/C4 deficiency were associated with the mildest clinical presentations of PG. Mutations in NFkB1, ITGB2, and PSTPIP1 were associated with the most heterogeneous clinical presentations.
CONCLUSIONS
Human inborn errors of immunity may be implicated in the genetic predisposition to PG and may influence the clinical presentation. Due to the rarity of these diseases, further work must be done to describe the association between inborn errors of immunity and PG. Identifying inborn errors of immunity that may contribute to the development of PG may assist in further elucidating the mechanism of PG, guiding targeted treatment, and improving clinical outcomes for these patients.
PubMed: 38951460
DOI: 10.1007/s40257-024-00875-y