Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although sunscreens are widely used to photoprotect patients with photosensitive lupus erythematosus (LE), standardized controlled studies that can prove their efficacy for this indication have been lacking. Therefore, in the present study, the capacity of three different, commercially available sunscreens to prevent the development of skin lesions that have been induced in LE patients under standardized, reproducible conditions by employing a provocative phototest was assessed. In a double blind, intraindividual comparative study, 11 patients with LE were photoprovoked according to a standard protocol. All patients developed LE-specific skin lesions upon photoprovocation with a combination of UVA plus UVB radiation. Each of the sunscreens tested prevented the development of skin lesions in this assay, but to various extents. Suncreen A (UVB: Octocrylene; UVA: Mexoryl SX, Mexoryl XL, Parsol 1789; TiO2) was by far the most effective by protecting in 11/11 patients. This protective capacity was corroborated by studies in which strong ICAM-1 mRNA expression was found in unprotected test areas, but not in sunscreen A pretreated sites. In contrast to sunscreen A, sunscreen B (UVB: Eusolex 6300, Parsol MCX, Uvinul T150, Neohelipan; UVA: Parsol 1789; TiO2) protected in 5 patients and sunscreen C (Eusolex 6300, Parsol MCX, Uvinul T150; UVA: Parsol 1789; TiO2) in 3 out of 11 patients. These studies indicate that the use of sunscreens is beneficial to LE patients because it can prevent the development of UV radiation-induced skin lesions. Effective protection, however, might vary considerably between different sunscreens.
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PMID:Evaluation of the capacity of sunscreens to photoprotect lupus erythematosus patients by employing the photoprovocation test. 1113 28

The genetic backgrounds of lupus-prone murine models are a valuable resource for studying the influence of environmental exposure on autoimmune diseases in sensitive populations. Epidemiological studies have shown associations between silica exposure and several autoimmune diseases, including scleroderma and systemic lupus erythematosus. To determine whether silica exposure can exacerbate systemic autoimmunity in genetically predisposed animals, New Zealand mixed mice were intranasally instilled twice with saline or saline suspensions of 1 mg silica or 500 micro g TiO2, a dose equivalent in surface area, and were evaluated with respect to health and immune status. Survival in silica exposed NZM mice was decreased compared to saline and TiO2 exposed mice. Proteinuria levels were elevated in silica exposed mice. Levels of circulating immune complexes, autoantibodies to nuclear antigen (ANA), histone, and double stranded DNA were measured every two weeks by ELISA. Circulating immune complexes showed a trend towards an increased acceleration in levels in the silica exposed mice compared to saline and TiO2 exposed mice. ANA levels were significantly higher in silica exposed animals compared to saline and TiO2 exposed animals (0.237 +/- 0.03 versus 0.140 +/- 0.029 and 0.125 +/- 0.03, P < 0.05) 16 weeks postexposure. Autoantibodies to histone were also significantly elevated after 16 weeks in silica exposed animals compared to saline and TiO2 exposed animals (0.227 +/- 0.03 versus 0.073 +/- 0.015 and 0.05 +/- 0.03, P < 0.05). In contrast, serum IgG levels were decreased in silica exposed NZM mice compared to the saline controls, however, IgM levels were unaffected. Lungs of the silica-exposed mice had increased inflammatory infiltrates as well as fibrotic lesions characterized by excess collagen deposition. Therefore, although NZM mice are susceptible to SLE, silica exposure significantly exacerbated the course of disease.
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PMID:Silica accelerated systemic autoimmune disease in lupus-prone New Zealand mixed mice. 1260 93