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Lupus erythematosus

Lupus erythematosus (also known as systemic lupus erythematosus or SLE) is an autoimmune disorder in which antibodies are created against the patient's own DNA. It can cause various symptoms, but the main ones relate to the skin, kidney (lupus nephritis), joints, blood and immune system. more...

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It is named for the Latin lupus, meaning "wolf", perhaps due to a crude similarity between the facial rash associated with the illness, and a wolf's face, although various explanations exist.

Signs and symptoms

Common initial and chronic complaints are fever, malaise, joint pains, myalgias and fatigue. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms, however, they are considered suggestive.

Dermatological manifestations

As many as 30% of patients present with some dermatological symptoms (and 65% suffer such symptoms at some point), with 30% to 50% suffering from the classic malar (or butterfly) rash associated with the disease. Patients may present with discoid lupus (thick, red scaly patches on the skin). Alopecia, mouth and vaginal ulcers, and lesions on the skin are also possible manifestations.

Musculoskeletal manifestations

Patients most often seek medical attention for joint pain, with small joints of the hand and wrist usually affected, although any joint is at risk. Unlike rheumatoid arthritis, SLE arthropathy is not usually destructive of bone, however, deformities caused by the disease may become irreversible in as many as 20% of patients.

Hematological manifestations

Anemia and iron deficiency may develop in as many as half of patients. Low platelet and white blood cell counts may be due to the disease or a side-effect of pharmacological treatment.

Cardiac manifestations

Patients may present with inflammation of various parts of the heart: pericarditis, myocarditis and endocarditis. The endocarditis of SLE is characteristically non-infective (Libman-Sacks endocarditis), and involves either the mitral valve or the tricuspid valve. Atherosclerosis also tends to occur more often and advance more rapidly in SLE patients than in the general population. (Asanuma et al 2003, Bevra 2003, Roman et al 2003).

Renal involvement

Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end stage renal failure. Because of early recognition and management of SLE, end stage renal failure occurs in less than 5% of patients.

Neurological manifestations

About 10% of patients may present with seizures or psychosis. A third may test positive for abnormalities in the cerebrospinal fluid.

T-cell abnormalities

Abnormalities in T cell signaling are associated with SLE, including deficiency in CD45 phosphatase, increased expression of CD40 ligand. Also associated with SLE is increased expression of FcεRIγ, which replaces the TCR ζ chain, which is deficient in some SLE patients. Other abnormalities include:


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Effect of environmental changes on oxidative deoxyribonucleic acid damage in systemic lupus erythematosus - DNA
From Archives of Environmental Health, 9/1/02 by Etsuko Maeshima

OXIDATIVE DEOXYRIBONUCLEIC ACID (DNA) DAMAGE from reactive oxygen species (ROS) is apparent in inflammation, malignant tumors, the aging process, and autoimmune diseases. (1) Often, urinary 8-hydroxydeoxyguanosine (8-OHdG) is the indicator of such oxidative DNA damage. An important target for ROS within a cell is DNA, the result of which is a broad range of alterations--including base and sugar modifications, covalent crosslinks with proteins, and single- and double-strand breaks. (1) The hypothesis that ROS modification of DNA is involved in the development of autoantibodies in systemic lupus erythematosus (SLE) has been supported by enhanced reactivity of SLE anti-DNA antibodies to ROS-denatured DNA. (2-5) In SLE, anti-double--stranded DNA (anti-ds-DNA) antibody--an autoantibody specific for double-stranded DNA--is a marker for the presence of disease and is an indicator of disease activity. (6) Anti-ds-DNA antibodies exist at high concentrations during active periods of SLE. The effect of exposure to sunlight (i.e., high-intensity vs. low-intensity sunlight), a well-established environmental factor in the induction and exacerbation of SLE, (7) on urinary excretion of 8-OHdG has not been considered in previous reports of oxidative DNA damage in SLE patients.

In the current study we measured urinary 8-OHdG levels to determine the effects of exposure to low-intensity and high-intensity sunlight on oxidative DNA damage in individuals with SLE.

Materials and Method

Study design and subjects. We first measured urinary 8-OHdG in consenting SLE patients and volunteers without any past diseases and present illnesses during 2 time periods: (1) late May to early September, a period of high-intensity sunlight in Japan; or (2) late November to early March, a period of low-intensity sunlight. We compared results obtained during both time periods for patients and controls. All patients with SLE fulfilled the American Rheumatism Association's 1987 revised criteria for the diagnosis of SLE. (8)

Strong sunlight period group. A total of 22 patients with SLE and 11 volunteers agreed to participate in this study. The ages for the SLE patients ranged from 23 yr to 63 yr (mean [[bar]x] [+ or -] standard deviation [SD] = 31.1 [+ or -] 11.7 yr). The volunteers' ages ranged from 23 yr to 57 yr ([bar]x [+ or -] SD = 29.8 [+ or -] 10.1 yr). In this group, age did not differ significantly between the volunteers and the SLE patients. All patients with SLE and volunteers in this group were female.

Weak sunlight period group. We enrolled 19 patients with SLE; their ages ranged from 23.0 yr to 63.0 yr ([bar]x [+ or -] SD = 37.8 [+ or -] 12.6 yr). Twelve volunteers who were 23.0-58.0 yr of age ([bar]x [+ or -] SD = 29.4 [+ or -] 10.0 yr) were also enrolled. Again, no significant difference in age was noted between the 2 groups. All patients with SLE and volunteers in this group were female.

Measurement of urinary 8-OHdG levels and anti-ds-DNA antibodies. We measured urinary 8-OHdG and anti-ds-DNA antibodies in a group of 39 patients with SLE during both high-intensity and low-intensity sunlight periods to evaluate seasonal changes. Seasonal changes in 8-OHdG levels among SLE patients were compared with levels in healthy volunteers who agreed to being studied for more than 1 yr. Among the SLE patients, 3 were male and 36 were female; their ages ranged from 1 6.0 yr to 64.0 yr ([bar]x [+ or -] SD = 39.4 [+ or -] 13.2 yr). Healthy volunteers were 8 females between the ages of 23.0 yr and 57.0 yr ([bar]x [+ or -] SD = 31.1 [+ or -] 11.7 yr). No significant age differences were noted between the low-intensity and high-intensity sunlight groups.

Urine samples. Participants with SLE provided urine samples during follow-up at an outpatient clinic; urine samples were provided by healthy controls at the time they reported to our laboratory. Urine samples were centrifuged at 3,000 g for 5 min, during which time suspended cell debris was removed. Subsequently, the supernatant was stored at -80[degrees]C until time of analysis.

Determination of 8-OHdG. Prior to examination, we again centrifuged urine samples at 3,000 g for 5 min to remove any suspended cell debris. We assayed the supernatant with a kit that included competitive enzyme-linked immunosorbent assay (ELISA; 8-OHdG Check, Japan institute for the Control of Aging [Fukuroi, Japan]). The specificity of monoclonal antibody N45.1 used in the competitive ELISA kit has been established previously. (9) At the conclusion of the assay, absorbance was measured at 450 nm with a computer-controlled ELISA reader (MPR Model 550; Bio-Rad [Tokyo, Japan]). The 8-OHdG standards used for the assay ranged between 0.5 and 200.0 ng/ml. The concentration of 8-OHdG in the test samples was interpolated from a standard curve drawn with the assistance of logarithmic transformation. Urinary creatinine was determined by the alkaline picrate method. (10) Data herein are expressed as the urinary 8-OHdG (ng/ml)-to-creatinine (mg/dl) ratio (ng/mg). (11)

Determination of anti-ds-DNA antibodies. We evaluated the activity or inactivity of SLE among patients by measuring serum anti-ds-DNA antibodies. We used an ELISA kit (Mesacup DNA-II test-ds [Nagoya, Japan]) to determine anti-ds-DNA antibodies.


Patients with SLE vs. controls, by season. Urinary 8-OHdG levels in the SLE patients and healthy controls were compared for the high-intensity and low-intensity sunlight periods. Among the patients with SLE, levels of 8-OHdG (31.0 [+ or -] 20.6 ng/mg [[bar]x [+ or -] SD]) were significantly higher than levels in volunteers (15.4 [+ or -] 7.2 ng/mg [p < .05]) during the high-intensity sunlight period. Nonetheless, no significant difference was observed between the SLE patients (15.4 [+ or -] 5.5 ng/mg [[bar]x [+ or -] SD]) and the volunteers (16.3 [+ or -] 4.6 ng/mg) during the low-intensity sunlight period (Fig. 1).


Season, 8-OHdG levels, and anti-ds-DNA antibodies. Seasonal changes in urinary 8-OHdG and serum anti-ds-DNA antibodies were examined in the SLE patients. Urinary 8-OHdG levels and serum anti-ds--DNA antibodies were 21.3 [+ or -] 20.6 ng/mg (values are [bar]x [+ or -] SD, unless noted otherwise) and 50.5 [+ or -] 65.8 IU/I, respectively, during the high-intensity sunlight period. During the low-intensity sunlight period, the respective values were only 12.6 [+ or -] 6.7 ng/mg and 42.1 [+ or -] 51.6 IU/I. Urinary 8-OHdG levels and anti-ds--DNA antibodies were significantly higher during the high-intensity sunlight period than during the low-intensity sunlight period (p < .01 and p < .05, respectively). In healthy control subjects, however, urinary 8-OHdG was 16.2 [+ or -] 8.0 ng/mg and 15.7 [+ or -] 5.1 ng/mg for high-intensity and low-intensity sunlight periods, respectively, thus providing no evidence of a seasonal change (Fig. 2).



In only a few studies have investigators compared urinary 8-OHdG between SLE patients and healthy persons. In 1994, Lunec et al. (12) used high-performance liquid chromatography in an attempt to measure urinary 8-OHdG in patients with SLE. Lunec et al. (12) did not detect 8-OHdG in the SLE patients. Recently, Evans et al. (13) used ELISA to reexamine urinary 8-OHdG levels in SLE patients; no difference between SLE patients and controls was detected. (13) It should be noted that the effect of sunlight intensity on urinary 8-OHdG levels was not considered in the study by Evans et al. (13) In our study, in addition to the influence of sunlight, fragments of DNA in urine that contained 8-OHdG may have gone undetected had we used chromatography, but use of ELISA permitted detection. Additional reasons for the differences between our study and others may involve disease activity or steroid therapy. In our study, urinary 8-OHdG levels in patients with SLE were significantly higher than in healthy persons during the period of high-intensity sunlight, although no significant difference was found for the period of low-intensity sunlight. This difference indicated that urinary 8-OHdG varied with seasonal changes in sunlight intensity. Environmental factors, especially the effect of sunlight, may be important in the evaluation of oxidative DNA damage in patients with SLE. In addition, oxidative DNA damage in our study was greater during high-intensity sunlight, which was associated with disease activity. Both urinary 8-OHdG levels and anti-ds-DNA antibodies were significantly higher in patients with SLE during periods of high-intensity sunlight than during periods of low-intensity sunlight. These results suggest that oxidative DNA damage from sunlight plays an important role in development and exacerbation of SLE.

Requests for reprints should be sent to Maeshima Etsuko, M.D., Ph.D., Third Department of Internal Medicine, Wakayama Medical University, Wakayama City, Wakayama 640-0012, Japan.


(1.) Cooke MS, Evans MD, Herbert KE, et al. Urinary 8-oxo-2'-deoxyguanosine source, significance and supplements. Free Rad Res 2000; 22:381-97.

(2.) Cooke MS, Mistry N, Wood C, et al. Immunogenicity of DNA damaged by reactive oxygen species--implication for anti-DNA antibodies in lupus. Free Radic Biol Med 1997; 22:151-59.

(3.) Bount S, Griffiths HR, Emery P, et al. Reactive oxygen species modify human DNA, eliciting a more discriminating antigen for the diagnosis of systemic lupus erythematosus. Clin Exp Immunol 1990; 81:384-89.

(4.) Bashir S, Harris G, Denman MA, et al. Oxidative DNA damage and cellular sensitivity to oxidative stress in human autoimmune diseases. Ann Rheum Dis 1993; 52:659-66.

(5.) Bount S, Griffiths HR, Emery P, et al. Reactive oxygen species damage to DNA and its role in systemic lupus erythematosus. Mol Aspects Med 1991; 12:93-105.

(6.) Ter Borg EJ, Horst G, Hummel EJ, et al. Measurement of increases in anti-double-stranded antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus. Arthritis Rheum 1990; 33: 634-43.

(7.) Mongy AB, Hess EV. The role of environment in systemic lupus erythematosus and associated disorders. In: Wallace DJ, Hahn BH (Eds). Dubois' Lupus Erythematosus, 5th ed. Baltimore, MD: Williams & Wilkins Press, 1997; pp 31-47.

(8.) Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the clasification of systemic lupus erythematosus. Arthritis Rheum 1982; 25:1271-77.

(9.) Toyokuni S, Tanaka T, Hattori Y, et al. Quantitative immunohistochemical determination of 8-hydroxyl-2'-deoxyguanosine by a monoclonal antibody N45.1: its application to ferric nitrilotriacetate-induced renal carcinogenesis model. Lab Invest 1997; 76: 365-74.

(10.) Taussky HH. A microcolormetric determination of creatinine in urine by the Jaffe reaction. J Biol Chem 1954; 208: 853-61.

(11.) Erhola M, Toyokuni S, Okada K, et al. Biomarker evidence of DNA oxidation in lung cancer patients: association of urinary-hydroxy-2'-deoxyguanosine excretion with radiotherapy, chemotherapy, and response to treatment. FEBS Lett 1994; 409:287-91.

(12.) Lunec J, Herbert K, Blount S, et al. 8-hydroxydeoxyguanosine. A marker of oxidative DNA damage in systemic lupus erythematosus. FEBS Lett 1994; 348:126-30.

(13.) Evans MD, Cooke MS, Akil M, et al. Aberrant processing of oxidative DNA damage in systemic lupus erythematosus. Biochem Biophys Res Commun 2000; 273:894-98.

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