and Goerz 1987), whereas SCLE is found in 7-32% of the patients (Sonthei-meret al. 1979; Molad 1987; Weinstein 1987; Mooney and Wade 1989).

Risk Factors that Induce SLE

Risk factors might be divided into factors that induce the disease and risk factors that effect the prognosis of the disease. Several risk factors have been evaluated and identified for SLE (Table 5). One risk factor is the presence of CDLE and/or SLE in the family. Lawrence et al. reported (1987) that 3.9% of first degree relatives of SLE patients and 2.6% of first degree relatives of CDLE patients developed SLE, compared with only 0.3% of the controls. Similar results were obtained by Cooper et al. who found a history of lupus in a parent or sibling in 15 (6%) cases and 7 (2%) controls (2002b). In contrast, there was no elevated risk for first degree relatives of SLE patients to develop CDLE whereas 3.5% of CDLE family members compared with 0.5% of the controls developed CDLE (Lawrence et al. 1987).

Smoking is also discussed to be a risk factor for both SLE and CDLE. Nagata et al. (1995) were able to show an increased risk of SLE for smoking (OR: 2.31; 95% confidence interval (CI) 1.34-3.97). However, in a recent study Cooper et al (2001) were not able reproduce these results for either current and previous smokers. Smoking is also discussed to be a risk factor for CDLE. Gallego et al. (1999) showed in a case-control-study based on 28 CDLE patients and 112 matched controls, and in addition by comparing a second set of 20 CDLE patients to statewide smoking prevalence data that smoking

Table 5. Risk Factors that May Induce Systemic Lupus Erythematosus

Risk factor studied (author, year)

Study design Size of study

Odds Ratio (95% CI)

Positive family history (Nagata et al. 1995)

Case-control study 282 cases/292 controls

5.20 (1.08-24.95)

History of lupus in parents or siblings (Cooper et al 2002b)

Case-control study 265 cases/355 controls

(Nagata et al. 1995)

Case-control study Case-control study

2.31 (1.34-3.97)

Current smoking (Cooper et al. 2001)

Case-control study 265 cases/355 controls

1.1 (0.7-1.7)*

Crystalline silica dust (Parks et al. 2002)

Case-control study 265 cases/355 controls

4.6 (1.4-15.4) high exposure*

Postmenopausal Estrogen Therapy (Sánchez-Guerrero et al. 1995a) (Meier et al. 1998)

Prospective cohort study 69,435

Case-control study 75 cases/295 controls

2.1 (1.1-4.0) 2.8 (0.9-9.0)

Use of oral contraceptives (Cooper et al. 2002a)

Case-control study 240 cases/321 controls

1.3 (0.9, 2.1)

Breast feeding (Cooper et al. 2002a)

Case-control study 240 cases/321 controls

0.6 (0.4, 0.9)

Allergy to medications Particularly to antibiotics (Cooper et al. 2002b)

Case-control study 265 cases/355 controls

3.1 (2.1-4.5)*

History of shingles (Cooper et al. 2002b)

Case-control study 265 cases/355 controls

2.5 (1.1-5.9)*

Cold sores (Cooper et al. 2002b)

Case-control study 265 cases/355 controls

2.8 (1.4-5.4)*

is a risk factor for CDLE, too. In the CDLE patients, the prevalence of smoking was 83% (23 of 28) compared to 22% (25 of 112) in the control group (OR = 12.2, with p = 0.001). They also found, that the 23 CDLE smokers smoked significantly more than the 25 control smokers (mean, standard deviation and range: CDLE 1.43 (0.56) 0.5 to 2.5 packs/day; control 0.71 (0.44) 0.05 to 1.5 packs/day; p = 0.0001, Wilcoxon's rank sum test). The second set of patients showed 15 of 20 to be smokers, resulting in a smoking rate of 75% which exceeded three times the 1992 to 1993 smoking rate for the general population of Minnesota (25,1%) (Shopland et al. 1996; Gallego et al. 1999). These results suggest that CDLE is largely a disease of chronic, particularly heavy smokers. Nevertheless other potential confounding factors as alcohol were not considered in this study.

Besides smoking, female hormones seem to be an important risk factor. Sánchez-Guerrero et al. (1995a) reported an increased relative risk of developing SLE for longer term (5-10 years) postmenopausal estrogen users compared with nonusers of 2.7 (95% CI 1.2-6.4). In a population-based, case-control study, using the UK-based General Practice Research Database (GPRD) (Jick et al. 1991; Walley and Mantgani 1997), Meier et al. (1998) analyzed 34 cases with CDLE, 41 cases with SLE and 295 age, gender and practice matched controls. After adjusting for body mass index, hysterectomy, oophorectomy, and smoking status, the RR estimate for current use versus nonuse was 1.5 (95%, CI 0.7-3.7) for SLE, 2.3 (0.8-6.7) for CDLE, and 1.7 (0.9-3.2) for CDLE and SLE combined. Never and former users were combined into a single group of nonusers, because former users did not show an increased risk. The adjusted OR for current estrogen use of a duration of less than 25 months and of 25 months or more, as compared to nonuse, were 0.7 (0.3-2.1) and 2.8 (1.3-5.8; p = 0.008), respectively. Exposure to 1200 or more cumulative defined daily doses (DDD) resulted in elevated RR estimates (adjusted OR 2.8, 95% CI 1.1-7.2), whereas low cumulative estrogen doses of 500 or less DDD did not increase the relative risk estimates compared to nonuse. These results have been confirmed by other authors. In the Nurses Health Study, the long-term use of opposed estrogens was associated with a 2- to 3- fold increased age adjusted RR estimate (Sánchez-Guerrero et al. 1995). In addition Meier et al. (1998) found an increased risk of developing SLE and CDLE for current estrogen users compared to nonusers. This effect showed a distinct dose and duration dependency, which has been documented independently for SLE and for DLE. In contrast Cooper et al (2002a) found only little evidence that estrogen- or prolactin-related exposures were associated with an increased risk of lupus. In this study an inverse association of breast feeding and lupus was found (OR 0.6, CI 0.4-0.9). Cooper et al. (2002a) also states that natural menopause occurred earlier in women with SLE and that this finding was not considered in the Nurses Health Study.

A role for infectious agents as a risk factor for SLE has been postulated for many years (Strom et al. 1994). SLE may be the cause of an aberrant response or lack of immune control of a response to a pathogen. Cooper et al. (2002b) focused in one of her recent case-control studies on infections. She was able to show an increased risk for SLE with a past history of shingles 2.5 (95%, CI 1.1-5.9) as well as cold sores 2.8 (95%, CI 1.4-5.4).

Several studies dealt with the question whether breast implants increase the risk of acquiring any of the connective tissue diseases or not. The results will be reported in more detail in the part about systemic sclerosis. However, in studies of good grades of recommendation (Ball et al. 1999), no evidence has been found that silicone gel-filled breast implants increase the risk of developing SLE.

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