Epidemiology Distribution and Incidence

Reviews of the proportion of cases of DLE in the clientele of dermatology clinics began to be reported at the beginning of this century. An incidence of between 0.25 percent and 0.75 percent has been consistently found in various parts of the world (Gahan 1942). The early belief that the disease is rare in the tropics and among black populations has been disproved in Africa and in the United States (Rothfield et al. 1963; Findlay and Lups 1967).

The only epidemiological conclusion about SLE reached until the 1950s was that the disease occurs predominantly in young women. In 1952 an ethnic predisposition was postulated, based on the observation of the often deleterious effect of sun exposure: Redheaded, freckled persons with an inability to tan were deemed most susceptible (Brunsting 1952). This conclusion was contradicted, however, by M. Siegel and his colleagues (1964), whose epidemiological data indicated that SLE is actually more common among blacks. Studies in San Francisco (Fessel 1974) and Baltimore (Hochberg 1987) substantiated this increased susceptibility of blacks, particularly among black women. National data from Veterans Administration hospitals have confirmed the racial difference among men as well (Siegel and Lee 1973). Unlike infectious diseases such as rheumatic fever or tuberculosis, the occurrence of SLE appears not to be related to socioeconomic factors. In terms of total population, the annual incidence of SLE in the United States has been estimated at about 5 per 100,000, with black females about three times more susceptible and black males two times more susceptible than their white counterparts. The mean age of onset is 28 to 30 years, but the preponderance of female patients varies with age. About twice as many females as males suffer from the disease during the first decade of life and from the seventh decade on. But between ages 20 and 40, there are 8 female patients for every male.

The prevalence, sex ratio, and mortality rates for SLE in northern Europe resemble those of U.S. white populations (Helve 1985; Hochberg 1987). In other parts of the world, as recognition of the disease has increased, more cases are being diagnosed. For example, SLE was rarely diagnosed in India before 1970, but from 1974 to 1985, 181 cases were seen in one hospital in New Delhi (Malaviya et al. 1987). Studies in Hawaii (Serdula and Rhoads 1979) and Malaysia (Frank 1980) indicate greater susceptibility of Chinese than other ethnic groups, and the death rate due to SLE for Oriental women in the United States (nearly three times that of white women) is similar to that of black women (Kaslow 1982). The prevalence of SLE among Polynesians also exceeds that of Caucasians (Serdula and Rhoads 1979; Hart, Grigor, and Caughey 1983).

In the predominantly black population of Jamaica, SLE constitutes a remarkably large proportion of treated rheumatic diseases. Indeed, 22 percent of all outpatients and 37 percent of inpatients with rheumatic disease suffer from SLE (Wilson and Hughes 1979). In view of the prevalence of SLE among non-white populations elsewhere, the apparent rarity of the disease among African blacks has been perplexing. The first case was reported from Senegal in 1960. Between 1967 and 1978, only 21 cases were recorded in Kampala, Uganda. A 5-year prospective analysis of cases of polyarthritis in Zimbabwe reported in 1969 found no case of SLE, whereas another study during 1979-84 discovered 31 cases (30 female, ages 13 to 46 years) (Taylor and Stein 1986). The possibility of differences in susceptibility of various African ethnic groups must be considered. During 1960-72, for example, 130 cases of SLE were admitted to two hospitals in Cape Town, South Africa. These included 86 "coloureds" (mainly Indian), 36 whites, and only 8 "Bantu." In terms of each 1,000 female admissions, this meant a rate of 4.9 "coloured," 3.8 "Bantu," and 2.3 white (Jessop and Meyers 1973). The data from much of the world remain inadequate to draw firm conclusions about ethnic and other possible variables related to SLE.

Thomas G. Benedek

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