Psoriasis: Epidemiology

Epidemiology can be defined as “the study of a disease in relation to populations.” Epidemiologic research can be understood in the light of its main interest, i.e., prevention of the disease and its consequences in man. The following areas will be covered in this review: (i) descriptive epidemiology; (ii) analytic epidemiology; and (iii) natural history and prognosis.

The measures usually adopted are incidence and prevalence. A preliminary step is to obtain a valid definition of what constitutes a “case.” Unfortunately, up to now, no widely employed diagnostic criteria have been developed for clinical and population based studies of psoriasis. The first diagnosis made by a physician and the first appearance of skin lesions as reported by the patient have both been taken as markers of “onset” in epidemiologic studies.

The incidence rate is the number of new cases per population in a given time period. There are few studies concerning psoriasis. In a pilot study conducted in Rochester, Minnesota¹ in the period 1980–1983, incident cases were defined as patients requiring, for the first time in their life, medical care for a condition diagnosed as psoriasis. The age- and sex-adjusted (1980 United States white population) annual incidence rate was 60.4 per 100,000 people. The crude rates were 54.4 for men and 60.2 for women. In another study from the United States, a cohort of 1,633 adult subjects was followed up from 1970 to 2000. Incidence rates adjusted to the 2,000 United States population increased significantly over time from 50.8 in the period 1970–74 to 100.5 per 100,000 in the period 1995–1999.² In a third study from United States, a cohort of people younger than 18 years was followed up between 1970 and 1999. The overall incidence of psoriasis age- and sex-adjusted to the 2000 United States population was 40.8 per 100,000. The incidence increased steadily with increasing age. Moreover, incidence increased in most recent years in both boys and girls.³ In a study based on data from the United Kingdom General Practice Research Database (UKGPRD) where cases were recorded by general practitioners from January 1996 to December 1997, a rate as high as 14 per 10,000 person-years was estimated, much higher than rates in the United States.⁴ Finally, in an Italian study based on a general practice database an incidence as high as 230/100,000 person-years in 2005 were estimated.⁵ Reasons for the large variations in estimates observed in different countries are not fully clear, and may involve, among the others, case definition and ascertainment procedures.

A new case (incident case) enters the prevalence pool and remains there until either recovery or death. If recovery and death are not frequent, even low incidence rates (as those calculated for psoriasis) produce high prevalence. Prevalence measures may be relative to a point in time (point prevalence) or to a longer period (period and lifetime prevalence).

Geographic and ethnic variations are observed. Mongoloid races in the Far East of Asia have remarkably low prevalence rates.¹³ Lower prevalence rates have been also documented in African-Americans compared with Caucasians in United States.²⁰ Duffy et al.,²⁴ analyzing cumulative incidence in 3,808 twin pairs, documented significantly higher prevalence rates in southern states of Australia with respect to northern areas. Geographical variations were also described by Braathen et al.⁸ with the northern regions of Troms and Finmark showing higher rates and Hedmark and Oppland regions in the south of the country showing lower rates.

Most prevalence studies suggest that psoriasis tends to be slightly more prevalent among men as compared to women. The few studies available providing age specific incidence rates of psoriasis suggest that incidence increases more or less steadily with age up to the seventh decade of life. If psoriasis appeared throughout life, then both point prevalence and lifetime prevalence would increase with age. However, prevalence estimates in several studies do not increase with age and even decreases,^7,8,24 suggesting higher mortality rates in older psoriatics compared to the general population. It has been reported that age-at-onset in large series of psoriatic patients has a bimodal distribution.²⁵ This has been taken as evidence for etiologic heterogeneity and type I and type II psoriasis have been proposed.

A history of psoriasis in first degree relatives is given by 20–30% of psoriatics. In a study, the prevalence of psoriasis increased with the number of first degree relatives affected from 3% with no relative affected, to about 40% with two relatives affected.⁶

The causative model of psoriasis involves interaction between genetic predisposition and environmental factors (i.e., multifactorial heredity).^24–37

The role of genetic factors is well established. Their review is outside the scope of this article. HLA-C remains the strongest susceptibility candidate gene in psoriasis.

Smoking has been consistently linked with psoriasis. Studies which examine the exposure before the onset of psoriasis and control for confounding factors offer the more convincing evidence (Table 2).^{4,27,29,31,33} There are indications that the risk for smoking may vary according to gender, with it being higher in women. Smoking and alcohol may alter the expression of psoriasis (e.g., pattern distribution, clinical varieties) and its clinical course. Smoking has been linked with acral lesions. Alcohol has been associated with severity of psoriasis and treatment failures.

It is well established that increased body mass index (BMI) and increased waist circumference are risk factors for developing psoriasis.^{27,28,31–33} The association has been documented also in infantile psoriasis.^32–34 Scanty data are available concerning diet. In an Italian case-control study, the risk of psoriasis increased with increasing BMI and was inversely related to the consumption of carrots, tomatoes, and fresh fruit, and to the index of beta-carotene intake.³⁵ A recent cohort study documented that vigorous physical activity was independently associated with a reduced risk of incident psoriasis.³⁶

Several drugs, e.g., lithium salts, beta-adrenergic blocking agents, and antimalarials have been reported to be responsible for the onset or exacerbation of psoriasis but evidence is inconclusive.³⁰ An infection with β-hemolytic streptococci often precedes the first manifestation of guttate psoriasis. Furthermore, a cohort study in the United States, involving 265,000 members of the Harvard Community Health Plan, demonstrated that chronic HIV infection is linked to a higher risk of psoriasis (relative risk 3.5). The risk increases with the progression of the disease from the asymptomatic phase to full-blown acquired immune deficiency syndrome.³⁷

Psychosomatic factors are deemed to play a role in psoriasis, and stressful life events have been linked with the risk of incident psoriasis. A major problem in this area is that virtually all the research is based on the recall of past events. People have a strong tendency to seek explanations in order to account for what happens to them and stress is commonly used for this.

Limited data are available concerning long-term outcome and prognosis. An analysis over a 20-year follow-up period of patients enrolled in the psoralen with ultraviolet A (PUVA) cohort study, documented that, on average, individuals with moderate to severe disease remained at these same levels for 11 or more years, and that, in spite of looking for a cure, consistent control of their psoriasis often had not been achieved.³⁸

The prevalence of psoriasis is relatively high in the general population, ranging between 0.6% and 4.8%, mainly as a result of chronicity and the absence of a cure. Genetic-environmental interaction has been proposed as a model for the causation of psoriasis. Environmental risk factors which have been documented in epidemiological studies include smoking, alcohol consumption, diet, overweight and physical inactivity, infection, drugs, and stressful life events. Psoriasis affects the quality of life to substantial degree. Apart from a few cross-sectional surveys of large series of psoriatic patients, there have been no formal studies of the natural history and prognosis of established psoriasis. By imposing methodologic control and a numerate approach, epidemiology can offer a major contribution to understand psoriasis.