Definition

Psoriasis is a chronic dermatological condition represented by epidermal thickening, hyperplasia, hyperkeratosis and inflammation. Of the two key types of psoriasis, type 1 is the most severe and the most resistant to treatment. Type 1 usually occurs in early adulthood and family history of the disease is common. Type 2 typically manifests in the fifth to sixth decade of life, is less severe and is not related to family history.¹ Overlapping these two types of psoriasis are a number of subtypes, including the erythrodermic, guttate, plaque and pustular variants.

Epidemiology

Psoriasis affects between one and five per cent of the population,² and even though the disease can occur at any age, it has a tendency to peak from late adolescence (i.e. 16 years) to 22 years and again between 57 and 60 years.¹

Aetiology and pathophysiology

Psoriasis is a disorder with a firm genetic basis.³ The lifetime prevalence of developing psoriasis in first-degree relatives ranges from four per cent if neither parent has the condition, to twenty-eight per cent if one parent has the condition and up to sixty-five per cent if both parents have psoriasis.⁴ Additional to this, almost half of sufferers report a positive family history of the condition.⁵

One factor that may increase the skin’s susceptibility to chronic plaque formation is a reduction in cyclic adenosine monophosphate (cAMP) levels. Reduced cAMP elevates proteinase activity, for instance, causing accelerated growth and thickening of the epidermis. Low cAMP levels also increase arachidonic acid production, leukotriene B₄ activation, neutrophil migration and epidermal inflammation.⁶

While changes in the levels of these chemical messengers may be genetically predetermined, they could also be influenced by several physiological factors, including incomplete protein digestion, bowel toxaemia and impaired liver function. According to one theory, inadequate protein digestion elevates the quantity of undigested amino acids in the intestinal lumen, which, upon exposure to intestinal flora, leads to the formation of toxic polyamines and a subsequent reduction in cAMP production.^7,8 The presence of gut-derived toxins from intestinal bacteria and fungi is believed to increase levels of cyclic guanidine monophosphate (cGMP), which may, in effect, increase cellular proliferation.⁸ Although the accumulation of toxins from abnormal digestive or hepatic function might contribute to and/or aggravate the symptoms of psoriasis, there is insufficient evidence to support these mechanisms of action.

Adding to the complexity of this disease are myriad intrinsic and extrinsic triggers of psoriasis. Some of the extrinsic triggers of this disease include alcohol, beta-hemolytic streptococcal infection, epidermal trauma, gluten, sunburn, viral infection and medications, including angiotensin converting enzyme inhibitors, beta-adrenergic blockers, chloroquine, interferon-alpha, lithium, non-steroidal anti-inflammatory drugs and terbinafine.^1,2 Intrinsic triggers, such as emotional stress, are considered to be a major aggravating factor of the disease.^1,9,10 Exactly how stress affects psoriasis is not clear. Findings from one study suggest it could relate to the adverse effects of cortisol on the immunological and integumentary systems. In this 3-year study of 95 sufferers of progressive psoriasis, stressful life events were found to precede a rise in cortisol levels, which was followed by the development of an infectious illness and the eruption of psoriasis over an average span of 8 weeks.¹¹ Corroborating evidence from larger studies may help to support this stress–psoriasis hypothesis.