Case 10 Psoriasis
Description of psoriasis
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.
Clinical manifestations
Psoriatic lesions and concomitant symptoms of the disease vary according to the type and subtype of psoriasis. Plaque psoriasis is the most common subtype and usually presents as demarcated, erythematous and thickened plaques covered with fine silvery scales. These lesions are often located on the scalp, trunk and extremities, and are frequently accompanied by pruritus and nail pitting. The pustular variant may manifest as erythematous, pustule-studded lesions to the palmar or plantar surfaces, though in some cases can be associated with pyrexia and malaise. Guttate psoriasis presents as distinct, scaly, erythematous, droplet-like lesions to the scalp, ears, face, trunk and proximal limbs. The other major variant, erythrodermic psoriasis, is a dermatological emergency, manifesting as severe and extensive erythema and exfoliation, malaise and reduced skin function. Sufferers of psoriasis can also develop psoriatic arthritis, although this tends to affect a relatively small proportion of psoriasis cases.1,12,13
Rapport
Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, as well as the accuracy and comprehensiveness of the clinical assessment.
Medical history
Family history
Father has psoriasis, paternal grandmother has rheumatoid arthritis.
Medications
Calcipotriol/betamethasone diproprionate 50/500 ointment twice a day, coal tar three times a week.
Lifestyle history
Illicit drug use
| Diet and fluid intake | |
| Breakfast | Corn Flakes® with full-cream milk. |
| Morning tea | Coffee. |
| Lunch | Meat pie, white roll with salad, hot chicken roll, iced coffee. |
| Afternoon tea | Coffee. |
| Dinner | Spaghetti bolognaise, meat lover’s pizza, beef schnitzel or sausages with mashed potato and peas. |
| Fluid intake | 1 cup of water daily, 2 cups of iced coffee daily, 1–2 cups of soft drink daily, 1 cup of milk daily, 2–3 cups of instant coffee daily. |
| Food frequency | |
| Fruit | 0–1 serve daily |
| Vegetables | 1–2 serves daily |
| Dairy | 1–2 serves daily |
| Cereals | 4–5 serves daily |
| Red meat | 8 serves a week |
| Chicken | 2 serves a week |
| Fish | 0 serves a week |
| Takeaway/fast food | 8 times a week |
Physical examination
Inspection
Skin lesions are evident on the scalp and both elbows, anterior knees and buttocks, ranging from 5 to 100 mm in diameter. All plaques are demarcated, erythematous, thickened and covered with fine silvery scales. Excoriation and lichenification are also present around the lesions. There is no exudation, bleeding, papules, pustules or ulceration. Pitting and mild onycholysis is evident to all fingernails.
Diagnostics
Pathology tests
Liver function test (LFT)
The LFT can provide useful information about hepatic function but cannot reliably detect impairments in liver detoxification because elevated blood ammonia, a sign of functional liver impairment, is unlikely to rise above the normal range in mild to moderate hepatic disease.14
Endomysial and gliadin antibodies
The accumulation of undigested gliadin and gluten within the intestinal tract can lead to the formation of immunoglobulin A (IgA) endomysial antibodies, and IgA/IgG gliadin antibodies. Elevated serum levels of these antibodies are suggestive of gluten-sensitive enteropathy,14 a possible trigger of psoriasis.2
Functional tests
The comprehensive detoxification profile (CDP) measures a person’s capacity to effectively clear toxic metabolites from the blood, which may help to ascertain whether impaired liver function is a contributing and/or aggravating factor of psoriasis.15
Invasive tests
A lesion biopsy may be required if a diagnosis of psoriasis is uncertain. Histological findings indicative of psoriatic disease include increased mitosis of endothelial cells, fibroblasts and keratinocytes, evidence of inflammatory cells within the dermis and epidermis, and acanthosis.16
