Psoriasis is a chronic skin condition that presents in a variety of ways among individuals. It is a genetic condition triggered by environmental factors such as infection, medications, and trauma. It is characterized by exaggerated and disordered epidermal cell proliferation and keratinization. Typical lesions are well-defined erythematous, indurated papules, and plaques with white or silvery scale. It may also involve the nails and joints (Figure 8-1).

A. Definition

1. Psoriasis is thought to be a T-lymphocyte-mediated autoimmune disease. The skin lesions of psoriasis are characterized by cells multiplying much more quickly than normal (epidermal hyperproliferation), cells that do not mature normally (abnormal keratinocyte differentiation), and the presence of proinflammatory cells (a lymphocyte inflammatory infiltrate).

B. Background and etiology

1. Affects about 1% to 3% of the population worldwide depending on the study reviewed. It is seen equally in men and women, and people of all races are affected. Prevalence estimates vary in relation to age and geographic region, being more frequent in countries farther from the equator.

2. US prevalence in Caucasians is 3.6%, in African Americans is 1.9%, in Hispanics is 1.6%, and in other groups is 1.4%.

3. Prevalence varies throughout the world. The highest rates are in Norway of 8.5%, and the lowest rates in Asia of less than 0.5%.

4. Age at onset ranges from infancy to the end of life. The incidence of psoriasis commonly peaks at two different times across the life span (the early peak is between 20 and 30 years and the late peak is 50 and 60 years). Early onset usually leads to a more severe course of the disease.

5. Multifactorial and polygenetically inherited disease. The role of hereditary transmission is supported by familial association, twin studies, and correlation with human leukocyte antigens (HLA). Numerous studies have proven that certain antigens are positively associated with psoriasis and that Cw6 antigen has been shown to be the most significant marker for the risk prediction of the disease.

6. On the basis of epidemiological studies, the theory of two distinct disease patterns of psoriasis has been suggested. In type I psoriasis, the disease has an early onset and familial inheritance. Type II psoriasis has a late onset and sporadic familial occurrence.

7. If one parent is affected, 8% of children will develop psoriasis. If both parents are affected, then 41% of children develop psoriasis. Twin studies by Farber et al. showed that monozygotic twin pairs tend to be similar with respect to age of onset and pattern of disease. This was not the case in concordant dizygotic twins. The fact that not all monozygotic twins exhibited the same
disease characteristics indicates the influence of environmental triggering factors.

8. Trigger factors. Multiple internal and external factors can trigger psoriasis in genetically susceptible people.

a. Infections: In some cases, bacterial infections are the initial trigger for psoriasis. A correlation between streptococcal infection and psoriasis has been identified using both clinical and epidemiological data. Acute streptococcal infections, often associated with pharyngitis, are the most common and are specifically associated with the guttate form of psoriasis (Figure 8-2). Children and adolescents are the most susceptible, but it may also precipitate pustular psoriasis or exacerbations of plaque psoriasis. HIV and other immune-suppressing infections can significantly worsen psoriasis. Other infections, such as respiratory, gastrointestinal, and genitourinary, may also trigger psoriasis, although less often.

b. Psychological stress: Stress is a well-known trigger for psoriasis. Zachariae et al. found that 66% of patients reported exacerbations of their psoriasis related to stress and 35% reported that the onset of their psoriasis occurred during a time of stress. Those who were the most stressed reported greater disease severity, psoriasis-related stress, and quality-of-life (QOL) impairment. Depression can be a significant barrier to improving the patient’s condition. When severe psoriasis is present or the patient expresses distress related to the psoriasis, depression screening should be considered at the initial visit, as well as follow-up visits. The PHQ-2 depression scale can be used as an initial screening tool for undiagnosed depression. It consists of the first two questions on the PHQ-9 depression questionnaire (PHQ-9 Depression Scale. AIMS Center: Advancing Integrated Mental Health Solutions). If the patient answers affirmatively to either question, the other seven questions should be asked. If depression is identified, the nurse or provider should connect the patient to his/her primary care provider or to behavioral health for follow-up. See Chapter 7 for additional information on psychosocial effects and nursing interventions for psoriasis.

c. Drugs: Multiple medications have been implicated as inducers of psoriasis including beta-blockers, lithium, antimalarials, interferon, NSAIDs, and tetracyclines. The degree of impact from each of these medications varies. Rapid discontinuation of corticosteroids can lead to exacerbations of plaque and pustular psoriasis. This is why oral prednisone is generally advised to be avoided, and topical steroids should be tapered instead of abruptly stopped.

d. Smoking and alcohol: Smoking and alcohol both have effects on psoriasis. Smoking seems to be a more significant trigger in women, while alcohol may have more impact on the evolution of the disease, particularly in men. Smoking is also strongly associated with pustular psoriasis. Helping patients understand the impact of alcohol and smoking on psoriasis has the potential to significantly impact the course of the disease.

e. Trauma: The Koebner phenomenon (Figure 8-3), a condition induced by trauma to the skin, is common in patients with psoriasis. It was first described by Heinrich Koebner in 1876 as the formation of psoriatic lesions in uninvolved skin of patients after cutaneous trauma. It can be triggered by virtually any form of trauma, such as scratching, picking, rubbing, sunburn, drug eruptions, and tattoos. Patient education is important in the prevention of this type of trigger.

C. Immunopathogenesis

1. Studies indicate that psoriasis is a T-lymphocyte-mediated autoimmune disease. Its pathophysiology is complex, involving parts of the innate and adaptive immune systems, genetics, and the environment. This
interaction of multiple systemic factors results in an increase in antigen presentation and the activation of T-helper cell type 1 (TH1) and T-helper cell type 17 (TH17), resulting in what we recognize as typical cutaneous plaques of psoriasis.

2. The skin lesions of psoriasis are characterized by cells multiplying much more quickly than normal (epidermal hyperproliferation), cells that do not mature normally (abnormal keratinocyte differentiation), and the presence of proinflammatory cells (a lymphocyte inflammatory infiltrate).

3. The T-lymphocyte subsets seen in the early phase of psoriasis and the response to T-lymphocyte targeting therapies strongly suggest that the T lymphocytes are the main players in the pathogenesis of psoriasis. Activated T cells in psoriasis secrete cytokines, which can account for many characteristics of the psoriasis lesions. See Chapter 5 to learn more about immunology and its influence on psoriasis treatment decisions.

D. Comorbidities

1. Since psoriasis and psoriatic arthritis are immunemediated inflammatory disorders, they are associated with multiple comorbidities and cardiovascular risk factors. Patients with psoriasis have an increased risk of atherosclerosis, myocardial infarction, stroke, and cardiovascular death. It has been suggested that overlapping mechanisms of systemic inflammation contribute to the connection between psoriasis and cardiovascular disease.

2. An association with metabolic dysfunction, including obesity and metabolic syndrome (ischemic heart disease, hypertension, nonalcoholic fatty liver disease, diabetes, and obesity), with subsequent effects on morbidity and mortality, has been documented in psoriasis. It is also associated with inflammatory bowel disease (Crohn disease).

3. Psychiatric/psychological comorbidities that are associated with psoriasis include depression, anxiety, suicidal ideation, and poor QOL. Psoriasis often causes significant psychosocial burden affecting all aspects of a person’s life—relationships, social activities, work, and emotional well-being. The collective effect may be self-perpetuating social withdrawal. Health-related QOL studies have measured the burden of psoriasis, and some new studies have attempted to assess the significant cumulative disability over a person’s lifetime. Psoriasis is known to affect QOL and emotional well-being in a way that is comparable with other major conditions, including diabetes, arthritis, and cancer. It is imperative to support patients to discuss their feelings and how the condition affects their lives.

E. Assessment

1. Clinical manifestations and therapeutic modalities: Psoriasis can be classified by its different phenotypes, which include the following:

a. Chronic plaque psoriasis: About 90% of psoriasis is the plaque type and is characterized by well-defined red or salmon-colored, scaly plaques that are usually fairly symmetrically distributed (Figure 8-4). The degree of body surface involvement varies from limited to extensive. The scalp, elbows, knees, and low back/sacral area are the most common sites (Figure 8-5). Hands and feet are also frequently involved. In about 30% of people, the genitals are affected. Treatments range from topical medications (e.g., corticosteroids, vitamin D preparations, coal tar, calcineurin inhibitors) to systemic medications (e.g., methotrexate, acitretin, biologics) and phototherapy for widespread and recalcitrant cases. Depending on the location and severity of the disease, the treatment will need to be individualized to meet the patient’s needs. In clinical trials, a method call Psoriasis Area and Severity Index (PASI) is used to evaluate the
percentage of body involvement and plaque severity evident on the day of the exam. The PASI scores are then evaluated over time. A PASI score is determined based on the amount of erythema, scaling, and thickness of an “average” plaque on the patient and the percentage of body areas affected. The evaluator must be well trained in how to determine the PASI score in order for the assessment to be accurate and consistent throughout the clinic trial. Because of the complexity and tediousness of PASI scoring, it is not typically used in most dermatology clinics.

b. Scalp: Well-demarcated red, scaly plaques on the scalp are usually classic for psoriasis, but it can sometimes be difficult to differentiate from seborrheic dermatitis (Figure 8-6). Posterior or temporal scalp involvement is often suggestive of psoriasis versus a frontal or diffuse scalp flaking that may be more suggestive of seborrheic dermatitis. There is certainly overlap between the two conditions. Scalp psoriasis can be especially distressing to patients due to itching, its visibility, and difficulty in treatment (Figure 8-7). The presence of hair can make application of topical medications very challenging. Solutions and gels are frequently utilized, but if the person has more course or very curly short hair, then oils, creams, or ointments may be appropriate. Very recalcitrant scalp psoriasis may require phototherapy or another systemic treatment such as methotrexate. When there are thick adherent scales, a keratolytic preparation such as salicylic acid and coal tar may be needed.

c. Guttate: Widespread erythematous papules with scale, which may be preceded by streptococcal infection. For this reason, underlying infection should be suspected and treated if present. Often, a throat culture is done in new cases whether or not patient complains of sore throat. Regardless of culture results, many patients are treated empirically for streptococcal infections in new cases of guttate psoriasis with a course of amoxicillin. Guttate lesions are often too widespread for topical therapy, so most patients are started on phototherapy (narrowband ultraviolet B [UVB]). It usually responds well so it is only occasionally necessary to use a more aggressive second-line therapy (Figure 8-8).

d. Inverse psoriasis: Characterized by plaques in the intertriginous areas (axillae, inframammary area, gluteal cleft, umbilicus, abdominal folds, and genital area). These plaques tend to be red, thinner, and without scale (Figure 8-9). The intertriginous areas are usually treated with mild topical steroids. Because they are more at risk for steroid atrophy and striae long term, continuous use of even mild steroids should be avoided, though short courses are appropriate.
Therefore, nonsteroid treatment is often appropriate, such as tacrolimus or pimecrolimus.

e. Erythrodermic: An uncommon but severe and disabling variant of psoriasis occurring in 1.5% of cases characterized by widespread deep erythema and scaling affecting the entire cutaneous surface (Figure 8-10). Withdrawal of systemic steroid therapy, infections, and drugs are frequent causes in erythrodermic exacerbations. Thus, use of systemic steroids in patients with psoriasis should be avoided. Punch biopsies are important to obtain in any erythrodermic patient to rule out erythrodermic T-cell lymphoma and other conditions that can mimic erythrodermic psoriasis. The protective functions of the skin are lost so these patients are susceptible to infection and loss of fluids and nutrients. Cyclosporine is often necessary for rapid control of this form of psoriasis. Methotrexate or biologics are useful for more long-term treatment, but caution is essential given the risk for complications due to immunosuppression and infection.

f. Pustular psoriasis: Localized or generalized noninfectious pustules. It is characterized by pustules, not papules, found on normal or erythematous skin. There are two types, palmoplantar (Figure 8-11) and generalized (Figure 8-12) acute pustular psoriasis. Incidence of palmoplantar is low compared to psoriasis vulgaris and is seen more frequently in smokers. It tends to be chronic with intermittent exacerbations that are limited to the palms and soles. The lesions are sterile, yellow, deep-seated pustules. It is known to be refractory to many therapeutic approaches. Generalized acute pustular psoriasis is rare and life threatening. It is characterized by burning erythema with widespread sterile pustules, fever, malaise, and leukocytosis. These patients are often admitted to the hospital or should be monitored very closely, and a dermatologist
should be called to distinguish this entity from a pustular drug eruption.

g. Nail disease: Occurs in about 50% of people with psoriasis and is more common in those with associated psoriatic arthritis. There are a variety of nail abnormalities associated with psoriasis. The most common change is pitting (Figure 8-13). Loosening of the nail plate from the underlying nail bed, onycholysis, is also fairly common (Figure 8-14). Oil spots may also be seen in the nail bed.

h. Psoriatic arthritis: Psoriatic arthritis is associated with cutaneous psoriasis in 7% to 26% of cases. It is a seronegative inflammatory arthritis that is usually asymmetric (60% to 70% of the time) and involves the proximal and distal joints of the fingers or toes (Figure 8-15). It may also manifest as sausage fingers (dactylitis). The axial form involves the vertebra and sacral joints and occurs approximately 5% of the time. It is a destructive arthritis; therefore, early diagnosis and treatment is critical for optimal control and averting joint destruction, functional disability, and reduced QOL.

2. Diagnostic tests

a. Diagnosis is most often based on clinical findings.

b. Punch biopsy may be considered if diagnosis is unclear.

F. Nursing considerations

1. Medical intervention overview

a. A variety of topical and systemic treatments exist for the management of psoriasis. It is a chronic, lifelong disease with natural exacerbations and remissions that require long-term treatment. There is a range of treatments available to manage the condition, but the response to treatment is unique to each individual. For that reason, finding an effective treatment plan can be a process of trial and error.

b. Eighty percent of psoriasis patients have mild-to-moderate disease, so topical therapies play a central role in the treatment of their psoriasis. Patients usually start with a single type of therapy; however, in more severe cases (>10% body surface area, severely impaired QOL, or recalcitrant psoriatic lesions), multiple treatment approaches may be used as part of combination, successive, or rotational therapeutic regimen.

c. The main treatment options include topical steroids, topical vitamin D, retinoids, phototherapy, oral systemic therapies (methotrexate, acitretin, cyclosporine), and biologic therapies. Recently, laser has been developed as another modality to treat psoriasis.

d. Other topical therapies include the following steroid-sparing agents: coal tar, anthralin, calcineurin inhibitors, keratolytics, and emollients.

e. Therapeutic approaches should take into consideration the main goal of improving the patient’s QOL, the individual patient’s likelihood of adherence, and promoting a therapeutic relationship with the patient (Table 8-1).

2. Medications

a. Topical corticosteroids were first introduced in the early 1950s and have been the most common treatment for psoriasis. They are often the first-line therapy in mild-to-moderate psoriasis but are also used as adjunct therapy in more severe psoriasis. For plaque psoriasis, medium- to high-potency steroids used one to two times a day can lead to significant improvements. Itching, scale, and inflammation improve quickly. Potent topical corticosteroids (e.g., betamethasone dipropionate) and very high-potency (e.g., clobetasol propionate) topical corticosteroids are most effective. Some studies compared vitamin D products directly with potent or very potent corticosteroids and found that they have comparable effects when applied to the body, but corticosteroids were more effective than vitamin D for scalp psoriasis. Combination therapy with a topical vitamin D with topical corticosteroid is more powerful than either alone. On both the body and the scalp, potent corticosteroids were less likely than vitamin D to cause local adverse events, such as skin irritation or burning, so people were consequently more likely to stop using vitamin D products.