Psoriasis and Its Treatment

FACULTY:

Sneha Baxi, PharmD
Clinical Assistant Professor
University of Connecticut School of Pharmacy
Storrs, Connecticut
Clinical Pharmacist
Hospital of Saint Raphael
New Haven, Connecticut

FACULTY DISCLOSURE STATEMENTS:

Dr. Baxi has no actual or potential conflict of interest in relation to this program.

U.S. Pharmacist does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors may express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.

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Pharmacy
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Program No.: 430-000-08-006-H01-P and 430-000-08-006-H01-T
Credits: 2.0 hours (0.20 ceu)

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DISCLAIMER:

Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications or dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities.

GOAL:

To recognize the symptoms of psoriasis, differentiate between the various treatments, and provide patient education.

OBJECTIVES:

At the completion of this article, the participant should be able to:

1. Identify the types of psoriasis.*
2. Recognize the different treatment strategies for the management of psoriasis and the role of topical versus systemic medications.*
3. Recommend nonpharmacologic therapy for treatment, including avoidance of the triggers that may exacerbate psoriasis.
4. Formulate a plan for the treatment of psoriasis that includes dosing, monitoring parameters, and patient education.

*Also applies to pharmacy technicians.

Psoriasis is a chronic disease with a variety of treatment options and strategies. The 18th-century English physician Robert Willan, considered the father of dermatology, is credited with being the first to accurately describe psoriasis.¹ This multifactorial disorder affects 1% to 3% of the population; it is most prevalent in Caucasians and occurs equally among men and women. Age of onset varies according to type of psoriasis, generally occurring at age 20 to 30 years or 50 to 60 years.^1,2

Multiple genetic and environmental factors are involved in psoriasis. The genetic component is not well understood; however, the disease affects more than one immediate family member in approximately 30% of patients with psoriasis, and the incidence is higher in monozygotic twins than in dizygotic twins. There is an 8.1% chance of developing psoriasis when one parent has the disease; the risk increases to 41% when both parents have it. Additionally, certain genes have been identified that increase the likelihood of developing psoriasis by nine to 15 times normal.²

Exogenous factors may precipitate or aggravate psoriasis. See TABLE 1 for the various psoriasis triggers. Cold weather is thought to increase dry skin (conversely, warm weather and sunlight may improve psoriasis in 80% of patients). Koebner’s phenomenon is the development of psoriasis after injury to the skin. These injuries include endogenous and exogenous causes such as photosensitivity, dermatitis, herpes zoster, abrasions, burns, bites, shaving, surgery, and tattoos, among others. Streptococcal pharyngitis and HIV type 1 appear to be triggers. Stress is thought to worsen psoriasis in approximately 40% of patients. Certain medications may trigger or exacerbate the disease.^3-7

Psoriasis is a lifelong condition with both physical and psychological effects. Patients may experience anywhere from one or two localized, scaly patches to widespread patches on the skin’s surface that can cause itching, burning, and pain. Quality of life frequently is affected. Patients often are embarrassed by the plaques and may become depressed or withdrawn. Patients with psoriasis have been found to have lower self-confidence and increased rates of substance abuse.⁸

Table 1

Precipitating/Exacerbating Triggers for Psoriasis

Environment Cold weather

Physical trauma (Koebner’s response)

Infection

Stress

Medication Lithium, beta-blockers, antimalarials, systemic steroids, nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, tetracyclines, interferons

Allergy

Diet

Alcohol binge

Smoking

Pathophysiology

Psoriasis is a tissue-specific autoimmune disorder in which there is interplay between infiltrating leukocytes, resident skin cells, many proinflammatory cytokines, chemokines, and chemical mediators. Psoriasis has both a genetic and a cellular basis. The human leukocyte antigen Cw*0602 was found in about 50% of patients with psoriasis versus 10% of healthy controls in a study conducted in northern Europe.⁹ Genetic analysis has shown that certain chromosomes contain susceptible loci for psoriasis. On a cellular level, much histopathologic action takes place. The redness of the plaques is due to the growth and dilation of superficial blood vessels. Additionally, hyperplasia of the epidermis occurs that involves acanthosis (thickening) and differentiation changes. In psoriasis, the life cycle of the skin cells is altered; the keratinocytes proliferate and mature rapidly, and therefore terminal differentiation is incomplete. There is a proliferation of keratinocytes secondary to activation of T lymphocytes that leads to cytokine release. The stratum corneum is formed with improper adhesion, leading to the scales or flakes of the lesions. Normally, the skin cell’s life cycle is 28 to 30 days; in psoriasis, the life cycle may be three to four days, and therefore the cells build up on one another, forming the scales.

Types of Psoriasis⁸

There are several different types of psoriasis: plaque, guttate, flexural (inverse), pustular (localized or generalized), erythrodermic, palmar-plantar, scalp, and nail psoriasis, in addition to psoriatic arthritis (TABLE 2). Diagnosis is generally made according to the characteristic features of each type. Depending on the type of psoriasis, lesions may occur on the face, ears, hands, feet, genitalia, intertriginous areas, scalp, nails, trunk, or extremities. Plaque psoriasis is the most common form, occurring about 80% to 90% of the time.¹⁰

Table 2
Some Types of Psoriasis and Their Therapies
Type	Characteristics	Areas of Involvement	Therapies
Plaque	Deeply erythematous Sharply demarcated Oval Moderate: Heavy, silvery-white surface	Scalp Extensor surface Fold areas (abdomen, gluteal)	Mild: Topical therapies • Corticosteroids • Tazarotene • Calcipotriene • Anthralin • Coal tar • Keratolytic agents • EmollientsModerate-to-severe: Phototherapy, MTX, cyclosporine, oral retinoids, SC etanercept, IM/IV alefacept, biological agents
Guttate	Acute eruption Teardrop-like Erythematous Scaly	Trunk (mainly) Face Scalp Hands Feet	Phototherapy +/– tar Photochemotherapy Topical agents Systemic agents prn
Flexural (Inverse)	Smooth, inflamed patches	Skin folds (axillae, breasts, groin)	Topical steroids Emollients MTX
Pustular	Pus-filled Blister-like patches	Hands Feet Palms/soles (palmar-plantar pustulosis)	Oral retinoids MTX Cyclosporine Phototherapy Immunobiologicals Hospitalization
Erythrodermic	Skin surface red & scaly	Nearly all of body	Hospitalization Cyclosporine MTX Oral retinoids +/– photo(chemo)therapy
MTX: methotrexate; SC: subcutaneous; IM: intramuscular.

Effect of Diet on Psoriasis¹¹

Although there is no definitive evidence that certain foods worsen psoriasis, some studies have shown a link between psoriasis and diet. Psoriasis may be improved with a low-calorie or vegetarian diet, possibly secondary to decreased arachidonic acid intake, which increases anti-inflammatory cytokines. Additionally, alcohol intake can aggravate skin lesions by causing a release of histamine.

Some researchers believe that a subgroup of patients with psoriasis may also have gluten intolerance, but currently there is no recommendation to avoid gluten-containing foods (e.g., pasta, cereal, bread, pastries). In general, if a patient notices that his or her psoriasis worsens after certain foods, those foods should be avoided. Further research is being conducted regarding the link between foods and psoriasis.

Treatment

Nonpharmacologic treatments are generally utilized in conjunction with pharmacotherapy. Self-care is limited to those patients with mild cases of psoriasis. In cases where 10% or more of the body-surface area is involved, in children less than 2 years of age, or in recalcitrant cases, patients should be referred to their primary care physician.^2,12

Patients should be counseled to avoid triggers such as stress, smoking, and alcohol. Dry skin is a trigger factor, and therefore emollients may be used to hydrate the stratum corneum to minimize water loss, lubricate the skin, and relieve pruritus. Emollients need to be administered several times a day and should be applied to the lesions within three minutes of bathing for the most occlusive effect. Side effects of emollient use are fairly uncommon, but may include folliculitis or contact dermatitis. Patients should bathe in warm water with lubricating bath products two to three times a week.²

Sunlight and tanning-bed treatment may improve psoriatic lesions. Patients should apply sunblock to the unaffected areas to protect their skin. If a tanning bed is used, treatment should start at a few minutes a day and be gradually increased as tolerated.

Balneotherapy is the treatment of disease by means of bathing in therapeutic water, thereby stimulating circulatory processes, accelerating cell activity, and dilating the tissues and vessels. Balneotherapy has a high success rate because of the salinity of the water, and the natural exposure to ultraviolet (UV) A in these places has been shown to be safe, effective, and pleasant. The Dead Sea in Israel, the Kangal Hot Springs in Turkey, and the Blue Lagoon in Iceland are some places where balneotherapy is practiced.^2,13

Narrowband UVB phototherapy and excimer laser phototherapy are other nonpharmacologic options for the treatment of psoriasis. Natural sunlight often improves psoriasis; similarly, UVB phototherapy at wavelengths of 310 to 315 nm (narrowband UVB) has proven to be effective for treating plaque-type psoriasis. It is thought that UVB phototherapy slows keratinization and induces apoptosis of pathogenic T cells. Excimer lasers mainly treat isolated plaques, and the method requires fewer treatments at a smaller UV radiation dose.² Phototherapy that combines a systemic psoralen and UVA (PUVA; developed in the 1970s) works on the hyperproliferative effects of psoriasis. Topical and systemic therapies may be combined with PUVA to increase effectiveness. The various treatments also may be rotated to reduce PUVA side effects.¹⁴ PUVA has been associated with squamous cell carcinomas; in general, UVB therapy is considered safer than PUVA.¹⁵ Patients should be instructed to wear protective clothing and avoid sunlight the day after UVB or PUVA treatment and to get an ophthalmic examination yearly.⁵

Pharmacotherapy includes both topical and systemic medications. Topical treatment is generally considered first-line therapy and is usually utilized in localized psoriasis. In generalized psoriasis, topical and systemic treatment may be combined. Different strategies for treatment—sequential therapy, rotational therapy, and combination therapy—also may be used. In combination therapy, agents that have different mechanisms of action are administered together to provide synergistic or additive efficacy; this improved efficacy, in turn, allows lower doses or concentrations to be used, thereby potentially decreasing the adverse effects. Sequential therapy has three phases: clearing, transitional, and maintenance. In the clearing phase, a rapid-acting agent (which usually correlates to higher toxicity) is used; then, in the transitional phase, the rapid-acting agent is tapered and the longer-term medication, which will be used in the maintenance phase, is initiated. Rotational therapy means starting with one medication and then switching to another medication in order to minimize the cumulative toxic effects.^2,16,17

Topical corticosteroids affect gene transcription by anti-inflammatory, antiproliferative, and immunosuppressive actions, thereby decreasing erythema, scaling, and pruritus. Topical steroids take rapid effect and are available in multiple dosage forms (ointment, cream, lotion, and solution) and different strengths (TABLE 3), both prescription and OTC. The Stoughton-Cornell classification system ranks the topical steroids by vasoconstriction potency. Class I agents have the highest potency and are reserved for short-term use on small body-surface areas. High-potency agents are used when the psoriasis is refractory to treatment with lower-potency agents or for the short-term treatment of thick, chronic plaques. Class VII agents are considered the safest and are recommended for longer-term use and in infants and young children. These lower-strength agents are used on the face, groin, axillae, and any other area where the skin is thinner because natural occlusion occurs, thus increasing the agent’s potency. On other areas of the body, therapy is usually initiated with medium-potency agents. Although topical steroids have limited systemic adverse effects, their long-term use may cause side effects including cutaneous atrophy, telangiectasia, striae, acne, hypothalamus-pituitary-adrenal axis suppression, and growth retardation in children. Rapid flare-up of disease is common upon treatment discontinuation.^2,16,17

Vitamin D and its analogs are thought to have hypoproliferative effects on epidermal cells and to normalize keratinocytes. Calcipotriene 0.005% (available as ointment, cream, or solution) is indicated for plaque, scalp, and nail psoriasis as monotherapy or as combination therapy with topical corticosteroids. It is shown to work on the lesions by reducing the thickness and scaling. Due to its slow onset of action, it may take six to eight weeks of therapy to see an outcome. Adverse effects are mild and include dermatitis, dry skin, skin irritation, and burning sensation. A more serious side effect is hypercalcemia, which may occur with long-term use of higher-strength calcipotriene.^2,18

Table 3

Potencies of Various Topical Steroidsa

Low Potency

Dexamethasone Hydrocortisone, hydrocortisone acetate—     all strengths & formulations Methylprednisolone acetateMedium Potency

Betamethasone valerate Hydrocortisone butyrate, hydrocortisone valerate Mometasone furoate Triamcinolone acetonide 0.025%-0.1% High Potency

Triamcinolone acetonide 0.5% Kenalog cream & ointment Aristocort ointment 0.1% Diflorasone diacetate Clobetasol propionate Betamethasone dipropionate

aBased on USP potency ratings and vasoconstrictive potency ratings. Source: Reference 2.

Coal tar is one of the oldest therapies for the treatment of psoriasis and is thought to work by suppressing epidermal DNA synthesis. Coal tar is available OTC and in the following dosage forms: cream, ointment, lotion, shampoo, bath oil, and soap. It is usually used in conjunction with UV therapy, but it can be used as monotherapy or with topical corticosteroids. Coal tar’s adverse effects are minimal and usually limited to folliculitis; however, because of its messiness, odor, and tendency to stain clothing, this therapy may be unappealing to some patients. Bedtime application is recommended to minimize staining of fabric.

Salicylic acid 1.8% to 3% may be used for treatment because it loosens the psoriatic plaques by decreasing skin pH and increasing keratin hydration. Topical application to thick scales and scalp psoriasis usually is effective in seven to 10 days; the lowest possible concentration should be used to minimize adverse effects. Salicylic acid should not be used in intertriginous areas such as the armpits and genitals.¹²

Second-line topical agents for psoriasis are anthralin and tazarotene. Anthralin 0.1% to 1% is available in cream, ointment, and solution forms. It works by resolving hyperproliferation, hyper- and parakeratosis, epidermal accumulation of polymorphonuclear leukocytes, and dermal inflammation. A cotton-tipped applicator or a gloved hand should be used to apply anthralin directly to thick, large plaques for a short contact time, initially once daily. Contact time is usually initiated at one minute and may be gradually increased to 10 to 30 minutes. The cream should be removed by washing or showering with acidic soap; the ointment should be removed by gently swabbing the area with a soft paper towel and then washing with acidic soap and applying an emollient. Anthralin stains most surfaces and may irritate any skin around the plaque it contacts. Anthralin is generally safe and effective; because of the staining and irritation, however, patients may be hesitant to utilize it first-line.

The first receptor-selective retinoid approved for the topical treatment of psoriasis is tazarotene gel, available in 0.05% to 0.1% concentrations. The gel, which is applied once daily, works by decreasing inflammation and normalizing the proliferation and differentiation of keratinocytes. It is used to reduce plaque elevation in mild-to-moderate psoriasis and is usually combined with topical corticosteroid therapy. Unlike corticosteroids, tazarotene has been shown to maintain clinical response.¹⁹ Side effects include skin irritation and increased photosensitivity. Similar to the oral retinoids, tazarotene is a Pregnancy Category X drug.^2,19,20

Systemic agents are generally recommended for patients with moderate-to-severe disease. Moderate disease is defined as greater than 5% body-surface area involvement; severe disease is defined by greater than 10%. Other factors must be considered when classifying psoriasis, including how disabling it is and how it affects the patient’s quality of life.¹⁸

The oral retinoid acitretin is indicated for patients with severe erythrodermic and generalized pustular psoriasis and for adjunctive treatment in plaque psoriasis. Acitretin is a derivative of vitamin A and is thought to correct abnormal cell differentiation in the keratinocyte nucleus. Acitretin may be combined with UVB or photochemotherapy to achieve higher response rates, better tolerance, and lower UV exposure.

Cyclosporine is a T-cell suppressor, inhibiting the first phase of T-cell activation as well as the release of inflammatory mediators for certain cells. Cyclosporine should be initiated at 2.5 mg/kg/day and may be increased to 5 mg/kg/day. Doses greater than 5 mg/kg/day are associated with increased risk of nephrotoxicity, and use for more than two years is associated with increased risk of malignancies. Additionally, cyclosporine interacts with many medications because it is extensively metabolized in the liver by the CYP450 3A enzyme system.^2,20

Methotrexate is a folic-acid antagonist with effectiveness similar to that of cyclosporine in the treatment of severe psoriasis, especially if refractive to topical or phototherapy; it also is used to treat psoriatic arthritis and nail disease. It is thought to have antiproliferative effects on DNA synthesis as well as immunosuppressive effects on activated T cells. Methotrexate is dosed weekly orally or by injection and may be incrementally increased as needed.

Table 4
FDA-Approved Systemic Medications for Psoriasis
Medication	Dose	Monitoring Parameters	Adverse Effects	Patient Education
Acitretin	25-50 mg/day po	Lipids (especially TG); liver function; blood glucose; pregnancy	Dry lips/cheilitis; dry mouth, nose, eyes, skin; pruritus; scaling; alopecia	• Wait 3y after discontinuing   before becoming pregnant. • Food increases absorption,   tolerability.
Cyclosporine	2.5-50 mg/day po	Liver & renal functions; BP; lipids; serum electrolytes	GI discomfort; hypertrichosis; gingival hyperplasia; headaches	• Grapefruit juice may   increase drug concentration. • Many drug-drug interactions
MTX	Initial: 7.5-15 mg/wk po; increase by 2.5 mg every 2-4 wk	CBC; liver & renal function; chest x-ray	Nausea & vomiting	• May supplement with oral   folic acid.
Infliximab (Remicade)	Induction: 5 mg/kg IV at wk 0, 2, 6 Maintenance: 5 mg/kg every 8 wk	Liver function; TB skin test; BP	Abdominal pain; fatigue; headache	• May bleed more easily. • Monitor for signs of   infection, allergic reaction.
Etanercept (Enbrel)	(Plaque) Initial: 50 mg SC twice weekly (3-4 days apart) × 3 mo Maintenance: 50 mg SC weekly	Serum chemistry; signs/symptoms of infection	Headache; tiredness; mild skin rash/itching	• Rotate injection site. • Keep refrigerated.
Alefacept (Amevive)	IM: 15 mg once weekly x 12 wk IV: 7.5 mg once weekly x 12 wk	CD4+ T-lymphocyte count weekly	Chills; dizziness; headache; nausea	• Monitor for signs of   infection, allergic reaction.
Efalizumab (Raptiva)	0.7 mg/kg SC initially, then 1 mg/kg/wk	Platelet count	Headache; infection; chills; nausea; pain	• Monitor for signs of   thrombocytopenia.
TG: triglycerides; GI: gastrointestinal; BP: blood pressure; MTX: methotrexate; CBC: complete blood count; TB: tuberculosis; SC: subcutaneous; IM: intramuscular.

Another antimetabolite that can be used as an alternative treatment for psoriasis (although not FDA-approved for this use) is 6-thioguanine initiated at 80 mg twice daily to a maximum of 160 mg three times a week. This agent may be beneficial in patients with liver complications because it seems to be less hepatotoxic than methotrexate. Common adverse effects include bone marrow suppression, nausea, vomiting, and stomatitis. Additionally, hydroxyurea 1 g/day increased to 2 g/day may be considered for patients with liver disease or for patients at risk for adverse effects from other agents. Hydroxyurea works by inhibiting the S phase of the DNA cycle. It is not as effective as methotrexate, but it is an option for patients who are unable to tolerate methotrexate.²⁰ Similar to the other antimetabolites, hydroxyurea may cause bone marrow suppression as well as cutaneous reactions and leg ulcers.

Two other medications utilized for alternative treatment of severe psoriasis are mycophenolate mofetil and tacrolimus, which are most commonly prescribed for organ-transplant rejection. These medications are not FDA-approved for psoriasis treatment. Tacrolimus is dosed orally at 0.05 mg/kg/day, up to 0.15 mg/kg/day, for the treatment of recalcitrant plaque-type psoriasis. Tacrolimus ointment has been studied for descaling and occlusion but appears not to be effective in clinical practice.² Mycophenolate mofetil has antiproliferative effects on specific lymphocytes and it reversibly blocks de novo synthesis of guanine nucleotides. Further clinical trials of these medications are needed to determine their safety and efficacy. Both tacrolimus and mycophenolate mofetil have numerous toxicities and drug interactions.^2,20

Infliximab, etanercept, alefacept, and efalizumab are biologic therapies that alter the immune response and are used in the treatment of psoriasis. Infliximab (a chimeric monoclonal antibody) and etanercept (a dimeric) are tumor necrosis factor (TNF)-alpha blockers. TNF-alpha is found in large amounts in psoriatic lesions, and infliximab and etanercept work in different ways to inhibit the synthesis of cytokines and induction of the expression of intracellular adhesion molecules. Etanercept 50 mg subcutaneously one to two times a week is approved for the treatment of chronic moderate-to-severe plaque psoriasis and psoriasis with arthropathy. Common adverse effects are local injection-site reaction, infections in the respiratory and gastrointestinal tract, gastrointestinal disturbances, and rash. Infliximab is approved for severe chronic plaque psoriasis and psoriasis with arthropathy. The induction therapy is 5 mg/kg IV at weeks 0, 2, and 6, followed by administration every eight weeks. Hypersensitivity reactions, headaches, fever, chills, fatigue, and diarrhea are common adverse effects. Alefacept is a recombinant fusion protein that works by preventing T-cell activation and, perhaps, the apoptosis of T cells as well, by binding to CD2 on memory effector T cells. It is approved for the treatment of plaque psoriasis and may be given as a once-weekly dose IV or intramuscularly for a total of 12 weeks. CD4+ T-lymphocyte count should be monitored; if it falls below 250 cells/mL, treatment should be withheld. Patients also should be monitored for allergic reactions and signs and symptoms of infection. An additional 12-week course of therapy may be considered after a 12-week break from Cycle 1.^20-23

Efalizumab, an immunosuppressant, binds to CD11a, thereby inhibiting T-cell activation in the epidermis and dermis. It is indicated for treatment of moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy. Initial conditioning dose is 0.7 mg/kg, with a subsequent dose of 1 mg/kg/wk subcutaneously (maximum total dose 200 mg).²⁴

Herbal Remedies^24,25

Some patients may be using herbal remedies for their psoriasis; these substances are not well studied or proven effective, however. Some herbs used for psoriasis are aloe vera, burdock, evening primrose, figwort, red clover, Chinese foxglove, Chinese angelica (dong quai), salvia (dan shen) root, and licorice. These substances are thought to relieve psoriasis by reducing inflammation, modulating cytokine production, or inhibiting angiogenesis. Before herbal remedies can be recommended, more studies examining their effectiveness and safety are needed.

Conclusion

Psoriasis is a chronic disease that affects a patient physically and psychologically. Many different treatments and strategies are available to achieve disease control. It is vital to consider the efficacy of the various treatments as well as their toxicities because it is the balance of the efficacy and toxicity, as well as tolerability and ease of use, that will determine the best course of treatment initially, during flare-ups, and for maintenance.

REFERENCES

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26. Barnes J, Anderson LA, Phillipson JD. Herbal Medicines. 2nd ed. London, England: Pharmaceutical Press; 2002.

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