Patients with psoriasis can present with multiple levels of involvement and with different types of the chronic condition. Accordingly, this author discusses the presentation of the condition, offers keys to diagnosis and reviews a variety of treatment options, including topical agents and combination therapy.
A patient presents to the office with symmetric, sharply demarcated, erythematous, silver-scaled patches on the back of the heels and ankles. The right foot is sore and has dried blood from constant scratching. Your immediate differential is tinea pedis, drug eruption, contact dermatitis, irritant dermatitis, eczema or psoriasis.
A history reveals the patient has siblings with similar issues only on other areas of the body. A full body exam reveals that there is some flaking of the scalp and scaling on the neck. The patient has some yellow toenails that have yet to respond to oral antifungals despite two courses of such medication. Clotrimazole (Lotrimin), recommended by the internist, has not provided any resolution of the scaling and pruritus. What is the likely diagnosis? Psoriasis.
As podiatrists, we can see all types of psoriasis from the most common plaque type to the least common pustular psoriasis form. The other types (guttate, inverse, erythrodermic) occur rarely in the foot and ankle. Once one recognizes psoriasis and rules it in as the correct dermatosis in question, the management/treatment depends on the type of psoriasis, extent of the disease, area of involvement and percentage of skin involved. Other factors include whether there is a known arthritis component or other comorbidities as well as the patient’s background or lifestyle. In podiatry, we generally will see those with localized psoriasis. The majority of patients with psoriasis have mild or limited psoriasis, which is generally defined as less than 20 percent body involvement.1
Psoriasis is characterized by inappropriate activation of the cellular immune system directed against self-antigens.2 It is mediated by the T lymphocyte of the skin and is the most prevalent T cell–mediated inflammatory disease in adults.3 Psoriasis occurs as part of a complex set of interactions among genetic, immunological, systemic and environmental factors.4
Psoriasis causes significant physical and psychosocial suffering. A study conducted in 2009 revealed that the psychosocial morbidity of psoriasis and impairment of quality of life is the same or worse than arthritis, diabetes or cancer.5
Psoriasis is one of the most prevalent immune diseases and affects nearly 2 to 3 percent of the Caucasian population, including over 7 million Americans and an estimated 125 million people worldwide.6,2 It affects approximately 1.3 percent of the African-American population in the United States. Generally, it is more common in individuals living at higher latitudes or in colder locales, and is less common in individuals who have greater sun exposure.
The incidence of psoriasis is much lower in dark-skinned West Africans and African-Americans than in light-skinned people of European ancestry. The incidence is also low in the Japanese and Eskimos, and is extremely low to non-existent in Native Americans in both North and South America.7
How Psoriasis Develops
In a normal human, skin cells normally take about a month to develop, mature and move to the skin’s surface, where they are continually shed. Turnover of the epidermis allows the skin to maintain its barrier function, repair injured skin in wound healing and receive the signals that stimulate or inhibit cell proliferation. In psoriasis, the skin cells mature in less than a week and move to the surface where they accumulate, resulting in the formation of scales among the red, inflamed tissues.8
Psoriasis is a hyperproliferative disorder of keratinocytes.9 The lesions of psoriasis are distinctive. They begin as red, scaling papules that coalesce to form round-to-oval plaques, easily distinguishable from the surrounding normal skin.10 The primary psoriatic lesion is an erythematous papule topped by a loosely adherent scale. Removing the silvery scales induces trauma to the underlying dilated capillaries and results in pinpoint bleeding at the site of the lesion, a finding known as the Auspitz sign.6 The scales “flake” off continuously and cause cracking, dryness and pain.
The old “academic” definition, seen on board exams and in class, notes that the silvery scales with pinpoint bleeding is not the norm for there is a wide range of skin presentations. These presentations are not in a vacuum as the individual may have rubbed, scratched, soaked or warmed the area. Before presenting to your office, the patient may have used an array of topical agents and the area may have cleared and relapsed several times.
Pruritus and burning are the main symptoms. Dogra and colleagues found pruritus to be present in 95 percent of their cases while burning was present in 15 percent.11 General measures for control of pruritus include keeping the skin cool and moisturized, and avoiding irritating fabrics. Ice packs may help stop the itching. Patients can apply a heavy moisturizing cream twice daily to help control scaling and pruritus. The podiatrist should prescribe specific pharmacologic measures on the basis of the patient’s history of psoriasis and overall medical condition.
What Factors Can Precipitate Or Exacerbate Psoriasis?
There are many “irritants,” both endogenous and exogenous, which affect psoriasis of the foot and lower legs. The endogenous irritants are varied. Some drugs may exacerbate or precipitate psoriasis. These include beta-adrenoceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, non-steroidal anti-inflammatory drugs and anti-malarial drugs. Chloroquine (Aralen, Sanofi Aventis), lithium and mepacrine have been linked with severe deterioration of psoriasis.12 Systemic oral steroids will rapidly clear the plaques but may also worsen the flare and evolve into pustular psoriasis when the steroid use stops. Smoking and alcohol consumption may contribute to worsening psoriasis.
Any object that comes in contact with the skin and rubs it or changes the “climate” of the skin can have an effect. The exogenous “irritants” that potentiate the skin response involve the Koebner phenomenon.13 The isomorphic response of Koebner occurs when skin lesions develop at the site of trauma and nowhere is there more trauma than the foot. Trauma can be the normal rubbing and scratching by the patient but it can also occur with orthotics, ankle foot orthotics, vascular hose or short and long leg casts. Therefore, any of our patients with psoriasis who need an orthotic or a cast are at potential risk for developing worsening skin conditions at that site. Other triggers that lead to the Koebner phenomenon are excoriation, sunburns and maceration.13
As surgeons, we should be aware of this entity and warn our patients about its possible occurrence.14 In podiatry, we routinely use knives and sanding discs to remove thick calluses. If there is a patient with cracks on the rim of the heel, it is not unusual to debride the skin so a moisturizer can “heal” the fissures. However, in psoriasis, the mere “debriding” or “burring” of the skin equates to “trauma” of the skin. This can potentiate or increase scale production, and negatively impact the patient.
A Guide To Making A Differential Diagnosis
Psoriasis may occasionally resemble atopic dermatitis or eczema. However, it will usually be thicker, redder and more sharply demarcated than eczematous lesions. Psoriasis usually affects the extensor surfaces whereas eczema typically involves the flexor surfaces.15
Psoriatic plaques may occasionally resemble seborrheic dermatitis, tinea infections, cutaneous T-cell lymphoma, ichthyosis, secondary syphilis and Reiter’s syndrome. Other differential diagnoses include contact dermatitis, stasis dermatitis, nummular dermatitis, candidiasis, drug eruption and mycosis fungoides.
As podiatric physicians, we may see patients before the internists or pediatrician. Accordingly, we are on the frontlines and often act as the “triage” doctor as we decide what other specialists are needed for the best care for the patient. When it comes to patients with psoriasis, you must look at the whole body for other sites of skin involvement to help key into their diagnosis or diagnoses. Look at the face, neckline, hairline, elbows and knees. Patients with psoriasis have increased cardiovascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, obesity and smoking.6 Those who have childhood obesity are also at risk.
In the cases in which physical examination and clinical history are not diagnostic, skin biopsy may be indicated to make the diagnosis. I would recommend two 2-mm or 3-mm punches in the center of the “inflamed” area. If the scaling only affects a small area of the foot and does not show up elsewhere on the body, it is advantageous to biopsy.
We are at a disadvantage in comparison to the dermatologists or internists who have a larger “playing field” and more skin to observe. While one does want to do full body exams, it is not always feasible in terms of time. In my practice, I routinely biopsy any skin that scales and skin for which I do not have a definite diagnosis. I would also make it a point to biopsy on the spot if the patient is in the office for the “skin” problem. If the finding is secondary to another issue of more concern, schedule the biopsy for another visit.
Pertinent Insights On The Classification Of Psoriasis
There are varied clinical presentations of psoriasis. It has been broadly classified into non-pustular and pustular psoriasis. Non-pustular psoriasis is more common and can be organized into plaque, guttate, inverse and erythrodermic psoriasis. The plaque type is more common and occurs in 85 to 90 percent of patients with psoriasis. It is also known as psoriasis vulgaris.16 The lesions are often symmetrical.16 As podiatrists, we see the following phenotypes: the classic plaque type, the palmoplantar type, the interdigital type and nail psoriasis.
Different studies show different results. Under the “plaque” phenotype, one study observed that the most common sites of involvement in descending order of frequency were trunk, limbs, scalp, face, palms-soles and flexures.17 The second most common clinical phenotype was palmoplantar psoriasis followed by flexural psoriasis.17 Kaur and co-workers reported the scalp (25 percent) as the most common first site of involvement followed by legs (20.6 percent) and arms (11.7 percent).18
Pustular psoriasis. This is an uncommon form of psoriasis and presents as studded with tiny, superficial, sterile pustular lesions. There are two forms of pustular psoriasis: localized and generalized. In the localized form, the disease is confined to hands and feet, and tends to be chronic.19 The usual bacterial organism in the blood of pustular psoriasis is Staphylococcus aureus. High dosages of oral corticosteroids for a period of time are among the more common precipitating factors. One may see pustular psoriasis of the nail unit, known as acrodermatitis continua, which starts as pustules under the nail and can result in extensive destruction of the nail plate.20
Palmoplantar psoriasis. Also uncommon, this disabling condition significantly impairs quality of life due to the fact that it can limit the use of one’s hand to do work and can cause significant pain with walking. Although palm and sole psoriasis affects a small (less than 5 percent) portion of the total cutaneous surface, the impact of palm and sole psoriasis on quality of life is out of proportion to the small percent of body surface area affected.21
The physical examination can show erythematous scaly patches and fissured hyperkeratotic psoriatic plaques of both the palmar and plantar surfaces. The differential for pustular psoriasis includes: chronic eczema, reactive arthritis (Reiter’s syndrome), paraneoplastic acrokeratosis and superficial fungal infection.
Nail psoriasis. Nail involvement is common in psoriasis and can be the initial and only site of involvement in some patients. The morphology of nail changes depends on whether the nail matrix, nail bed or hyponychium has been affected. Nail involvement is more common in those who have concurrent psoriatic arthritis. Bedi noted nail changes in 74 percent of patients with plaque or palmoplantar psoriasis while isolated nail affliction occurred in 6 percent of cases.17 Various nail changes observed in descending order of frequency were pitting, nail plate thickening, partial onycholysis, subungual hyperkeratosis, yellow-brown discoloration, paronychia and complete onycholysis.22
Changes in the nail matrix include: pitting, leukonychia (white patches under the nails), red spots in the lunula and nail plate crumbling. Within the nail bed, we see onycholysis, splinter hemorrhage, oil spot or oil drop patches (salmon or pink colored blotches on the surface of the nail) and hyperkeratosis.13 The oil-drop sign is virtually pathognomonic for psoriasis.23 Other changes include onychauxis, Beau’s lines and transverse depressions.
In psoriatic arthritis, an inflammatory reaction results in microtrauma to the joints and the entheses. Research has shown the nail to be functionally integrated with entheses associated with the distal phalanx that provides anchorage to the skin and joint.24
The finding of nail disease in the patient increases the possibility of the patient having psoriatic arthritis. Many studies have shown that 10 to 20 percent of those with psoriasis will get psoriatic arthritis.25 The same inflammatory changes, namely T-cell proliferation, that affect the skin can affect the joints. Among the most common joints affected are the hands and feet (distal interphalangeal joints), and the spine.26 Psoriatic arthritis can affect virtually any joint of the body, producing a wide variety of arthritic changes and joint deformity. Psoriatic arthritis can destroy joints, similar to rheumatoid arthritis.
Researchers have investigated the types and severity of nail disease by using the modified nail psoriasis severity score index (mNAPSI).27,28 The severity of fingernail disease in psoriatic arthritis patients was significantly associated with distal interphalangeal joint disease. The study authors felt treatment of the nail disease is more of an arthritis issue than a “dermatological” issue.
Essential Treatment Considerations
Since treatment depends on the type of psoriasis, let us take a closer look at the more common plaque psoriasis, palmoplantar psoriasis and nail psoriasis.
In plaque and palmoplantar psoriasis, the three pathogenic factors that we want to resolve are abnormal keratinocyte differentiation, epidermal hyperproliferation and inflammation of the skin. These three factors result in pruritus and burning.
It is helpful to understand the traditional therapies used for psoriasis before we review the newer modalities. The oldest one is coal tar. It is a first line treatment for scalp, hand and foot psoriasis. It has anti-inflammatory, antibacterial, antipruritic and antimitotic effects. Coal tar has been in use for more than 100 years and was the mainstay for treating inflammatory skin conditions before the development of topical steroids.29
The anti-inflammatory effects of tar are usually not as pronounced as those of topical glucocorticoids or calcineurin inhibitors. Tar preparations are useful in reducing the potency of topical glucocorticoids required in the long-term maintenance therapy of psoriasis.30
Soaking the area in water seems too easy but superficial hyperthermia delivered biweekly via simple water bath immersion can clear mild to moderate psoriatic lesions. It can also reduce edema and relieve pruritus for up to several months.31
Many individuals organize modalities into first, second and third lines of treatment. Emollients are a requirement in all of the different “tiers” of treatment. Emollients are the mainstay of all skincare regimens and help moisturize dry skin. In regard to psoriasis, emollients soften scaling and reduce irritation.13 Emollients are available as creams, ointments, lotions, shower gels, bath oils and aerosol sprays. They offer relief from dryness, scaling, itching and cracking, and may also have an anti-proliferative effect.
First-line treatment involves topical therapies. Second-line therapy includes phototherapy and systemic drugs. Third-line treatment involves biologic therapy. If you are comfortable with systemic medications, including biologics, this is within the scope of our expertise. However, a dermatologist may have more practice with the systemic medications and biologics from his or her training.
A Guide To Topical Agents For Psoriasis
First-line options include keratolytics, topical corticosteroids, topical retinoids (vitamin A analogues), vitamin D analogues such as calcipotriol (Daivonex, CSL Biotherapies), calcitriol (Rocaltrol, Roche) or tacalcitol, and coal tar preparations.
Keratolytics thin and soften the skin, and cause the stratum corneum to loosen and shed, removing the dead skin. Urea, salicylic acid and lactic acid are the more popular agents. These are present in many of the products we use such as Foot Miracle (Foot Miracle), 45% urea nail gel (Uramaxin, Medimetriks Pharmaceuticals) and Kerasal (Alterna). Use these at low concentrations for general thinning of skin.
Calcipotriene 0.005% (Dovonex, Warner Chilcott) is a vitamin D3 analogue that inhibits epidermal cell proliferation and enhances cell differentiation. It is available as a cream and recently came out as a foam. Most studies show that calcipotriene is not as effective as group I corticosteroids but regimens using calcipotriene and group I corticosteroids are superior over either agent alone.32
Most patients now use the following regimen. Apply calcipotriene in the morning and a group I corticosteroid in the evening for two weeks. Then begin a maintenance regimen using group I corticosteroids twice daily on weekends and calcipotriene twice daily on weekdays. Application for six to eight weeks gives a 60 to 70 percent improvement in plaque-type psoriasis.32
Topical steroids are in use most often for plaque and palmoplantar psoriasis. Topical steroids give fast but temporary relief. They are most useful for reducing inflammation and controlling itching. Initially, when the patient is introduced to topical steroids, one will usually see spontaneous clearing of the skin in a few treatments. However, tachyphylaxis or tolerance occurs, and the medication becomes less effective with continued use.
Ultrapotent topical corticosteroids are the mainstay of podiatric psoriasis treatment, whether one uses them as monotherapy or in combination with a topical vitamin D analogue. The more common ones include betamethasone dipropionate (Diprosone, Diprolene, Schering Plough) and clobetasol (Clobex, Galderma Laboratories). My patients use them twice a day for two weeks to resolve inflammation and pruritus.
When it comes to psoriasis, ointment is the most common treatment vehicle because of its soothing effect and occlusive nature. Ointments also provide the highest potency for any dermatoses. However, a recent study showed that betamethasone dipropionate 0.05% in optimized cream used once a day compared well with the standard betamethasone ointment.33
Recent studies demonstrate that poor adherence to topical treatment is common among patients with psoriasis and contributes to poor treatment outcomes. Non-ointment topical corticosteroid products exhibit excellent efficacy in clinical practice.
Much of the poor outcomes in psoriasis, even tachyphylaxis, likely relate less to actual medication failure and more to failure to apply the medication.34 Topical psoriasis treatment is likely to be more successful when podiatrists and patients discuss what type of vehicle the patient will use and plan treatment accordingly. Almost any lesion of psoriasis can completely resolve with topical therapy alone when clinicians use traditional tar preparations, anthralin (Dithranol) or topical corticosteroids with or without salicylic acid.35
Topical retinoids are thought to normalize abnormal keratinocyte differentiation, reduce epidermal hyperproliferation and decrease inflammation, resulting in a more normal expression of skin differentiation in psoriatic lesions. As podiatrists, we routinely use calcipotriene, a vitamin D analogue and less frequently use other active forms of vitamin D like calcitriol and tacalcitol (Curatoderm). One can also use the vitamin A analogues isotretinoin and acitretin (Soriatane, GlaxoSmithKline).
In one study, topical tazarotene (Stiefel), a topical retinoid (0.1% cream), was less effective than topical clobetasol propionate 0.05% cream in the treatment of plaque psoriasis.1
How Effective Is Combination Therapy?
The prevailing thinking is that a combination approach enhances the efficacy of the vitamin D analogue and limits the toxicity of the corticosteroid.
There is a multitude of topical preparations that can treat psoriasis. In one study, researchers used calcipotriol/betamethasone dipropionate (Dovobet) and compared it to calcipotriol alone.36 There was higher efficacy and a quicker onset of action with the Dovobet.
I will use Dovonex one day and the steroid the other day, or Dovonex in the morning and a steroid at night. One commonly used strategy is to use Dovonex twice a day on weekdays and a high- to super-potency topical steroid twice a day on weekends.
The two-compound ointment containing calcipotriene 50 mcg/gm plus betamethasone dipropionate 0.5 mg/gm (Dovobet or Daivobet and Taclonex, Leo Pharma) combines a vitamin D analogue and a corticosteroid. Patients apply this once each day and it is indicated for the topical treatment of psoriasis in adults 18 years and older. Patients can use the ointment acutely for four to eight weeks to bring psoriasis under control. After this, patients can maintain control of the disease with once-a-day application as needed.10
What You Should Know About Phototherapy And Lasers
Phototherapy is a mainstay in the treatment of extensive plaque type psoriasis. It is rarely in use in the podiatry community due to the facts that podiatrists rarely treat extensive plaque psoriasis and the cost of ultraviolet phototherapy equipment.
Phototherapy is available as psoralen plus UVA, broadband UVB and narrowband UVB. The typical regimen is three times a week for three months. For some people, psoriasis can deteriorate upon exposure to sunlight.37 Psoralens increases the skin’s sensitivity to ultraviolet light, including sunlight. One would use psoralens to improve the effectiveness of ultraviolet light therapy for psoriasis.
Some studies have found that the earliest changes in psoriatic lesions concern abnormal microvasculature. In these scenarios, laser therapy could be a possible treatment.38,39
One study looked at the Nd:YAG 1064 nm laser as this laser can penetrate up to the deeper abnormal psoriatic vasculature.38 The effects are comparable to treatment with the well established calcipotriol/betamethasone dipropionate ointment. The study found the use of the Nd:YAG laser was not of additional value in the array of treatment modalities for chronic localized plaque psoriasis.
In another study, researchers found the monochromatic excimer light (308-nm) to be an effective and safe treatment modality for patients with mild to moderate psoriasis vulgaris and palmoplantar psoriasis.39 The excimer laser is an example of targeted phototherapy and one can use it when a patient has more localized areas of plaques as one would find on the foot. An excimer laser uses a combination of an inert gas and a reactive gas to create an excited dimer or excimer, which gives rise to laser light in the ultraviolet range.40
Pulsed dye laser therapy can be effective in clearing psoriasis plaques but the mechanism of action is only partially understood.41 This therapy might be an alternative treatment for nail psoriasis.42
Key Insights On The Potential Of Biologics
Biologics comprise a new class of treatment for psoriasis and patients take them by intravenous infusion.
Different from the traditional systemic drugs that impact the entire immune system, biologics target specific parts of the immune system. The biologics treat psoriatic diseases by blocking the action of T cells or by blocking proteins (such as tumor necrosis factor-alpha or interleukins 12 and 23) in the immune system. These cells and proteins all play a major role in developing psoriasis and psoriatic arthritis.43
The more common biologics include: infliximab (Remicade, Janssen Biotech); etanercept (Enbrel, Amgen and Pfizer); adalimumab (Humira, Abbott Laboratories); and ustekinumab (Stelara, Janssen Biotech).
Matching The Best Treatment For The Type Of Psoriasis
Palmoplantar psoriasis tends to be resistant to conventional therapies and may last for several years. Treatment options remain unsatisfactory for patients with palmoplantar psoriasis and palmoplantar pustular psoriasis.44 Topical treatments are usually ineffective but, depending on the area of involvement of the sole/foot, one can try the topical combination of Dovonex and betamethasone as a first-line treatment. Systemic therapy with oral retinoids and psoralen plus ultraviolet A light phototherapy is frequently required although it rarely leads to remission.45 Biologics may also be effective in the treatment of sole psoriasis.
One of my patients had total resolution of her severely disabling plantar psoriasis with one year of phototherapy that was coupled with six months of etanercept. She is still plaque free at the time of this publication.
The treatment options for nail psoriasis include topical or interlesional steroids, photochemotherapy, topical fluorouracil, topical calcipotriol, topical anthralin, topical tazarotene, topical cyclosporine, avulsion therapy, and systemic therapy for severe cases. If all 10 nails are involved, do not try topical therapy and instead educate the patient or make a referral to a dermatologist who treats psoriasis. One should also remember the close association of nail disease and psoriatic arthritis, and contemplate a referral to a rheumatologist.
High-potency corticosteroid solution or ointment under occlusion with cellophane wrap at bedtime can improve nail psoriasis. A recent study tested a water-soluble nail lacquer, which contains hydroxypropyl chitosan (Vitivia, Innocutis), horsetail extract (Equisetum arvense) and methylsulfonylmethane (DMSO2).46 This product, which recently became available, was effective in strengthening the nails and reducing fragility and roughness in brittle nails. At the end of treatment, patients showed a 72 percent reduction in pitting, a 66 percent reduction in leukonychia, a 63 percent reduction in onycholysis and a reduction of 65 percent in the NAPSI score in comparison to baseline.
Another study also reviewed the use of tacalcitol ointment (a vitamin D3 analog) and a new formulation containing 8% clobetasol-17-propionate in a colorless nail lacquer vehicle that has produced good results for the control of nail psoriasis.46
Intralesional steroids with the use of triamcinolone acetonide suspension of 2.5 mg/mL into the proximal nail fold are very helpful for nail matrix psoriasis (e.g., pitting, ridging, leukonychia). One may administer this medication every four to six weeks. Clinicians would spray the proximal nail fold first with a refrigerant spray for anesthesia and give the injection with a 30-gauge needle. I have found that digital anesthesia makes the steroid injection less painful.
At present, there are three systemic medications (methotrexate, retinoids and cyclosporine) that clinicians most commonly use for nail psoriasis. A recent study found that a low dose of methotrexate (5 mg) once a week successfully treated severe nail psoriasis involving all 20 nails.47
One can perform surgical avulsion therapy for psoriatic nail disease when other treatments have failed. During surgery, one can cauterize or surgically remove the matrix to prevent regrowth of the nail. Whether this “traumatic” event will result in worsening of the condition is unknown.
Dr. Morse is the President of the American Society of Podiatric Dermatology. He is a Fellow of the American College of Foot and Ankle Surgeons, and the American College of Foot and Ankle Orthopedics and Medicine. Dr. Morse is board certified in foot surgery. He is on the Podiatric Residency Educational Committee at the Washington Hospital Center.
1. Angelo JS, Kar BR, Thomas J. Comparison of clinical efficacy of topical tazarotene 0.1% cream with topical clobetasol propionate 0.05% cream in chronic plaque psoriasis: A double-blind, randomized, right-left comparison study. Indian J Dermatol Venereol Leprol. 2007; 73(1):65.
2. Habif TP. Principles of Diagnosis and Anatomy. In: Clinical Dermatology, 5th Edition, Chapter 1, Elsevier, St. Louis, 2010.
3. Koo JYM, Siebenlist J. Vitamin D analogues in the treatment of psoriasis. In: Roenigk HH, Maibach HI, eds. Psoriasis, 3rd edition, Marcel Dekker, New York, 1998, pp. 497-510.
4. Green L. An overview and update of psoriasis. Nurs Stand. 2011; 25(35):47-55.
5. Warren R. Adalimumab for the treatment of psoriasis. Expert Rev Derm. 2009; 4(1):15–21.
6. Ferri F. Ferri’s Clinical Advisor, 1st edition, Mosby, St. Louis, 2012.
7. Available at http://www.skincarephysicians.com/psoriasisnet/faqs.html#14 .
8. Available at http://www.psoriasis.org/ .
9. Tuzun Y, Dolar N, Keskin S, Wolf R. Disorders of cell kinetics and differentiation. Dermatol Clin. 2007; 25(4):589-95.
10. Habif TP. Papulpsquamous Diseases. In: Clinical Dermatology, 5th Edition, Chapter 8, Elsevier, St. Louis, 2010.
11. Dogra S, Yadav S. Psoriasis in India: prevalence and pattern. Ind J Dermatol Venereol Leprol. 2010; 76(6):595-601.
12. British Association of Dermatologists, Primary Care Dermatology Society. Recommendations for the Initial Management of Psoriasis, 2009. Available at www.bad.org.uk/site/622/default.aspx .
13. Mendez-Fernandez MA. Koebner phenomenon: what you don’t know may hurt you. Ann Plast Surg. 2000; 44(6):644-5.
14. Gelmetti C. Therapeutic moisturizers as adjuvant therapy for psoriasis patients. Am J Clin Dermatol. 2009; 10 Suppl 1:7-12.
15. Levine D, Gottlieb A. Evaluation and management of psoriasis: an internist’s guide. Med Clin N Am. 2009; 93(6):1291-1303.
16. Sullivan-Whalen M, Gilleaudeau P. Psoriasis: Hope for the future. Nurs Clin N Am. 2007; 42(3):467-84.
17. Bedi TR. Clinical profile of psoriasis in North India. Indian J Dermatol Venereol Leprol. 1995; 61(4):202-5.
18. Kaur I, Handa S, Kumar B. Natural history of psoriasis: a study from the Indian subcontinent. J Dermatol. 1997; 24(4):230-4
19. Das J. Pustular psoriasis: treatment with antibiotics. Indian J Dermatol Venereol Leprol. 1996; 62(5):312-3.
20. Baden HP. Nail abnormalities associated with cutaneous diseases. In: Diseases of the hair and nails. Year Book Medical Publishers, Chicago, 1987, pp. 48-51.
21. Menter A, et al. Guidelines of care for the management of psoriasis. Dermatol Venereol Leprol. 1995; 61:202-5.
22. Jiaravuthisan MM, Sasseville D, Vender RB, et al. Psoriasis of the nail: Anatomy, pathology, clinical presentation, and a review of the literature on therapy. J Am Acad Dermatol. 2007; 57(1):1-27.
23. Scher RK. Psoriasis of the nail. Dermatol Clin. 1985; 3(3):387-94.
24. McGonagle D, Benjamin M, Tan. The pathogenesis of psoriatic arthritis and associated nail disease: not autoimmune after all? Curr Opin Rheum. 2009; 21(4):340-347.
25. Husni ME. Psoriatic Arthritis in Cleveland Clinic: Current Clinical Medicine, 2nd Edition, Saunders, Philadelphia, 2010.
26. Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis. J Am Acad Dermatol. 2008; 58(5):851-64.
27. Rich P, Scher RK. Nail psoriasis severity index: a useful tool for evaluation of nail psoriasis. J Am Acad Dermatol. 2003; 49(2):206-212.
28. Rich P, Scher RK. Modifications of the nail psoriasis severity index [author’s reply]. J Am Acad Dermatol. 2005; 53(4):746-747.
29. Leong L. How I use coal tar in dermatology. Singapore Medl J. 1990; 31(6):614-615.
30. Kliegman. Nelson’s Textbook of Pediatrics, 19th edition, Saunders, Philadelphia, 2011.
31. Boreham DR, Gasmann HC, Mitchel RE. Water bath hyperthermia is a simple therapy for psoriasis and also stimulates skin tanning in response to sunlight. Int J Hypertherm. 1995; 11(6):745-54.
32. Ye R, Hobson G, Loupenok L, Weiss S. Chemical compatibility of calcipotriene 0.005% foam in combination with topical steroids. J Am Acad Dermatol. 2011; 64(2 Supp 1):AB154.
33. Chuang TY, Samson CR. 0.05 percent betamethasone dipropionate in optimized cream vehicle for psoriasis. Cutis. 1989; 43(2):178-82.
34. Zivkovich AH, Feldman SR. Are ointments better than other vehicles for corticosteroid treatment of psoriasis? J Drugs Dermatol. 2009; 8(6):570-2.
35. Pasricha JS. Treatment of the so-called incurable skin diseases. Ind J Dermatol Venereol Leprol. 1993; 59:159-67.
36. Saraceno R. Efficacy, safety and quality of life of calcipotriol/betamethasone dipropionate (Dovobet) versus calcipotriol (Daivonex) in the treatment of psoriasis vulgaris: a randomized, multicentre, clinical trial. J Dermatol Treat. 2007; 18(6):361-5.
37. Nalluri R. Photoaggravated hand and foot psoriasis. Photodermatol Photoimmunol Photomed. 2010; 26(5):261-262.
38. Van Lingen RG, de Jong EM, van Erp PE, et al. Nd: YAG laser (1,064 nm) fails to improve localized plaque type psoriasis: a clinical and immunohistochemical pilot study. Eur J Dermatol. 2008; 18(6):671-6.
39. Han L. Evaluation of 308-nm monochromatic excimer light in the treatment of psoriasis vulgaris and palmoplantar psoriasis. Photodermatol Photoimmunol Photomed. 2008; 24(5):231-236.
40. Lapolla W. A review of phototherapy protocols for psoriasis treatment. J Am Acad Dermatol. 2011; 64(5):936-949.
41. Rácz E. Cellular and molecular effects of pulsed dye laser and local narrow-band UVB therapy in psoriasis. Lasers Surg Med. 2010; 42(3):201-10.
42. Oram Y. Pulsed dye laser in the treatment of nail psoriasis. Dermatol Surg. 2010; 36(3):377-81.
43. Available at http://www.psoriasis.org/page.aspx?pid=455 .
44. Brunasso AM, Salvini C, Massone C. Efalizumab for severe palmo-plantar psoriasis: an open-label pilot trial in five patients. J Eur Acad Dermatol Venereol. 2009; 23(4):415-419.
45. Guimera-Martin-Neda F, Rodriguez-Garcia C, Perez-Robayna N, et al. Adalimumab for severe palmoplantar psoriasis: An open-label pilot trial in nine patients. J Am Acad Dermatol. 2011; 64(2 Suppl 1):AB158.
46. Sanchez Regana M, Martin Ezquerra G, Umbert Millet P, Llambi Mateos F. Treatment of nail psoriasis with 8% clobetasol nail lacquer: positive experience in 10 patients. J Eur Acad Dermatol Venereol. 2005; 19(5):573-7.
47. Yu J, Lee Y. Severe nail psoriasis successfully treated by low dose methotrexate. Dermatology Online Journal. 2009:15(11). Available at http://dermatology.cdlib.org/ .