Vitamin D analogs (eg, calcitriol, calcipotriol, and tacalcitol) can be used as monotherapy or in combination with topical corticosteroids for added benefit and steroid-sparing effect.12 Tazarotene, a topical retinoid, is also best used in combination with a topical corticosteroid. Salicylic acid (2%–10%) is a keratolytic (removes scale) used to soften psoriatic plaques and enhance penetration of topical steroid preparations. A less messy coal tar derivative, liquor carbonis detergens, can be mixed with topical steroids in concentrations of 5% to 10% as a steroid-sparing measure.
Emollients, especially petrolatum-containing products, are considered a standard part of treatment, utilized to retain moisture in the stratum corneum, and they will increase the local penetration of topical steroid preparations. Petrolatum ointment bases also have an antipsoriatic effect and can be alternated with gradual withdrawal of topical steroids for the maintenance stage of topical plaque psoriasis treatment. Coal tars, although effective, are less frequently used in current practice because of their malodorous nature, associated folliculitis, and propensity to stain skin and clothing.5
Topical calcineurin inhibitors are occasionally used (eg, tacrolimus and pimecrolimus) and have large molecules, so they do not penetrate the skin as readily as topical corticosteroids and are therefore recommended for use on thin-skinned areas, such as the body folds.
Small, resistant plaques of psoriasis may respond to intralesional steroid injections. Triamcinolone is most commonly used, with a concentration of 2.5 to 10 mg/mL injected into the mid-dermis of psoriatic plaques with a maximum of 2 to 3 mL of local injections every 6 to 8 weeks. Small amounts (0.1- to 0.2-mL aliquots) of the topical steroid (diluted to the above concentrations with xylocaine, saline, or sterile water) are injected into the mid-dermis with a spacing of approximately 1 cm between injection sites.
Phototherapy is an integral aspect of psoriasis treatment used for both extensive disease and for limited disease with debilitating symptoms. Ultraviolet light is locally immunosuppressive but typically lacks the systemic immunosuppression encountered with traditional oral antipsoriatic drugs and biologic agents. All candidates for phototherapy or photochemotherapy should undergo a complete history and physical examination. Systemic lupus erythematosus and xeroderma pigmentosum are absolute contraindications to phototherapy, whereas extensive photodamage, photosensitivity disorders, history of melanoma, atypical nevi, and immunosuppression (especially organ transplantation), among others, are relative contraindications.16 A history or suspicion of porphyria is also a contraindication for phototherapy. Persons with blonde or red hair or freckles and who always sunburn but never tan generally should not have phototherapy. If they do, low doses should be administered with extreme caution.
Phototherapy often consists of traditional ultraviolet B (UVB) therapy. The cumulative dose administered needs to be calculated and the skin monitored, with treatments often 3 to 5 times a week. Narrow-band UVB may provide a faster response rate than traditional UVB light with a lower total number of joules of energy required for a response. Ultraviolet A (UVA) penetrates deeper into the skin and is combined with the administration of a topical or systemic psoralen that acts as a photosensitizer to increase the local effect of the UVA treatments. This band length is associated with pigment darkening and an increased long-term incidence of squamous cell carcinomas.
The 5 most commonly used traditional systemic medications are sulfasalazine, acitretin, methotrexate, oral psoralens combined with UVA light (PUVA), and cyclosporine. These agents should be considered when suboptimal response has been achieved from the use of topical steroids, steroid-sparing topical agents, intralesional steroids, or phototherapy. Sulfasalazine and acitretin have a low adverse effect profile with significant reduction in the PASI.17 Sulfasalazine has been associated with allergic drug reactions, and gastrointestinal intolerance may be limiting factors.
Acitretin is an effective systemic agent that complements topical treatments and can be used with phototherapy.18 Patients should be monitored for hypertriglyceridemia and dry eye, nose, mouth, and skin. Given the possibility of teratogenicity, acitretin should not be used in women of childbearing potential; 13 cis-retinoic acid can be considered for short periods as an alternative but should be combined with oral contraceptives and not used in pregnant patients. In addition, acitretin may delay the occurrence of skin cancers related to previous phototherapy or other sources of photodamage. Sulfasalazine may help psoriatic arthritis, but acitretin does not benefit arthritis symptoms.
Methotrexate can treat psoriatic arthritis symptomatically, often with lower doses than needed for skin clearing (0.2–0.4 mg/kg per week in a single dose). Patients must be carefully monitored for myelosuppression (low hemoglobin, white blood cell count, platelets) and hepatotoxicity when on methotrexate. Cyclosporine can be used in low doses (3–5 mg/kg per day) for 1 to 2 years, and patients should be monitored for nephrotoxicity, hypertension, and potential drug interactions. Oral psoralens can also photosensitize the skin and when combined with UVA light decrease the amount of light needed for a therapeutic response.
Biologic agents are the newest class of antipsoriatic agents (Tables 2 and 3). They are considerably more costly than traditional systemic agents, and drug plan coverage is important to consider before prescribing these agents. Biologic agents are indicated if more than 10% of the body is involved with psoriatic plaques, and an individual has failed on 2 or more systemic agents. Biologic agents (Tables 2 and 3) can be categorized into 3 main groups: (1) anti-T cells (eg, alefacept and efalizumab), (2) tumor necrosis factor α inhibitors (eg, adalimumab, etanercept, infliximab, ustekinumab), and (3) interleukin-12 and interleukin-23 inhibitors (ustekinemab). On the PASI scale, all biologic agents demonstrated efficacy in reducing moderate to severe psoriasis after a 12-week period of use as compared with placebo.18 Biologic agents target the immune system; therefore, patients must be periodically monitored for symptoms of infection and malignancy.19 These therapies are generally considered safe, but rare, serious adverse effects, such as infections, reactivation tuberculosis, malignancy, and demyelination of nerve fibers, have been reported.20,21
Intertriginous psoriasis (see Figure, Intertriginous psoriasis photo), also known as inverse psoriasis or flexural psoriasis, is characterized by thin, sharply demarcated, shiny erythematous plaques. Scale is minimal to absent, and as the name suggests, typical locations include the axillae, behind the ears, under the breast, intergluteal cleft, and inguinal crease.
Other causes of intertrigo that should be distinguished from IP include Candida intertrigo, erythrasma, fungal infection, seborrheic dermatitis in infants, and contact allergic or irritant dermatitis.22 Bacterial culture and sensitivity can be obtained if secondary bacterial infection (impetiginized crusts or local pain with secondary perianal cellulitis) is suspected, as Staphylococcus or Streptococcus is known to colonize psoriatic skin lesions.23 Microscopic KOH examination of surface scale (red annular border with central clearing) can distinguish IP from a fungal infection of the groin (tinea cruris).
Erythrasma presents with hyperpigmented, slightly erythematous, and scaly plaques due to corynebacterial infection. The involved skin will fluoresce coral red under Wood light examination, whereas tinea versicolor has a yellow fluorescence. Evaluation for seborrheic dermatitis and contact irritant or allergic dermatitis is usually confirmed on history or with examination of lesions elsewhere. Occasionally, the application of a suspected topical contact allergen to a normal patch of skin (the size of a silver dollar twice a day for 2 or 3 days) on the forearm below the elbow crease will confirm a diagnosis of contact allergy, and the specific agent can be confirmed with patch tests of the components in the topical preparation. A skin biopsy is occasionally required if the clinical presentation of an intertriginous eruption is not diagnostic and more unusual etiologies, such as lichen planus, are suspected.
Management of IP involves short-term treatment (2-4 weeks) with low- to mid-potency topical steroids. The frequency of application can be tapered and ultimately discontinued if the psoriasis improves. Frequent, long-term use of topical steroids in fold areas can result in atrophy, striae, and telangiectasias. For continued therapy beyond 2 to 4 weeks, other topical options (calcipotriene, calcitriol, pimecrolimus, or tacrolimus) should be initiated; alternatively, low-dose topical steroids can be used once or twice weekly for maintenance therapy.24
PUSTULAR PSORIASIS: LOCALIZED AND GENERALIZED
Pustular psoriasis is an uncommon manifestation of psoriasis characterized by an eruption of sterile pustules. Four patterns, 3 generalized and 1 localized, have been proposed:
- The von Zumbusch pattern is characterized by abrupt onset of erythema, pustule formation, and fever, followed by pustule resolution and extensive scaling. This form of psoriasis may be life threatening.
- Annular pattern consists of erythematous, scaly, annular lesions with pustules at the annular advancing border.
- The exanthem type presents as an acute eruption of small pustules that resolve within days often without systemic symptoms.13 If systemic symptoms are present, they include recurrent fever followed by a new wave of pustule formation, weakness, and weight loss.25
- The localized pattern (see Figure, Localized pustular photo), in which pustules appear predominantly on the palms or soles and often within or at the periphery of psoriatic plaques. This condition is more common in women, especially smokers. Smoking cessation may improve the clinical symptoms and signs.
Risk factors for PP include infections, pregnancy (historically referred to as impetigo herpetiformis and now more commonly called PP of pregnancy), oral corticosteroid therapy (relatively contraindicated in persons with psoriasis), hypocalcemia, stress, and irritating topical therapy.21 The most important differential diagnosis is acute generalized exanthematous pustulosis (AGEP). This condition is an acute, febrile drug reaction characterized by small, sterile pustules with a background of erythema. Unlike generalized pustular psoriasis (GPP), AGEP is often associated with intense pruritus and other skin manifestations, such as vesicles (fluid-filled blisters less than a cm), purpura, and erythema multiforme–like lesions. In addition, AGEP typically occurs within 1 to 2 days following ingestion of the offending drug. A skin biopsy may also help differentiate GPP and AGEP.21
A 2012 task force of the National Psoriasis Foundation Medical Board26 recently issued a consensus paper on the treatment of PP. According to this report, first-line therapies include cyclosporine, methotrexate, and acitretin with psoralens plus ultraviolet A (PUVA) and the biological agents’ (infliximab, etanercept, and adalimumab) are considered second-line agents. The authors stress that disease severity and patient comorbidities should govern therapeutic decision making, as factors such as teratogenicity need to be considered.26
Erythrodermic psoriasis (EP) (see Figure, Erythrodermic psoriasis) is a rare but potentially life-threatening form of psoriasis characterized by generalized erythema and scaling. It may occur in patients with preexisting psoriasis or present de novo as the initial sign of psoriasis. Precipitating factors include excessive application of topical steroids, withdrawal from systemic steroids, systemic illness, emotional stress, phototherapy burns, alcoholism, and irritating topical therapy.27
Erythrodermic psoriasis can be acute or chronic with variable severity; some patients present with a rapid, intense onset that necessitates hospitalization and aggressive intervention, whereas others experience a protracted, waxing-and-waning course. Nail involvement, if present, ranges from mild pitting to severe dystrophy. The most common systemic findings include fever, chills, malaise, fatigue, weight loss, pruritus, and peripheral edema.27 Depending on the extent of exfoliation, complications such as dehydration, protein loss, hypothermia, and infection may occur.
The differential diagnosis of EP encompasses other causes of generalized erythroderma, including contact allergic dermatitis, atopic dermatitis, and drug reactions, along with a number of less common causes (pityriasis rubra pilaris, sarcoidosis, infections, seborrheic dermatitis [especially in infants], and erythrodermic cutaneous T-cell lymphoma). A personal or family history of psoriasis, presence of plaque-type psoriatic lesions previously, psoriatic nail changes, and inflammatory arthritis suggest a diagnosis of EP. If the diagnosis is uncertain, punch skin biopsies (2 or 3 sites may be required) should be performed.28
Erythrodermic psoriasis is a rare disorder, and data on the efficacy of treatment options are consequently limited. According to a 2010 task force of the National Psoriasis Foundation27 Medical Board, first-line therapy for severe, acute cases includes the rapidly acting agents cyclosporine and infliximab. Methotrexate and acitretin are other first-line agents, but their slightly delayed onset of action renders them appropriate for less acute cases or for patients with a contraindication to cyclosporine or infliximab. Combination therapy (concomitant use of 2 of the aforementioned agents) may also be considered for severe or refractory disease.27 Evidence for the efficacy of biologics in the treatment of EP is limited to case reports and case series, with the exception of 1 multicenter, retrospective study that compared outcomes in 28 patients.29 In this study, 48% of cases treated with infliximab, 50% of cases treated with adalimumab, and 40% of cases treated with etanercept reported greater than 75% improvement based on the PASI scores.29
Regardless of the systemic therapy chosen, patients should be closely monitored for signs of infection, high output cardiac failure, malabsorption, anemia, and decreased liver/renal function. Supportive care may include warming blankets (as these individuals tend to lose thermoregulation), topical emollients (only expose a local region of the body at any time), sequential wet compresses or soaks, or oatmeal baths followed by emollient or other topical applications.29,30 Topical steroids (low potency for the face and intertriginous folds, and medium potency for the trunk and extremities) may be used, but high-potency topical steroids are best avoided as they can exacerbate erythroderma and may lead to adrenal insufficiency, especially on withdrawal.29 It is recommended that disease severity and comorbidities guide the treatment strategy.28
Guttate psoriasis typically manifests as an acute eruption of monomorphic, pink, oval papules with silvery scale on the trunk and extremities of adolescents and young adults. Like EP, GP can present as an acute flare of established psoriasis or as a harbinger of occult psoriatic disease in adolescents or young adults. Also similar to EP, GP can assume an acute or chronic form.30 Few studies have examined the clinical course of GP, but recent evidence suggests that 33% to 38% of patients progress to CPP.30,31 Although older individuals are less often affected, they appear to have a less favorable outcome with higher rates of progression to chronic disease.31 Nail involvement and arthritis are less common in GP compared with non-GP, affecting only 3% and 11%, respectively, of patients with GP versus 27% and 32% of patients with non-GP.32 The most commonly reported systemic symptom is pruritus.30
Other diseases that mimic GP include pityriasis rosea, nummular eczema, secondary syphilis, drug reactions, and viral rashes.33 Risk factors for an initial episode of GP include a family history of psoriasis, emotional stress, and recent streptococcal pharyngitis.34 An association between GP and an elevated antistreptolysin O titer or infection with Streptococcus pyogenes is well established in the literature, although a pathogenic mechanism that links these entities has yet to be elucidated. Evidence suggests that antistreptococcal therapies do not confer a therapeutic advantage in the treatment of GP.34–38 In addition, the development of scarlet fever or poststreptococcal sequelae in patients with GP has not been reported.37
There is no consensus on the optimal treatment for GP and no published trials examining efficacy of commonly used topical therapies or phototherapy.41 Thus, the therapeutic armamentarium for GP mirrors that of plaque psoriasis. Tar preparations, topical corticosteroids, vitamin D analogs, and phototherapy are frequently used, although comparative data are lacking.39
PSORIASIS FOR THE WOUND CARE SPECIALIST
Protection and effective management of periwound skin are an integral component of wound healing. It also poses a significant challenge for wound care specialists and is of major concern for patients. Periwound skin is a vulnerable area for psoriatic patients because of the Koebner phenomenon, where traumatized skin more easily flares with psoriasis 1 or 2 weeks later. Maceration of the skin (due to overhydrating the stratum corneum keratin) by wound exudate and skin stripping due to adhesive dressings is also a source of skin damage and trauma. Liquid barrier films (film-forming liquid acrylates) can be used as a protective but flexible coating to cover tissue at risk of maceration. Several small-scale studies have demonstrated the efficacy of these films in decreasing epidermal stripping when wound-dressing adhesives are removed.40,41 Other options include petrolatum, zinc oxide ointment, or windowed adhesive dressings.
Peristomal psoriasis is also a common problem (see Figure, Periostomal psoriasis photo), and psoriasis in this region is associated with chronic moisture and irritation. Topical or intralesional corticosteroids can be used for treatment of peristomal psoriasis, as well as selecting an adhesive that minimizes trauma.42 In order to protect the adhesion of the ostomy wafer, intralesional corticosteroids are often useful if a normal wear time of 5 to 7 days is expected; topical steroids in the form of a spray or lotion are often better suited to having an appliance applied with adhesive over the local site. To avoid atrophy, the intralesional steroid applications should be repeated no more frequently than every 4 to 6 weeks. Topical applications are also infrequent with moderate to potent steroids if applications are only with appliance change every 3 to 7 days. Clinicians should be aware that preparations with high alcohol content will often burn and sting with application to open skin with erosions or ulceration.
In a consensus statement regarding management of peristomal and periwound moisture-associated dermatitis, prevention was emphasized as a critical step in management of these patients. Stool leakage is a major causative factor in peristomal dermatitis and psoriasis. Prevention of leakage through use of an appropriate pouch system is critical to resolving the problem. The opening of the skin barrier device must also be individualized. This can be accomplished through cutting the device into the size and shape of the stoma. The use of a convex rather than a flat appliance can also be considered if the stoma lumen is below skin level or if the stoma is located in an area in which skin folds or creases obstruct the area when sitting or performing daily activities of living. Skin barrier paste, strips, rings, powder, and belts can also be used to optimize placement of the skin barrier and decrease local trauma and subsequent appearance of psoriasis with the Koebner phenomenon.43
Psoriasis in the orthopedic patient presents unique challenges. In postsurgical patients with psoriasis, infection rates can range from 17% to 21% postarthroplasty.44 In a series of 27 psoriatic patients undergoing arthroplasty, 11% developed immediate postoperative complications related to a severe exacerbation of psoriasis or skin necrosis.44 Patients with psoriatic arthritis undergoing orthopedic foot surgery also had higher rates of postoperative infections (9.1%) compared with those with osteoarthritis and rheumatoid arthritis.45
Psoriasis can be present with leg ulcers as a bilateral lower-extremity eruption with or without coexisting vascular disease. The differential diagnosis includes stasis dermatitis and contact dermatitis. These chronic skin outbreaks and associated venous, mixed, or arterial leg ulcers can have a significant impact on quality of life, with the majority of patients experiencing pain, reduction in outdoor mobility, and difficulty with finding appropriate footwear.46 Treatment includes high compression therapy in the absence of arterial disease (ankle brachial pressure index [ABPI] >0.8) or modified compression with mixed venous and arterial disease (ABPI 0.6–0.8) to control the edema, which will also help to improve the psoriasis. Because an abrasive contact layer dressing adhesive may trigger the Koebner phenomenon, nonadhesive or soft silicone products should be utilized. Therefore, the wound care physician must monitor the patient frequently to determine the appropriate treatment.
In summary, psoriasis can present in multiple forms: chronic plaques, intertriginous, pustular, erythrodermic, and guttate subtypes. Systemic associations include arthritis with the skin and joint disease having psychological sequelae. A thorough history and physical examination at the time of presentation should document the extent, severity, and subtype(s) of psoriasis. The examination should also include examination of the scalp, nails, and intertriginous skin.
Multiple topical and systemic treatment options are available, and therapy should be directed according to the type and severity of psoriasis. Mild to moderate psoriasis can often be treated with topical steroids and steroid-sparing topical agents that may need to be supplemented with intralesional steroids or ultraviolet light. Systemic drugs (>10% body surface area) and biologic agents (>10% and failure of 2 systemic treatments) are typically reserved for those with moderate to severe presentations with inadequate topical therapy responses.
1. von de Kerkof P, Schalkwijk J. Psoriasis. In: Rapini RP, Jorizzo JL, Bolognia JL, eds. Dermatology. 2nd ed. Mosby Elsevier: Spain; 2008: 125–49.
2. Farber EM, Bright RD, Nall ML. Psoriasis. A questionnaire survey of 2,144 patients. Arch Dermatol 1968; 98: 248–59.
3. Coimbra S, Figueiredo A, Castro E, Rocha-Pereira P, Santos-Silva A. The roles of cells and cytokines in the pathogenesis of psoriasis. Int J Dermatol 2012; 51: 389–95.
4. Raychaudhuri SP. A cutting edge overview: psoriatic disease. Clin Rev Allergy Immunol 2013; 44: 109–13.
5. Brazzelli V, Carugno A, Alborghetti A, et al. Prevalence, severity and clinical features of psoriasis in fingernails and toenails in adult patients: Italian experience. J Eur Acad Dermatol Venereol 2012; 26: 1354–9.
6. Leibovici V, Hershko K, Ingber A, Westerman M, Leviatan-Strauss N, Hochberg M. Increased prevalence of onychomycosis among psoriatic patients in Israel. Acta Derm Venereol 2008; 88 (1): 31–3.
7. Prey S, Paul C, Bronsard V, et al. Assessment of risk of psoriatic arthritis in patients with plaque psoriasis: a systematic review of the literature. J Eur Acad Dermatol Venereol 2010; 24 (Suppl 2): 31–35.
8. Ackermann C, Kavanaugh A. Economic burden of psoriatic arthritis. Pharmacoeconomics 2008; 26: 121–9.
9. Gelfand JM, Neimann AL, Shin DB, Wang X, Margolis DJ, Troxel AB. Risk of myocardial infarction in patients with psoriasis. JAMA 2006; 296: 1735–41.
10. Kaye JA, Li L, Jick SS. Incidence of risk factors for myocardial infarction and other vascular diseases in patients with psoriasis. Br J Dermatol 2008; 159: 895–902.
11. Christophers E. Comorbidities in psoriasis. Clin Dermatol 2007; 25: 529–34.
12. Cohen SN, Baron SE, Archer CB. Guidance on the diagnosis and clinical management of psoriasis. Clin Exp Dermatol 2012; 37 (Suppl 1): 13–18.
13. Naldi L, Gambini D. The clinical spectrum of psoriasis. Clin Dermatol 2007; 25: 510–8.
14. Langley R, Reich K. In touch with psoriasis: a patient-centred approach to therapy. J Eur Acad Dermatol Venereol 2011; 25 (Suppl 4): 1–2.
15. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad Dermatol 2009; 60: 643–59.
16. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy. J Am Acad Dermatol 2010; 62 (1): 114–35.
17. el-Mofty M, el-Darouti M, Rasheed H, et al. Sulfasalazine and pentoxyifylline in psoriasis: a possible safe alternative. J Dermatol Treat 2011; 22 (1): 31–7.
18. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. Guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol 2009; 61: 451–85.
19. Kim IH, West CE, Kwatra SG, Feldman SR, O’Neill JL. Comparative efficacy of biologics in psoriasis: a review. Am J Clin Dermatol 2012; 13: 365–74.
20. Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol 2008; 58: 826–50.
21. Papp KA, Dekoven J, Parsons L, et al. Biologic therapy in psoriasis: perspectives on associated risks and patient management. J Cutan Med Surg 2012; 16: 153–68.
22. Lisi P. Differential diagnosis of psoriasis. Reumatismo 2007; 59 (Suppl 1): 56–60.
23. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol 2007; 25: 606–15.
24. Kalb RE, Bagel J, Korman NJ, et al. Treatment of intertriginous psoriasis: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol 2009; 60 (1): 120–4.
25. Ayala F. Clinical presentation of psoriasis. Reumatismo 2007; 59 (Suppl 1): 40–5.
26. Robinson A, Van Voorhees AS, Hsu S, et al. Treatment of pustular psoriasis: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol 2011; 67: 279–88.
27. Rosenbach M, Hsu S, Korman NJ, et al. Treatment of erythrodermic psoriasis: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010; 62: 655–62.
28. Tomasini C, Aloi F, Solaroli C, Pippione M. Psoriatic erythroderma: a histopathologic study of forty-five patients. Dermatology 1997; 194: 102–6.
29. Viguier M, Pages C, Aubin F, et al. Efficacy and safety of biologics in erythrodermic psoriasis: a multicentre, retrospective study. Br J Dermatol 2012; 167: 417–23.
30. Chalmers RJ, O’Sullivan T, Owen CM, Griffith CE. A systemic review of treatment for guttate psoriasis. Br J Dermatol 2001; 145: 891–4.
31. Ko HC, Jwa SW, Song M, Kim MB, Kwon KS. Clinical course of guttate psoriasis: long-term follow-up study. J Dermatol 2010; 37: 894–9.
32. Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis? Arch Dermatol 1996; 132: 717–8.
33. Mallbris L, Larsson P, Bergqvist S, Vingard E, Granath F, Stahle M. Psoriasis phenotype at disease onset: clinical characterization of 400 adult cases. J Invest Dermatol 2005; 124: 499–504.
34. Potok O, Prajapati V, Barankin B. Dermacase. Can you identify this condition? Guttate psoriasis. Can Fam Physician 2011; 57 (1): 55–7.
35. Naldi L, Peli L, Parazzini F, Carrel CF. Family history of psoriasis, stressful life events, and recent infectious disease are risk factors for a first episode of acute guttate psoriasis: results of a case-control study. J Am Acad Dermatol 2001; 44: 433–8.
36. Dogan B, Karabudak O, Harmanyeri Y. Antistreptococcal treatment of guttate psoriasis: a controlled study. Int J Dermatol 2008; 47: 950–2.
37. Krishnamurthy K, Walker A, Gropper CA, Hoffman C. To treat or not to treat? Management of guttate psoriasis and pityriasis rosea in patients with evidence of group A streptococcal infection. J Drugs Dermatol 2010; 9: 241–50.
38. Owen CM, Chalmers RJ, O’Sullivan T, Griffiths CE. A systematic review of antistreptococcal interventions for guttate and chronic plaque psoriasis. Br J Dermatol 2001; 145: 886–90.
39. Chalmers RJ, O’Sullivan T, Owen CM, Griffiths CE. A systematic review of treatments for guttate psoriasis. Br J Dermatol 2001; 145: 891–4.
40. Hollinworth H. Challenges in protecting peri-wound skin. Nurs Stand 2009; 24 (7): 53–54, 56, 58 passim.
41. White RJ, Cutting KF. Interventions to avoid maceration of the skin and wound bed. Br J Nurs 2003; 12: 1186–1201.
42. Martins L, Tavernelli K, Sansom W, et al. Strategies to reduce treatment costs of periosteal skin complications. Br J Nurs 2012; 21: 1312–5.
43. Colwell JC, Ratliff CR, Goldberg M, et al. MASD part 3: peristomal moisture- associated dermatitis and periwound moisture-associated dermatitis: a consensus. J Wound Ostomy Continence Nurs 2011; 38: 541–53.
44. Stern SH, Insall JN, Windsor RE, Inglis AE, Dines DM. Total knee arthroplasty in patients with psoriasis. Clin Orthop Relat Res 1989; 248: 108–10.
45. Hicken GJ, Kitaoka HB, Valente RM. Foot and ankle surgery in patients with psoriasis. Clin Orthop Relat Res 1994; 300: 201–6.
46. Heinen MM, Persoon A, van de Kerkhof P, Otero M, van Achterberg T. Ulcer-related problems and health care needs in patients with venous leg ulceration: a descriptive, cross-sectional study. Int J Nurs Stud 2007; 44: 1296–1303.
Keywords:© 2013 Lippincott Williams & Wilkins, Inc.
chronic plaque psoriasis; intertriginous psoriasis; pustular psoriasis; erythrodermic psoriasis; guttate psoriasis