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The many variants of psoriasis
The “heartbreak of psoriasis,” coined by an advertiser in the 1960s, conveyed the notion that this disease was a cosmetic disorder mainly limited to skin involvement. John Updike’s article in the September 1985 issue of The New Yorker, “At War With My Skin,” detailed Mr. Updike’s feelings of isolation and stress related to his condition, helping to reframe the popular concept of psoriasis.1 Updike’s eloquent account describing his struggles to find effective treatment increased public awareness about psoriasis, which in fact affects other body systems as well.
The overall prevalence of psoriasis is 1.5% to 3.1% in the United States and United Kingdom.2,3 More than 6.5 million adults in the United States > 20 years of age are affected.3 The most commonly affected demographic group is non-Hispanic Caucasians.
Our expanding knowledge of pathogenesis
Studies of genetic linkage have identified genes and single nucleotide polymorphisms associated with psoriasis.4 The interaction between environmental triggers and the innate and adaptive immune systems leads to keratinocyte hyperproliferation. Tumor necrosis factor (TNF), interleukin (IL) 23, and IL-17 are important cytokines associated with psoriatic inflammation.4 There are common pathways of inflammation in both psoriasis and cardiovascular disease resulting in oxidative stress and endothelial cell dysfunction.4 Ninety percent of early-onset psoriasis is associated with human leukocyte antigen (HLA)-Cw6.4 And alterations in the microbiome of the skin may contribute, as reduced microbial diversity has been found in psoriatic lesions.5
Comorbidities are common
Psoriasis is an independent risk factor for diabetes and major adverse cardiovascular events.6 Hypertension, dyslipidemia, inflammatory bowel disease, nonalcoholic fatty liver disease, chronic kidney disease, and lymphoma (particularly cutaneous T-cell lymphoma) are also associated with psoriasis.6 Psoriatic arthritis is frequently encountered with cutaneous psoriasis; however, it is often not recognized until late in the disease course.
There also appears to be an association among psoriasis, dietary factors, and celiac disease.7-9 Positive testing for IgA anti-endomysial antibodies and IgA tissue transglutaminase antibodies should prompt consideration of starting a gluten-free diet, which has been shown to improve psoriatic
The different types of psoriasis
The classic presentation of psoriasis involves stubborn plaques with silvery scale on extensor surfaces such as the elbows and knees. The severity of the disease corresponds with the amount of body surface area affected. While plaque-type psoriasis is the most common form, other patterns exist. Individuals may exhibit 1 dominant pattern or multiple psoriatic variants simultaneously. Most types of psoriasis have 3 characteristic features: erythema, skin thickening, and scales.
Certain history and physical clues can aid in diagnosing psoriasis; these include the Koebner phenomenon, the Auspitz sign, and the Woronoff ring. The Koebner phenomenon refers to the development of psoriatic lesions in an area of trauma (FIGURE 1), frequently resulting in a linear streak-like appearance. The Auspitz sign describes the pinpoint bleeding that may be encountered with the removal of a psoriatic plaque. The Woronoff ring is a pale blanching ring that may surround a psoriatic lesion.
Continue to: Chronic plaque-type psoriasis
Chronic plaque-type psoriasis (Figures 2A and 2B), the most common variant, is characterized by sharply demarcated pink papules and plaques with a silvery scale in a symmetric distribution on the extensor surfaces, scalp, trunk, and lumbosacral areas.
Guttate psoriasis (FIGURE 3) features small (often < 1 cm) pink scaly papules that appear suddenly. It is more commonly seen in children and is usually preceded by an upper respiratory tract infection, often with Streptococcus.10 If strep testing is positive, guttate psoriasis may improve after appropriate antibiotic treatment.
Erythrodermic psoriasis (FIGUREs 4A and 4B) involves at least 75% of the body with erythema and scaling.11 Erythroderma can be caused by many other conditions such as atopic dermatitis, a drug reaction, Sezary syndrome, seborrheic dermatitis, and pityriasis rubra pilaris. Treatments for other conditions in the differential diagnosis can potentially make psoriasis worse. Unfortunately, findings on a skin biopsy are often nonspecific, making careful clinical observation crucial to arriving at an accurate diagnosis.
Pustular psoriasis is characterized by bright erythema and sterile pustules. Pustular psoriasis can be triggered by pregnancy, sudden tapering of corticosteroids, hypocalcemia, and infection. Involvement of the palms and soles with severe desquamation can drastically impact daily functioning and quality of life.
Inverse or flexural psoriasis (FIGUREs 5A and 5B) is characterized by shiny, pink-to-red sharply demarcated plaques involving intertriginous areas, typically the groin, inguinal crease, axilla, inframammary regions, and intergluteal cleft.
Continue to: Geographic tongue
Geographic tongue describes psoriasis of the tongue. The mucosa of the tongue has white plaques with a geographic border. Instead of scale, the moisture on the tongue causes areas of hyperkeratosis that appear white.
Nail psoriasis can manifest as nail pitting (FIGURE 6), oil staining, onycholysis (distal lifting of the nail), and subungual hyperkeratosis. Nail psoriasis is often quite distressing for patients and can be difficult to treat.
Palmoplantar psoriasis (FIGUREs 7A and 7B) can be painful due to the involvement of the palms of the hands and soles of the feet. Lesions will either be similar to other psoriatic plaques with well-demarcated erythematous scaling lesions or involve thickening and scale without associated erythema.
Psoriatic arthritis can cause significant joint damage and disability. Most affected individuals with psoriatic arthritis have a history of preceding skin disease.12 There are no specific lab tests for psoriasis; radiologic studies can show bulky syndesmophytes, central and marginal erosions, and periostitis. Patterns of joint involvement are variable. Psoriatic arthritis is more likely to affect the distal interphalangeal joints than rheumatoid arthritis and is more likely to affect the metacarpophalangeal joints than osteoarthritis.13
Psoriatic arthritis often progresses insidiously and is commonly described as causing discomfort rather than acute pain. Enthesitis, inflammation at the site where tendons or ligaments insert into the bone, is often present. Joint destruction may lead to the telescoping “opera glass” digit (FIGURE 8).
Continue to: Drug-provoked psoriasis
Drug-provoked psoriasis is divided into 2 groups: drug-induced and drug-aggravated. Drug-induced psoriasis will improve after discontinuation of the causative drug and tends to occur in patients without a personal or family history of psoriasis. Drug-aggravated psoriasis continues to progress after the discontinuation of the offending drug and is more often seen in patients with a history of psoriasis.14 Drugs that most commonly provoke psoriasis are beta-blockers, lithium, and antimalarials.10 Other potentially aggravating agents include antibiotics, digoxin, and nonsteroidal anti-inflammatory drugs.10
Consider these skin disorders in the differential diagnosis
The diagnosis of psoriasis is usually clinical, and a skin biopsy is rarely needed. However, a range of other skin disorders should be kept in mind when considering the differential diagnosis.
Mycosis fungoides is a type of cutaneous T-cell lymphoma that forms erythematous plaques that may show wrinkling and epidermal atrophy in sun-protected sites. Onset usually occurs among the elderly.
Pityriasis rubra pilaris is characterized by salmon-colored patches that may have small areas of normal skin (“islands of sparing”), hyperkeratotic follicular papules, and hyperkeratosis of the palms and soles.
Seborrheic dermatitis, dandruff of the skin, usually involves the scalp and nasolabial areas and the T-zone of the face.
Continue to: Lichen planus
Lichen planus usually appears slightly more purple than psoriasis and typically involves the mouth, flexural surfaces of the wrists, genitals, and ankles.
Other conditions in the differential include pityriasis lichenoides chronica, which may be identified on skin biopsy. Inverse psoriasis can be difficult to differentiate from candida intertrigo, erythrasma, or tinea cruris.
A potassium hydroxide (KOH) preparation can help differentiate psoriasis from candida or tinea. In psoriasis, a KOH test will be negative for fungal elements. Mycology culture on skin scrapings may be performed to rule out fungal infection. Erythrasma may exhibit a coral red appearance under Wood lamp examination.
If a lesion fails to respond to appropriate treatment, a careful drug history and biopsy can help clarify the diagnosis.
Document disease
It’s important to thoroughly document the extent and severity of the psoriasis and to monitor the impact of treatment. The Psoriasis Area and Severity Index is a commonly used method that calculates a score based on the area (extent) of involvement surrounding 4 major anatomical regions (head, upper extremities, trunk, and lower extremities), as well as the degree of erythema, induration, and scaling of lesions. The average redness, thickness, and scaling are graded on a scale of 0 to 4 and the extent of involvement is calculated to form a total numerical score ranging from 0 (no disease) to 72 (maximal disease).
Continue to: Many options in the treatment arsenal
Many options in the treatment arsenal
Many treatments can improve psoriasis.9,15-19 Most affected individuals discover that emollients and exposure to natural sunlight can be effective, as are soothing baths (balneotherapy) or topical coal tar application. More persistent disease requires prescription therapy. Individualize therapy according to the severity of disease, location of the lesions, involvement of joints, and comorbidities (FIGURE 9).15
If ≤ 10% of the body surface area is involved, treatment options generally are explored in a stepwise progression from safest and most affordable to more involved therapies as needed: moisturization and avoidance of repetitive trauma, topical corticosteroids (TCS), vitamin D analogs, topical calcineurin inhibitors, and vitamin A creams. Recalcitrant disease will likely require ultraviolet (UV) light treatment or a systemic agent.15
If > 10% of the body surface area is involved, but joints are not involved, consider UV light treatment or a combination of alcitretin and TCS. If the joints are involved, likely initial options would be methotrexate, cyclosporine, or TNF-α inhibitor. Additional options to consider are anti-IL-17 or anti-IL-23 agents.15
If there’s joint involvement. In individuals with mild peripheral arthritis involving fewer than 4 joints without evidence of joint damage on imaging, nonsteroidal anti-inflammatory drugs are the mainstay of treatment. If the peripheral arthritis persists, or if it is associated with moderate-to-severe erosions or with substantial functional limitations, initiate treatment with a conventional disease-modifying antirheumatic drug. If the disease remains active, consider biologic agents.
Case studies
Mild-to-moderate psoriasis
Patient A is a 19-year-old woman presenting for evaluation of a persistently dry, flaking scalp. She has had the itchy scalp for years, as well as several small “patches” across her elbows, legs, knees, and abdomen. Over-the-counter emollients have not helped. The patient also says she has had brittle nails on several of her fingers, which she keeps covered with thick polish.
Continue to: The condition exemplified...
The condition exemplified by Patient A can typically be managed with topical products.
Topical steroids may be classified by different delivery vehicles, active ingredients, and potencies. The National Psoriasis Foundation's Topical Steroids Potency Chart can provide guidance (visit www.psoriasis.org/about-psoriasis/treatments/topicals/steroids/potency-chart and scroll down). Prescribing an appropriate amount is important; the standard 30-g prescription tube is generally required to cover the entire skin surface. Ointments have a greasy consistency (typically a petroleum base), which enhances potency and hydrates the skin. Creams and lotions are easier to rub on and spread. Gels are alcohol based and readily absorbed.16 Solutions, foams, and shampoos are particularly useful to treat psoriasis in hairy areas such as the scalp.
Corticosteroid potency ranges from Class I to Class VII, with the former being the most potent. While TCS products are typically effective with minimal systemic absorption, it is important to counsel patients on the risk of skin atrophy, impaired wound healing, and skin pigmentation changes with chronic use. With nail psoriasis, a potent topical steroid (including flurandrenolide [Cordran] tape) applied to the proximal nail fold has shown benefit.20
Topical calcineurin inhibitors (TCIs; eg, tacrolimus ointment and pimecrolimus cream) are anti-inflammatory agents often used in conjunction with topical steroids to minimize steroid use and associated adverse effects.15 A possible steroid-sparing regimen includes using a TCI Monday through Friday and a topical steroid on the weekend.
Topical vitamin D analogs (calcipotriene, calcipotriol, calcitriol) inhibit proliferation of keratinocytes and decrease the production of inflammatory mediators.15,17-19,21 Application of a vitamin D analog in combination with a high-potency TCS, systemic treatment, or phototherapy can provide greater efficacy, a more rapid onset of action, and less irritation than can the vitamin D analog used alone.21 If used in combination with UV light, apply topical vitamin D after the light therapy to prevent degradation.
Continue to: UV light therapy
UV light therapy is often used in cases refractory to topical therapy. Patients are typically prescribed 2 to 3 treatments per week with narrowband UVB (311-313 nm), the excimer laser (308 nm), or, less commonly, PUVA (UV treatment with psoralens). Treatment begins with a minimal erythema dose—the lowest dose to achieve minimal erythema of the skin before burning. When that is determined, exposure is increased as needed—depending on the response. If this is impractical or too time-consuming for the patient, an alternative recommendation would be increased exposure to natural sunlight or even use of a tanning booth. However, patients must then be cautioned about the increased risk of skin cancer.
Refractory/severe psoriasis
Patient B is a 35-year-old man with a longstanding history of psoriasis affecting his scalp and nails. Over the past 10 years, psoriatic lesions have also appeared and grown across his lower back, gluteal fold, legs, abdomen, and arms. He is now being evaluated by a rheumatologist for worsening symmetric joint pain that includes his lower back.
Methotrexate has been used to treat psoriasis and psoriatic arthritis since the 1950s. Methotrexate is a competitive inhibitor of dihydrofolate reductase and is typically given as an oral medication dosed once weekly with folic acid supplementation on the other 6 days.17 The most common adverse effects encountered with methotrexate are gastrointestinal upset and oral ulcers; however, routine monitoring for myelosuppression and hepatotoxicity is required.
Biologic therapy. When conventional therapies fail, immune-targeted treatment with “biologics” may be initiated. As knowledge of signaling pathways and the immunopathogenesis of psoriasis has increased, so has the number of biologic agents, which are generally well tolerated and effective in managing plaque psoriasis and psoriatic arthritis. Although their use, which requires monitoring, is handled primarily by specialists, familiarizing yourself with available agents can be helpful (TABLE).22
Nutritional modification and supplementation in treating skin disease still requires further investigation. Fish oil has shown benefit for cutaneous psoriasis in randomized controlled trials.7,8 Oral vitamin D supplementation requires further study, whereas selenium and B12 supplementation have not conferred consistent benefit.7 Given that several studies have demonstrated a relationship between body mass index and psoriatic disease severity, weight loss may be helpful in the management of psoriasis as well as psoriatic arthritis.8
Continue to: Other systemic agents
Other systemic agents—for individuals who cannot tolerate the biologic agents—include acitretin, azathioprine, mycophenolate mofetil, and cyclosporine.15,17
Paradoxical psoriatic reactions
When a psoriatic condition develops during biologic drug therapy, it is known as a paradoxical psoriatic reaction. The onset of de novo psoriasis has been documented during TNF-α inhibitor therapy for individuals with underlying rheumatoid arthritis.23 Skin biopsy reveals the same findings as common plaque psoriasis.
Using immunosuppressive Tx? Screen for tuberculosis
Testing to exclude a diagnosis of latent or undiagnosed tuberculosis must be performed prior to initiating immunosuppressive therapy with methotrexate or a biologic agent. Tuberculin skin testing, QuantiFERON-TB gold test, and the T-SPOT.TB test are accepted screening modalities. Discordance between tuberculin skin tests and the interferon gamma release assays in latent TB highlights the need for further study using the available QuantiFERON-TB gold test and the T-SPOT.TB test.24
CORRESPONDENCE
Karl T. Clebak, MD, FAAFP, Penn State Health Milton S. Hershey Medical Center, Department of Family and Community Medicine, 500 University Drive, Hershey, PA 17033; [email protected].
1. Jackson R. John Updike on psoriasis. At war with my skin, from the journal of a leper. J Cutan Med Surg. 2000;4:113-115.
2. Gelfand JM, Weinstein R, Porter SB, et al. Prevalence and treatment of psoriasis in the United Kingdom: a population-based study. Arch Dermatol. 2005;141:1537-1541.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Alexander H, Nestle FO. Pathogenesis and immunotherapy in cutaneous psoriasis: what can rheumatologists learn? Curr Opin Rheumatol. 2017;29:71-78.
5. Fahlén A, Engstrand L, Baker BS, et al. Comparison of bacterial microbiota in skin biopsies from normal and psoriatic skin. Arch Dermatol Res. 2012;304:15-22.
6. Takeshita J, Grewal S, Langan SM, et al. Psoriasis and comorbid diseases: epidemiology. J Am Acad Dermatol. 2017;76:377-390.
7. Millsop JW, Bhatia BK, Debbaneh M, et al. Diet and psoriasis, part III: role of nutritional supplements. J Am Acad Dermatol. 2014;71:561-569.
8. Debbaneh M, Millsop JW, Bhatia BK, et al. Diet and psoriasis, part I: impact of weight loss interventions. J Am Acad Dermatol. 2014;71:133-140.
9. Bhatia BK, Millsop JW, Debbaneh M, et al. Diet and psoriasis, part II: celiac disease and role of a gluten-free diet. J Am Acad Dermatol. 2014;71:350-358.
10. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
11. Singh RK, Lee KM, Ucmak D, et al. Erythrodermic psoriasis: pathophysiology and current treatment perspectives. Psoriasis (Aukl). 2016;6:93-104.
12. Garg A, Gladman D. Recognizing psoriatic arthritis in the dermatology clinic. J Am Acad Dermatol. 2010;63:733-748.
13. McGonagle D, Hermann KG, Tan AL. Differentiation between osteoarthritis and psoriatic arthritis: implications for pathogenesis and treatment in the biologic therapy era. Rheumatology. 2015;54:29-38.
14. Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug aggravated?: understanding pathophysiology and clinical relevance. J Clin Aesthet Dermatol. 2010;3:32-38.
15. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidence-based guide for primary care. J Am Board Fam Med. 2013;26:787-801.
16. Helm MF, Farah JB, Carvalho M, et al. Compounded topical medications for diseases of the skin: a long tradition still relevant today. N Am J Med Sci. 2017;10:116-118.
17. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013;87:626-633.
18. Helfrich YR, Sachs DL, Kang S. Topical vitamin D3. In: Wolverton SE, ed. Comprehensive Dermatologic Drug Therapy. 2nd ed. Philadelphia, PA: Saunders; 2007:691-695.
19. Lebwohl M, Siskin SB, Epinette W, et al. A multicenter trial of calcipotriene ointment and halobetasol ointment compared with either agent alone for the treatment of psoriasis. J Am Acad Dermatol. 1996;35:268-269.
20. Pasch MC. Nail psoriasis: a review of treatment options. Drugs. 2016;76:675-705.
21. Bagel J, Gold LS. Combining topical psoriasis treatment to enhance systemic and phototherapy: a review of the literature. J Drugs Dermatol. 2017;16:1209-1222.
22. Rønholt K, Iversen L. Old and new biological therapies for psoriasis. Int J Mol Sci. 2017;18:e2297.
23. Toussirot É, Aubin F. Paradoxical reactions under TNF-alpha blocking agents and other biologic agents given for chronic immune-mediated diseases: an analytical and comprehensive overview. RMD Open. 2016;2:e000239.
24. Connell TG, Ritz N, Paxton GA, et al. A three-way comparison of tuberculin skin testing, QuantiFERON-TB gold and T-SPOT.TB in children. PLoS One. 2008;3:e2624.
The “heartbreak of psoriasis,” coined by an advertiser in the 1960s, conveyed the notion that this disease was a cosmetic disorder mainly limited to skin involvement. John Updike’s article in the September 1985 issue of The New Yorker, “At War With My Skin,” detailed Mr. Updike’s feelings of isolation and stress related to his condition, helping to reframe the popular concept of psoriasis.1 Updike’s eloquent account describing his struggles to find effective treatment increased public awareness about psoriasis, which in fact affects other body systems as well.
The overall prevalence of psoriasis is 1.5% to 3.1% in the United States and United Kingdom.2,3 More than 6.5 million adults in the United States > 20 years of age are affected.3 The most commonly affected demographic group is non-Hispanic Caucasians.
Our expanding knowledge of pathogenesis
Studies of genetic linkage have identified genes and single nucleotide polymorphisms associated with psoriasis.4 The interaction between environmental triggers and the innate and adaptive immune systems leads to keratinocyte hyperproliferation. Tumor necrosis factor (TNF), interleukin (IL) 23, and IL-17 are important cytokines associated with psoriatic inflammation.4 There are common pathways of inflammation in both psoriasis and cardiovascular disease resulting in oxidative stress and endothelial cell dysfunction.4 Ninety percent of early-onset psoriasis is associated with human leukocyte antigen (HLA)-Cw6.4 And alterations in the microbiome of the skin may contribute, as reduced microbial diversity has been found in psoriatic lesions.5
Comorbidities are common
Psoriasis is an independent risk factor for diabetes and major adverse cardiovascular events.6 Hypertension, dyslipidemia, inflammatory bowel disease, nonalcoholic fatty liver disease, chronic kidney disease, and lymphoma (particularly cutaneous T-cell lymphoma) are also associated with psoriasis.6 Psoriatic arthritis is frequently encountered with cutaneous psoriasis; however, it is often not recognized until late in the disease course.
There also appears to be an association among psoriasis, dietary factors, and celiac disease.7-9 Positive testing for IgA anti-endomysial antibodies and IgA tissue transglutaminase antibodies should prompt consideration of starting a gluten-free diet, which has been shown to improve psoriatic
The different types of psoriasis
The classic presentation of psoriasis involves stubborn plaques with silvery scale on extensor surfaces such as the elbows and knees. The severity of the disease corresponds with the amount of body surface area affected. While plaque-type psoriasis is the most common form, other patterns exist. Individuals may exhibit 1 dominant pattern or multiple psoriatic variants simultaneously. Most types of psoriasis have 3 characteristic features: erythema, skin thickening, and scales.
Certain history and physical clues can aid in diagnosing psoriasis; these include the Koebner phenomenon, the Auspitz sign, and the Woronoff ring. The Koebner phenomenon refers to the development of psoriatic lesions in an area of trauma (FIGURE 1), frequently resulting in a linear streak-like appearance. The Auspitz sign describes the pinpoint bleeding that may be encountered with the removal of a psoriatic plaque. The Woronoff ring is a pale blanching ring that may surround a psoriatic lesion.
Continue to: Chronic plaque-type psoriasis
Chronic plaque-type psoriasis (Figures 2A and 2B), the most common variant, is characterized by sharply demarcated pink papules and plaques with a silvery scale in a symmetric distribution on the extensor surfaces, scalp, trunk, and lumbosacral areas.
Guttate psoriasis (FIGURE 3) features small (often < 1 cm) pink scaly papules that appear suddenly. It is more commonly seen in children and is usually preceded by an upper respiratory tract infection, often with Streptococcus.10 If strep testing is positive, guttate psoriasis may improve after appropriate antibiotic treatment.
Erythrodermic psoriasis (FIGUREs 4A and 4B) involves at least 75% of the body with erythema and scaling.11 Erythroderma can be caused by many other conditions such as atopic dermatitis, a drug reaction, Sezary syndrome, seborrheic dermatitis, and pityriasis rubra pilaris. Treatments for other conditions in the differential diagnosis can potentially make psoriasis worse. Unfortunately, findings on a skin biopsy are often nonspecific, making careful clinical observation crucial to arriving at an accurate diagnosis.
Pustular psoriasis is characterized by bright erythema and sterile pustules. Pustular psoriasis can be triggered by pregnancy, sudden tapering of corticosteroids, hypocalcemia, and infection. Involvement of the palms and soles with severe desquamation can drastically impact daily functioning and quality of life.
Inverse or flexural psoriasis (FIGUREs 5A and 5B) is characterized by shiny, pink-to-red sharply demarcated plaques involving intertriginous areas, typically the groin, inguinal crease, axilla, inframammary regions, and intergluteal cleft.
Continue to: Geographic tongue
Geographic tongue describes psoriasis of the tongue. The mucosa of the tongue has white plaques with a geographic border. Instead of scale, the moisture on the tongue causes areas of hyperkeratosis that appear white.
Nail psoriasis can manifest as nail pitting (FIGURE 6), oil staining, onycholysis (distal lifting of the nail), and subungual hyperkeratosis. Nail psoriasis is often quite distressing for patients and can be difficult to treat.
Palmoplantar psoriasis (FIGUREs 7A and 7B) can be painful due to the involvement of the palms of the hands and soles of the feet. Lesions will either be similar to other psoriatic plaques with well-demarcated erythematous scaling lesions or involve thickening and scale without associated erythema.
Psoriatic arthritis can cause significant joint damage and disability. Most affected individuals with psoriatic arthritis have a history of preceding skin disease.12 There are no specific lab tests for psoriasis; radiologic studies can show bulky syndesmophytes, central and marginal erosions, and periostitis. Patterns of joint involvement are variable. Psoriatic arthritis is more likely to affect the distal interphalangeal joints than rheumatoid arthritis and is more likely to affect the metacarpophalangeal joints than osteoarthritis.13
Psoriatic arthritis often progresses insidiously and is commonly described as causing discomfort rather than acute pain. Enthesitis, inflammation at the site where tendons or ligaments insert into the bone, is often present. Joint destruction may lead to the telescoping “opera glass” digit (FIGURE 8).
Continue to: Drug-provoked psoriasis
Drug-provoked psoriasis is divided into 2 groups: drug-induced and drug-aggravated. Drug-induced psoriasis will improve after discontinuation of the causative drug and tends to occur in patients without a personal or family history of psoriasis. Drug-aggravated psoriasis continues to progress after the discontinuation of the offending drug and is more often seen in patients with a history of psoriasis.14 Drugs that most commonly provoke psoriasis are beta-blockers, lithium, and antimalarials.10 Other potentially aggravating agents include antibiotics, digoxin, and nonsteroidal anti-inflammatory drugs.10
Consider these skin disorders in the differential diagnosis
The diagnosis of psoriasis is usually clinical, and a skin biopsy is rarely needed. However, a range of other skin disorders should be kept in mind when considering the differential diagnosis.
Mycosis fungoides is a type of cutaneous T-cell lymphoma that forms erythematous plaques that may show wrinkling and epidermal atrophy in sun-protected sites. Onset usually occurs among the elderly.
Pityriasis rubra pilaris is characterized by salmon-colored patches that may have small areas of normal skin (“islands of sparing”), hyperkeratotic follicular papules, and hyperkeratosis of the palms and soles.
Seborrheic dermatitis, dandruff of the skin, usually involves the scalp and nasolabial areas and the T-zone of the face.
Continue to: Lichen planus
Lichen planus usually appears slightly more purple than psoriasis and typically involves the mouth, flexural surfaces of the wrists, genitals, and ankles.
Other conditions in the differential include pityriasis lichenoides chronica, which may be identified on skin biopsy. Inverse psoriasis can be difficult to differentiate from candida intertrigo, erythrasma, or tinea cruris.
A potassium hydroxide (KOH) preparation can help differentiate psoriasis from candida or tinea. In psoriasis, a KOH test will be negative for fungal elements. Mycology culture on skin scrapings may be performed to rule out fungal infection. Erythrasma may exhibit a coral red appearance under Wood lamp examination.
If a lesion fails to respond to appropriate treatment, a careful drug history and biopsy can help clarify the diagnosis.
Document disease
It’s important to thoroughly document the extent and severity of the psoriasis and to monitor the impact of treatment. The Psoriasis Area and Severity Index is a commonly used method that calculates a score based on the area (extent) of involvement surrounding 4 major anatomical regions (head, upper extremities, trunk, and lower extremities), as well as the degree of erythema, induration, and scaling of lesions. The average redness, thickness, and scaling are graded on a scale of 0 to 4 and the extent of involvement is calculated to form a total numerical score ranging from 0 (no disease) to 72 (maximal disease).
Continue to: Many options in the treatment arsenal
Many options in the treatment arsenal
Many treatments can improve psoriasis.9,15-19 Most affected individuals discover that emollients and exposure to natural sunlight can be effective, as are soothing baths (balneotherapy) or topical coal tar application. More persistent disease requires prescription therapy. Individualize therapy according to the severity of disease, location of the lesions, involvement of joints, and comorbidities (FIGURE 9).15
If ≤ 10% of the body surface area is involved, treatment options generally are explored in a stepwise progression from safest and most affordable to more involved therapies as needed: moisturization and avoidance of repetitive trauma, topical corticosteroids (TCS), vitamin D analogs, topical calcineurin inhibitors, and vitamin A creams. Recalcitrant disease will likely require ultraviolet (UV) light treatment or a systemic agent.15
If > 10% of the body surface area is involved, but joints are not involved, consider UV light treatment or a combination of alcitretin and TCS. If the joints are involved, likely initial options would be methotrexate, cyclosporine, or TNF-α inhibitor. Additional options to consider are anti-IL-17 or anti-IL-23 agents.15
If there’s joint involvement. In individuals with mild peripheral arthritis involving fewer than 4 joints without evidence of joint damage on imaging, nonsteroidal anti-inflammatory drugs are the mainstay of treatment. If the peripheral arthritis persists, or if it is associated with moderate-to-severe erosions or with substantial functional limitations, initiate treatment with a conventional disease-modifying antirheumatic drug. If the disease remains active, consider biologic agents.
Case studies
Mild-to-moderate psoriasis
Patient A is a 19-year-old woman presenting for evaluation of a persistently dry, flaking scalp. She has had the itchy scalp for years, as well as several small “patches” across her elbows, legs, knees, and abdomen. Over-the-counter emollients have not helped. The patient also says she has had brittle nails on several of her fingers, which she keeps covered with thick polish.
Continue to: The condition exemplified...
The condition exemplified by Patient A can typically be managed with topical products.
Topical steroids may be classified by different delivery vehicles, active ingredients, and potencies. The National Psoriasis Foundation's Topical Steroids Potency Chart can provide guidance (visit www.psoriasis.org/about-psoriasis/treatments/topicals/steroids/potency-chart and scroll down). Prescribing an appropriate amount is important; the standard 30-g prescription tube is generally required to cover the entire skin surface. Ointments have a greasy consistency (typically a petroleum base), which enhances potency and hydrates the skin. Creams and lotions are easier to rub on and spread. Gels are alcohol based and readily absorbed.16 Solutions, foams, and shampoos are particularly useful to treat psoriasis in hairy areas such as the scalp.
Corticosteroid potency ranges from Class I to Class VII, with the former being the most potent. While TCS products are typically effective with minimal systemic absorption, it is important to counsel patients on the risk of skin atrophy, impaired wound healing, and skin pigmentation changes with chronic use. With nail psoriasis, a potent topical steroid (including flurandrenolide [Cordran] tape) applied to the proximal nail fold has shown benefit.20
Topical calcineurin inhibitors (TCIs; eg, tacrolimus ointment and pimecrolimus cream) are anti-inflammatory agents often used in conjunction with topical steroids to minimize steroid use and associated adverse effects.15 A possible steroid-sparing regimen includes using a TCI Monday through Friday and a topical steroid on the weekend.
Topical vitamin D analogs (calcipotriene, calcipotriol, calcitriol) inhibit proliferation of keratinocytes and decrease the production of inflammatory mediators.15,17-19,21 Application of a vitamin D analog in combination with a high-potency TCS, systemic treatment, or phototherapy can provide greater efficacy, a more rapid onset of action, and less irritation than can the vitamin D analog used alone.21 If used in combination with UV light, apply topical vitamin D after the light therapy to prevent degradation.
Continue to: UV light therapy
UV light therapy is often used in cases refractory to topical therapy. Patients are typically prescribed 2 to 3 treatments per week with narrowband UVB (311-313 nm), the excimer laser (308 nm), or, less commonly, PUVA (UV treatment with psoralens). Treatment begins with a minimal erythema dose—the lowest dose to achieve minimal erythema of the skin before burning. When that is determined, exposure is increased as needed—depending on the response. If this is impractical or too time-consuming for the patient, an alternative recommendation would be increased exposure to natural sunlight or even use of a tanning booth. However, patients must then be cautioned about the increased risk of skin cancer.
Refractory/severe psoriasis
Patient B is a 35-year-old man with a longstanding history of psoriasis affecting his scalp and nails. Over the past 10 years, psoriatic lesions have also appeared and grown across his lower back, gluteal fold, legs, abdomen, and arms. He is now being evaluated by a rheumatologist for worsening symmetric joint pain that includes his lower back.
Methotrexate has been used to treat psoriasis and psoriatic arthritis since the 1950s. Methotrexate is a competitive inhibitor of dihydrofolate reductase and is typically given as an oral medication dosed once weekly with folic acid supplementation on the other 6 days.17 The most common adverse effects encountered with methotrexate are gastrointestinal upset and oral ulcers; however, routine monitoring for myelosuppression and hepatotoxicity is required.
Biologic therapy. When conventional therapies fail, immune-targeted treatment with “biologics” may be initiated. As knowledge of signaling pathways and the immunopathogenesis of psoriasis has increased, so has the number of biologic agents, which are generally well tolerated and effective in managing plaque psoriasis and psoriatic arthritis. Although their use, which requires monitoring, is handled primarily by specialists, familiarizing yourself with available agents can be helpful (TABLE).22
Nutritional modification and supplementation in treating skin disease still requires further investigation. Fish oil has shown benefit for cutaneous psoriasis in randomized controlled trials.7,8 Oral vitamin D supplementation requires further study, whereas selenium and B12 supplementation have not conferred consistent benefit.7 Given that several studies have demonstrated a relationship between body mass index and psoriatic disease severity, weight loss may be helpful in the management of psoriasis as well as psoriatic arthritis.8
Continue to: Other systemic agents
Other systemic agents—for individuals who cannot tolerate the biologic agents—include acitretin, azathioprine, mycophenolate mofetil, and cyclosporine.15,17
Paradoxical psoriatic reactions
When a psoriatic condition develops during biologic drug therapy, it is known as a paradoxical psoriatic reaction. The onset of de novo psoriasis has been documented during TNF-α inhibitor therapy for individuals with underlying rheumatoid arthritis.23 Skin biopsy reveals the same findings as common plaque psoriasis.
Using immunosuppressive Tx? Screen for tuberculosis
Testing to exclude a diagnosis of latent or undiagnosed tuberculosis must be performed prior to initiating immunosuppressive therapy with methotrexate or a biologic agent. Tuberculin skin testing, QuantiFERON-TB gold test, and the T-SPOT.TB test are accepted screening modalities. Discordance between tuberculin skin tests and the interferon gamma release assays in latent TB highlights the need for further study using the available QuantiFERON-TB gold test and the T-SPOT.TB test.24
CORRESPONDENCE
Karl T. Clebak, MD, FAAFP, Penn State Health Milton S. Hershey Medical Center, Department of Family and Community Medicine, 500 University Drive, Hershey, PA 17033; [email protected].
The “heartbreak of psoriasis,” coined by an advertiser in the 1960s, conveyed the notion that this disease was a cosmetic disorder mainly limited to skin involvement. John Updike’s article in the September 1985 issue of The New Yorker, “At War With My Skin,” detailed Mr. Updike’s feelings of isolation and stress related to his condition, helping to reframe the popular concept of psoriasis.1 Updike’s eloquent account describing his struggles to find effective treatment increased public awareness about psoriasis, which in fact affects other body systems as well.
The overall prevalence of psoriasis is 1.5% to 3.1% in the United States and United Kingdom.2,3 More than 6.5 million adults in the United States > 20 years of age are affected.3 The most commonly affected demographic group is non-Hispanic Caucasians.
Our expanding knowledge of pathogenesis
Studies of genetic linkage have identified genes and single nucleotide polymorphisms associated with psoriasis.4 The interaction between environmental triggers and the innate and adaptive immune systems leads to keratinocyte hyperproliferation. Tumor necrosis factor (TNF), interleukin (IL) 23, and IL-17 are important cytokines associated with psoriatic inflammation.4 There are common pathways of inflammation in both psoriasis and cardiovascular disease resulting in oxidative stress and endothelial cell dysfunction.4 Ninety percent of early-onset psoriasis is associated with human leukocyte antigen (HLA)-Cw6.4 And alterations in the microbiome of the skin may contribute, as reduced microbial diversity has been found in psoriatic lesions.5
Comorbidities are common
Psoriasis is an independent risk factor for diabetes and major adverse cardiovascular events.6 Hypertension, dyslipidemia, inflammatory bowel disease, nonalcoholic fatty liver disease, chronic kidney disease, and lymphoma (particularly cutaneous T-cell lymphoma) are also associated with psoriasis.6 Psoriatic arthritis is frequently encountered with cutaneous psoriasis; however, it is often not recognized until late in the disease course.
There also appears to be an association among psoriasis, dietary factors, and celiac disease.7-9 Positive testing for IgA anti-endomysial antibodies and IgA tissue transglutaminase antibodies should prompt consideration of starting a gluten-free diet, which has been shown to improve psoriatic
The different types of psoriasis
The classic presentation of psoriasis involves stubborn plaques with silvery scale on extensor surfaces such as the elbows and knees. The severity of the disease corresponds with the amount of body surface area affected. While plaque-type psoriasis is the most common form, other patterns exist. Individuals may exhibit 1 dominant pattern or multiple psoriatic variants simultaneously. Most types of psoriasis have 3 characteristic features: erythema, skin thickening, and scales.
Certain history and physical clues can aid in diagnosing psoriasis; these include the Koebner phenomenon, the Auspitz sign, and the Woronoff ring. The Koebner phenomenon refers to the development of psoriatic lesions in an area of trauma (FIGURE 1), frequently resulting in a linear streak-like appearance. The Auspitz sign describes the pinpoint bleeding that may be encountered with the removal of a psoriatic plaque. The Woronoff ring is a pale blanching ring that may surround a psoriatic lesion.
Continue to: Chronic plaque-type psoriasis
Chronic plaque-type psoriasis (Figures 2A and 2B), the most common variant, is characterized by sharply demarcated pink papules and plaques with a silvery scale in a symmetric distribution on the extensor surfaces, scalp, trunk, and lumbosacral areas.
Guttate psoriasis (FIGURE 3) features small (often < 1 cm) pink scaly papules that appear suddenly. It is more commonly seen in children and is usually preceded by an upper respiratory tract infection, often with Streptococcus.10 If strep testing is positive, guttate psoriasis may improve after appropriate antibiotic treatment.
Erythrodermic psoriasis (FIGUREs 4A and 4B) involves at least 75% of the body with erythema and scaling.11 Erythroderma can be caused by many other conditions such as atopic dermatitis, a drug reaction, Sezary syndrome, seborrheic dermatitis, and pityriasis rubra pilaris. Treatments for other conditions in the differential diagnosis can potentially make psoriasis worse. Unfortunately, findings on a skin biopsy are often nonspecific, making careful clinical observation crucial to arriving at an accurate diagnosis.
Pustular psoriasis is characterized by bright erythema and sterile pustules. Pustular psoriasis can be triggered by pregnancy, sudden tapering of corticosteroids, hypocalcemia, and infection. Involvement of the palms and soles with severe desquamation can drastically impact daily functioning and quality of life.
Inverse or flexural psoriasis (FIGUREs 5A and 5B) is characterized by shiny, pink-to-red sharply demarcated plaques involving intertriginous areas, typically the groin, inguinal crease, axilla, inframammary regions, and intergluteal cleft.
Continue to: Geographic tongue
Geographic tongue describes psoriasis of the tongue. The mucosa of the tongue has white plaques with a geographic border. Instead of scale, the moisture on the tongue causes areas of hyperkeratosis that appear white.
Nail psoriasis can manifest as nail pitting (FIGURE 6), oil staining, onycholysis (distal lifting of the nail), and subungual hyperkeratosis. Nail psoriasis is often quite distressing for patients and can be difficult to treat.
Palmoplantar psoriasis (FIGUREs 7A and 7B) can be painful due to the involvement of the palms of the hands and soles of the feet. Lesions will either be similar to other psoriatic plaques with well-demarcated erythematous scaling lesions or involve thickening and scale without associated erythema.
Psoriatic arthritis can cause significant joint damage and disability. Most affected individuals with psoriatic arthritis have a history of preceding skin disease.12 There are no specific lab tests for psoriasis; radiologic studies can show bulky syndesmophytes, central and marginal erosions, and periostitis. Patterns of joint involvement are variable. Psoriatic arthritis is more likely to affect the distal interphalangeal joints than rheumatoid arthritis and is more likely to affect the metacarpophalangeal joints than osteoarthritis.13
Psoriatic arthritis often progresses insidiously and is commonly described as causing discomfort rather than acute pain. Enthesitis, inflammation at the site where tendons or ligaments insert into the bone, is often present. Joint destruction may lead to the telescoping “opera glass” digit (FIGURE 8).
Continue to: Drug-provoked psoriasis
Drug-provoked psoriasis is divided into 2 groups: drug-induced and drug-aggravated. Drug-induced psoriasis will improve after discontinuation of the causative drug and tends to occur in patients without a personal or family history of psoriasis. Drug-aggravated psoriasis continues to progress after the discontinuation of the offending drug and is more often seen in patients with a history of psoriasis.14 Drugs that most commonly provoke psoriasis are beta-blockers, lithium, and antimalarials.10 Other potentially aggravating agents include antibiotics, digoxin, and nonsteroidal anti-inflammatory drugs.10
Consider these skin disorders in the differential diagnosis
The diagnosis of psoriasis is usually clinical, and a skin biopsy is rarely needed. However, a range of other skin disorders should be kept in mind when considering the differential diagnosis.
Mycosis fungoides is a type of cutaneous T-cell lymphoma that forms erythematous plaques that may show wrinkling and epidermal atrophy in sun-protected sites. Onset usually occurs among the elderly.
Pityriasis rubra pilaris is characterized by salmon-colored patches that may have small areas of normal skin (“islands of sparing”), hyperkeratotic follicular papules, and hyperkeratosis of the palms and soles.
Seborrheic dermatitis, dandruff of the skin, usually involves the scalp and nasolabial areas and the T-zone of the face.
Continue to: Lichen planus
Lichen planus usually appears slightly more purple than psoriasis and typically involves the mouth, flexural surfaces of the wrists, genitals, and ankles.
Other conditions in the differential include pityriasis lichenoides chronica, which may be identified on skin biopsy. Inverse psoriasis can be difficult to differentiate from candida intertrigo, erythrasma, or tinea cruris.
A potassium hydroxide (KOH) preparation can help differentiate psoriasis from candida or tinea. In psoriasis, a KOH test will be negative for fungal elements. Mycology culture on skin scrapings may be performed to rule out fungal infection. Erythrasma may exhibit a coral red appearance under Wood lamp examination.
If a lesion fails to respond to appropriate treatment, a careful drug history and biopsy can help clarify the diagnosis.
Document disease
It’s important to thoroughly document the extent and severity of the psoriasis and to monitor the impact of treatment. The Psoriasis Area and Severity Index is a commonly used method that calculates a score based on the area (extent) of involvement surrounding 4 major anatomical regions (head, upper extremities, trunk, and lower extremities), as well as the degree of erythema, induration, and scaling of lesions. The average redness, thickness, and scaling are graded on a scale of 0 to 4 and the extent of involvement is calculated to form a total numerical score ranging from 0 (no disease) to 72 (maximal disease).
Continue to: Many options in the treatment arsenal
Many options in the treatment arsenal
Many treatments can improve psoriasis.9,15-19 Most affected individuals discover that emollients and exposure to natural sunlight can be effective, as are soothing baths (balneotherapy) or topical coal tar application. More persistent disease requires prescription therapy. Individualize therapy according to the severity of disease, location of the lesions, involvement of joints, and comorbidities (FIGURE 9).15
If ≤ 10% of the body surface area is involved, treatment options generally are explored in a stepwise progression from safest and most affordable to more involved therapies as needed: moisturization and avoidance of repetitive trauma, topical corticosteroids (TCS), vitamin D analogs, topical calcineurin inhibitors, and vitamin A creams. Recalcitrant disease will likely require ultraviolet (UV) light treatment or a systemic agent.15
If > 10% of the body surface area is involved, but joints are not involved, consider UV light treatment or a combination of alcitretin and TCS. If the joints are involved, likely initial options would be methotrexate, cyclosporine, or TNF-α inhibitor. Additional options to consider are anti-IL-17 or anti-IL-23 agents.15
If there’s joint involvement. In individuals with mild peripheral arthritis involving fewer than 4 joints without evidence of joint damage on imaging, nonsteroidal anti-inflammatory drugs are the mainstay of treatment. If the peripheral arthritis persists, or if it is associated with moderate-to-severe erosions or with substantial functional limitations, initiate treatment with a conventional disease-modifying antirheumatic drug. If the disease remains active, consider biologic agents.
Case studies
Mild-to-moderate psoriasis
Patient A is a 19-year-old woman presenting for evaluation of a persistently dry, flaking scalp. She has had the itchy scalp for years, as well as several small “patches” across her elbows, legs, knees, and abdomen. Over-the-counter emollients have not helped. The patient also says she has had brittle nails on several of her fingers, which she keeps covered with thick polish.
Continue to: The condition exemplified...
The condition exemplified by Patient A can typically be managed with topical products.
Topical steroids may be classified by different delivery vehicles, active ingredients, and potencies. The National Psoriasis Foundation's Topical Steroids Potency Chart can provide guidance (visit www.psoriasis.org/about-psoriasis/treatments/topicals/steroids/potency-chart and scroll down). Prescribing an appropriate amount is important; the standard 30-g prescription tube is generally required to cover the entire skin surface. Ointments have a greasy consistency (typically a petroleum base), which enhances potency and hydrates the skin. Creams and lotions are easier to rub on and spread. Gels are alcohol based and readily absorbed.16 Solutions, foams, and shampoos are particularly useful to treat psoriasis in hairy areas such as the scalp.
Corticosteroid potency ranges from Class I to Class VII, with the former being the most potent. While TCS products are typically effective with minimal systemic absorption, it is important to counsel patients on the risk of skin atrophy, impaired wound healing, and skin pigmentation changes with chronic use. With nail psoriasis, a potent topical steroid (including flurandrenolide [Cordran] tape) applied to the proximal nail fold has shown benefit.20
Topical calcineurin inhibitors (TCIs; eg, tacrolimus ointment and pimecrolimus cream) are anti-inflammatory agents often used in conjunction with topical steroids to minimize steroid use and associated adverse effects.15 A possible steroid-sparing regimen includes using a TCI Monday through Friday and a topical steroid on the weekend.
Topical vitamin D analogs (calcipotriene, calcipotriol, calcitriol) inhibit proliferation of keratinocytes and decrease the production of inflammatory mediators.15,17-19,21 Application of a vitamin D analog in combination with a high-potency TCS, systemic treatment, or phototherapy can provide greater efficacy, a more rapid onset of action, and less irritation than can the vitamin D analog used alone.21 If used in combination with UV light, apply topical vitamin D after the light therapy to prevent degradation.
Continue to: UV light therapy
UV light therapy is often used in cases refractory to topical therapy. Patients are typically prescribed 2 to 3 treatments per week with narrowband UVB (311-313 nm), the excimer laser (308 nm), or, less commonly, PUVA (UV treatment with psoralens). Treatment begins with a minimal erythema dose—the lowest dose to achieve minimal erythema of the skin before burning. When that is determined, exposure is increased as needed—depending on the response. If this is impractical or too time-consuming for the patient, an alternative recommendation would be increased exposure to natural sunlight or even use of a tanning booth. However, patients must then be cautioned about the increased risk of skin cancer.
Refractory/severe psoriasis
Patient B is a 35-year-old man with a longstanding history of psoriasis affecting his scalp and nails. Over the past 10 years, psoriatic lesions have also appeared and grown across his lower back, gluteal fold, legs, abdomen, and arms. He is now being evaluated by a rheumatologist for worsening symmetric joint pain that includes his lower back.
Methotrexate has been used to treat psoriasis and psoriatic arthritis since the 1950s. Methotrexate is a competitive inhibitor of dihydrofolate reductase and is typically given as an oral medication dosed once weekly with folic acid supplementation on the other 6 days.17 The most common adverse effects encountered with methotrexate are gastrointestinal upset and oral ulcers; however, routine monitoring for myelosuppression and hepatotoxicity is required.
Biologic therapy. When conventional therapies fail, immune-targeted treatment with “biologics” may be initiated. As knowledge of signaling pathways and the immunopathogenesis of psoriasis has increased, so has the number of biologic agents, which are generally well tolerated and effective in managing plaque psoriasis and psoriatic arthritis. Although their use, which requires monitoring, is handled primarily by specialists, familiarizing yourself with available agents can be helpful (TABLE).22
Nutritional modification and supplementation in treating skin disease still requires further investigation. Fish oil has shown benefit for cutaneous psoriasis in randomized controlled trials.7,8 Oral vitamin D supplementation requires further study, whereas selenium and B12 supplementation have not conferred consistent benefit.7 Given that several studies have demonstrated a relationship between body mass index and psoriatic disease severity, weight loss may be helpful in the management of psoriasis as well as psoriatic arthritis.8
Continue to: Other systemic agents
Other systemic agents—for individuals who cannot tolerate the biologic agents—include acitretin, azathioprine, mycophenolate mofetil, and cyclosporine.15,17
Paradoxical psoriatic reactions
When a psoriatic condition develops during biologic drug therapy, it is known as a paradoxical psoriatic reaction. The onset of de novo psoriasis has been documented during TNF-α inhibitor therapy for individuals with underlying rheumatoid arthritis.23 Skin biopsy reveals the same findings as common plaque psoriasis.
Using immunosuppressive Tx? Screen for tuberculosis
Testing to exclude a diagnosis of latent or undiagnosed tuberculosis must be performed prior to initiating immunosuppressive therapy with methotrexate or a biologic agent. Tuberculin skin testing, QuantiFERON-TB gold test, and the T-SPOT.TB test are accepted screening modalities. Discordance between tuberculin skin tests and the interferon gamma release assays in latent TB highlights the need for further study using the available QuantiFERON-TB gold test and the T-SPOT.TB test.24
CORRESPONDENCE
Karl T. Clebak, MD, FAAFP, Penn State Health Milton S. Hershey Medical Center, Department of Family and Community Medicine, 500 University Drive, Hershey, PA 17033; [email protected].
1. Jackson R. John Updike on psoriasis. At war with my skin, from the journal of a leper. J Cutan Med Surg. 2000;4:113-115.
2. Gelfand JM, Weinstein R, Porter SB, et al. Prevalence and treatment of psoriasis in the United Kingdom: a population-based study. Arch Dermatol. 2005;141:1537-1541.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Alexander H, Nestle FO. Pathogenesis and immunotherapy in cutaneous psoriasis: what can rheumatologists learn? Curr Opin Rheumatol. 2017;29:71-78.
5. Fahlén A, Engstrand L, Baker BS, et al. Comparison of bacterial microbiota in skin biopsies from normal and psoriatic skin. Arch Dermatol Res. 2012;304:15-22.
6. Takeshita J, Grewal S, Langan SM, et al. Psoriasis and comorbid diseases: epidemiology. J Am Acad Dermatol. 2017;76:377-390.
7. Millsop JW, Bhatia BK, Debbaneh M, et al. Diet and psoriasis, part III: role of nutritional supplements. J Am Acad Dermatol. 2014;71:561-569.
8. Debbaneh M, Millsop JW, Bhatia BK, et al. Diet and psoriasis, part I: impact of weight loss interventions. J Am Acad Dermatol. 2014;71:133-140.
9. Bhatia BK, Millsop JW, Debbaneh M, et al. Diet and psoriasis, part II: celiac disease and role of a gluten-free diet. J Am Acad Dermatol. 2014;71:350-358.
10. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
11. Singh RK, Lee KM, Ucmak D, et al. Erythrodermic psoriasis: pathophysiology and current treatment perspectives. Psoriasis (Aukl). 2016;6:93-104.
12. Garg A, Gladman D. Recognizing psoriatic arthritis in the dermatology clinic. J Am Acad Dermatol. 2010;63:733-748.
13. McGonagle D, Hermann KG, Tan AL. Differentiation between osteoarthritis and psoriatic arthritis: implications for pathogenesis and treatment in the biologic therapy era. Rheumatology. 2015;54:29-38.
14. Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug aggravated?: understanding pathophysiology and clinical relevance. J Clin Aesthet Dermatol. 2010;3:32-38.
15. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidence-based guide for primary care. J Am Board Fam Med. 2013;26:787-801.
16. Helm MF, Farah JB, Carvalho M, et al. Compounded topical medications for diseases of the skin: a long tradition still relevant today. N Am J Med Sci. 2017;10:116-118.
17. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013;87:626-633.
18. Helfrich YR, Sachs DL, Kang S. Topical vitamin D3. In: Wolverton SE, ed. Comprehensive Dermatologic Drug Therapy. 2nd ed. Philadelphia, PA: Saunders; 2007:691-695.
19. Lebwohl M, Siskin SB, Epinette W, et al. A multicenter trial of calcipotriene ointment and halobetasol ointment compared with either agent alone for the treatment of psoriasis. J Am Acad Dermatol. 1996;35:268-269.
20. Pasch MC. Nail psoriasis: a review of treatment options. Drugs. 2016;76:675-705.
21. Bagel J, Gold LS. Combining topical psoriasis treatment to enhance systemic and phototherapy: a review of the literature. J Drugs Dermatol. 2017;16:1209-1222.
22. Rønholt K, Iversen L. Old and new biological therapies for psoriasis. Int J Mol Sci. 2017;18:e2297.
23. Toussirot É, Aubin F. Paradoxical reactions under TNF-alpha blocking agents and other biologic agents given for chronic immune-mediated diseases: an analytical and comprehensive overview. RMD Open. 2016;2:e000239.
24. Connell TG, Ritz N, Paxton GA, et al. A three-way comparison of tuberculin skin testing, QuantiFERON-TB gold and T-SPOT.TB in children. PLoS One. 2008;3:e2624.
1. Jackson R. John Updike on psoriasis. At war with my skin, from the journal of a leper. J Cutan Med Surg. 2000;4:113-115.
2. Gelfand JM, Weinstein R, Porter SB, et al. Prevalence and treatment of psoriasis in the United Kingdom: a population-based study. Arch Dermatol. 2005;141:1537-1541.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Alexander H, Nestle FO. Pathogenesis and immunotherapy in cutaneous psoriasis: what can rheumatologists learn? Curr Opin Rheumatol. 2017;29:71-78.
5. Fahlén A, Engstrand L, Baker BS, et al. Comparison of bacterial microbiota in skin biopsies from normal and psoriatic skin. Arch Dermatol Res. 2012;304:15-22.
6. Takeshita J, Grewal S, Langan SM, et al. Psoriasis and comorbid diseases: epidemiology. J Am Acad Dermatol. 2017;76:377-390.
7. Millsop JW, Bhatia BK, Debbaneh M, et al. Diet and psoriasis, part III: role of nutritional supplements. J Am Acad Dermatol. 2014;71:561-569.
8. Debbaneh M, Millsop JW, Bhatia BK, et al. Diet and psoriasis, part I: impact of weight loss interventions. J Am Acad Dermatol. 2014;71:133-140.
9. Bhatia BK, Millsop JW, Debbaneh M, et al. Diet and psoriasis, part II: celiac disease and role of a gluten-free diet. J Am Acad Dermatol. 2014;71:350-358.
10. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
11. Singh RK, Lee KM, Ucmak D, et al. Erythrodermic psoriasis: pathophysiology and current treatment perspectives. Psoriasis (Aukl). 2016;6:93-104.
12. Garg A, Gladman D. Recognizing psoriatic arthritis in the dermatology clinic. J Am Acad Dermatol. 2010;63:733-748.
13. McGonagle D, Hermann KG, Tan AL. Differentiation between osteoarthritis and psoriatic arthritis: implications for pathogenesis and treatment in the biologic therapy era. Rheumatology. 2015;54:29-38.
14. Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug aggravated?: understanding pathophysiology and clinical relevance. J Clin Aesthet Dermatol. 2010;3:32-38.
15. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidence-based guide for primary care. J Am Board Fam Med. 2013;26:787-801.
16. Helm MF, Farah JB, Carvalho M, et al. Compounded topical medications for diseases of the skin: a long tradition still relevant today. N Am J Med Sci. 2017;10:116-118.
17. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013;87:626-633.
18. Helfrich YR, Sachs DL, Kang S. Topical vitamin D3. In: Wolverton SE, ed. Comprehensive Dermatologic Drug Therapy. 2nd ed. Philadelphia, PA: Saunders; 2007:691-695.
19. Lebwohl M, Siskin SB, Epinette W, et al. A multicenter trial of calcipotriene ointment and halobetasol ointment compared with either agent alone for the treatment of psoriasis. J Am Acad Dermatol. 1996;35:268-269.
20. Pasch MC. Nail psoriasis: a review of treatment options. Drugs. 2016;76:675-705.
21. Bagel J, Gold LS. Combining topical psoriasis treatment to enhance systemic and phototherapy: a review of the literature. J Drugs Dermatol. 2017;16:1209-1222.
22. Rønholt K, Iversen L. Old and new biological therapies for psoriasis. Int J Mol Sci. 2017;18:e2297.
23. Toussirot É, Aubin F. Paradoxical reactions under TNF-alpha blocking agents and other biologic agents given for chronic immune-mediated diseases: an analytical and comprehensive overview. RMD Open. 2016;2:e000239.
24. Connell TG, Ritz N, Paxton GA, et al. A three-way comparison of tuberculin skin testing, QuantiFERON-TB gold and T-SPOT.TB in children. PLoS One. 2008;3:e2624.
PRACTICE RECOMMENDATIONS
› Consider guttate psoriasis if small (often < 1 cm) pink scaly papules appear suddenly, particularly in a child who has an upper respiratory tract infection. C
› Document extent of disease using a tool such as the Psoriasis Area and Severity Index, which calculates a score based on the area (extent) of involvement surrounding 4 major anatomical regions. C
› Consider prescribing UV light treatment or a combination of alcitretin and topical corticosteroid if > 10% of the body surface area is involved but joints are not affected. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Progressive discoloration over the right shoulder
A 15-year-old Caucasian boy presented for evaluation of an asymptomatic brown patch on his right shoulder. While the patient’s mother first noticed the patch when he was 5 years old, the discolored area had recently been expanding in size and had developed hypertrichosis. The patient was otherwise healthy; he took no medications and denied any symptoms or history of trauma to the area. None of his siblings were similarly affected.
A physical examination revealed a well-demarcated hyperpigmented patch with an irregularly shaped border and an increased number of terminal hairs (FIGURE 1). The affected area was not indurated, and there were no muscular or skeletal abnormalities on inspection. Examination of the patch under a dermatoscope revealed islands of reticular (lattice-like) hyperpigmentation, focal hypopigmentation, and prominent follicles (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
DIAGNOSIS: Becker melanosis
Becker melanosis (also called Becker’s nevus or Becker’s pigmentary hamartoma) is an organoid hamartoma that is most common among males.1 This benign area of hyperpigmentation typically manifests as a circumscribed patch with an irregular border on the upper trunk, shoulders, or upper arms of young men. Becker melanosis is usually acquired and typically comes to medical attention around the time of puberty, although there may be a history of discoloration (as was true in this case).
A diagnosis that’s usually made clinically
Androgenic origin. Because of the male predominance and association with hypertrichosis (and for that matter, acne), androgens have been thought to play a role in the development of Becker melanosis.2 The condition affects about 1 in 200 young men.1 To date, no specific gene defect has been identified.
Underlying hypoplasia of the breast or musculoskeletal abnormalities are uncommonly associated with Becker melanosis. When these abnormalities are present, the condition is known as Becker’s nevus syndrome.3
Look for the pattern. Becker melanosis is associated with homogenous brown patches with perifollicular hypopigmentation, sometimes with a faint reticular pattern.4,5 The diagnosis can usually be made clinically, but a skin biopsy can be helpful to confirm questionable cases. Dermoscopy can also assist in diagnosis. In this case, our patient’s presentation was typical, and additional studies were not needed.
Other causes of hyperpigmentation
The differential diagnosis includes other localized disorders associated with hyperpigmentation (TABLE1,3,4).
Continue to: Morphea
Morphea represents a thickening of collagen bundles in the skin. Although morphea can affect the shoulder and trunk, as Becker melanosis does, lesions of morphea feel firm to the touch and are not associated with hypertrichosis.
Localized post-inflammatory hyperpigmentation occurs following a traumatic event, such as a burn, or a prior dermatosis, such as zoster. Careful history-taking can uncover an antecedent inflammatory condition. Post-inflammatory pigment changes do not typically result in hypertrichosis.
Café-au-lait macules can manifest as isolated areas of discoloration. These macules can be an important indicator of neurofibromatosis, a genetic disorder in which tumors grow in the nervous system. Melanocytic hamartomas of the iris (Lisch nodules), axillary freckling (Crowe’s sign), or multiple cutaneous neurofibromas serve as additional clues to neurofibromatosis. In ambiguous cases, a skin biopsy can help differentiate a café au lait macule from Becker melanosis.
To treat or not to treat?
No treatment other than reassurance is needed in most cases of Becker melanosis, as it is a benign condition. Protecting the area from sunlight can minimize darkening and contrast with the surrounding skin. Electrolysis and laser therapy can be used to treat the associated hypertrichosis; laser therapy can also reduce the hyperpigmentation. Nonablative fractional resurfacing accompanied by laser hair removal is also reported to be of value.6
Our patient was satisfied with reassurance of the benign nature of the condition and did not elect treatment.
CORRESPONDENCE
Matthew F. Helm, MD, 500 University Drive, Suite 4300, Department of Dermatology, HU14, UPC II, Hershey, PA 17033-2360; [email protected]
1. Rabinovitz HS, Barnhill RL. Benign melanocytic neoplasms. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012;112:1853-1854.
2. Person JR, Longcope C. Becker’s nevus: an androgen-mediated hyperplasia with increased androgen receptors. J Am Acad Dermatol. 1984;10:235-238.
3. Cosendey FE, Martinez NS, Bernhard GA, et al. Becker nevus syndrome. An Bras Dermatol. 2010;85:379-384.
4. Ingordo V, Iannazzone SS, Cusano F, et al. Dermoscopic features of congenital melanocytic nevus and Becker nevus in an adult male population: an analysis with 10-fold magnification. Dermatology. 2006;212:354-360.
5. Luk DC, Lam SY, Cheung PC, et al. Dermoscopy for common skin problems in Chinese children using a novel Hong Kong-made dermoscope. Hong Kong Med J. 2014;20:495-503.
6. Balaraman B, Friedman PM. Hypertrichotic Becker’s nevi treated with combination 1,550nm non-ablative fractional photothermolysis and laser hair removal. Lasers Surg Med. 2016;48:350-353.
A 15-year-old Caucasian boy presented for evaluation of an asymptomatic brown patch on his right shoulder. While the patient’s mother first noticed the patch when he was 5 years old, the discolored area had recently been expanding in size and had developed hypertrichosis. The patient was otherwise healthy; he took no medications and denied any symptoms or history of trauma to the area. None of his siblings were similarly affected.
A physical examination revealed a well-demarcated hyperpigmented patch with an irregularly shaped border and an increased number of terminal hairs (FIGURE 1). The affected area was not indurated, and there were no muscular or skeletal abnormalities on inspection. Examination of the patch under a dermatoscope revealed islands of reticular (lattice-like) hyperpigmentation, focal hypopigmentation, and prominent follicles (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
DIAGNOSIS: Becker melanosis
Becker melanosis (also called Becker’s nevus or Becker’s pigmentary hamartoma) is an organoid hamartoma that is most common among males.1 This benign area of hyperpigmentation typically manifests as a circumscribed patch with an irregular border on the upper trunk, shoulders, or upper arms of young men. Becker melanosis is usually acquired and typically comes to medical attention around the time of puberty, although there may be a history of discoloration (as was true in this case).
A diagnosis that’s usually made clinically
Androgenic origin. Because of the male predominance and association with hypertrichosis (and for that matter, acne), androgens have been thought to play a role in the development of Becker melanosis.2 The condition affects about 1 in 200 young men.1 To date, no specific gene defect has been identified.
Underlying hypoplasia of the breast or musculoskeletal abnormalities are uncommonly associated with Becker melanosis. When these abnormalities are present, the condition is known as Becker’s nevus syndrome.3
Look for the pattern. Becker melanosis is associated with homogenous brown patches with perifollicular hypopigmentation, sometimes with a faint reticular pattern.4,5 The diagnosis can usually be made clinically, but a skin biopsy can be helpful to confirm questionable cases. Dermoscopy can also assist in diagnosis. In this case, our patient’s presentation was typical, and additional studies were not needed.
Other causes of hyperpigmentation
The differential diagnosis includes other localized disorders associated with hyperpigmentation (TABLE1,3,4).
Continue to: Morphea
Morphea represents a thickening of collagen bundles in the skin. Although morphea can affect the shoulder and trunk, as Becker melanosis does, lesions of morphea feel firm to the touch and are not associated with hypertrichosis.
Localized post-inflammatory hyperpigmentation occurs following a traumatic event, such as a burn, or a prior dermatosis, such as zoster. Careful history-taking can uncover an antecedent inflammatory condition. Post-inflammatory pigment changes do not typically result in hypertrichosis.
Café-au-lait macules can manifest as isolated areas of discoloration. These macules can be an important indicator of neurofibromatosis, a genetic disorder in which tumors grow in the nervous system. Melanocytic hamartomas of the iris (Lisch nodules), axillary freckling (Crowe’s sign), or multiple cutaneous neurofibromas serve as additional clues to neurofibromatosis. In ambiguous cases, a skin biopsy can help differentiate a café au lait macule from Becker melanosis.
To treat or not to treat?
No treatment other than reassurance is needed in most cases of Becker melanosis, as it is a benign condition. Protecting the area from sunlight can minimize darkening and contrast with the surrounding skin. Electrolysis and laser therapy can be used to treat the associated hypertrichosis; laser therapy can also reduce the hyperpigmentation. Nonablative fractional resurfacing accompanied by laser hair removal is also reported to be of value.6
Our patient was satisfied with reassurance of the benign nature of the condition and did not elect treatment.
CORRESPONDENCE
Matthew F. Helm, MD, 500 University Drive, Suite 4300, Department of Dermatology, HU14, UPC II, Hershey, PA 17033-2360; [email protected]
A 15-year-old Caucasian boy presented for evaluation of an asymptomatic brown patch on his right shoulder. While the patient’s mother first noticed the patch when he was 5 years old, the discolored area had recently been expanding in size and had developed hypertrichosis. The patient was otherwise healthy; he took no medications and denied any symptoms or history of trauma to the area. None of his siblings were similarly affected.
A physical examination revealed a well-demarcated hyperpigmented patch with an irregularly shaped border and an increased number of terminal hairs (FIGURE 1). The affected area was not indurated, and there were no muscular or skeletal abnormalities on inspection. Examination of the patch under a dermatoscope revealed islands of reticular (lattice-like) hyperpigmentation, focal hypopigmentation, and prominent follicles (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
DIAGNOSIS: Becker melanosis
Becker melanosis (also called Becker’s nevus or Becker’s pigmentary hamartoma) is an organoid hamartoma that is most common among males.1 This benign area of hyperpigmentation typically manifests as a circumscribed patch with an irregular border on the upper trunk, shoulders, or upper arms of young men. Becker melanosis is usually acquired and typically comes to medical attention around the time of puberty, although there may be a history of discoloration (as was true in this case).
A diagnosis that’s usually made clinically
Androgenic origin. Because of the male predominance and association with hypertrichosis (and for that matter, acne), androgens have been thought to play a role in the development of Becker melanosis.2 The condition affects about 1 in 200 young men.1 To date, no specific gene defect has been identified.
Underlying hypoplasia of the breast or musculoskeletal abnormalities are uncommonly associated with Becker melanosis. When these abnormalities are present, the condition is known as Becker’s nevus syndrome.3
Look for the pattern. Becker melanosis is associated with homogenous brown patches with perifollicular hypopigmentation, sometimes with a faint reticular pattern.4,5 The diagnosis can usually be made clinically, but a skin biopsy can be helpful to confirm questionable cases. Dermoscopy can also assist in diagnosis. In this case, our patient’s presentation was typical, and additional studies were not needed.
Other causes of hyperpigmentation
The differential diagnosis includes other localized disorders associated with hyperpigmentation (TABLE1,3,4).
Continue to: Morphea
Morphea represents a thickening of collagen bundles in the skin. Although morphea can affect the shoulder and trunk, as Becker melanosis does, lesions of morphea feel firm to the touch and are not associated with hypertrichosis.
Localized post-inflammatory hyperpigmentation occurs following a traumatic event, such as a burn, or a prior dermatosis, such as zoster. Careful history-taking can uncover an antecedent inflammatory condition. Post-inflammatory pigment changes do not typically result in hypertrichosis.
Café-au-lait macules can manifest as isolated areas of discoloration. These macules can be an important indicator of neurofibromatosis, a genetic disorder in which tumors grow in the nervous system. Melanocytic hamartomas of the iris (Lisch nodules), axillary freckling (Crowe’s sign), or multiple cutaneous neurofibromas serve as additional clues to neurofibromatosis. In ambiguous cases, a skin biopsy can help differentiate a café au lait macule from Becker melanosis.
To treat or not to treat?
No treatment other than reassurance is needed in most cases of Becker melanosis, as it is a benign condition. Protecting the area from sunlight can minimize darkening and contrast with the surrounding skin. Electrolysis and laser therapy can be used to treat the associated hypertrichosis; laser therapy can also reduce the hyperpigmentation. Nonablative fractional resurfacing accompanied by laser hair removal is also reported to be of value.6
Our patient was satisfied with reassurance of the benign nature of the condition and did not elect treatment.
CORRESPONDENCE
Matthew F. Helm, MD, 500 University Drive, Suite 4300, Department of Dermatology, HU14, UPC II, Hershey, PA 17033-2360; [email protected]
1. Rabinovitz HS, Barnhill RL. Benign melanocytic neoplasms. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012;112:1853-1854.
2. Person JR, Longcope C. Becker’s nevus: an androgen-mediated hyperplasia with increased androgen receptors. J Am Acad Dermatol. 1984;10:235-238.
3. Cosendey FE, Martinez NS, Bernhard GA, et al. Becker nevus syndrome. An Bras Dermatol. 2010;85:379-384.
4. Ingordo V, Iannazzone SS, Cusano F, et al. Dermoscopic features of congenital melanocytic nevus and Becker nevus in an adult male population: an analysis with 10-fold magnification. Dermatology. 2006;212:354-360.
5. Luk DC, Lam SY, Cheung PC, et al. Dermoscopy for common skin problems in Chinese children using a novel Hong Kong-made dermoscope. Hong Kong Med J. 2014;20:495-503.
6. Balaraman B, Friedman PM. Hypertrichotic Becker’s nevi treated with combination 1,550nm non-ablative fractional photothermolysis and laser hair removal. Lasers Surg Med. 2016;48:350-353.
1. Rabinovitz HS, Barnhill RL. Benign melanocytic neoplasms. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012;112:1853-1854.
2. Person JR, Longcope C. Becker’s nevus: an androgen-mediated hyperplasia with increased androgen receptors. J Am Acad Dermatol. 1984;10:235-238.
3. Cosendey FE, Martinez NS, Bernhard GA, et al. Becker nevus syndrome. An Bras Dermatol. 2010;85:379-384.
4. Ingordo V, Iannazzone SS, Cusano F, et al. Dermoscopic features of congenital melanocytic nevus and Becker nevus in an adult male population: an analysis with 10-fold magnification. Dermatology. 2006;212:354-360.
5. Luk DC, Lam SY, Cheung PC, et al. Dermoscopy for common skin problems in Chinese children using a novel Hong Kong-made dermoscope. Hong Kong Med J. 2014;20:495-503.
6. Balaraman B, Friedman PM. Hypertrichotic Becker’s nevi treated with combination 1,550nm non-ablative fractional photothermolysis and laser hair removal. Lasers Surg Med. 2016;48:350-353.
Biopsies for skin cancer detection: Dispelling the myths
Once it’s determined that a growth requires a biopsy, there is often uncertainty about which type of biopsy to perform. Insufficient knowledge of, and/or experience with, the various biopsy modalities may deter FPs from performing skin biopsies when they are indicated. To help fill the knowledge gaps and better position FPs to tackle skin cancer in its earliest stages, this article identifies and dispels 5 of the most common myths surrounding skin biopsies for the detection of basal and squamous cell carcinoma and melanoma.
MYTH #1
A punch biopsy is always preferred for suspected melanoma because it gets full depth.
A deep shave biopsy (saucerization)—not a punch biopsy—is usually the procedure of choice when biopsying a lesion suspected to be melanoma.2 The National Comprehensive Cancer Network (NCCN) "Melanoma Clinical Practice Guidelines in Oncology" state that an excisional biopsy (elliptical, punch, or saucerization) with a 1- to 3-mm margin is the preferred method of biopsy for suspected melanoma.3 However, a punch biopsy should be performed only if a 1- to 3-mm margin all around a suspected melanoma can be obtained. Otherwise, a saucerization or elliptical excision is preferred.3
The saucerization technique generally permits optimal sampling in terms of both the breadth and depth of the growth, providing the pathologist with sufficient tissue from both the epidermis and dermis (FIGURE 1).
Why are breadth/depth important? Breadth is important because showing the pathologist the epidermis (especially the edge) of a suspected melanocytic tumor allows for detection of pagetoid spread (upward movement through the epidermis) of melanocytes and of single melanocytes at the edge of a tumor. Single melanocytes at the edge of a tumor and pagetoid spread are histologic features of melanoma that help to distinguish these lesions from nevi, which tend to have nested melanocytes.2
Depth is important because it predicts prognosis and impacts management. For tumors 0.8 mm to 1 mm deep, a sentinel lymph node biopsy (SLNB) should be considered.3,4 Although the tumor depth threshold for a SLNB is still debated, most skin cancer experts in the United States agree that a melanoma thicker than 1 mm qualifies for this procedure. Some melanomas with high-risk features (such as ulceration) qualify for an SNLB even if they are <1 mm in depth.5 An SLNB provides prognostic information, and a positive SLNB directly affects staging.
[polldaddy:9990508]
Avoid partial biopsies. For tumors that have been partially biopsied with a punch or shallow shave biopsy, evaluation of the remaining neoplasm after subsequent excision leads to tumor upstaging in 21% of patients, with 10% qualifying for an SLNB.6 Thus, the goal should always be to obtain the entire depth of the tumor with the initial biopsy.
In addition, surgical margins are determined by primary tumor depth. To ensure a depth greater than 1 mm, aim to obtain a tissue specimen that is at least as thick as a dime (1.3 mm).
Because the goal is to avoid partial sampling, a challenge exists when the suspicious growth is large. Many melanomas are broader than a centimeter. And while punch biopsies ensure a depth of 1 mm or more, they risk missing the thickest portion of the tumor.7
Partial sampling of large melanocytic tumors with punch biopsies can lead to sampling error.8 Ng et al9 found there was a significant increase in histopathologic misdiagnosis with a punch biopsy of part of a melanoma (odds ratio [OR]=16.6; 95% confidence interval [CI], 10-27; P<.001) and with shallow shave biopsy (OR=2.6; 95% CI, 1.2-5.7; P=.02) compared with excisional biopsy (including saucerization).9 Punch biopsy of part of a melanoma was also associated with increased odds of misdiagnosis with an adverse outcome (OR=20; 95% CI, 10-41; P<.001).
Punch biopsies do, however, offer a reasonable alternative when the melanoma is too broad for a complete saucerization. In these cases, consider multiple 4- to 6-mm punch biopsies to reduce the risk of sampling error.
Avoid performing punch biopsies <4 mm, as the breadth of tissue is inadequate. For example, even with dermoscopy, facial lentigo maligna melanoma is often difficult to differentiate from pigmented actinic keratosis and solar lentigines. (See JFP’s Watch and Learn Video on dermoscopy.) A broad shave biopsy is the preferred method of biopsy for lentigo maligna melanoma in situ according to the NCCN.3 And there have been several reports showing that the results of shave biopsies of melanocytic lesions are cosmetically acceptable to patients.10,11
If the biopsy confirms malignancy, a larger surgery with suturing will be needed. The most important issue to keep in mind is that if partial sampling leads to a benign diagnosis of a suspicious lesion, then the remainder of the lesion must be excised and sent for pathology.
Saucerization is also the preferred biopsy type for basal cell and squamous cell carcinomas (SCCs). Studies have shown tumor depth is the most important factor in predicting metastasis of SCC, as well as tumor relapse rate, making accurate identification of the depth of the tumor important for both management and prognosis.12,13 Determining the thickness of the SCC is important for guiding management. SCC in situ is more amenable than invasive SCC to topical therapy or electrodesiccation and curettage.
What you’ll need. FPs can perform saucerization quickly and easily in the office during a standard 15-minute visit. Of course, it is essential to have all the necessary materials available. The key materials needed are lidocaine and epinephrine, a sharp razor blade such as a DermaBlade, and something for hemostasis (aluminum chloride and/or an electrosurgical instrument). Cotton-tipped applicators to apply the aluminum chloride and needles and syringes to administer the local anesthetic are also needed. (See JFP’s Watch and Learn Video on shave biopsy.) A quick saucerization eliminates the need for the patient to return for an elliptical excision and prevents a delayed diagnosis that can occur as a result of a long wait to see a dermatologist.
As a final note, the pathology order form should be completed with information on biopsy type, clinical presentation, differential diagnosis, and whether or not the full lesion was excised.
MYTH #2
A wide excisional biopsy is required for a suspected melanoma.
While complete excision of the entire tumor does allow the pathologist to evaluate the entire growth, wide (>3 mm) margins on the initial biopsy are not necessary. In fact, there are potential disadvantages to full excisional biopsy.
For example, seborrheic keratoses and other benign growths can mimic melanoma. Neither the physician nor the patient wants to learn that a large elliptical wound was created for a growth that turned out to be a benign seborrheic keratosis. Saucerization provides the pathologist with the entire lesion, and the resulting shallow wound heals as a round scar that is most often acceptable to patients.10,11,14 In addition, excisional biopsies carry a higher risk of infection than does saucerization.
Even when the index of suspicion is high for melanoma, a wide margin is not indicated. NCCN guidelines suggest that the margins around a suspected melanoma on initial biopsy not exceed 3 mm to avoid disrupting the accuracy of an SLNB (FIGURE 2).3
In addition, time constraints (elliptical excisional biopsies can take up to one hour, especially when a layered closure is performed) and a lack of surgical training may prohibit FPs from performing excisions.
One study found that while dermatologists prefer shave biopsies (80.5%), surgeons prefer excisional biopsies (46.3%) and primary care physicians prefer punch biopsies (44%) for biopsy of a growth suspicious for melanoma.7 In fact, of the biopsies FPs perform, only 29% are of the shave variety.7
However, deep shave biopsies can be performed quickly, with the whole process taking less than 5 minutes. We advocate performing them at the time of presentation, as the evidence shows that deep shave biopsies of suspected melanoma are reliable and accurate in 97% of cases.15
MYTH #3
A partial biopsy can make the cancer spread.
There is no evidence to support that a partial biopsy has any effect on the local recurrence or metastatic potential of malignant melanoma.16 In fact, a biopsy elicits an inflammatory response that activates the patient’s immune system and often causes tumor lysis. Some tumors may even resolve after biopsy. In our clinical practice, we have had several cases of basal cell carcinoma resolve after a biopsy without additional treatment.
MYTH #4
If after performing a deep shave biopsy, tumor or pigment remains, you must leave it because a second biopsy specimen can’t be added to the first.
If pigment is visible after an initial shave or punch biopsy, it is reasonable to obtain additional tissue from the base of the biopsy site. While the deeper tissue cannot be added to the initial specimen for the purposes of Breslow’s depth, it is still helpful for the pathologist to have the sample so that he or she can analyze the tumor cells in the dermis. (Melanoma tumor depth is measured as the maximum distance between malignant cells and the top of the granular layer.17) In these situations, be sure to let the pathologist know that there are 2 specimens in the container.
In general, it is valuable to get as much of the tissue as possible at the time of the initial biopsy. One way to avoid leaving tumor at the base of the biopsy is to look at
MYTH #5
Epinephrine cannot be used for biopsies on the fingers, toes, nose, or penis.
Lidocaine with epinephrine is safe to use in areas with end-arteries, such as the fingers, toes, nose (FIGURE 4), and penis. There is no evidence to support the notion that local anesthesia with vasoconstriction can cause necrosis in these areas, and no case of necrosis has been reported since the introduction of commercial lidocaine with epinephrine in 1948.18
In addition to an absence of complications, epinephrine supplementation results in a relatively bloodless operating field and longer effectiveness of local anesthesia, as a study of more than 10,000 ear and nose surgeries using epinephrine-supplemented local anesthetics showed.19 The relative absence of blood in the operating field significantly reduces the duration of surgery and increases the healing rate because less electrocautery is needed.19
Similarly, the addition of epinephrine in digital blocks minimizes the need for tourniquets and large volumes of anesthetic and provides better and longer pain control during procedures.20 This topic was addressed by Prabhakar et al in a Cochrane Review in 2015.21 While digital surgeries are common, there were only 4 randomized controlled studies addressing the use of epinephrine in digital blocks. In these studies, there were no reports of adverse events, such as ischemia distal to the injection site. Evidence suggests that epinephrine in digital blocks can even be used safely in patients with vascular disease.22
And while the use of epinephrine with lidocaine in sites with end-arteries is beneficial for hemostasis and does not seem to pose a risk of ischemia, it is prudent to use the smallest volume of epinephrine (with lidocaine) needed to achieve anesthesia for the site.
CORRESPONDENCE
Elizabeth V. Seiverling, MD, 300 Southborough Drive, Suite 201, South Portland, ME 04106; [email protected].
1. Kerr OA, Tidman MJ, Walker JJ, et al. The profile of dermatological problems in primary care. Clin Exp Dermatol. 2010;35:380-383.
2. Hosler GA, Patterson JW. Lentigines, nevi, and melanomas. In: Patterson JW, ed. Weedon’s Skin Pathology. Elsevier; 2015:32,837-901.
3. Coit DG, Andtbacka R, Bichakjian CK, et al. Melanoma. J Natl Compr Canc Netw. 2009;7:250-275.
4. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer Staging Manual. Springer International Publishing; 2017;8:563-585.
5. American Joint Committee on Cancer. Implementation of AJCC 8th Edition Cancer Staging System. Available at: https://cancerstaging.org/About/news/Pages/Implementation-of-AJCC-8th-Edition-Cancer-Staging-System.aspx. Accessed April 2, 2018.
6. Karimipour DJ, Schwartz JL, Wang TS, et al. Microstaging accuracy after subtotal incisional biopsy of cutaneous melanoma. J Am Acad Dermatol. 2005;52:798-802.
7. Kaiser S, Vassell R, Pinckney RG, et al. Clinical impact of biopsy method on the quality of surgical management in melanoma. J Surg Oncol. 2014;109:775-779.
8. Montgomery BD, Sadler GM. Punch biopsy of pigmented lesions is potentially hazardous. Can Fam Physician. 2009;55:24.
9. Ng JC, Swain S, Dowling JP, et al. The impact of partial biopsy on histopathologic diagnosis of cutaneous melanoma: experience of an Australian tertiary referral service. Arch Dermatol. 2010;146:234-239.
10. Gambichler T, Senger E, Rapp S, et al. Deep shave excision of macular melanocytic nevi with the razor blade biopsy technique. Dermatol Surg. 2000;26:662-666.
11. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg. 2005;31(9 Pt 1):1112-1115.
12. D'souza G, Carey TE, William WN Jr, et al. Epidemiology of head and neck squamous cell cancer among HIV-infected patients. J Acquir Immune Defic Syndr. 2014;65:603-610.
13. Edge SB, Byrd DR, Compton CC, et al, eds. AJCC Cancer Staging Handbook. 7th ed. New York, NY: Springer; 2010.
14. Elston DM, Stratman EJ, Miller SJ, et al. Skin biopsy. J Am Acad Dermatol. 2016;74:1-16.
15. Zager JS, Hochwald SN, Marzban SS, et al. Shave biopsy is a safe and accurate method for the initial evaluation of melanoma. J Am Coll Surg. 2011;212:454-460.
16. Chanda JJ, Callen JP. Adverse effect of melanoma incision. J Am Acad Dermatol. 1985;13:519-522.
17. Noroozi N, Zakerolhosseini A. Computerized measurement of melanocytic tumor depth in skin histopathological images. Micron. 2015;77:44-56.
18. Nielsen LJ, Lumholt P, Hölmich LR. [Local anaesthesia with vasoconstrictor is safe to use in areas with end-arteries in fingers, toes, noses and ears]. Ugeskr Laeger. 2014;176(44).
19. Häfner HM, Röcken M, Breuninger H. Epinephrine-supplemented local anesthetics for ear and nose surgery: clinical use without complications in more than 10,000 surgical procedures. J Dtsch Dermatol Ges. 2005;3:195-199.
20. Krunic AL, Wang LC, Soltani K, et al. Digital anesthesia with epinephrine: an old myth revisited. J Am Acad Dermatol. 2004;51:755-759.
21. Prabhakar H, Rath S, Kalaivani M, et al. Adrenaline with lidocaine for digital nerve blocks. Cochrane Database Syst Rev. 2015;(3):CD010645.
22. Ilicki J. Safety of epinephrine in digital nerve blocks: a literature review. J Emerg Med. 2015;49:799-809.
Once it’s determined that a growth requires a biopsy, there is often uncertainty about which type of biopsy to perform. Insufficient knowledge of, and/or experience with, the various biopsy modalities may deter FPs from performing skin biopsies when they are indicated. To help fill the knowledge gaps and better position FPs to tackle skin cancer in its earliest stages, this article identifies and dispels 5 of the most common myths surrounding skin biopsies for the detection of basal and squamous cell carcinoma and melanoma.
MYTH #1
A punch biopsy is always preferred for suspected melanoma because it gets full depth.
A deep shave biopsy (saucerization)—not a punch biopsy—is usually the procedure of choice when biopsying a lesion suspected to be melanoma.2 The National Comprehensive Cancer Network (NCCN) "Melanoma Clinical Practice Guidelines in Oncology" state that an excisional biopsy (elliptical, punch, or saucerization) with a 1- to 3-mm margin is the preferred method of biopsy for suspected melanoma.3 However, a punch biopsy should be performed only if a 1- to 3-mm margin all around a suspected melanoma can be obtained. Otherwise, a saucerization or elliptical excision is preferred.3
The saucerization technique generally permits optimal sampling in terms of both the breadth and depth of the growth, providing the pathologist with sufficient tissue from both the epidermis and dermis (FIGURE 1).
Why are breadth/depth important? Breadth is important because showing the pathologist the epidermis (especially the edge) of a suspected melanocytic tumor allows for detection of pagetoid spread (upward movement through the epidermis) of melanocytes and of single melanocytes at the edge of a tumor. Single melanocytes at the edge of a tumor and pagetoid spread are histologic features of melanoma that help to distinguish these lesions from nevi, which tend to have nested melanocytes.2
Depth is important because it predicts prognosis and impacts management. For tumors 0.8 mm to 1 mm deep, a sentinel lymph node biopsy (SLNB) should be considered.3,4 Although the tumor depth threshold for a SLNB is still debated, most skin cancer experts in the United States agree that a melanoma thicker than 1 mm qualifies for this procedure. Some melanomas with high-risk features (such as ulceration) qualify for an SNLB even if they are <1 mm in depth.5 An SLNB provides prognostic information, and a positive SLNB directly affects staging.
[polldaddy:9990508]
Avoid partial biopsies. For tumors that have been partially biopsied with a punch or shallow shave biopsy, evaluation of the remaining neoplasm after subsequent excision leads to tumor upstaging in 21% of patients, with 10% qualifying for an SLNB.6 Thus, the goal should always be to obtain the entire depth of the tumor with the initial biopsy.
In addition, surgical margins are determined by primary tumor depth. To ensure a depth greater than 1 mm, aim to obtain a tissue specimen that is at least as thick as a dime (1.3 mm).
Because the goal is to avoid partial sampling, a challenge exists when the suspicious growth is large. Many melanomas are broader than a centimeter. And while punch biopsies ensure a depth of 1 mm or more, they risk missing the thickest portion of the tumor.7
Partial sampling of large melanocytic tumors with punch biopsies can lead to sampling error.8 Ng et al9 found there was a significant increase in histopathologic misdiagnosis with a punch biopsy of part of a melanoma (odds ratio [OR]=16.6; 95% confidence interval [CI], 10-27; P<.001) and with shallow shave biopsy (OR=2.6; 95% CI, 1.2-5.7; P=.02) compared with excisional biopsy (including saucerization).9 Punch biopsy of part of a melanoma was also associated with increased odds of misdiagnosis with an adverse outcome (OR=20; 95% CI, 10-41; P<.001).
Punch biopsies do, however, offer a reasonable alternative when the melanoma is too broad for a complete saucerization. In these cases, consider multiple 4- to 6-mm punch biopsies to reduce the risk of sampling error.
Avoid performing punch biopsies <4 mm, as the breadth of tissue is inadequate. For example, even with dermoscopy, facial lentigo maligna melanoma is often difficult to differentiate from pigmented actinic keratosis and solar lentigines. (See JFP’s Watch and Learn Video on dermoscopy.) A broad shave biopsy is the preferred method of biopsy for lentigo maligna melanoma in situ according to the NCCN.3 And there have been several reports showing that the results of shave biopsies of melanocytic lesions are cosmetically acceptable to patients.10,11
If the biopsy confirms malignancy, a larger surgery with suturing will be needed. The most important issue to keep in mind is that if partial sampling leads to a benign diagnosis of a suspicious lesion, then the remainder of the lesion must be excised and sent for pathology.
Saucerization is also the preferred biopsy type for basal cell and squamous cell carcinomas (SCCs). Studies have shown tumor depth is the most important factor in predicting metastasis of SCC, as well as tumor relapse rate, making accurate identification of the depth of the tumor important for both management and prognosis.12,13 Determining the thickness of the SCC is important for guiding management. SCC in situ is more amenable than invasive SCC to topical therapy or electrodesiccation and curettage.
What you’ll need. FPs can perform saucerization quickly and easily in the office during a standard 15-minute visit. Of course, it is essential to have all the necessary materials available. The key materials needed are lidocaine and epinephrine, a sharp razor blade such as a DermaBlade, and something for hemostasis (aluminum chloride and/or an electrosurgical instrument). Cotton-tipped applicators to apply the aluminum chloride and needles and syringes to administer the local anesthetic are also needed. (See JFP’s Watch and Learn Video on shave biopsy.) A quick saucerization eliminates the need for the patient to return for an elliptical excision and prevents a delayed diagnosis that can occur as a result of a long wait to see a dermatologist.
As a final note, the pathology order form should be completed with information on biopsy type, clinical presentation, differential diagnosis, and whether or not the full lesion was excised.
MYTH #2
A wide excisional biopsy is required for a suspected melanoma.
While complete excision of the entire tumor does allow the pathologist to evaluate the entire growth, wide (>3 mm) margins on the initial biopsy are not necessary. In fact, there are potential disadvantages to full excisional biopsy.
For example, seborrheic keratoses and other benign growths can mimic melanoma. Neither the physician nor the patient wants to learn that a large elliptical wound was created for a growth that turned out to be a benign seborrheic keratosis. Saucerization provides the pathologist with the entire lesion, and the resulting shallow wound heals as a round scar that is most often acceptable to patients.10,11,14 In addition, excisional biopsies carry a higher risk of infection than does saucerization.
Even when the index of suspicion is high for melanoma, a wide margin is not indicated. NCCN guidelines suggest that the margins around a suspected melanoma on initial biopsy not exceed 3 mm to avoid disrupting the accuracy of an SLNB (FIGURE 2).3
In addition, time constraints (elliptical excisional biopsies can take up to one hour, especially when a layered closure is performed) and a lack of surgical training may prohibit FPs from performing excisions.
One study found that while dermatologists prefer shave biopsies (80.5%), surgeons prefer excisional biopsies (46.3%) and primary care physicians prefer punch biopsies (44%) for biopsy of a growth suspicious for melanoma.7 In fact, of the biopsies FPs perform, only 29% are of the shave variety.7
However, deep shave biopsies can be performed quickly, with the whole process taking less than 5 minutes. We advocate performing them at the time of presentation, as the evidence shows that deep shave biopsies of suspected melanoma are reliable and accurate in 97% of cases.15
MYTH #3
A partial biopsy can make the cancer spread.
There is no evidence to support that a partial biopsy has any effect on the local recurrence or metastatic potential of malignant melanoma.16 In fact, a biopsy elicits an inflammatory response that activates the patient’s immune system and often causes tumor lysis. Some tumors may even resolve after biopsy. In our clinical practice, we have had several cases of basal cell carcinoma resolve after a biopsy without additional treatment.
MYTH #4
If after performing a deep shave biopsy, tumor or pigment remains, you must leave it because a second biopsy specimen can’t be added to the first.
If pigment is visible after an initial shave or punch biopsy, it is reasonable to obtain additional tissue from the base of the biopsy site. While the deeper tissue cannot be added to the initial specimen for the purposes of Breslow’s depth, it is still helpful for the pathologist to have the sample so that he or she can analyze the tumor cells in the dermis. (Melanoma tumor depth is measured as the maximum distance between malignant cells and the top of the granular layer.17) In these situations, be sure to let the pathologist know that there are 2 specimens in the container.
In general, it is valuable to get as much of the tissue as possible at the time of the initial biopsy. One way to avoid leaving tumor at the base of the biopsy is to look at
MYTH #5
Epinephrine cannot be used for biopsies on the fingers, toes, nose, or penis.
Lidocaine with epinephrine is safe to use in areas with end-arteries, such as the fingers, toes, nose (FIGURE 4), and penis. There is no evidence to support the notion that local anesthesia with vasoconstriction can cause necrosis in these areas, and no case of necrosis has been reported since the introduction of commercial lidocaine with epinephrine in 1948.18
In addition to an absence of complications, epinephrine supplementation results in a relatively bloodless operating field and longer effectiveness of local anesthesia, as a study of more than 10,000 ear and nose surgeries using epinephrine-supplemented local anesthetics showed.19 The relative absence of blood in the operating field significantly reduces the duration of surgery and increases the healing rate because less electrocautery is needed.19
Similarly, the addition of epinephrine in digital blocks minimizes the need for tourniquets and large volumes of anesthetic and provides better and longer pain control during procedures.20 This topic was addressed by Prabhakar et al in a Cochrane Review in 2015.21 While digital surgeries are common, there were only 4 randomized controlled studies addressing the use of epinephrine in digital blocks. In these studies, there were no reports of adverse events, such as ischemia distal to the injection site. Evidence suggests that epinephrine in digital blocks can even be used safely in patients with vascular disease.22
And while the use of epinephrine with lidocaine in sites with end-arteries is beneficial for hemostasis and does not seem to pose a risk of ischemia, it is prudent to use the smallest volume of epinephrine (with lidocaine) needed to achieve anesthesia for the site.
CORRESPONDENCE
Elizabeth V. Seiverling, MD, 300 Southborough Drive, Suite 201, South Portland, ME 04106; [email protected].
Once it’s determined that a growth requires a biopsy, there is often uncertainty about which type of biopsy to perform. Insufficient knowledge of, and/or experience with, the various biopsy modalities may deter FPs from performing skin biopsies when they are indicated. To help fill the knowledge gaps and better position FPs to tackle skin cancer in its earliest stages, this article identifies and dispels 5 of the most common myths surrounding skin biopsies for the detection of basal and squamous cell carcinoma and melanoma.
MYTH #1
A punch biopsy is always preferred for suspected melanoma because it gets full depth.
A deep shave biopsy (saucerization)—not a punch biopsy—is usually the procedure of choice when biopsying a lesion suspected to be melanoma.2 The National Comprehensive Cancer Network (NCCN) "Melanoma Clinical Practice Guidelines in Oncology" state that an excisional biopsy (elliptical, punch, or saucerization) with a 1- to 3-mm margin is the preferred method of biopsy for suspected melanoma.3 However, a punch biopsy should be performed only if a 1- to 3-mm margin all around a suspected melanoma can be obtained. Otherwise, a saucerization or elliptical excision is preferred.3
The saucerization technique generally permits optimal sampling in terms of both the breadth and depth of the growth, providing the pathologist with sufficient tissue from both the epidermis and dermis (FIGURE 1).
Why are breadth/depth important? Breadth is important because showing the pathologist the epidermis (especially the edge) of a suspected melanocytic tumor allows for detection of pagetoid spread (upward movement through the epidermis) of melanocytes and of single melanocytes at the edge of a tumor. Single melanocytes at the edge of a tumor and pagetoid spread are histologic features of melanoma that help to distinguish these lesions from nevi, which tend to have nested melanocytes.2
Depth is important because it predicts prognosis and impacts management. For tumors 0.8 mm to 1 mm deep, a sentinel lymph node biopsy (SLNB) should be considered.3,4 Although the tumor depth threshold for a SLNB is still debated, most skin cancer experts in the United States agree that a melanoma thicker than 1 mm qualifies for this procedure. Some melanomas with high-risk features (such as ulceration) qualify for an SNLB even if they are <1 mm in depth.5 An SLNB provides prognostic information, and a positive SLNB directly affects staging.
[polldaddy:9990508]
Avoid partial biopsies. For tumors that have been partially biopsied with a punch or shallow shave biopsy, evaluation of the remaining neoplasm after subsequent excision leads to tumor upstaging in 21% of patients, with 10% qualifying for an SLNB.6 Thus, the goal should always be to obtain the entire depth of the tumor with the initial biopsy.
In addition, surgical margins are determined by primary tumor depth. To ensure a depth greater than 1 mm, aim to obtain a tissue specimen that is at least as thick as a dime (1.3 mm).
Because the goal is to avoid partial sampling, a challenge exists when the suspicious growth is large. Many melanomas are broader than a centimeter. And while punch biopsies ensure a depth of 1 mm or more, they risk missing the thickest portion of the tumor.7
Partial sampling of large melanocytic tumors with punch biopsies can lead to sampling error.8 Ng et al9 found there was a significant increase in histopathologic misdiagnosis with a punch biopsy of part of a melanoma (odds ratio [OR]=16.6; 95% confidence interval [CI], 10-27; P<.001) and with shallow shave biopsy (OR=2.6; 95% CI, 1.2-5.7; P=.02) compared with excisional biopsy (including saucerization).9 Punch biopsy of part of a melanoma was also associated with increased odds of misdiagnosis with an adverse outcome (OR=20; 95% CI, 10-41; P<.001).
Punch biopsies do, however, offer a reasonable alternative when the melanoma is too broad for a complete saucerization. In these cases, consider multiple 4- to 6-mm punch biopsies to reduce the risk of sampling error.
Avoid performing punch biopsies <4 mm, as the breadth of tissue is inadequate. For example, even with dermoscopy, facial lentigo maligna melanoma is often difficult to differentiate from pigmented actinic keratosis and solar lentigines. (See JFP’s Watch and Learn Video on dermoscopy.) A broad shave biopsy is the preferred method of biopsy for lentigo maligna melanoma in situ according to the NCCN.3 And there have been several reports showing that the results of shave biopsies of melanocytic lesions are cosmetically acceptable to patients.10,11
If the biopsy confirms malignancy, a larger surgery with suturing will be needed. The most important issue to keep in mind is that if partial sampling leads to a benign diagnosis of a suspicious lesion, then the remainder of the lesion must be excised and sent for pathology.
Saucerization is also the preferred biopsy type for basal cell and squamous cell carcinomas (SCCs). Studies have shown tumor depth is the most important factor in predicting metastasis of SCC, as well as tumor relapse rate, making accurate identification of the depth of the tumor important for both management and prognosis.12,13 Determining the thickness of the SCC is important for guiding management. SCC in situ is more amenable than invasive SCC to topical therapy or electrodesiccation and curettage.
What you’ll need. FPs can perform saucerization quickly and easily in the office during a standard 15-minute visit. Of course, it is essential to have all the necessary materials available. The key materials needed are lidocaine and epinephrine, a sharp razor blade such as a DermaBlade, and something for hemostasis (aluminum chloride and/or an electrosurgical instrument). Cotton-tipped applicators to apply the aluminum chloride and needles and syringes to administer the local anesthetic are also needed. (See JFP’s Watch and Learn Video on shave biopsy.) A quick saucerization eliminates the need for the patient to return for an elliptical excision and prevents a delayed diagnosis that can occur as a result of a long wait to see a dermatologist.
As a final note, the pathology order form should be completed with information on biopsy type, clinical presentation, differential diagnosis, and whether or not the full lesion was excised.
MYTH #2
A wide excisional biopsy is required for a suspected melanoma.
While complete excision of the entire tumor does allow the pathologist to evaluate the entire growth, wide (>3 mm) margins on the initial biopsy are not necessary. In fact, there are potential disadvantages to full excisional biopsy.
For example, seborrheic keratoses and other benign growths can mimic melanoma. Neither the physician nor the patient wants to learn that a large elliptical wound was created for a growth that turned out to be a benign seborrheic keratosis. Saucerization provides the pathologist with the entire lesion, and the resulting shallow wound heals as a round scar that is most often acceptable to patients.10,11,14 In addition, excisional biopsies carry a higher risk of infection than does saucerization.
Even when the index of suspicion is high for melanoma, a wide margin is not indicated. NCCN guidelines suggest that the margins around a suspected melanoma on initial biopsy not exceed 3 mm to avoid disrupting the accuracy of an SLNB (FIGURE 2).3
In addition, time constraints (elliptical excisional biopsies can take up to one hour, especially when a layered closure is performed) and a lack of surgical training may prohibit FPs from performing excisions.
One study found that while dermatologists prefer shave biopsies (80.5%), surgeons prefer excisional biopsies (46.3%) and primary care physicians prefer punch biopsies (44%) for biopsy of a growth suspicious for melanoma.7 In fact, of the biopsies FPs perform, only 29% are of the shave variety.7
However, deep shave biopsies can be performed quickly, with the whole process taking less than 5 minutes. We advocate performing them at the time of presentation, as the evidence shows that deep shave biopsies of suspected melanoma are reliable and accurate in 97% of cases.15
MYTH #3
A partial biopsy can make the cancer spread.
There is no evidence to support that a partial biopsy has any effect on the local recurrence or metastatic potential of malignant melanoma.16 In fact, a biopsy elicits an inflammatory response that activates the patient’s immune system and often causes tumor lysis. Some tumors may even resolve after biopsy. In our clinical practice, we have had several cases of basal cell carcinoma resolve after a biopsy without additional treatment.
MYTH #4
If after performing a deep shave biopsy, tumor or pigment remains, you must leave it because a second biopsy specimen can’t be added to the first.
If pigment is visible after an initial shave or punch biopsy, it is reasonable to obtain additional tissue from the base of the biopsy site. While the deeper tissue cannot be added to the initial specimen for the purposes of Breslow’s depth, it is still helpful for the pathologist to have the sample so that he or she can analyze the tumor cells in the dermis. (Melanoma tumor depth is measured as the maximum distance between malignant cells and the top of the granular layer.17) In these situations, be sure to let the pathologist know that there are 2 specimens in the container.
In general, it is valuable to get as much of the tissue as possible at the time of the initial biopsy. One way to avoid leaving tumor at the base of the biopsy is to look at
MYTH #5
Epinephrine cannot be used for biopsies on the fingers, toes, nose, or penis.
Lidocaine with epinephrine is safe to use in areas with end-arteries, such as the fingers, toes, nose (FIGURE 4), and penis. There is no evidence to support the notion that local anesthesia with vasoconstriction can cause necrosis in these areas, and no case of necrosis has been reported since the introduction of commercial lidocaine with epinephrine in 1948.18
In addition to an absence of complications, epinephrine supplementation results in a relatively bloodless operating field and longer effectiveness of local anesthesia, as a study of more than 10,000 ear and nose surgeries using epinephrine-supplemented local anesthetics showed.19 The relative absence of blood in the operating field significantly reduces the duration of surgery and increases the healing rate because less electrocautery is needed.19
Similarly, the addition of epinephrine in digital blocks minimizes the need for tourniquets and large volumes of anesthetic and provides better and longer pain control during procedures.20 This topic was addressed by Prabhakar et al in a Cochrane Review in 2015.21 While digital surgeries are common, there were only 4 randomized controlled studies addressing the use of epinephrine in digital blocks. In these studies, there were no reports of adverse events, such as ischemia distal to the injection site. Evidence suggests that epinephrine in digital blocks can even be used safely in patients with vascular disease.22
And while the use of epinephrine with lidocaine in sites with end-arteries is beneficial for hemostasis and does not seem to pose a risk of ischemia, it is prudent to use the smallest volume of epinephrine (with lidocaine) needed to achieve anesthesia for the site.
CORRESPONDENCE
Elizabeth V. Seiverling, MD, 300 Southborough Drive, Suite 201, South Portland, ME 04106; [email protected].
1. Kerr OA, Tidman MJ, Walker JJ, et al. The profile of dermatological problems in primary care. Clin Exp Dermatol. 2010;35:380-383.
2. Hosler GA, Patterson JW. Lentigines, nevi, and melanomas. In: Patterson JW, ed. Weedon’s Skin Pathology. Elsevier; 2015:32,837-901.
3. Coit DG, Andtbacka R, Bichakjian CK, et al. Melanoma. J Natl Compr Canc Netw. 2009;7:250-275.
4. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer Staging Manual. Springer International Publishing; 2017;8:563-585.
5. American Joint Committee on Cancer. Implementation of AJCC 8th Edition Cancer Staging System. Available at: https://cancerstaging.org/About/news/Pages/Implementation-of-AJCC-8th-Edition-Cancer-Staging-System.aspx. Accessed April 2, 2018.
6. Karimipour DJ, Schwartz JL, Wang TS, et al. Microstaging accuracy after subtotal incisional biopsy of cutaneous melanoma. J Am Acad Dermatol. 2005;52:798-802.
7. Kaiser S, Vassell R, Pinckney RG, et al. Clinical impact of biopsy method on the quality of surgical management in melanoma. J Surg Oncol. 2014;109:775-779.
8. Montgomery BD, Sadler GM. Punch biopsy of pigmented lesions is potentially hazardous. Can Fam Physician. 2009;55:24.
9. Ng JC, Swain S, Dowling JP, et al. The impact of partial biopsy on histopathologic diagnosis of cutaneous melanoma: experience of an Australian tertiary referral service. Arch Dermatol. 2010;146:234-239.
10. Gambichler T, Senger E, Rapp S, et al. Deep shave excision of macular melanocytic nevi with the razor blade biopsy technique. Dermatol Surg. 2000;26:662-666.
11. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg. 2005;31(9 Pt 1):1112-1115.
12. D'souza G, Carey TE, William WN Jr, et al. Epidemiology of head and neck squamous cell cancer among HIV-infected patients. J Acquir Immune Defic Syndr. 2014;65:603-610.
13. Edge SB, Byrd DR, Compton CC, et al, eds. AJCC Cancer Staging Handbook. 7th ed. New York, NY: Springer; 2010.
14. Elston DM, Stratman EJ, Miller SJ, et al. Skin biopsy. J Am Acad Dermatol. 2016;74:1-16.
15. Zager JS, Hochwald SN, Marzban SS, et al. Shave biopsy is a safe and accurate method for the initial evaluation of melanoma. J Am Coll Surg. 2011;212:454-460.
16. Chanda JJ, Callen JP. Adverse effect of melanoma incision. J Am Acad Dermatol. 1985;13:519-522.
17. Noroozi N, Zakerolhosseini A. Computerized measurement of melanocytic tumor depth in skin histopathological images. Micron. 2015;77:44-56.
18. Nielsen LJ, Lumholt P, Hölmich LR. [Local anaesthesia with vasoconstrictor is safe to use in areas with end-arteries in fingers, toes, noses and ears]. Ugeskr Laeger. 2014;176(44).
19. Häfner HM, Röcken M, Breuninger H. Epinephrine-supplemented local anesthetics for ear and nose surgery: clinical use without complications in more than 10,000 surgical procedures. J Dtsch Dermatol Ges. 2005;3:195-199.
20. Krunic AL, Wang LC, Soltani K, et al. Digital anesthesia with epinephrine: an old myth revisited. J Am Acad Dermatol. 2004;51:755-759.
21. Prabhakar H, Rath S, Kalaivani M, et al. Adrenaline with lidocaine for digital nerve blocks. Cochrane Database Syst Rev. 2015;(3):CD010645.
22. Ilicki J. Safety of epinephrine in digital nerve blocks: a literature review. J Emerg Med. 2015;49:799-809.
1. Kerr OA, Tidman MJ, Walker JJ, et al. The profile of dermatological problems in primary care. Clin Exp Dermatol. 2010;35:380-383.
2. Hosler GA, Patterson JW. Lentigines, nevi, and melanomas. In: Patterson JW, ed. Weedon’s Skin Pathology. Elsevier; 2015:32,837-901.
3. Coit DG, Andtbacka R, Bichakjian CK, et al. Melanoma. J Natl Compr Canc Netw. 2009;7:250-275.
4. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer Staging Manual. Springer International Publishing; 2017;8:563-585.
5. American Joint Committee on Cancer. Implementation of AJCC 8th Edition Cancer Staging System. Available at: https://cancerstaging.org/About/news/Pages/Implementation-of-AJCC-8th-Edition-Cancer-Staging-System.aspx. Accessed April 2, 2018.
6. Karimipour DJ, Schwartz JL, Wang TS, et al. Microstaging accuracy after subtotal incisional biopsy of cutaneous melanoma. J Am Acad Dermatol. 2005;52:798-802.
7. Kaiser S, Vassell R, Pinckney RG, et al. Clinical impact of biopsy method on the quality of surgical management in melanoma. J Surg Oncol. 2014;109:775-779.
8. Montgomery BD, Sadler GM. Punch biopsy of pigmented lesions is potentially hazardous. Can Fam Physician. 2009;55:24.
9. Ng JC, Swain S, Dowling JP, et al. The impact of partial biopsy on histopathologic diagnosis of cutaneous melanoma: experience of an Australian tertiary referral service. Arch Dermatol. 2010;146:234-239.
10. Gambichler T, Senger E, Rapp S, et al. Deep shave excision of macular melanocytic nevi with the razor blade biopsy technique. Dermatol Surg. 2000;26:662-666.
11. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg. 2005;31(9 Pt 1):1112-1115.
12. D'souza G, Carey TE, William WN Jr, et al. Epidemiology of head and neck squamous cell cancer among HIV-infected patients. J Acquir Immune Defic Syndr. 2014;65:603-610.
13. Edge SB, Byrd DR, Compton CC, et al, eds. AJCC Cancer Staging Handbook. 7th ed. New York, NY: Springer; 2010.
14. Elston DM, Stratman EJ, Miller SJ, et al. Skin biopsy. J Am Acad Dermatol. 2016;74:1-16.
15. Zager JS, Hochwald SN, Marzban SS, et al. Shave biopsy is a safe and accurate method for the initial evaluation of melanoma. J Am Coll Surg. 2011;212:454-460.
16. Chanda JJ, Callen JP. Adverse effect of melanoma incision. J Am Acad Dermatol. 1985;13:519-522.
17. Noroozi N, Zakerolhosseini A. Computerized measurement of melanocytic tumor depth in skin histopathological images. Micron. 2015;77:44-56.
18. Nielsen LJ, Lumholt P, Hölmich LR. [Local anaesthesia with vasoconstrictor is safe to use in areas with end-arteries in fingers, toes, noses and ears]. Ugeskr Laeger. 2014;176(44).
19. Häfner HM, Röcken M, Breuninger H. Epinephrine-supplemented local anesthetics for ear and nose surgery: clinical use without complications in more than 10,000 surgical procedures. J Dtsch Dermatol Ges. 2005;3:195-199.
20. Krunic AL, Wang LC, Soltani K, et al. Digital anesthesia with epinephrine: an old myth revisited. J Am Acad Dermatol. 2004;51:755-759.
21. Prabhakar H, Rath S, Kalaivani M, et al. Adrenaline with lidocaine for digital nerve blocks. Cochrane Database Syst Rev. 2015;(3):CD010645.
22. Ilicki J. Safety of epinephrine in digital nerve blocks: a literature review. J Emerg Med. 2015;49:799-809.
From The Journal of Family Practice | 2018;67(5):270-274.
Scaly Pink Patches: Differentiating Psoriasis From Basal Cell Carcinoma
Dermoscopy increases diagnostic accuracy in the analysis of skin growths.1,2 Recently the use of dermoscopy has broadened to include inflammatory dermatoses and skin infections.3 To substantiate the value of dermoscopy in assessing psoriasis, we performed a systematic review of the literature and briefly reviewed 31 articles. We also report a case that highlights the differences between psoriasis and basal cell carcinoma (BCC) under dermoscopic examination, and we discuss the literature on the dermoscopic findings of psoriasis with an emphasis on the relative sensitivities and specificities of dermoscopic findings for psoriasis and for BCC.
Case Report
A 63-year-old man with psoriasis and a history of BCC presented for follow-up of psoriasis, which was well-controlled on etanercept. The physical examination was remarkable for scaly pink papules scattered on the trunk and extremities. A new larger red-pink patch was located on the left lower back (Figure 1). Dermoscopic evaluation of the new patch revealed shiny white lines and branching blood vessels (Figure 2).
Comment
The clinical morphology of psoriasis and BCC can be similar, and dermoscopy can help in differentiating between the 2 conditions.
Literature Search on Dermoscopy and Psoriasis
We performed a PubMed search of articles indexed for MEDLINE to review the published literature on dermoscopy and psoriasis. Two reviewers (C.H. and L.C.) searched for psoriasis paired with the terms dermoscopy or dermatoscopy or epiluminescence microscopy. Only English-language articles published between 1996 and 2016 were included in the search. Articles that focused solely on confocal microscopy were excluded. Article titles and abstracts were evaluated and articles that omitted mention of dermoscopy and psoriasis were excluded, yielding a total of 31 articles. Of these articles, only 2 discussed the specificity or sensitivity of the dermoscopic findings of psoriasis.4,5 Most of the articles were case reports and descriptive cross-sectional studies. The reports addressed multiple subtypes of psoriasis, but reports on psoriasis vulgaris and scalp psoriasis were most common (Table). Lallas et al6 provided a comprehensive descriptive review of the main findings on dermoscopy for psoriasis and other inflammatory skin conditions, but it lacked a comparison between psoriasis and BCC or data on the sensitivity and specificity of the findings. Two studies reported sensitivity and specificity values for the dermoscopic findings of psoriasis.4,5 Pan et al5 reported a 98% diagnostic probability of psoriasis if red dots, homogeneous vascular pattern, and a light red background are all present. Additionally, they reported that the presence of 4 of 6 criteria for BCC—scattered vascular pattern, arborizing microvessels, telangiectatic or atypical vessels, milky-pink background, and brown dots⁄globules—yielded a diagnostic probability of 99%.5 Similarly, Lallas et al6 demonstrated that the presence of dotted vessels alone is not sufficient to presume a diagnosis of psoriasis, as this finding can be seen in other inflammatory skin conditions. However, “the combination of regularly distributed dotted vessels over a light red background associated with diffuse white scales was highly predictive of [plaque psoriasis] and allowed a correct diagnosis with 88.0% specificity and 84.9% sensitivity.”4 Figure 3 shows a dermoscopic image of plaque psoriasis that demonstrates these findings. The remaining literature corroborated this evidence, with the most commonly reported dermoscopic findings of psoriasis being red dots, red globules, glomerular vessels (also known as twisted capillary loops), red globular ring
Dermoscopy and BCC
Much has been published on the dermoscopic findings of BCC.5,13-15 The dermoscopic findings of BCC include large blue-gray ovoid nests, leaflike areas, spoke-wheel–like areas, arborizing vessels (telangiectasia), and ulceration.15 Superficial BCC is characterized by short fine or arborizing telangiectasia, shallow erosions, and shiny white areas.15 The positive predictive value of dermoscopy in BCC is as high as 97%.16 Additionally, multiple studies report a sensitivity of 95% to 99%5,13,14 and a specificity of 79% to 99% in the use of dermoscopy for identifying BCC. According to Pan et al,5 the most sensitive finding for BCC is a scattered vascular pattern (97%), while the most specific finding is arborizing microvessels (99%).
Utility of Dermoscopy
Our case of a 63-year-old man with a history of psoriasis and BCC highlights the usefulness of dermoscopy in accurately determining the features of each condition. Additionally, dermoscopy aids in differentiating between psoriasis and squamous cell carcinoma. In contrast to the dotted vessels seen in psoriasis, squamous cell carcinomas often have peripheral hairpin (glomerular) vessels.17
If future reports confirm dermoscopy’s utility in accurately diagnosing psoriasis, fewer biopsies may be needed when evaluating patients with new rashes. Furthermore, dermoscopy may expedite treatment of psoriasis (as it can for malignant conditions) by obviating the wait for pathology results currently needed to initiate systemic treatment. For patients with psoriasis who also have sun-damaged skin, dermoscopy may assist in differentiating pink patches and plaques of psoriasis from skin cancer, such as superficial BCCs, which often have shiny white lines not seen in psoriasis.15
- Kittler H, Pehamberger H, Wolff K, et al. Diagnostic accuracy of dermoscopy. Lancet Oncol. 2002;3:159-165.
- Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
- Lallas A, Giacomel J, Argenziano G, et al. Dermoscopy in general dermatology: practical tips for the clinician. Br J Dermatol. 2014;170:514-526.
- Lallas A, Kyrgidis A, Tzellos TG, et al. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus and pityriasis rosea. Br J Dermatol. 2012;166:1198-1205.
- Pan Y, Chamberlain AJ, Bailey M, et al. Dermatoscopy aids in the diagnosis of the solitary red scaly patch or plaque–features distinguishing superficial basal cell carcinoma, intraepidermal carcinoma, and psoriasis. J Am Acad Dermatol. 2008;59:268-274.
- Lallas A, Apalla Z, Argenziano G, et al. Dermoscopic pattern of psoriatic lesions on specific body sites. Dermatology. 2014;228:250-254.
- Almeida MC, Romiti R, Doche I, et al. Psoriatic scarring alopecia. An Bras Dermatol. 2013;88:29-31.
- Zalaudek I, Argenziano G. Dermoscopy subpatterns of inflammatory skin disorders. Arch Dermatol. 2006;142:808.
- Miteva M, Tosti A. Hair and scalp dermatoscopy. J Am Acad Dermatol. 2012;67:1040-1048.
- Vázquez-López F, Zaballos P, Fueyo-Casado A, et al. A dermoscopy subpattern of plaque-type psoriasis: red globular rings. Arch Dermatol. 2007;143:1612.
- Lacarrubba F, Nasca MR, Micali G. Videodermatoscopy enhances diagnostic capability in psoriatic balanitis. J Am Acad Dermatol. 2009;61:1084-1086.
- Liebman TN, Wang SQ. Detection of early basal cell carcinoma with dermoscopy in a patient with psoriasis. Dermatol Online J. 2011;17:12.
- Menzies SW, Westerhoff K, Rabinovitz H, et al. Surface microscopy of pigmented basal cell carcinoma. Arch Dermatol. 2000;136:1012-1016.
- Altamura D, Menzies SW, Argenziano G, et al. Dermatoscopy of basal cell carcinoma: morphologic variability of global and local features and accuracy of diagnosis. J Am Acad Dermatol. 2010;62:67-75.
- Marghoob AA, Malvehy J, Braun RP, eds. An Atlas of Dermoscopy. 2nd ed. Boca Raton, FL: CRC Press; 2012.
- Nelson SA, Scope A, Rishpon A, et al. Accuracy and confidence in the clinical diagnosis of basal cell cancer using dermoscopy and reflex confocal microscopy. Int J Dermatol. 2016;55:1351-1356.
- Zalaudek I, Kreusch J, Giacomel J, et al. How to diagnose nonpigmented skin tumors: a review of vascular structures seen with dermoscopy: part I. melanocytic skin tumors. J Am Acad Dermatol. 2010;63:361-374.
Dermoscopy increases diagnostic accuracy in the analysis of skin growths.1,2 Recently the use of dermoscopy has broadened to include inflammatory dermatoses and skin infections.3 To substantiate the value of dermoscopy in assessing psoriasis, we performed a systematic review of the literature and briefly reviewed 31 articles. We also report a case that highlights the differences between psoriasis and basal cell carcinoma (BCC) under dermoscopic examination, and we discuss the literature on the dermoscopic findings of psoriasis with an emphasis on the relative sensitivities and specificities of dermoscopic findings for psoriasis and for BCC.
Case Report
A 63-year-old man with psoriasis and a history of BCC presented for follow-up of psoriasis, which was well-controlled on etanercept. The physical examination was remarkable for scaly pink papules scattered on the trunk and extremities. A new larger red-pink patch was located on the left lower back (Figure 1). Dermoscopic evaluation of the new patch revealed shiny white lines and branching blood vessels (Figure 2).
Comment
The clinical morphology of psoriasis and BCC can be similar, and dermoscopy can help in differentiating between the 2 conditions.
Literature Search on Dermoscopy and Psoriasis
We performed a PubMed search of articles indexed for MEDLINE to review the published literature on dermoscopy and psoriasis. Two reviewers (C.H. and L.C.) searched for psoriasis paired with the terms dermoscopy or dermatoscopy or epiluminescence microscopy. Only English-language articles published between 1996 and 2016 were included in the search. Articles that focused solely on confocal microscopy were excluded. Article titles and abstracts were evaluated and articles that omitted mention of dermoscopy and psoriasis were excluded, yielding a total of 31 articles. Of these articles, only 2 discussed the specificity or sensitivity of the dermoscopic findings of psoriasis.4,5 Most of the articles were case reports and descriptive cross-sectional studies. The reports addressed multiple subtypes of psoriasis, but reports on psoriasis vulgaris and scalp psoriasis were most common (Table). Lallas et al6 provided a comprehensive descriptive review of the main findings on dermoscopy for psoriasis and other inflammatory skin conditions, but it lacked a comparison between psoriasis and BCC or data on the sensitivity and specificity of the findings. Two studies reported sensitivity and specificity values for the dermoscopic findings of psoriasis.4,5 Pan et al5 reported a 98% diagnostic probability of psoriasis if red dots, homogeneous vascular pattern, and a light red background are all present. Additionally, they reported that the presence of 4 of 6 criteria for BCC—scattered vascular pattern, arborizing microvessels, telangiectatic or atypical vessels, milky-pink background, and brown dots⁄globules—yielded a diagnostic probability of 99%.5 Similarly, Lallas et al6 demonstrated that the presence of dotted vessels alone is not sufficient to presume a diagnosis of psoriasis, as this finding can be seen in other inflammatory skin conditions. However, “the combination of regularly distributed dotted vessels over a light red background associated with diffuse white scales was highly predictive of [plaque psoriasis] and allowed a correct diagnosis with 88.0% specificity and 84.9% sensitivity.”4 Figure 3 shows a dermoscopic image of plaque psoriasis that demonstrates these findings. The remaining literature corroborated this evidence, with the most commonly reported dermoscopic findings of psoriasis being red dots, red globules, glomerular vessels (also known as twisted capillary loops), red globular ring
Dermoscopy and BCC
Much has been published on the dermoscopic findings of BCC.5,13-15 The dermoscopic findings of BCC include large blue-gray ovoid nests, leaflike areas, spoke-wheel–like areas, arborizing vessels (telangiectasia), and ulceration.15 Superficial BCC is characterized by short fine or arborizing telangiectasia, shallow erosions, and shiny white areas.15 The positive predictive value of dermoscopy in BCC is as high as 97%.16 Additionally, multiple studies report a sensitivity of 95% to 99%5,13,14 and a specificity of 79% to 99% in the use of dermoscopy for identifying BCC. According to Pan et al,5 the most sensitive finding for BCC is a scattered vascular pattern (97%), while the most specific finding is arborizing microvessels (99%).
Utility of Dermoscopy
Our case of a 63-year-old man with a history of psoriasis and BCC highlights the usefulness of dermoscopy in accurately determining the features of each condition. Additionally, dermoscopy aids in differentiating between psoriasis and squamous cell carcinoma. In contrast to the dotted vessels seen in psoriasis, squamous cell carcinomas often have peripheral hairpin (glomerular) vessels.17
If future reports confirm dermoscopy’s utility in accurately diagnosing psoriasis, fewer biopsies may be needed when evaluating patients with new rashes. Furthermore, dermoscopy may expedite treatment of psoriasis (as it can for malignant conditions) by obviating the wait for pathology results currently needed to initiate systemic treatment. For patients with psoriasis who also have sun-damaged skin, dermoscopy may assist in differentiating pink patches and plaques of psoriasis from skin cancer, such as superficial BCCs, which often have shiny white lines not seen in psoriasis.15
Dermoscopy increases diagnostic accuracy in the analysis of skin growths.1,2 Recently the use of dermoscopy has broadened to include inflammatory dermatoses and skin infections.3 To substantiate the value of dermoscopy in assessing psoriasis, we performed a systematic review of the literature and briefly reviewed 31 articles. We also report a case that highlights the differences between psoriasis and basal cell carcinoma (BCC) under dermoscopic examination, and we discuss the literature on the dermoscopic findings of psoriasis with an emphasis on the relative sensitivities and specificities of dermoscopic findings for psoriasis and for BCC.
Case Report
A 63-year-old man with psoriasis and a history of BCC presented for follow-up of psoriasis, which was well-controlled on etanercept. The physical examination was remarkable for scaly pink papules scattered on the trunk and extremities. A new larger red-pink patch was located on the left lower back (Figure 1). Dermoscopic evaluation of the new patch revealed shiny white lines and branching blood vessels (Figure 2).
Comment
The clinical morphology of psoriasis and BCC can be similar, and dermoscopy can help in differentiating between the 2 conditions.
Literature Search on Dermoscopy and Psoriasis
We performed a PubMed search of articles indexed for MEDLINE to review the published literature on dermoscopy and psoriasis. Two reviewers (C.H. and L.C.) searched for psoriasis paired with the terms dermoscopy or dermatoscopy or epiluminescence microscopy. Only English-language articles published between 1996 and 2016 were included in the search. Articles that focused solely on confocal microscopy were excluded. Article titles and abstracts were evaluated and articles that omitted mention of dermoscopy and psoriasis were excluded, yielding a total of 31 articles. Of these articles, only 2 discussed the specificity or sensitivity of the dermoscopic findings of psoriasis.4,5 Most of the articles were case reports and descriptive cross-sectional studies. The reports addressed multiple subtypes of psoriasis, but reports on psoriasis vulgaris and scalp psoriasis were most common (Table). Lallas et al6 provided a comprehensive descriptive review of the main findings on dermoscopy for psoriasis and other inflammatory skin conditions, but it lacked a comparison between psoriasis and BCC or data on the sensitivity and specificity of the findings. Two studies reported sensitivity and specificity values for the dermoscopic findings of psoriasis.4,5 Pan et al5 reported a 98% diagnostic probability of psoriasis if red dots, homogeneous vascular pattern, and a light red background are all present. Additionally, they reported that the presence of 4 of 6 criteria for BCC—scattered vascular pattern, arborizing microvessels, telangiectatic or atypical vessels, milky-pink background, and brown dots⁄globules—yielded a diagnostic probability of 99%.5 Similarly, Lallas et al6 demonstrated that the presence of dotted vessels alone is not sufficient to presume a diagnosis of psoriasis, as this finding can be seen in other inflammatory skin conditions. However, “the combination of regularly distributed dotted vessels over a light red background associated with diffuse white scales was highly predictive of [plaque psoriasis] and allowed a correct diagnosis with 88.0% specificity and 84.9% sensitivity.”4 Figure 3 shows a dermoscopic image of plaque psoriasis that demonstrates these findings. The remaining literature corroborated this evidence, with the most commonly reported dermoscopic findings of psoriasis being red dots, red globules, glomerular vessels (also known as twisted capillary loops), red globular ring
Dermoscopy and BCC
Much has been published on the dermoscopic findings of BCC.5,13-15 The dermoscopic findings of BCC include large blue-gray ovoid nests, leaflike areas, spoke-wheel–like areas, arborizing vessels (telangiectasia), and ulceration.15 Superficial BCC is characterized by short fine or arborizing telangiectasia, shallow erosions, and shiny white areas.15 The positive predictive value of dermoscopy in BCC is as high as 97%.16 Additionally, multiple studies report a sensitivity of 95% to 99%5,13,14 and a specificity of 79% to 99% in the use of dermoscopy for identifying BCC. According to Pan et al,5 the most sensitive finding for BCC is a scattered vascular pattern (97%), while the most specific finding is arborizing microvessels (99%).
Utility of Dermoscopy
Our case of a 63-year-old man with a history of psoriasis and BCC highlights the usefulness of dermoscopy in accurately determining the features of each condition. Additionally, dermoscopy aids in differentiating between psoriasis and squamous cell carcinoma. In contrast to the dotted vessels seen in psoriasis, squamous cell carcinomas often have peripheral hairpin (glomerular) vessels.17
If future reports confirm dermoscopy’s utility in accurately diagnosing psoriasis, fewer biopsies may be needed when evaluating patients with new rashes. Furthermore, dermoscopy may expedite treatment of psoriasis (as it can for malignant conditions) by obviating the wait for pathology results currently needed to initiate systemic treatment. For patients with psoriasis who also have sun-damaged skin, dermoscopy may assist in differentiating pink patches and plaques of psoriasis from skin cancer, such as superficial BCCs, which often have shiny white lines not seen in psoriasis.15
- Kittler H, Pehamberger H, Wolff K, et al. Diagnostic accuracy of dermoscopy. Lancet Oncol. 2002;3:159-165.
- Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
- Lallas A, Giacomel J, Argenziano G, et al. Dermoscopy in general dermatology: practical tips for the clinician. Br J Dermatol. 2014;170:514-526.
- Lallas A, Kyrgidis A, Tzellos TG, et al. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus and pityriasis rosea. Br J Dermatol. 2012;166:1198-1205.
- Pan Y, Chamberlain AJ, Bailey M, et al. Dermatoscopy aids in the diagnosis of the solitary red scaly patch or plaque–features distinguishing superficial basal cell carcinoma, intraepidermal carcinoma, and psoriasis. J Am Acad Dermatol. 2008;59:268-274.
- Lallas A, Apalla Z, Argenziano G, et al. Dermoscopic pattern of psoriatic lesions on specific body sites. Dermatology. 2014;228:250-254.
- Almeida MC, Romiti R, Doche I, et al. Psoriatic scarring alopecia. An Bras Dermatol. 2013;88:29-31.
- Zalaudek I, Argenziano G. Dermoscopy subpatterns of inflammatory skin disorders. Arch Dermatol. 2006;142:808.
- Miteva M, Tosti A. Hair and scalp dermatoscopy. J Am Acad Dermatol. 2012;67:1040-1048.
- Vázquez-López F, Zaballos P, Fueyo-Casado A, et al. A dermoscopy subpattern of plaque-type psoriasis: red globular rings. Arch Dermatol. 2007;143:1612.
- Lacarrubba F, Nasca MR, Micali G. Videodermatoscopy enhances diagnostic capability in psoriatic balanitis. J Am Acad Dermatol. 2009;61:1084-1086.
- Liebman TN, Wang SQ. Detection of early basal cell carcinoma with dermoscopy in a patient with psoriasis. Dermatol Online J. 2011;17:12.
- Menzies SW, Westerhoff K, Rabinovitz H, et al. Surface microscopy of pigmented basal cell carcinoma. Arch Dermatol. 2000;136:1012-1016.
- Altamura D, Menzies SW, Argenziano G, et al. Dermatoscopy of basal cell carcinoma: morphologic variability of global and local features and accuracy of diagnosis. J Am Acad Dermatol. 2010;62:67-75.
- Marghoob AA, Malvehy J, Braun RP, eds. An Atlas of Dermoscopy. 2nd ed. Boca Raton, FL: CRC Press; 2012.
- Nelson SA, Scope A, Rishpon A, et al. Accuracy and confidence in the clinical diagnosis of basal cell cancer using dermoscopy and reflex confocal microscopy. Int J Dermatol. 2016;55:1351-1356.
- Zalaudek I, Kreusch J, Giacomel J, et al. How to diagnose nonpigmented skin tumors: a review of vascular structures seen with dermoscopy: part I. melanocytic skin tumors. J Am Acad Dermatol. 2010;63:361-374.
- Kittler H, Pehamberger H, Wolff K, et al. Diagnostic accuracy of dermoscopy. Lancet Oncol. 2002;3:159-165.
- Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
- Lallas A, Giacomel J, Argenziano G, et al. Dermoscopy in general dermatology: practical tips for the clinician. Br J Dermatol. 2014;170:514-526.
- Lallas A, Kyrgidis A, Tzellos TG, et al. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus and pityriasis rosea. Br J Dermatol. 2012;166:1198-1205.
- Pan Y, Chamberlain AJ, Bailey M, et al. Dermatoscopy aids in the diagnosis of the solitary red scaly patch or plaque–features distinguishing superficial basal cell carcinoma, intraepidermal carcinoma, and psoriasis. J Am Acad Dermatol. 2008;59:268-274.
- Lallas A, Apalla Z, Argenziano G, et al. Dermoscopic pattern of psoriatic lesions on specific body sites. Dermatology. 2014;228:250-254.
- Almeida MC, Romiti R, Doche I, et al. Psoriatic scarring alopecia. An Bras Dermatol. 2013;88:29-31.
- Zalaudek I, Argenziano G. Dermoscopy subpatterns of inflammatory skin disorders. Arch Dermatol. 2006;142:808.
- Miteva M, Tosti A. Hair and scalp dermatoscopy. J Am Acad Dermatol. 2012;67:1040-1048.
- Vázquez-López F, Zaballos P, Fueyo-Casado A, et al. A dermoscopy subpattern of plaque-type psoriasis: red globular rings. Arch Dermatol. 2007;143:1612.
- Lacarrubba F, Nasca MR, Micali G. Videodermatoscopy enhances diagnostic capability in psoriatic balanitis. J Am Acad Dermatol. 2009;61:1084-1086.
- Liebman TN, Wang SQ. Detection of early basal cell carcinoma with dermoscopy in a patient with psoriasis. Dermatol Online J. 2011;17:12.
- Menzies SW, Westerhoff K, Rabinovitz H, et al. Surface microscopy of pigmented basal cell carcinoma. Arch Dermatol. 2000;136:1012-1016.
- Altamura D, Menzies SW, Argenziano G, et al. Dermatoscopy of basal cell carcinoma: morphologic variability of global and local features and accuracy of diagnosis. J Am Acad Dermatol. 2010;62:67-75.
- Marghoob AA, Malvehy J, Braun RP, eds. An Atlas of Dermoscopy. 2nd ed. Boca Raton, FL: CRC Press; 2012.
- Nelson SA, Scope A, Rishpon A, et al. Accuracy and confidence in the clinical diagnosis of basal cell cancer using dermoscopy and reflex confocal microscopy. Int J Dermatol. 2016;55:1351-1356.
- Zalaudek I, Kreusch J, Giacomel J, et al. How to diagnose nonpigmented skin tumors: a review of vascular structures seen with dermoscopy: part I. melanocytic skin tumors. J Am Acad Dermatol. 2010;63:361-374.
Practice Points
- Dermoscopy has been largely utilized for the evaluation of malignant lesions. It also is gaining traction in the evaluation of inflammatory dermatoses.
- Early distinction between basal cell carcinoma and psoriasis is important for both treatment options and health care costs.