Plaque Psoriasis
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Psoriasis, which manifests most often as plaque psoriasis, is a chronic, relapsing, inflammatory skin disorder with a strong genetic basis. Plaque psoriasis (see the image below) is rarely life threatening, but it often is intractable to treatment.
See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.
Psoriatic plaques are characterized as follows:
Raised and easily palpable – Owing to the thickened epidermis, expanded dermal vascular compartment, as well as infiltrate of neutrophils and lymphocytes
Irregular to oval in shape
One to several centimeters in size
Well defined, with sharply demarcated boundaries
Very distinctive rich, full red color; lesions on the legs sometimes carry a blue or violaceous tint
Typically have a dry, thin, silvery-white or micaceous scale
Typically have a high degree of uniformity, with few morphologic differences between the 2 sides
Range in number from a few to many at any given time
Most often located on the scalp, trunk, and limbs, with a predilection for extensor surfaces, such as the elbows and knees
Symmetrically distributed over the body
May, in the case of smaller plaques, coalesce into larger lesions, especially on the legs and sacral regions
Other manifestations of plaque psoriasis include the following:
Pruritus – One of the main symptoms of plaque psoriasis
Nail psoriasis – Nails may exhibit pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign
Inverse psoriasis – A variant of psoriasis that spares the typical extensor surfaces and affects intertriginous areas (ie, axillae, inguinal folds, inframammary creases) with minimal scale
Psoriatic arthritis – Occurs in approximately 10-20% of all cases of plaque psoriasis
Manifestations of the psoriatic arthritis include the following:
Red, warm, tender, and inflamed joints
Joint deformity
Dactylitis
Sausage digits
Children
In children with plaque psoriasis, plaques are not as thick, and the lesions are less scaly. Psoriasis often appears in the diaper region in infancy and in flexural areas in children. The disease more commonly affects the face in children than it does in adults.
Laboratory studies
The diagnosis of psoriasis is almost always made on the basis of clinical findings. Laboratory investigations are rarely indicated.
Skin biopsy
Skin biopsy can confirm the diagnosis of plaque psoriasis. This procedure, however, is usually reserved for the evaluation of atypical cases or for excluding other conditions in cases of diagnostic uncertainty.
Histology
Histologic epidermal findings include the following:
Mitotic activity of basal keratinocytes is increased almost 50-fold, with keratinocytes migrating from the basal to the cornified layers in only 3-5 days rather than the normal 28-30 days
The epidermis becomes thickened or acanthotic in appearance, and the rete ridges increase in size
Abnormal keratinocyte differentiation is noted throughout the psoriatic plaques, as manifested by the loss of the granular layer
Alternating collections of neutrophils are sandwiched between layers of parakeratotic stratum corneum, which is virtually pathognomonic for psoriasis
Histologic dermal findings include the following:
Signs of inflammation can be observed throughout the dermis
Marked hypervascularity and an increase in the size of the dermal papillae occur
An activated CD3+ lymphocytic infiltrate is noted around blood vessels
An aggregation of neutrophils in the dermis occurs that extends up into the epidermis
Topical therapy
Topical agents used (often concurrently) to treat plaque psoriasis include the following:
Corticosteroids
Coal tar
Anthralin
Calcipotriene
Tazarotene
Phototherapy
The 2 main forms of phototherapy are as follows:
Ultraviolet B (UVB) irradiation – UVB therapy is usually combined with one or more topical treatments
Psoralen plus ultraviolet A irradiation (PUVA) – This treatment uses the photosensitizing drug methoxsalen (8-methoxypsoralen) in combination with UVA irradiation to treat patients with more extensive disease
Systemic therapy
Systemic treatment is initiated only after topical treatments and phototherapy have proved unsuccessful. Systemic therapy should also be considered for patients with very active psoriatic arthritis, as well as for patients whose disease is physically, psychologically, socially, or economically disabling. [1, 2, 3, 4]
Biologic therapy
Biologic therapies provide selective, systemic, immunologically directed interventions, including the following, at key steps in the pathogenesis of plaque psoriasis [5] :
Inhibition of the initial cytokine release and Langerhans cell migration
Targeting of activated T cells, prevention of further T-cell activation, and elimination of pathologic T cells
Blockage of interactions that lead to T-cell activation or migration into tissue
Alteration of the balance of T-cell types
Inhibition of proinflammatory cytokines, such as tumor necrosis factor (TNF), [6] interleukin (IL)–12, IL-17, and IL-23 [7, 8, 9]
Psoriasis is a common, chronic, relapsing, inflammatory skin disorder with a strong genetic basis. The plaque type of psoriasis is the most common, although several other distinctive clinical variants of psoriasis are recognized (eg, Guttate Psoriasis; Psoriasis, Nails; Psoriasis, Pustular; Psoriatric Arthritis).
Plaque psoriasis is most typically characterized by circular-to-oval red plaques distributed over extensor body surfaces and the scalp. The plaques usually exhibit scaling as a result of epidermal hyperproliferation and dermal inflammation. The extent and duration of plaque psoriasis is highly variable from patient to patient. Acute flares or relapses of plaque psoriasis may also evolve into more severe disease, such as pustular or erythrodermic psoriasis.
Up to 10-20% of patients with plaque psoriasis also experience psoriatic arthritis. A population-based study by Wilson et al that spanned more than 30 years reported that less than 10% of psoriasis patients develop clinically recognized psoriatic arthritis. The clinical features that were associated with an increased chance of leading to psoriatic arthritis were reported as being scalp lesions, nail dystrophy, and intergluteal or perianal psoriasis. [10]
For more information, see Psoriasis.
The pathophysiology of psoriasis must be understood in terms of the prominent pathologies occurring in both major components of the skin—the epidermis and the dermis.
Psoriasis is fundamentally an inflammatory skin condition with reactive abnormal epidermal differentiation and hyperproliferation. Current research suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained primarily by T cells in the dermis. [11]
In this model, antigen-presenting cells in the skin, such as Langerhans cells, are believed to migrate from the skin to regional lymph nodes, where they interact with T cells. Presentation of an as yet unidentified antigen to the T cells, as well as a number of co-stimulatory signals, triggers an immune response, leading to T-cell activation and the release of cytokines.
Co-stimulatory signals are initiated via the interaction of adhesion molecules on the antigen-presenting cells, such as lymphocyte function–associated antigen (LFA)–3 and intercellular adhesion molecule-1, with their respective receptors CD2 and LFA-1 on T cells. These T cells are released into the circulation and traffic back into the skin.
Reactivation of T cells in the dermis and epidermis and the local effects of cytokines such as tumor necrosis factor lead to the inflammation, cell-mediated immune responses, and epidermal hyperproliferation observed in persons with psoriasis.
An interleukin (IL)-12–related cytokine, IL-23, is involved in the establishment of chronic inflammation and in the development of a T helper (Th)–cell subset producing IL-17. These cells, which are designated Th17, are distinct from Th1 and Th2 populations. Th17 cells are now recognized as a third T-effector cell subset, and the IL-23/IL-17 pathway has been implicated in the induction and progression of a number of inflammatory diseases, including psoriasis. [12]
Infection and a number of physical agents (eg, HIV infection, alcoholism, smoking, UV light) all can affect the course, duration, and clinical appearance of plaque psoriasis. See Etiology of Plaque Psoriasis, below, for more details on the role of environmental factors.
HLA-B13, -B17, and -Cw6 are all associated with plaque psoriasis. Multifactorial inheritance mechanisms and etiologies without any genetic component have not yet been excluded, although many families appear to exhibit autosomal dominant patterns of inheritance with decreased penetrance. Studies of twin siblings have shown concordant disease in 73% of monozygotic twins compared with 20% in dizygotic twins.
Several putative genetic susceptibility loci have also been identified, including psoriasis susceptibility 1 (PSOR1) on chromosome 6, which is associated with up to 50% of cases. Six other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7) have been discovered, as well as the transcription factor RUNX1. While this certainly points to genetic mechanisms, the absence of 100% concordance among monozygotes suggests that environmental factors must play a role in the pathophysiology of this disease.
All types of trauma have been associated with the development of plaque psoriasis (eg, physical, chemical, electrical, surgical, infective, and inflammatory injury). Even excessive scratching can aggravate or precipitate localized psoriasis. The development of psoriatic plaques at a site of injury is known as the Koebner reaction.
Most patients consider sunlight to be beneficial for their psoriasis; they report a decrease in illness severity during the summer months or periods of increased sun exposure. However, a small minority of patients find that their symptoms are aggravated by strong sunlight, and these individuals actually experience a worsening of their disease in the summer. A severe sunburn can lead to an exacerbation of plaque psoriasis via the Koebner reaction.
Pharyngeal streptococcal infections have been shown to produce a clinically distinctive disease flare known as guttate psoriasis. Some evidence suggests that subclinical streptococcal colonization or overgrowth could be responsible for refractory plaque psoriasis.
An increase in psoriasis activity has been observed in patients who are infected, or become infected, with HIV. The extent and severity of skin disease initially appears to parallel the disease stage. Psoriasis often becomes less active in advanced HIV infection.
A number of medications have been shown to cause an exacerbation of psoriasis. Lithium and withdrawal from systemic corticosteroids are well known to cause flares of disease. Beta-blockers, antimalarials, and nonsteroidal anti-inflammatory drugs (NSAIDs) have also been implicated.
Many patients report an increase in psoriasis severity with psychological stress. A clear cause-and-effect relationship between disease exacerbation and stress unfortunately has not been proven. Patients may show a decreased capacity to cope with their treatment regimen with higher levels of stress. Pruritus in the setting of increased anxiety or depression may promote scratching and a Koebner reaction.
An increased risk of chronic plaque psoriasis exists in persons who smoke cigarettes.
Alcohol consumption is considered a risk factor for psoriasis, particularly in young to middle-aged men.
Psoriasis severity has been noted to fluctuate with hormonal changes. Disease incidence peaks at puberty and during menopause. During pregnancy, symptoms are more likely to improve than worsen, if any changes occur at all. In contrast, the disease is more likely to flare in the postpartum period, again if any changes occur at all.
Plaque psoriasis occurs worldwide, although its prevalence varies with race, geography, and environmental factors (eg, sun exposure). In the United States, 1-2% of the population has plaque psoriasis.
Family history has been shown to predict disease occurrence. When both parents are affected by psoriasis, the rate in siblings of probands is as high as 50%. When one parent is affected, the rate is 16.4%. When neither parent has psoriasis, only 7.8% of siblings of probands are affected.
Of patients with psoriasis, 36-71% have one relative who is also affected by psoriasis. For siblings of patients whose psoriasis appeared before age 15 years, a 3-fold higher risk exists of developing disease compared with siblings of patients who first presented after age 30 years.
Psoriasis affects adult males and females equally. Among children and adolescents, plaque psoriasis has been found to affect females more than males, but this observation may be due to the earlier age of onset in females.
Plaque psoriasis first appears during 2 peak age ranges. The first peak occurs in persons aged 16-22 years, and the second occurs in persons aged 57-60 years. Females develop plaque psoriasis earlier than males, and patients with a positive family history for psoriasis also tend to have an earlier age of onset.
Disease-related mortality is exceedingly rare in psoriasis. Even then, mortality is related primarily to therapy: systemic corticosteroid therapy may provoke pustular flares of disease, which can be fatal; methotrexate therapy may result in hepatic fibrosis; and phototherapy (eg, psoralen plus UVA [PUVA]) may induce skin cancers, with subsequent metastasis.
Morbidity is a much greater problem in patients with psoriasis; it includes pruritus, dry and peeling skin, fissuring, self-consciousness and embarrassment about appearance, inconvenience, and the adverse effects and high cost of antipsoriatic treatment regimens. By far, reduced quality of life is the most significant morbidity. Studies have demonstrated that patients with psoriasis have deficiencies in quality of life similar to those for persons with congestive heart failure.
An association between psoriasis, obesity, and cardiovascular comorbidity was been recognized amongst patients with plaque psoriasis. This appears to be strongest in younger patients with severe disease. The association seems to be related to the metabolic syndrome, a state of chronic systemic inflammation characterized by at least 3 of the following:
Abdominal obesity
Impaired glucose regulation
Hypertriglyceridemia
Reduced high-density lipoprotein levels
Hypertension
Psoriasis and obesity are now believed to share similar mediators (eg, cytokines tumor necrosis factor [TNF]–alpha and IL-6) that drive the inflammatory process in these conditions. This finding, as it becomes further elucidated, may have future implications on health screening and treatment of patients with psoriasis. [13]
Psoriasis can affect persons of any race; however, epidemiologic studies have shown a higher prevalence in western European and Scandinavian populations. In these groups, 1.5-3% of the population is affected by the disease.
The highest documented disease prevalence is in Arctic Kasach’ye, with 12% of the population affected, followed by Norway, where 4.8% of the population has psoriasis. Lower prevalence rates for psoriasis have been reported among Japanese and Inuit populations.
Psoriasis is thought to be rare in West Africans and African Americans and is nearly absent in North American Indians. Psoriasis was undetected in the Samoan population and in a study that examined 26,000 South American Indians.
The typical history given by a patient with plaque psoriasis is relatively straightforward: patients report prominent itchy, red areas with increased skin scaling and peeling. Patients are particularly aware of lesions on the scalp and extensor surfaces. Patients typically are self-conscious about their lesions and commonly report using clothing to cover affected sites and avoiding potentially embarrassing social activities.
Patients commonly recognize that new lesions appear at sites of injury or trauma to the skin. This isomorphic phenomenon (Koebner reaction) typically occurs 7-14 days after the skin has been injured and has been found in 38-76% of patients with plaque psoriasis. In some patients, so-called reverse-Koebner reactions have also been noted in which preexisting psoriatic plaques actually clear after injury or trauma to the skin.
Patients may report that their disease worsens in the winter and improves in the summer.
Significant joint pain, stiffness, and deformity are reported in the 10-20% of patients with psoriasis who develop psoriatic arthritis.
Several cardinal features of plaque psoriasis can be readily observed during the physical examination.
Psoriasis manifests as elevated lesions that vary in size from one to several centimeters (see image below). The thickened epidermis, expanded dermal vascular compartment, and infiltrate of neutrophils and lymphocytes account for the psoriatic lesions being raised and easily palpable. The number of lesions may range from few to many at any given time.
The plaques are irregular to oval and are most often located on the scalp, trunk, and limbs, with a predilection for extensor surfaces such as the elbows and knees. Smaller plaques may coalesce into larger lesions, especially on the legs and sacral regions (see image below). Fissuring within plaques can occur when lesions are present over joint lines or on the palms and soles.
Psoriatic plaques are well defined and have sharply demarcated boundaries. Psoriatic plaques occasionally appear to be immediately encircled by a paler peripheral zone referred to as the halo or ring of Woronoff.
The color of psoriatic lesions is a very distinctive rich, full, red color. Lesions on the legs sometimes carry a blue or violaceous tint.
Psoriatic plaques typically have a dry, thin, silvery-white or micaceous scale; however, the amount and thickness of this scale is quite variable. Removing the scale reveals a smooth, red, glossy membrane with tiny punctate bleeding points. These points represent bleeding from enlarged dermal capillaries after removal of the overlying suprapapillary epithelium. This phenomenon is known as the Auspitz sign.
Psoriatic plaques tend to be symmetrically distributed over the body. Lesions typically have a high degree of uniformity with few morphologic differences between the 2 sides.
Pruritus, one of the main symptoms of plaque psoriasis, is quite variable in intensity but should not be ignored. Emotional instability (eg, high levels of anxiety, depression) that might be induced by the disease often manifests as an increased tendency to scratch.
Nail changes are commonly observed in patients with plaque psoriasis. Nails may exhibit pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign. A proper assessment of any patient suspected of having psoriasis should include careful examination of the nails.
Plaque psoriasis manifests slightly differently in children. Plaques are not as thick, and the lesions are less scaly. Psoriasis may often appear in the diaper region in infancy and in flexural areas in children. The disease more commonly affects the face in children compared with adults.
This is a variant of psoriasis that spares the typical extensor surfaces and affects intertriginous (ie, axillae, inguinal folds, inframammary creases) areas with minimal scale.
Approximately 10-20% of all cases of plaque psoriasis are associated with psoriatic arthritis. Signs of psoriatic arthritis include the following:
Red, warm, tender, and inflamed joints
Joint deformity
Dactylitis
Sausage digits
Patients with obesity and psoriasis may have an increased risk of cardiovascular disease. This association appears to be strongest in younger patients with severe disease and may be related to the metabolic syndrome. [13]
Alcoholism can be considered a complication of psoriasis. Male patients with severe disease are particularly at risk for this type of substance abuse.
The differential diagnosis of plaque psoriasis includes the following:
The diagnosis of psoriasis is almost always made on the basis of clinical findings. Laboratory investigations are rarely indicated. In severe cases, patients may have mild hyperuricemia and low folate levels, presumably because of enhanced epidermopoiesis.
Skin biopsies can confirm the diagnosis of plaque psoriasis; however, this is usually reserved for the evaluation of atypical cases or for excluding other conditions in cases of diagnostic uncertainty. See Histologic Findings, below, for more details on plaque histology.
Mitotic activity of basal keratinocytes is increased almost 50-fold, with keratinocytes migrating from the basal to the cornified layers in only 3-5 days rather than the normal 28-30 days. With hyperproliferation of skin cells, the epidermis becomes thickened or acanthotic in appearance and the rete ridges increase in size.
Abnormal keratinocyte differentiation is noted throughout the psoriatic plaques, as manifested by the loss of the granular layer. The stratum corneum is also thickened, and the retention of cell nuclei in this layer is referred to as parakeratosis.
Neutrophils and lymphocytes can be observed migrating upwards from the dermis into the acanthotic epidermis. Neutrophils may form localized collections known as Munro microabscesses. The presence of alternating collections of neutrophils sandwiched between layers of parakeratotic stratum corneum is virtually pathognomonic for psoriasis. (See image below.)
Signs of inflammation can be observed throughout the dermis in persons with plaque psoriasis. Marked hypervascularity and an increase in the size of the dermal papillae occur. An activated CD3+ lymphocytic infiltrate is noted around blood vessels, with T cells expressing cutaneous lymphocyte–associated antigen, co-stimulatory molecules such as CD2, and lymphocyte function-associated antigen–1 (LFA-1) adhesion molecules. An aggregation of neutrophils in the dermis occurs that extends up into the epidermis.
Plaque psoriasis is a chronic skin condition. Any approach to the treatment of this disease must be considered for the long term. Treatment regimens must be individualized according to age, sex, occupation, personal motivation, other health conditions, and available resources.
Disease severity is defined not only by the number and extent of plaques present but also by the patient’s perception and acceptance of the disease. Treatment, therefore, must be designed with the patient’s specific expectations in mind rather than the extent of the body surface area involved. [14]
Many treatments exist for psoriasis; however, the construction of an effective therapeutic regimen is not necessarily complicated. Three basic treatment modalities are available for the overall management of psoriasis: topical agents; phototherapy; and systemic agents, including biologic therapies. All of these treatments may be used alone or in combination.
The American Academy of Dermatology has published guidelines of care for the management of psoriasis and psoriatic arthritis. See the following sections:
Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics [15]
Section 2. Psoriatic arthritis: overview and guidelines of care for treatment with an emphasis on the biologics [16]
Section 3. Guidelines of care for the management and treatmentof psoriasis with topical therapies [17]
Section 4. Guidelines of care for the management and treatment of psoriasis with traditional systemic agents [18]
Section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy [19]
Section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: Case-based presentations and evidence-based conclusions [20]
Outpatient topical therapy is the first-line treatment of plaque psoriasis. A number of topical treatments are available (eg, corticosteroids, coal tar, anthralin, calcipotriene, tazarotene). [21]
No single topical agent is ideal for plaque psoriasis, and many are often used concurrently in a combined approach. With the different adverse effect profiles for the various agents, using a rotational therapeutic approach in which different topical agents are used sequentially over time in the same patient is common.
In general, the effects of topical therapy should become evident within the first 2-3 weeks of use. Clearing of scale is usually observed first, followed by flattening of the treated plaques. Resolution of erythema may take 6-8 weeks.
Auxiliary agents such as keratolytics can often be added to these preparations. However, some auxiliary agents are incompatible with the active ingredients of these preparations. For example, salicylic acid inactivates calcipotriene. On the other hand, agents such as anthralin require the auxiliary agent salicylic acid for chemical stability.
Initiate phototherapy only in the presence of extensive and widespread disease (generally practically defined as more lesions than can be easily counted). Resistance to topical treatment is another indication for phototherapy.
The 2 main forms of phototherapy are ultraviolet B (UVB) irradiation and psoralen plus ultraviolet A irradiation (PUVA). Proper facilities are required for both UVB irradiation and PUVA photochemotherapy.
UVB irradiation uses light with wavelengths of 290-320 nm (in comparison, the visible light range is 400-700 nm). Narrow-band UVB phototherapy uses a fluorescent bulb with a narrow emission spectrum that peaks at 311 nm. This selective and relatively longer wavelength is more effective than broadband UVB for the treatment of plaque-type psoriasis, and poses less risk of burning. [22] Excimer laser UVB therapy can deliver high-dose light to limited plaques.
UVB therapy is usually combined with one or more topical treatments. The Goeckerman regimen uses coal tar followed by UVB exposure and has been shown to induce disease remission in more than 80% of patients. The Ingram method comprises anthralin application following a tar bath and UVB treatment. At present, UVB is more commonly combined with topical corticosteroids, calcipotriene, tazarotene, or simply bland emollients. Etanercept and narrow-band UVB combination therapy reportedly was successful. [23]
UVB phototherapy is extremely effective for treating moderate-to-severe plaque psoriasis. The major drawback of this therapy is the time commitment required for treatments and the accessibility of the UVB equipment. Patients may dislike the unpleasant odor when coal tar is added.
Home ultraviolet therapy can overcome some of the logistical problems associated with phototherapy. Because of the expense of the home units, it is most suitable for patients who require long-term maintenance therapy.
PUVA photochemotherapy, also known as PUVA, uses the photosensitizing drug methoxsalen (8-methoxypsoralen) in combination with UVA irradiation to treat patients with more extensive disease. UVA irradiation uses light with wavelengths of 320-400 nm. PUVA interferes with DNA synthesis, decreases cellular proliferation, and induces apoptosis of cutaneous lymphocytes, leading to a localized immunosuppression.
More than 85% of patients report relief of disease symptoms with 20-30 treatments. Therapy is usually administered 2-3 times per week in an outpatient setting, with maintenance treatments every 2-4 weeks until remission.
Adverse effects of PUVA therapy include nausea, pruritus, and a burning sensation. Long-term complications include increased risks of photo damage to the skin and (more importantly) skin cancer. PUVA has been combined with oral retinoid derivatives to decrease the cumulative dose of UVA radiation to the skin.
Initiate systemic treatment only after both topical treatments and phototherapy have proved unsuccessful. Consider systemic therapy for patients with very active psoriatic arthritis. Patients who have disease that is physically, psychologically, socially, or economically disabling are also considered candidates for systemic treatment. All patients must be informed of the risks and adverse effects of systemic therapy before treatment is initiated. [2, 3, 4]
Plaque psoriasis appears to respond better to combination topical/systemic therapy than to systemic treatment alone. In a randomized study, adding a topical corticosteroid to etanercept therapy in patients with moderate to severe plaque psoriasis proved to be a more effective treatment than etanercept alone. [24] In the study, which involved 592 adult patients with a Psoriasis Area and Severity Index (PASI) score of 10 or higher and with 10% or more of their body surface area affected by psoriasis, treatment consisted of either etanercept alone or etanercept plus topical clobetasol propionate foam. Significant differences favoring combination therapy were seen at week 12, including percentage of improvement in the PASI score (76.5% for combination therapy vs 68.2% for etanercept alone). [24]
Two clinical studies, ESTEEM 1 and ESTEEM 2, showed that patients treated with apremilast experienced significant, clinically meaningful improvement in plaque psoriasis at week 16 as measured by the PASI score. Apremilast was approved by the FDA for the treatment of plaque psoriasis in September 2014. [1]
These relatively new systemic therapies provide selective, immunologically directed intervention at key steps in the pathogenesis of the disease. [5] These steps include the following:
Inhibiting the initial cytokine release and Langerhans cell migration
Targeting activated T cells, preventing further T-cell activation, and eliminating pathologic T cells
Blocking the interactions that lead to T-cell activation or migration into tissue
Altering the balance of T-cell types
Inhibiting proinflammatory cytokines such as tumor necrosis factor (TNF), [6] IL-12, IL-17, and IL-23 [7, 25]
As with the systemic agents, biologic therapies are typically reserved for more severe and recalcitrant cases. [26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37] Patients with active psoriatic arthritis in addition to their skin disease should also be considered.
In a study completed by the Psoriatic Arthritis Study Group, beneficial effects were observed for patients with psoriasis and psoriatic arthritis on stable doses of methotrexate when one or more courses of intramuscular alefacept were added. Further benefit in psoriatic arthritis was apparent after a second course of alefacept, and no additional toxicity was observed. [38]
Psoriasis of the palms and soles is more difficult to treat than psoriasis on other body sites. Adalimumab is effective, but only 31% of patients treated with adalimumab for hand or foot psoriasis in a placebo-controlled trial achieved clear or almost clear. [39]
In 2017, the US Food and Drug Administration (FDA) approved the addition of moderate-to-severe fingernail psoriasis data to the adalimumab (Humira) prescribing information, based on results from a phase 3, multicenter, randomized, double-blind, parallel-arm, placebo-controlled clinical trial. [40] It is indicated for moderate-to-severe chronic plaque psoriasis in patients who are candidates for systemic therapy or phototherapy and for whom other systemic therapies are inappropriate. Several adalimumab biosimilar products are also approved for plaque psoriasis.
Certolizumab pegol (Cimzia) was approved by the FDA in May 2018 for use in moderate-to-severe plaque psoriasis. Approval was based on data from the CIMPASI-1, CIMPASI-2, and CIMPACT phase 3 clinical trials (n >1000). Nearly one third of participants had prior biologic exposure. The trials included an assessment of patients who achieved at least 75% and 90% improvement from baseline as measured by the Psoriasis Area and Severity Index (PASI) compared with placebo (CIMPASI-1 and CIMPASI-2) and/or etanercept (CIMPACT). Significant improvement was observed by week 16 and meaningful improvements were maintained through 48 weeks. [41, 42]
Ustekinumab (Stelara), a fully human IL-12 and IL-23 antagonist, is FDA approved to treat adults with moderate or severe psoriasis who may benefit from systemic or phototherapy. Approval was based on data from the phase 3 ACCEPT trial that revealed ustekinumab (administered as 2 subcutaneous injections at weeks 0 and 4) was significantly more effective than etanercept (50 mg injected subcutaneous twice weekly for 12 weeks) for achieving a 75% or greater reduction in psoriasis at week 12, as measured by the PASI 75. At week 12, 68% and 74% of patients receiving ustekinumab 45 mg and 90 mg, respectively, achieved a PASI 75 compared with 57% of patients receiving etanercept. [43]
In October 2017, the FDA expanded its approval to include patients aged 12 years or older. Approval of ustekinumab for adolescents aged 12-17 years with moderate-to-severe plague psoriasis was based on the phase 3, double-blind, placebo-controlled, multicenter CADMUS trial (n=110). Patients were randomly assigned to receive ustekinumab standard dosing (SD) or half-standard dosing (HSD) at weeks 0 and 4 and every 12 weeks thereafter or placebo at weeks 0 and 4 with crossover to either SD or HSD at week 12 and 16 and then every 12 weeks. At week 12, 67.7% and 69.4% of patients receiving ustekinumab HSD and SD achieved Physician’s Global Assessment (PGA) of cleared/minimal psoriasis (PGA 0/1) compared with 5.4% for placebo (P<.001). PASI 75 was 78.4% and 80.6% in HSD and SD, respectively, compared with 10.8% for placebo; PASI 90 was 54.1% and 61.1% in HSD and SD, respectively, compared with 5.4% for placebo. [44]
Guselkumab (Tremfya) was approved by the FDA in July 2017 for adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. It is a human monoclonal IgG1-lambda antibody that selectively binds to the p19 subunit of interleukin (IL)–23. IL-23 is a natural cytokine associated with inflammatory and immune responses. Guselkumab inhibits the proinflammatory actions of IL-23, thereby decreasing cytokine and chemokine release.
Approval was based on three phase 3 studies that included more than 2000 patients. In the VOYAGE 1 trial, guselkumab was compared with adalimumab. At 16 weeks, at least 7 of 10 patients treated with guselkumab achieved at least 90% clearer skin (Psoriasis Area and Severity Index [PASI 90]) and more than 80% demonstrated cleared or almost cleared skin. Patients who achieved PASI 90 at week 28 maintained that response at week 48. [45] Similar results were shown in the VOYAGE 2 trial that included adalimumab nonresponders. [46]
Guselkumab also demonstrated effectiveness in patients who had an inadequate response to ustekinumab. [47]
The first IL-17A inhibitor, secukinumab (Cosyntex), was approved by the FDA in January 2015. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses and plays a key role in the pathogenesis of plaque psoriasis. Approval was based on the efficacy and safety outcomes that included more than 3990 patients.
In two pivotal trials, secukinumab was shown to be superior compared with placebo at week 12 with respect to the proportion of patients who had a reduction of greater than 75% from baseline in the PASI score (PASI 75). The proportion of patients who met the criterion for PASI 75 at week 12 was higher with each secukinumab dose than with placebo or etanercept. In the ERASURE study (Efficacy of Response And Safety of two fixed secUkinumab REgimens in psoriasis), the rates were 81.6% with 300 mg of secukinumab, 71.6% with 150 mg of secukinumab, and 4.5% with placebo. In the FIXTURE study (Full year Investigative eXamination of secukinumab vs. eTanercept Using 2 dosing Regimens to determine Efficacy in psoriasis), the rates were 77.1% with 300 mg of secukinumab, 67% with 150 mg of secukinumab, 44% with etanercept, and 4.9% with placebo (P<.001 for each secukinumab dose vs comparators). [25]
A second IL-17A inhibitor, ixekizumab (Taltz), was approved in March 2016. Efficacy was observed in two prospective, double-blind, multicenter, phase 3 trials (UNCOVER 2, UNCOVER 3) that compared ixekizumab to placebo and etanercept. Ixekizumab (q2wk or q4wk) showed greater efficacy (measured by PASI 75) compared with placebo or etanercept (P<.0001). Greater proportions of patients given ixekizumab achieved PASI 90 by week 2 compared with etanercept in both studies (UNCOVER 2: P=.0002 [ixekizumab q4wk] and P<.0001 [ixekizumab q2wk]; UNCOVER 3: P <.0001 [ixekizumab q4wk] and P=.0001 [ixekizumab q2wk]). [8] IL-17 inhibitors may be associated with a small increase in the incidence of Candida infections. [48] Additionally, ixekizumab’s prescribing information includes data supporting use for genital plaque psoriasis.
Brodalumab (Siliq), another monoclonal antibody that targets IL-17, was approved in February 2017. Approval was contingent upon including a boxed warning in the prescribing information warning of the risk of suicide and suicidal ideation, particularly in patients with a history of suicidality or depression. Because of the observed suicidal behavior, brodalumab is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS).
Approval of brodalumab was based on data from the AMAGINE phase III pivotal studies. At the 210-mg dose, brodalumab was shown to be effective in total skin clearance of psoriasis compared with placebo and superior to ustekinumab at week 12 in two replicate comparator trials involving over 3500 patients. [9]
Tildrakizumab (Ilumya), a high-affinity, humanized, IgG1/κ, anti–IL-23p19 monoclonal antibody that does not bind human IL-12 or p40, is being developed for the treatment of chronic plaque psoriasis. In March 2018, the FDA approved tildrakizumab-asmn for moderate-to-severe plaque psoriasis, which is supported by the two pivotal phase 3 trials (reSURFACE 1 and 2). [49] The two multicenter, randomized, double-blind, placebo-controlled trials involved 926 adults with moderate-to-severe plaque psoriasis, with 616 treated with tildrakizumab-asmn and 310 receiving placebo. Both studies met the primary efficacy endpoints, demonstrating significant clinical improvement with tildrakizumab-asmn compared with placebo when measured by at least a 75% reduction in PASI 75 and PGA score of “clear” or “minimal” at week 12 after two doses.
In the reSURFACE 1 study, 74% of patients achieved PASI 75 at week 28 after three doses of tildrakizumab-asmn and 84% of patients who continued on the drug maintained PASI 75 at week 64, compared with 22% of patients who were rerandomized to placebo. In reSURFACE 2, 66% of the 200-mg group and 61% of the 100-mg group achieved PASI 75, compared with 6% of the placebo group and 48% of the etanercept group at week 12.
Guidelines on psoriasis biologic therapy from the British Association of Dermatologists [50]
Offer biologic therapy to people with psoriasis who require systemic therapy if methotrexate and cyclosporine have failed; if these agents are not tolerated or are contraindicated; and if the psoriasis has a large impact on physical, psychological, or social functioning (eg, Dermatology Life Quality Index [DLQI] or Children’s DLQI score >10 or clinically relevant depressive or anxiety symptoms) and one or more of the following disease severity criteria apply:
Consider biologic therapy earlier in the treatment plan (eg, if methotrexate has failed, is not tolerated, or is contraindicated) in people with psoriasis who fulfill the disease severity criteria and who also have active psoriatic arthritis or who have psoriasis that is persistent (ie, that relapses rapidly, defined as >50% baseline disease severity within 3 mo of completion of any treatment) while not on a therapy that cannot be continued in the long term (eg, narrow-band UVB).
Assess whether the minimal response criteria have been met, which are defined by the following:
Specific agents should be used as follows:
Advise women of childbearing potential who are starting biologic therapy for psoriasis to use effective contraception and discuss conception plans with the consultant supervising their care. There are no known interactions between biologic therapies and contraceptive methods.
Advise mothers who have received biologic therapy for psoriasis beyond 16 weeks’ gestation that their infants should not receive any live vaccinations until they have reached age 6 months (eg, rotavirus and BCG). Do not give live vaccines to people on biologic therapy or to infants (up to age 6 mo) whose mothers have received biologic therapy beyond 16 weeks’ gestation. Stop biologic therapy for at least 6 months before giving live vaccines and for 12 months in the case of the shingles (herpes zoster) vaccine. In general, biologic therapy can be started 4 weeks after administration of a live vaccine. Whenever possible, complete all required vaccinations prior to the initiation of biologic therapy, and review vaccination requirements during therapy with reference to the Green Book and the clinical risk category of “immunosuppression.”
Do not use TNF antagonists in people with demyelinating diseases, and review alternative interventions in people who have an affected first-degree relative with demyelinating disease. Stop treatment and seek specialist advice if neurologic symptoms suggestive of demyelinating disease develop during TNF antagonist therapy. Symptoms include loss or reduction of vision in one eye with painful eye movements; double vision; ascending sensory disturbance and/or weakness; problems with balance, unsteadiness, or clumsiness; and altered sensation traveling down the back and sometimes into the limbs when bending the neck forward.
Avoid TNF antagonist therapy in people with severe cardiac failure. Stop TNF antagonist therapy in the event of new or worsening preexisting heart failure and seek specialist advice.
Exercise caution and consult a gastroenterology specialist before using secukinumab or ixekizumab in people with inflammatory bowel disease.
Consider consultation with a rheumatologist for patients who have evidence of psoriatic arthritis. Patients with cardiovascular comorbidities should be considered for referral to a cardiologist. Evidence-based guidelines have been published on the management of cardiovascular morbidities. [51]
Alcohol is considered a risk factor for psoriasis in young to middle-aged males. All patients with psoriasis should avoid or minimize alcohol use; patients with dependency states should be appropriately treated. Otherwise, specific dietary restrictions or supplements other than a well-balanced and adequate diet are unimportant in the management of plaque psoriasis.
Avoiding specific exacerbating factors (see Etiology of Plaque Psoriasis for details) may help prevent or minimize flare-ups of psoriasis in some patients, although the cause of disease exacerbation in many patients often is unknown.
Overly aggressive use of topical steroids could produce progression from plaque psoriasis to generalized pustular or erythrodermic forms. Topical steroids used with occlusion increase the risk of developing cutaneous atrophy. Potential adverse effects of systemic agents and phototherapy should be monitored on a regular basis and treated as soon as possible.
Patient education is one of the foundations for managing this chronic and typically relapsing disorder. Not only is psoriasis associated with morbidity, its treatment can also cause significant adverse effects (even death in rare instances). Patients should be familiar with these details in order to make proper and informed decisions about therapy.
The National Psoriasis Foundation is an excellent organization that provides support to patients with psoriasis.
For patient education information, see the Psoriasis Center, as well as What Is Psoriasis?, Plaque Psoriasis, Types of Psoriasis, Understanding Psoriasis Medications, and Nail Psoriasis.
The course of plaque psoriasis is unpredictable. Predicting the duration of active disease, the time or the frequency of relapses, or the duration of a remission is impossible. The disease rarely is life threatening but often is intractable to treatment, with relapses occurring in most patients.
Both early onset and a family history of disease are considered poor prognostic indicators. Some suggest that stress is also associated with an unfavorable prognosis.
Environmental factors (particularly sunlight and warm weather) help alleviate the disease and are considered advantageous. Methotrexate, PUVA, cyclosporine, oral retinoids, and biologic therapies all have helped induce and maintain remission in severe cases of plaque psoriasis.
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Harvey Lui, MD, FRCPC Professor and Head, Department of Dermatology and Skin Science, Vancouver General Hospital, University of British Columbia; Medical Director, The Skin Centre, Lions Laser Skin Centre and Psoriasis and Phototherapy Clinic, Vancouver General Hospital
Harvey Lui, MD, FRCPC is a member of the following medical societies: Canadian Medical Association, American Society for Photobiology, Photomedicine Society, European Academy of Dermatology and Venereology, National Psoriasis Foundation, Canadian Dermatology Association, College of Physicians and Surgeons of British Columbia, North American Hair Research Society, Canadian Dermatology Foundation, American Academy of Dermatology, American Society for Laser Medicine and Surgery
Disclosure: Received consulting fee from Astellas for review panel membership; Received consulting fee from Amgen/Wyeth for speaking and teaching; Received honoraria from LEO Pharma for speaking and teaching; Received grant/research funds from LEO Pharma for investigator; Received grant/research funds from Galderma for other.
Adam J Mamelak, MD, FRCPC Attending Physician, Division of Dermatology, The Ottawa Hospital, University of Ottawa
Adam J Mamelak, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery, Canadian Dermatology Association
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society
Disclosure: Nothing to disclose.
Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Mark G Lebwohl, MD Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Received none from Amgen for consultant & investigator; Received none from Novartis for consultant & investigator; Received none from Pfizer for consultant & investigator; Received none from Celgene Corporation for consultant & investigator; Received none from Clinuvel for consultant & investigator; Received none from Eli Lilly & Co. for consultant & investigator; Received none from Janssen Ortho Biotech for consultant & investigator; Received none from LEO Pharmaceuticals for consultant & inves.
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