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Psoriasis

Updated: Mar 27, 2018

Author

Jacquiline Habashy, DO, MSc Resident Physician, Department of Dermatology,


Western University of Health Sciences College of Osteopathic Medicine of the Pacific

Jacquiline Habashy, DO, MSc is a member of the following medical societies: American
Osteopathic College of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

David T Robles, MD, PhD Dermatologist, Chaparral Medical Group

David T Robles, MD, PhD is a member of the following medical societies: American
Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman,


Residency Program Director, Department of Dermatology, University of Pennsylvania
School of Medicine

William D James, MD is a member of the following medical societies: American


Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier;
WebMD.

Additional Contributors

Jeffrey Meffert, MD † Former Associate Clinical Professor of Dermatology, University


of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy


of Dermatology, American Medical Association, Association of Military Dermatologists,
Texas Dermatological Society

Disclosure: Nothing to disclose.


Acknowledgements

Robert Arffa, MD Clinical Assistant Professor, University of Pittsburgh School of


Medicine

Robert Arffa, MD is a member of the following medical societies: American Academy of


Ophthalmology

Disclosure: Nothing to disclose.

Richard Gordon Jr, MD Staff Physician, Department of Emergency Medicine, Detroit


Receiving Hospital University Health Center

Richard Gordon Jr, MD is a member of the following medical societies: American


College of Emergency Physicians, American College of Physicians, American Medical
Student Association/Foundation, Emergency Medicine Residents Association, and
Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan I Huffman, MD Resident Physician, Department of Ophthalmology, Yale-New


Haven Hospital

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of


Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David
Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American
Academy of Ophthalmology, American Glaucoma Society, and Association for
Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Randy Park, MD Chair, Associate Professor, Department of Emergency Medicine,


Denton Regional Medical Center

Disclosure: Nothing to disclose.

Brian A Phillpotts, MD Former Vitreo-Retinal Service Director, Former Program


Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University
College of Medicine
Brian A Phillpotts, MD is a member of the following medical societies: American
Academy of Ophthalmology, American Diabetes Association, American Medical
Association, and National Medical Association

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson


Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-
Director of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American


Academy of Ophthalmology, American Society of Cataract and Refractive Surgery,
Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association
of America, and International Society of Refractive Surgery

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee


Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other;
Bausch & Lomb Honoraria Speaking and teaching; Merck Consulting fee Consulting;
Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Adam J Rosh, MD Assistant Professor, Program Director, Emergency Medicine


Residency, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne
State University School of Medicine

Adam J Rosh, MD is a member of the following medical societies: American Academy


of Emergency Medicine, American College of Emergency Physicians, and Society for
Academic Emergency Medicine

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology,


University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American


Academy of Ophthalmology, American College of Surgeons, and Pan-American
Association of Ophthalmology

Disclosure: Nothing to disclose.

Dana A Stearns, MD Assistant Director of Undergraduate Education, Department of


Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery,
Harvard Medical School

Dana A Stearns, MD is a member of the following medical societies: American College


of Emergency Physicians
Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of


Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug
Reference

Disclosure: Medscape Salary Employment

Practice Essentials

Psoriasis is a complex, chronic, multifactorial, inflammatory disease that involves


hyperproliferation of the keratinocytes in the epidermis, with an increase in the
epidermal cell turnover rate (see the image below). Environmental, genetic, and
immunologic factors appear to play a role. The disease most commonly manifests on
the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans
penis. In up to 30% of patients, the joints are also affected.

Treatment is based on surface areas of involvement, body site(s) affected, the presence
or absence of arthritis, and the thickness of the plaques and scale.

Plaque psoriasis is raised,


roughened, and covered with white or silver scale with underlying erythema.
Contributed by Randy Park, MD.

View Media Gallery

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.
Signs and symptoms

Signs and symptoms of psoriasis may include the following:

 Worsening of a long-term erythematous scaly area


 Sudden onset of many small areas of scaly redness
 Recent streptococcal throat infection, viral infection, immunization, use of
antimalarial drug, or trauma
 Pain (especially in erythrodermic psoriasis and in some cases of traumatized
plaques or in the joints affected by psoriatic arthritis)
 Pruritus (especially in eruptive, guttate psoriasis)
 Afebrile (except in pustular or erythrodermic psoriasis, in which the patient may
have high fever)
 Dystrophic nails, which may resemble onychomycosis
 Long-term, steroid-responsive rash with recent presentation of joint pain
 Joint pain (psoriatic arthritis) without any visible skin findings
 Conjunctivitis or blepharitis

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of psoriasis is clinical, and the type of psoriasis present affects the
physical examination findings.

Types of psoriasis

Common types of psoriasis include the following:

 Chronic stationary psoriasis (psoriasis vulgaris): Most common type of psoriasis;


involves the scalp, extensor surfaces, genitals, umbilicus, and lumbosacral and
retroauricular regions
 Plaque psoriasis: Most commonly affects the extensor surfaces of the knees,
elbows, scalp, and trunk
 Guttate psoriasis: Presents predominantly on the trunk; frequently appears
suddenly, 2-3 weeks after an upper respiratory tract infection with group A beta-
hemolytic streptococci; this variant is more likely to itch, sometimes severely
 Inverse psoriasis: Occurs on the flexural surfaces, armpit, and groin; under the
breast; and in the skin folds; this is often misdiagnosed as a fungal infection
 Pustular psoriasis: Presents on the palms and soles or diffusely over the body
 Erythrodermic psoriasis: Typically encompasses nearly the entire body surface
area with red skin and a diffuse, fine, peeling scale
 Scalp psoriasis: Affects approximately 50% of patients
 Nail psoriasis: May be indistinguishable from, and more prone to developing,
onychomycosis
 Psoriatic arthritis: Affects approximately 10-30% of those with skin symptoms;
usually in the hands and feet and, occasionally, the large joints
 Oral psoriasis: May present as severe cheilosis, with extension onto the
surrounding skin, crossing the vermillion border
 Eruptive psoriasis: Involves the upper trunk and upper extremities; most often
seen in younger patients
 Napkin psoriasis: Presence of psoriasis in children's diaper region
 Linear psoriasis: Psoriasis that occurs within a dermatome

Examination in patients with psoriasis includes the following:

 Dermatologic: Most commonly, scaling erythematous macules, papules, and


plaques; area of skin involvement varies with the form of psoriasis
 Ocular: Ectropion and trichiasis, conjunctivitis and conjunctival hyperemia, and
corneal dryness with punctate keratitis and corneal melt [1] ; blepharitis
 Musculoskeletal: Stiffness, pain, throbbing, swelling, or tenderness of the joints;
distal joints most often affected (eg, fingers, toes, wrists, knees, ankles); may
progress to a severe and mutilating arthritis of the hands, especially if treatment
has been suboptimal

Testing

There is no specific or diagnostic blood test for psoriasis. Laboratory studies and
findings for patients with psoriasis may include the following:

 Rheumatoid factor level: Negative


 Erythrocyte sedimentation rate: Usually normal, except in pustular and
erythrodermic psoriasis, where it may be elevated along with the white blood cell
count
 Uric acid level: May be elevated in psoriasis (especially in pustular psoriasis)
 Examination of fluid from pustules: Sterile bacterial culture with neutrophilic
infiltrate
 Fungal studies: Especially important in cases of hand and foot psoriasis that
seem to be worsening with the use of topical steroids or to determine if psoriatic
nails are also infected with fungus
 Conjunctival impression cytology: Increased incidence of squamous metaplasia,
neutrophil clumping, and snakelike chromatin

The differentiation of psoriatic arthritis from rheumatoid arthritis and gout can be
facilitated by the absence of the typical laboratory findings of those conditions.

Consider obtaining the following baseline laboratory studies in patients being initiated
on systemic therapies (eg, immunologic inhibitors):

 CBC count
 BUN and creatinine levels
 Liver function tests
 Hepatitis panel
 TB screening
 HIV testing
 Pregnancy test

Other studies

 Radiographs of affected joints: Can be helpful in differentiating types of arthritis


 Joint radiographs: Can facilitate the diagnosis of psoriatic arthritis
 Bone scans: Can identify joint involvement early
 Dermatologic biopsy: Can be used to make the diagnosis when some cases of
psoriasis are difficult to recognize (eg, pustular forms)

See Workup for more detail.

Management

Pharmacotherapy

Medications used in the management of psoriasis include the following:

 Topical corticosteroids (eg, triamcinolone acetonide 0.025-0.1% cream,


betamethasone 0.025-0.1% cream
 Ophthalmic corticosteroids (eg, prednisolone acetate 1% ophthalmic,
dexamethasone ophthalmic)
 Intramuscular corticosteroids (eg, triamcinolone): Requires caution because the
patient may have a significant flare as the medication wears off; 3 months should
elapse between injections
 Intralesional corticosteroids: May be useful for resistant plaques and for the
treatment of psoriatic nails
 Coal tar 0.5-33%
 Keratolytic agents (eg, anthralin, urea): Use of these medications may facilitate
more direct steroid contact with the skin
 Vitamin D analogs (eg, calcitriol ointment, calcipotriene, calcipotriene and
betamethasone topical ointment)
 Topical retinoids (eg, tazarotene aqueous gel and cream 0.05% and 0.1%)
 Antimetabolites (eg, methotrexate)
 Immunomodulators (eg, tacrolimus topical 0.1%, cyclosporine, alefacept,
ustekinumab)
 TNF inhibitors (eg, infliximab, etanercept, adalimumab)
 Phosphodiesterase-4 inhibitors (eg, apremilast)
 Interleukin inhibitors (eg, ustekinumab, secukinumab, ixekizumab, brodalumab) [2,
3, 4]

 Artificial tears
The American Academy of Dermatology (AAD) guidelines recommend treatment with
methotrexate, cyclosporine, and acitretin, with consideration of contraindications and
drug interactions. [5]

A 2013 international consensus report on treatment optimization and transitioning for


moderate-to-severe plaque psoriasis include the following recommendations [6] :

 Methotrexate, for as long as it remains effective and well-tolerated


 Cyclosporine, generally used intermittently for inducing a clinical response with
one or several courses over 3-6 months
 Transition from conventional systemic therapy to a biologic agent, either directly
or with an overlap if transitioning is needed due to lack of efficacy, or with a
treatment-free interval if transitioning is needed for safety reasons
 Combination therapy
 Continuous therapy for patients receiving biologic agents
 Switching biologic agents: If due to lack of efficacy, perform without a washout
period; if for safety reasons, a treatment-free interval may be required
 Combinations of multiple agents (eg, methotrexate and a biologic) are necessary
in some patients but the long-term safety and optimal laboratory monitoring have
yet to be defined

Other therapies

Management of psoriasis may also involve the following nondrug therapies:

 Light therapy with solar or ultraviolet radiation


 Stress reduction
 Biofeedback
 Climatotherapy
 Adjuncts, such as sunshine, sea bathing, moisturizers, oatmeal baths
 Punctal occlusion (and ocular lubricants): For keratoconjunctivitis sicca
 Bandage contact lens: To retard corneal melting

Surgical option

Ocular manifestations such as trichiasis and cicatricial ectropion usually require surgical
treatment. Progression of corneal melting, inflammation, and vascularization may
require lamellar or penetrating keratoplasty.

See Treatment and Medication for more detail.

Background

Psoriasis is a chronic, noncontagious, multisystem, inflammatory disorder. Patients with


psoriasis have a genetic predisposition for the illness, which most commonly manifests
itself on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and
glans penis. The joints are also affected by psoriasis in up to 30% of patients with the
disease. (See Pathophysiology and Etiology.)

Psoriasis has a tendency to wax and wane with flares related to systemic or
environmental factors, including life stress events and infection. It impacts quality of life
and potentially long-term survival. There should be a higher clinical suspicion for
depression in the patient with psoriasis. (See Prognosis.)

Multiple types of psoriasis are identified, with plaque-type psoriasis, also known as
discoid psoriasis, being the most common type. Plaque psoriasis usually presents with
plaques on the scalp, trunk, and limbs (see the image below). These plaques appear as
focal, raised, inflamed, edematous lesions covered with silvery-white “micaceous”
scales. (See Clinical Presentation.)

Plaque psoriasis is most common


on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.

View Media Gallery

Ocular signs occur in approximately 10% of psoriasis patients, and they are more
common in men than in women. Patients with ocular findings almost always have
psoriatic skin disease; however, it is rare for the eye to become involved before the skin.
[7]

The diagnosis of psoriasis is clinical. (See Workup.) Management of psoriasis may


involve topical or systemic medications, light therapy, stress reduction, climatotherapy,
and various adjuncts such as sunshine, moisturizers, and salicylic acid. (See Treatment
and Management.)

For more information, see the following:

 Guttate Psoriasis
 Nail Psoriasis
 Plaque Psoriasis
 Pustular Psoriasis
 Psoriatic Arthritis
 Imaging of Psoriatic Arthritis
 Parapsoriasis

Pathophysiology

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic


and immune-mediated components. This is supported by the successful treatment of
psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist
regarding triggers of the disease process including an infectious episode, traumatic
insult, and stressful life event. In many patients, no obvious trigger exists at all.
However, once triggered, there appears to be substantial leukocyte recruitment to the
dermis and epidermis resulting in the characteristic psoriatic plaques.

Specifically, the epidermis is infiltrated by a large number of activated T cells, which


appear to be capable of inducing keratinocyte proliferation. This is supported by
histologic examination and immunohistochemical staining of psoriatic plaques revealing
large populations of T cells within the psoriasis lesions. One report calculated that a
patient with 20% body surface area affected with psoriasis lesions has around 8 billion
blood circulating T cells compared with approximately 20 billion T cells located in the
dermis and epidermis of psoriasis plaques. [8]

Ultimately, a ramped-up, deregulated inflammatory process ensues with a large


production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma,
interleukin-12). Many of the clinical features of psoriasis are explained by the large
production of such mediators. Interestingly, elevated levels of TNF-α specifically are
found to correlate with flares of psoriasis.

One study adds further support that T-cell hyperactivity and the resulting
proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis
of psoriasis. [9]

Key findings in the affected skin of patients with psoriasis include vascular engorgement
due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal
hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to
improper cell maturation.

Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a
condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells
fail to release adequate levels of lipids, which normally cement adhesions of
corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the
flaking, scaly presentation of psoriasis lesions, the surface of which often resembles
silver scales.

Conjunctival impression cytology demonstrated a higher incidence of squamous


metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with
psoriasis. [10]

Etiology

Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an


increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the
loss of control of keratinocyte turnover is unknown. However, environmental, genetic,
and immunologic factors appear to play a role.

Environmental factors

Many factors besides stress have also been observed to trigger exacerbations,
including cold, trauma, infections (eg, streptococcal, staphylococcal, human
immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin,
lithium, beta-blockers, botulinum A, antimalarials). One study showed an increased
incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the
gingivitis led to improved control of the psoriasis but did not influence longterm
incidence, highlighting the multifactorial and genetic influences of this disease. [11]

Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not
universal. Perceived stress can exacerbate psoriasis. Some authors suggest that
psoriasis is a stress-related disease and offer findings of increased concentrations of
neurotransmitters in psoriatic plaques.

Genetic factors

Patients with psoriasis have a genetic predisposition for the disease. The gene locus is
determined. The triggering event may be unknown in most cases, but it is likely
immunologic. The first lesion commonly appears after an upper respiratory tract
infection.

Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, the
strongest being human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis
is an autosomal dominant trait. Additional HLA antigens that have shown associations
with psoriasis and psoriatic subtypes include HLA-B27, HLA-B13, HLA-B17, and HLA-
DR7. [12]

A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE)


genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in
different populations. [13]
Obesity is another factor associated with psoriasis. Whether it is related to weight alone,
genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or
worsening of psoriasis with weight gain and/or improvement with weight loss is
observed.

Immunologic factors

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels
of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful.
Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by


stimulation with streptococcal superantigen, which cross-reacts with dermal collagen.
This small peptide has been shown to cause increased activity among T cells in patients
with psoriasis but not in control groups. Some of the newer drugs used to treat severe
psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with
decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the
pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce
T-cell counts help reduce psoriasis severity. This finding is possibly explained by a
decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the
worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of


superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as
streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.

Epidemiology

According to the National Institutes of Health (NIH), approximately 2.2% of the United
States population has psoriasis. Internationally, the incidence of psoriasis varies
dramatically. A study of 26,000 South American Indians did not reveal a single case of
psoriasis, whereas in the Faeroe Islands, an incidence of 2.8% was observed. Overall,
approximately 2-3% of people are affected by psoriasis worldwide. Psoriasis can begin
at any age, yet there is a bimodal peak between age 20-30 years and 50-60 years.
Approximately 10-15% of new cases begin in children younger than 10 years. The
median age at onset is 28 years.

Psoriasis appears to be slightly more prevalent among women than among men;
however, men are thought to be more likely to experience the ocular disease. Psoriasis
is slightly more common in women than in men.
The incidence of psoriasis is dependent on the climate and genetic heritage of the
population. It is less common in the tropics and in dark-skinned persons. Psoriasis
prevalence in African Americans is 1.3% compared with 2.5% in whites. [14]

Psoriasis, even severe psoriasis, may occur in the pediatric age group, with a
prevalence of 0.5-2% of children. Both biologic and immunomodulating therapies may
be used safely and effectively. [15]

Prognosis

Although psoriasis is usually benign, it is a lifelong illness with remissions and


exacerbations and is sometimes refractory to treatment. It progresses to arthritis in
about 10% of cases. About 17-55% of patients experience remissions of varying
lengths.

Mild psoriasis does not appear to increase risk of death. [16] However, men with severe
psoriasis died 3.5 years earlier compared with men without the disease. Women with
severe psoriasis died 4.4 years earlier compared with women without the disease. [16]

Psoriasis is associated with smoking, alcohol, metabolic syndrome, lymphoma,


depression, suicide, potentially harmful drug and light therapies, and possibly
melanoma and nonmelanoma skin cancers.

In a population-based cross-sectional study of 9035 psoriasis patients and 90,350


matched controls without psoriasis, those with more extensive psoriatic skin disease
were at greater risk for major medical comorbidities, including heart and blood vessel
disease, chronic lung disease, diabetes, kidney disease, joint problems, and other
health conditions. [17, 18] Overall, the risk for any other type of serious illness was 11%
higher for people with mild psoriasis, 15% higher for patients with moderate psoriasis,
and 35% higher for those with severe psoriasis. [17, 18]

Heart disease

A systematic review of 90 studies confirmed that patients with psoriasis had a higher
risk of ischemic heart disease, stroke, and peripheral arterial disease but also a greater
prevalence of risk factors for cardiovascular disease, compared with controls. The
authors concluded that large prospective studies with long-term followup are required to
determine whether psoriasis is an independent risk factor for vascular disease or is
merely associated with known risk factors. [19] Another study identified psoriasis as an
independent risk factor for cardiovascular disease in women, especially if they had
psoriatic arthritis and suffered from psoriasis for a longer time period (>9 y). [20]

Hypertension

In a population-based cross-sectional study of 1322 hypertensive patients with psoriasis


and 11,977 controls without psoriasis, Takeshita et al found that patients with psoriasis
were more likely to suffer from uncontrolled hypertension than those without psoriasis.
[21, 22] Patients with moderate-to-severe psoriasis affecting more than 3% of their body

surface area were at the greatest risk.

The dose-response relation between uncontrolled hypertension and psoriasis severity


remained significant after adjustment for age, sex, body mass index, smoking status,
alcohol use, comorbid conditions, and current use of antihypertensive medications and
nonsteroidal anti-inflammatory drugs, with odds ratios of 1.20 (95% confidence interval
[CI], 0.99-1.45) for moderate psoriasis and 1.48 (95% CI, 1.08-2.04) for severe
psoriasis. [22]

Kidney disease

Severe psoriasis was associated with a greatly increased risk of chronic kidney disease
(CKD) in a recent study of more than 800,000 patients, including 142,883 with psoriasis,
7354 with severe psoriasis, and 689,702 without psoriasis. After adjustment for age,
sex, cardiovascular disease, diabetes mellitus, hyperlipidemia, hypertension, use of
nonsteroidal anti-inflammatory drugs, and body mass index, the adjusted hazard ratio
for CKD among patients with severe psoriasis was 1.93. [23, 24]

In a nested analysis of 8731 psoriasis patients and 87,310 controls, the odds ratio of
CKD after adjustment for age, sex, cardiovascular disease, diabetes, hypertension,
hyperlipidemia, body mass index, use of nonsteroidal anti-inflammatory drugs, and
duration of observation was 1.36 in patients with moderate psoriasis and 1.58 in those
with severe psoriasis. The relative risk for CKD was highest in younger patients. [23, 24]

Quality of life

Psoriasis can significantly influence a person’s quality of life. The physical and mental
disability experienced with this disease can be comparable or in excess of that found in
patients with other chronic illnesses such as cancer, arthritis, hypertension, heart
disease, diabetes, and depression. A study by Kurd et al further supports the notion that
psoriasis impacts quality of life and potentially long-term survival. [25] There should be a
higher clinical suspicion for depression in the patient with psoriasis.

While the clinical presentation of psoriasis, and whatever improvements are made
during therapy, is usually measured using the PASI (Psoriasis Area and Severity Index)
score, measurement of the effect on the quality of life of the psoriasis patient may be
better assessed by the DLQI (Dermatology Life Quality Index) or the CDLQI (Children’s
Dermatology Life Quality Index). Measurements using these tools generally show
improved quality of life with more aggressive treatment such as systemic agents. [26, 27]

Studies show that psoriasis of the palms and soles tend to have greater impact on the
patient’s quality of life compared to those with more extensive psoriatic involvement not
involving the palms and soles. [28, 29]
Patient Education

Dry eye and its manifestations may be present. Avoiding drying conditions and using
lubricants can be effective. Patient recognition of these symptoms is vital for effective
early treatment of this disease. Most cases of psoriasis can be controlled at a tolerable
level with the regular application of care measures.

For patient education resources, see the Psoriasis Center, as well as Psoriasis, What Is
Psoriasis?, Types of Psoriasis, Nail Psoriasis, and Understanding Psoriasis
Medications.

History

Symptoms of psoriasis may include the following:

 Worsening of a long-term erythematous scaly area


 Sudden onset of many small areas of scaly redness
 Recent streptococcal throat infection, viral infection, immunization, use of
antimalarial drug, or trauma
 Family history of similar skin condition
 Pain (especially in erythrodermic psoriasis and in some cases of traumatized
plaques or in the joints affected by psoriatic arthritis)
 Pruritus (especially in eruptive, guttate psoriasis)
 Afebrile (except in pustular or erythrodermic psoriasis in which the patient may
have high fever)
 Dystrophic nails
 Long-term rash with recent presentation of joint pain
 Joint pain without any visible skin findings

The skin almost always is affected before the eyes. Ocular findings occur in
approximately 10% of patients. The most common ocular symptoms are redness and
tearing due to conjunctivitis or blepharitis.

The nonocular symptoms are related to rash and psoriatic arthritis. The rash can be
uncomfortable or even painful. Psoriatic arthritis can cause stiffness, pain, throbbing,
swelling, or tenderness of the joints. The distal joints, such as the fingers, toes, wrists,
knees, and ankles, are most often affected.

Physical Examination

Findings on physical examination depend on the type of psoriasis present.

The most common skin manifestations are scaling, salmon-colored/erythematous


macules, papules, and plaques. Typically, the macules are seen first, and these
progress to maculopapules and ultimately well-demarcated, noncoherent, silvery
plaques overlying a glossy homogeneous erythema. The area of skin involvement
varies with the form of psoriasis.

Chronic stationary psoriasis (psoriasis vulgaris) is the most common type of psoriasis.
This involves the scalp, extensor surfaces, genitals, umbilicus, and lumbosacral and
retroauricular regions.

Plaque psoriasis is characterized by raised, inflamed lesions covered with a silvery


white scale. The scale may be scraped away to reveal inflamed skin beneath. This is
most common on the extensor surfaces of the knees, elbows, scalp, and trunk.

Guttate psoriasis presents as small salmon-pink papules, 1-10 mm in diameter,


predominately on the trunk; the lesions may be scaly (see the image below). It
frequently appears suddenly, 2-3 weeks after an upper respiratory infection (URI) with
group A beta-hemolytic streptococci.

Guttate psoriasis erupted in this


patient after topical steroid therapy was withdrawn during a pregnancy. Contributed by
Randy Park, MD.

View Media Gallery

Inverse psoriasis occurs on the flexural surfaces, armpit, groin, under the breast, and in
the skin folds. It is characterized by smooth, inflamed lesions without scaling due to the
moist nature of the area where this type of psoriasis is located.

Pustular psoriasis presents as sterile pustules appearing on the palms and soles or
diffusely over the body. Pustular psoriasis may cycle through erythema, pustules, then
scaling. The diffuse variant is termed von Zumbusch variant, which is accompanied by
fever and intense ill feeling in addition to the widespread pustules. Acrodermatitis
continua of Hallopeau is considered a form of pustular psoriasis that affects the hands
and feet. It may prove resistant to topical and other therapies.

Erythrodermic psoriasis presents as generalized erythema, pain, itching, and fine


scaling; various pustular forms also exist. It typically encompasses nearly the entire
body surface area. It may be accompanied by fever, chills, hypothermia, and
dehydration secondary to the large body surface area involvement. Patients with severe
pustular or erythrodermic psoriasis may require hospital admission for metabolic and
pain management. Older patients with erythrodermic psoriasis may experience cardiac
instability and hypotension due to massive vascular shunting in the skin.

Scalp psoriasis affects approximately 50% of patients. It presents as erythematous


raised plaques with silvery white scales on the scalp.

Nail psoriasis may cause pits on the nails, which often become thickened and yellowish;
this is considered the most common nail finding. Oil spots, caused by exocytosis of
leukocytes beneath the nail plate, are considered the most specific nail finding in
psoriasis. Nails may separate from the nail bed, known as onycholysis, due to the
parakeratosis of the distal nail bed. Psoriatic nails may be indistinguishable from fungal
nails and, at the same time, may be more prone to developing onychomycosis because
of the nail separation and subungual debris.

A retrospective study from 2014 reports that nail involvement in psoriasis is a significant
predictor of the patient also having psoriatic arthritis. [30] The study looked at
retrospective data from three German cross-sectional independent national studies on
patients with psoriasis and psoriatic arthritis. Data on the patient’s history of psoriasis
and psoriatic arthritis, clinical findings, nail involvement, and patient- and practitioner-
reported outcomes were collected from standardized questionnaires. In the results, the
regression model of 4146 patients indicated one of the strongest predictors of
concomitant psoriatic arthritis was nail involvement.

Psoriatic arthritis affects approximately 10-30% of those with skin symptoms. The
arthritis is usually in the hands and feet and, occasionally, the large joints. It produces
stiffness, pain, and progressive joint damage.

Oral psoriasis may present with whitish lesions on the oral mucosa, which may appear
to change in severity daily. It may also present as severe cheilosis with extension onto
the surrounding skin, crossing the vermillion border. Geographic tongue is considered
by many to be an oral form of psoriasis.

Eruptive psoriasis involves the upper trunk and upper extremities. Most often, it is seen
in younger patients.
Ocular Manifestations

In addition to skin manifestations, psoriasis may also affect the lid, conjunctiva, or
cornea and give rise to ocular manifestations, including ectropion and trichiasis,
conjunctivitis and conjunctival hyperemia, and corneal dryness with punctate keratitis
and corneal melt. [1]

Blepharitis is the most common ocular finding in psoriasis. Erythema, edema, and
psoriatic plaques may develop, and they can result in madarosis, cicatricial ectropion,
trichiasis, and even loss of the lid tissue.

A chronic nonspecific conjunctivitis is fairly common. It usually occurs in association


with eyelid margin involvement. Psoriatic plaques can extend from the lid onto the
conjunctiva. Chronic conjunctivitis can lead to symblepharon, keratoconjunctivitis sicca,
and trichiasis. Nodular episcleritis and limbal lesions resembling phlyctenules also can
be seen.

Corneal disease is relatively rare. Most often, it is secondary to lid or conjunctival


complications, such as dryness, trichiasis, or exposure. The most common finding is
punctate keratitis. Filaments, epithelial thickening, recurrent erosions, vascularization,
ulceration, and scarring can occur. The vascularization tends to be superficial,
peripheral, and interpalpebral or inferior. Rarely, peripheral infiltration and melting can
occur in the absence of trichiasis and exposure. [31]

In one case, recurrent nasolacrimal duct occlusion was observed, presumably caused
by washing of the scales into the lacrimal sac.

Usually, anterior uveitis can be seen in association with psoriatic arthritis. Acute
psoriatic uveitis tends to be bilateral, prolonged, and more severe than nonpsoriatic
cases. [32, 33]

Complications

Complications of psoriasis may include the following:

 Secondary infections
 Possible increased risk of lymphoma
 Possible increased risk of cardiovascular and ischemic heart disease
 Psoriatic arthritis
 Mitral valve prolapse

Even after plaques have cleared, there may be a longstanding or permanent


dyschromia. Arthritis, if not controlled, may be mutilating and crippling. Arthritic changes
cannot be reversed; therefore, initiation of treatment is imperative to slow, or even halt,
progression of disease. It is suggested that psoriatic patients have a higher incidence of
cancer, especially lymphoma, but how much of this increased risk can be ascribed to
the psoriasis and how much to the medications used for psoriasis is less certain.
Psoriatic patients have a higher incidence of depression and anxiety, and, while these
conditions usually improve with successful treatment, it is not guaranteed. Many other
potential complications are directly related to the treatment, such as a higher incidence
of skin cancer in patients treated with phototherapy and a higher incidence of infections,
mild and serious, in patients on immune-suppressing medications.

Differential Diagnoses

 Adult Blepharitis
 Allergic Contact Dermatitis
 Atopic Dermatitis in Emergency Medicine
 Atopic Keratoconjunctivitis (AKC)
 Cutaneous Squamous Cell Carcinoma
 Diaper Dermatitis
 Dry Eye Disease (Keratoconjunctivitis Sicca)
 Gout and Pseudogout
 Lichen Planus
 Lichen Simplex Chronicus
 Mycosis Fungoides
 Nummular Dermatitis
 Onychomycosis
 Pityriasis Alba
 Pityriasis Rosea
 Pustular Eruptions
 Reactive Arthritis
 Seborrheic Dermatitis
 Sicca Keratoconjunctivitis
 Subcorneal Pustulosis
 Syphilis
 Tinea in Emergency Medicine

Approach Considerations

The diagnosis of psoriasis is clinical. The differentiation of psoriatic arthritis from


rheumatoid arthritis and gout can be facilitated by the absence of the typical laboratory
findings of those conditions. Overlap with other arthritic syndromes is possible,
however.

Laboratory Studies

Laboratory studies and findings for patients with psoriasis may include the following:

 Test result for rheumatoid factor (RF) is negative.


 Erythrocyte sedimentation rate (ESR) is usually normal (except in pustular and
erythrodermic psoriasis).
 Uric acid level may be elevated in psoriasis (especially in pustular psoriasis),
causing confusion with gout in psoriatic arthritis.
 Fluid from pustules is sterile with neutrophilic infiltrate.
 Perform fungal studies. (This is especially important in cases of hand and foot
psoriasis that seem to be worsening with the use of topical steroids.)

If starting systemic therapies such as immunological inhibitors, consider obtaining


baseline laboratory studies (ie, complete blood cell [CBC] count, blood urea nitrogen
[BUN]/creatinine, liver function tests [LFTs], hepatitis panel, tuberculosis [TB] screening,
and pregnancy test).

Other Tests

Although most cases of psoriasis are diagnosed clinically, some, particularly the
pustular forms, can be difficult to recognize. In these cases, dermatologic biopsy can be
used to make diagnosis. Biopsy of the skin lesion may reveal basal cell hyperplasia,
proliferation of subepidermal vasculature, absence of normal cell maturation, and
keratinization. A large number of activated T cells are present in the epidermis. Biopsy
of acral skin may be less useful as chronic eczematous dermatitis may be psoriasiform
and psoriasis of the palms and soles may show spongiosis more often associated with
eczema.

Radiographs of affected joints can be helpful in differentiating types of arthritis. Joint x-


rays can facilitate the diagnosis of psoriatic arthritis. Bone scans can identify joint
involvement early.

Conjunctival impression cytology has demonstrated an increased incidence of


squamous metaplasia, neutrophil clumping, and snakelike chromatin.

When the scales are removed, small droplets of blood appear within a few seconds
from exposed vessels in the dermal papillae; this is known as the Auspitz sign.

Procedures

Punch biopsy of the skin may act as a confirmatory workup procedure.

Histologic Findings

Histopathology findings include the following [34] :

 Regular acanthosis of the epidermis


 Parakeratosis
 Kogoj spongiotic pustules
 Munro microabscesses
Approach Considerations

Management of psoriasis may involve topical and systemic medication, phototherapy,


stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers,
salicylic acid, and other keratolytics such as urea.

Expert dermatologists from across the globe released a consensus report on treatment
optimization and transitioning for moderate-to-severe plaque psoriasis.
Recommendations of the 2013 consensus report include the following:

 Methotrexate may be used for as long as it remains effective and well-tolerated.


 Cyclosporine is generally used intermittently for inducing a clinical response with
one or several courses over a 3–6 month period.
 Transition from conventional systemic therapy to a biological agent may be done
directly or with an overlap if transitioning is needed because of lack of efficacy, or
with a treatment-free interval if transitioning is needed for safety reasons.
 Combination therapy may be helpful.
 Continuous therapy for patients receiving biologicals is recommended.
 Switching biologicals because of lack of efficacy should be performed without a
washout period while switching biologicals for safety reasons may require a
treatment-free interval.

The American Academy of Dermatology (AAD) is developing a series of


recommendations under the umbrella title, Guidelines of Care for the Management of
Psoriasis and Psoriatic Arthritis. The most recent addition was Section 6 (published
online in November 2010; in print 2011.) All 6 sections are available online at the AAD
website. [5, 35, 36, 37, 38] Section 6 of the AAD guideline recommends that psoriasis
treatment be personalized for each patient’s clinical situation and discusses examples
of this approach to treatment. [38]

A summary of biologic therapy guidelines from the British Association of Dermatologists


can be found in Guideline Summary.

Treatment of Skin Lesions

Patients with guttate, erythrodermic, or generalized pustular psoriasis may present to


the emergency department. In each of these cases, restoration of the barrier function of
the skin is of prime concern. This can be performed with cleaning and bandaging.

Plaque and scalp lesions are frequently encountered in patients seeking care for other
problems, and initial treatment of the lesions should be offered.

The simplest treatment of psoriasis is daily sun exposure, sea bathing, topical
moisturizers, and relaxation. Moisturizers, such as petrolatum jelly, are helpful. Daily
application of moisturizing cream to the affected area is inexpensive and successful
adjunct to psoriasis treatment. Application immediately after a bath or shower helps to
minimize itching and tenderness. Section 3 (2009) of the AAD guideline discusses
topical agents and recommends their use adjunctively but not as monotherapy if the
disease is extensive or recalcitrant. [36]

Nonprescription tar preparations are available and have therapeutic success, especially
when used in conjunction with topical corticosteroids; the newer foams are less messy
preparations than some of the older ones. Anthralin, tazarotene, salicylic acid, phenolic
compounds, and calcipotriene (a vitamin D analog) also may be effective especially
when used in combination with topical corticosteroids. Systemic corticosteroids are
generally ineffective, and they can significantly exacerbate the disease upon withdrawal.

Combination therapy with a vitamin D analog (calcipotriol and calcipotriene) or a retinoid


such as tazarotene and a topical corticosteroid is more effective than therapy with either
agent alone. [39] Oatmeal baths may be helpful for itching.

Solar or therapeutic ultraviolet (UV) radiation may be helpful. Various UV light


treatments are used—now most commonly, UVB, although psoralen + UVB (PUVA) is
still used. Among phototherapy options, Section 5 (2010) of the AAD guideline gives the
highest recommendation to oral PUVA or a combination of PUVA and topical agents. [37]

Psoralen is a photosensitizer that is ingested prior to light exposure. PUVA treatment


results in conjunctival hyperemia and dry eye, particularly if sun protection is not used.
With proper eye protection, there does not appear to be a risk of cataract. Psoralens for
either topical (bath) or systemic use may occasionally be difficult to obtain because of
intermittent availability issues.

According to the AAD guidelines, PUVA can result in long remissions, but long-term use
of PUVA in Caucasians may increase the risk of squamous cell carcinoma (SCC) and
possibly malignant melanoma. [35, 37] A prospective study of 1380 patients found a strong
correlation between number of PUVA treatments and risk of developing one or more
SCC. According to the study, exposure to more than 350 PUVA treatments greatly
increases the risk of SCC. [40]

In a retrospective study of 48 patients (mean age, 51 yr; 33 women, 15 men), psoralen-


UVA (PUVA) therapy was found to be an appropriate treatment alternative for
palmoplantar psoriasis, according to Carrascosa et al. It provided similar response rates
to systemic treatment and often with increased tolerance and safety. PUVA was found
to be effective in 63% of cases of palmoplantar psoriasis. Systemic therapy, however,
was required in 47.9% of patients, with acitretin being the drug most often used.
Adverse events occurred in 25% of patients, with the most common one being mild
erythema (18%). [41]

Narrowband UVB therapy has always been accepted as a good treatment modality of
psoriasis, [42] and the AAD guidelines recommend it over broad-band (UVB), although
both are less effective than PUVA. [35, 37] As with PUVA, the guidelines also recommend
treatment with combinations of UVB and topical or systemic agents. [37] However, a
study by Keaney and Kirsner gives objective reasoning for the benefit of narrowband
UV therapy by showing decreases in T cells, dendritic cells, and interleukins within
responsive psoriatic plaques compared with plaques that did not respond to therapy. [9]
UVB also has the advantage of not leaving the patient with a prolonged period of
photosensitivity as PUVA does.

Guttate psoriasis may prove especially responsive to phototherapy. Therapies such as


UVB and PUVA have low efficacy for the treatment of nail psoriasis because of the
blockage of the UV radiation by the intervening nail plate, so that systemic therapy or
intralesional steroids may be best for these. [43] In 2017, the US Food and Drug
Administration (FDA) approved the addition of moderate-to-severe fingernail psoriasis
data to the adalimumab prescribing information, based on results from a phase 3,
multicenter, randomized, double-blind, parallel-arm, placebo-controlled clinical trial. [44]

Patients with psoriasis should avoid injury to skin, including sunburn and other physical
trauma, as these areas may develop psoriasis. The appearance of psoriatic lesions in
previously uninvolved areas after irritation or trauma is known as the Köbner
phenomenon. Patients with psoriasis should also, when feasible, avoid drugs known to
worsen the problem (eg, chloroquine, beta-blockers, aspirin or other NSAIDs). They
should also avoid alcohol to excess. An association has been made between
nonalcoholic fatty liver disease and moderate-to-severe psoriasis. What is related to
treatment and what is related to psoriasis itself is still being studied. [45]

In severe cases, systemic medications such as retinoids (acitretin), methotrexate,


cyclosporine, 6-thioguanine, azathioprine, a biologic, or hydroxyurea may be necessary
for adequate control. Retinoids have been reported to cause dry eye, blepharitis,
corneal opacities, cataracts, and decreased night vision. All of these may be associated
with gastrointestinal intolerance, hepatic damage (acitretin, 6-thioguanine, azathioprine,
methotrexate), marrow suppression (6-thioguanine, methotrexate, azathioprine,
hydroxyurea) or renal damage (cyclosporine).

The use of biologic agents (proteins with pharmacologic activity) is discussed in Section
1 (2008) and reviewed, with updated safety information, in Section 6 of the AAD
guidelines. The AAD recommends a set of baseline laboratory studies before starting
treatment with a biologic agent to ensure any underlying conditions or risk factors are
understood. [35, 38] Some patients with chronic hepatitis C may be safely treated with
biologic agents, [46] while active hepatitis B is still considered a contraindication.

The use of these systemic medications, with appropriate safety considerations, is


supported by Section 4 (2009) of the AAD guidelines. [5] Increased risk of infection
applies to all systemic immune-suppressing medications, especially when used in
combinations. Many of the therapies for psoriasis manipulate the function of the immune
system and expose the patient to risk of severe infections while blunting the body’s
response. In these patients, findings suggestive of minor infections must be taken
seriously, and the risk versus the benefit of continuing the drug in the face of the
infection must be weighed.
In addition, systemic retinoids and hydroxyurea may interfere with proper wound healing
and elective procedures, including dental surgery, which are best performed before the
start of the medications. Acitretin appears more effective than isotretinoin in psoriasis
and does not require enrollment in the IPledge program. On the other hand, there is a 3-
year pregnancy prohibition after its use, and many will not use this medication in any
patient capable of ever becoming pregnant. Combination therapies, such as a biologic
plus another immunosuppressive medication, have been used with good effect but data
detailing the safest way to do this are scant. All of the systemic medications except
acitretin may increase the risk of infection.

Abruptly stopping steroid therapy in psoriasis or adding known irritant drugs can result
in the sudden worsening of psoriasis or appearance of a new form. Commonly, this new
form is guttate psoriasis, which is much more severe and cosmetically problematic than
the preexisting plaque type. It may also present with a more threatening pustular or
erythrodermic psoriatic flare.

Because of concerns that immune-suppressing medications may blunt the body


response to malignancies, most consider active or untreated cancer a contraindication
to starting such medications.

Treatment of Ocular Complications

Keratoconjunctivitis sicca can be treated with ocular lubricants and punctal occlusion.
Trichiasis and cicatricial ectropion usually require surgical treatment. Conjunctival,
corneal, and anterior chamber inflammation can be treated with topical corticosteroids.
Nonsteroidal anti-inflammatory agents or oral corticosteroids are occasionally
necessary. Whether systemic immunosuppression is effective for ocular disease is not
clear. Corneal melting, inflammation, and vascularization can be difficult to treat. A
bandage contact lens may retard the melting. Topical corticosteroids can control the
infiltration and delay the vascularization. In some cases, progression can occur in spite
of these treatments and can lead to the need for lamellar or penetrating keratoplasty.

Consultations

Psoriasis is a chronic problem, and consultation for follow-up with a dermatologist or a


rheumatologist is appropriate. Close follow-up is necessary to design an optimal
treatment plan in accordance with the severity of disease.

Severity of psoriasis can be classified as follows:

 Mild - Less than 2% of the body is affected


 Moderate - From 3-10% of the body is affected
 Severe - More than 10% of the body is affected

Of note, the palm of the patient’s hand is equal to 1% body surface area.
Determining the severity of psoriasis requires combining objective measures, such as
body surface area involvement; disease location; symptoms; and presence of psoriatic
arthritis with subjective measures such as the physical, financial, and emotional impact
of the disease.

Patients with infectious diseases and psoriasis may be using drugs that modify
immunologic response and render them immunocompromised. Investigation into the
type of therapy is important and, if such an agent is identified, referral and close follow-
up is needed.

Many suggest that because of the comorbidities of heart disease and cardiovascular
disease that if adult patients have not been recently evaluated and screened for these,
they should either be tested or referred back to their primary care provider to consider
what is appropriate for any particular patient.

Patients with psoriasis, especially widespread and severe, have a higher incidence of
depression, which may require medical intervention. If this cannot be managed by their
primary care provider, referral to a mental health specialist might be appropriate.

Autoimmune diseases are generally associated with increased rates of lymphoma and
myelodysplastic disease. Whether this is related to the disease itself or to its treatment
is not yet determined. Patients who have laboratory abnormalities or physical findings of
hematologic disease or malignancy should be evaluated by a hematologist and/or
oncologist as appropriate. [47]

Surgical Care

No specific surgical treatments are available for psoriasis, other than procedures
relating to ophthalmic complications as described in other sections. The development of
psoriasis at surgical sites (and after sunburn) is a recognized phenomenon.

Medical Costs

See above Treatment of Skin Lesions for a discussion on different treatment options. All
newer medications, especially the biologic therapies, are extremely expensive, with
cash prices ranging from $30,000 per year to over $80,000 per year. Other medications,
topical and systemic, that have been available for decades have been subjected to
regular price increases, which, while keeping them less expensive than a newer biologic
agent, has still resulted in them being very expensive. This usually includes generic
medications, when generics are available.

Industry communications reveal that the list cost of a new medication has little to do with
the cost of research and manufacturing expenses, but more to do with target income
goals and considerations of what the market will bear. For this reason, most insurance
plans do not do blanket approval of any and all FDA-approved medications and will
often require a staged approval process, where a patient will have to have been
unresponsive or have had significant adverse effects to less expensive medications
before more expensive treatments are considered. This is even more problematic when
there are attempts to do off-label psoriasis treatment using medications indicated for
other inflammatory and arthritic conditions. Such use, even if supported by the scientific
literature, is often be branded "experimental", and insurance coverage may be difficult
or impossible to obtain.

Difficulty in reliably obtaining, storing, and using some of these newer medications may
explain why the biologics seem to be less efficacious in patients with lower
socioeconomic status. [48]

Diet

Ample literature suggests that weight loss can help psoriasis, but other attempts to
show improvement with more specific diets, such as a gluten-free diet, are less
conclusive. Studies of very-low-calorie diets and the “Mediterranean Diet" have both
shown improvement in anecdotal reports and small studies. [49, 50] Nutritional
supplements have shown limited benefit, with the exception of fish oil. [51] Vitamin D itself
has also been reported to be of benefit in small studies. [52] Much more work needs to be
done before enthusiastic support of any particular supplement or dietary plan may be
offered.

Activity

Any restrictions on activity would relate to concomitant arthritis and how well it is being
controlled. Natural sunlight can help psoriasis and may explain why it is relatively rare
on the face. It has been suggested that a more active lifestyle can help psoriasis, but
whether this is an independent factor or more related to better weight control is less
certain.

Prevention

No specific strategies prevent psoriasis, although healthy lifestyles that avoid obesity
and reduced alcohol use can make control easier and increase the chances of at least
temporary remission. Whenever possible, patients who are currently being treated for
psoriasis or have a history of psoriasis should avoid over-the-counter and prescription
medications known to exacerbate it. This includes the use of over-the-counter NSAIDs
such as ibuprofen and naproxen.

Long-Term Monitoring

Other than age-appropriate screening for cardiovascular disease, long-term monitoring


is generally treatment specific (eg, skin cancer in phototherapy patients, liver disease in
methotrexate patients, tuberculosis exposure in patients on biologic medications).
Guidelines on screening for comorbidities in pediatric patients with psoriasis have been
issued by the Pediatric Dermatology Research Alliance and National Psoriasis
Foundation. [53] Features include the following:

 Overweight or obesity - Start at age 2 years; use body mass index criteria
 Type 2 diabetes -Starting at age 10 years or puberty onset in overweight patients
with two risk factors, screen every 3 years; screen obese patients every 3 years
regardless of risk factors; use fasting serum glucose value for screening
 Dyslipidemia - Start at age 9-11 years and then again at age 17-21 years; use
universal lipid screening; fasting lipid panel recommended
 Hypertension - Starting at age 3 years, screen yearly using age, sex, and height
reference charts
 Nonalcoholic fatty liver disease (NAFLD) - Starting at age 9-11 years, use
alanine aminotransferase in overweight or obese children with risk factors (eg,
insulin resistance, prediabetes or diabetes, central adiposity, dyslipidemia, sleep
apnea, family history of NAFLD/nonalcoholic steatohepatitis (NASH); consider
screening at a younger age if patients have greater risk factors (eg, severe
obesity, family history of NAFLD/NASH, hypopituitarism); with normal screening
results, repeat alanine aminotransferase screening every 2-3 years based on risk
factors (or sooner if they increase in number or severity)
 Polycystic ovary syndrome - Consider screening in patients with symptoms (eg,
oligomenorrhea, hirsutism)
 Gastrointestinal disease - Considering evaluating patients with decreased growth
rate, unexplained weight loss, or symptoms of inflammatory bowel disease
 Arthritis - Screen periodically with review of systems and physical examination
 Uveitis - Only warranted in psoriatic arthritis.
 Mood disorders and substance abuse - Regardless of age, annually for
depression and anxiety; at age 11 years, annually for substance abuse
 Quality of life - Consider using formal instrument (eg, Children's Dermatology Life
Quality Index)

Guidelines Summary

Guidelines on psoriasis biologic therapy from the British Association of


Dermatologists [56]

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:

 Psoriasis is extensive (defined as body surface area [BSA] >10% or PASI ≥10)
 Psoriasis is severe at localized sites and associated with significant functional
impairment and/or high levels of distress (eg, nail disease or involvement of high-
impact and difficult-to-treat sites such as the face, scalp, palms, soles, flexures,
and genitals)

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:

 Fifty percent or greater reduction in baseline disease severity (eg, PASI 50


response, or percentage BSA where PASI is not applicable) and
 Clinically relevant improvement in physical, psychological, or social functioning
(eg, ≥4-point improvement in DLQI or resolution of low mood)

Specific agents should be used as follows:

 Ustekinumab: Offer ustekinumab as a first-line biologic agent to adults with


psoriasis who fulfil the criteria for biologic therapy.
 Adalimumab: Offer adalimumab as a first-line biologic agent to adults with
psoriasis, particularly when psoriatic arthropathy is a consideration.
 Secukinumab: Consider secukinumab as a first-line biologic agent in adults with
psoriasis, with or without psoriatic arthritis.
 Infliximab: Reserve infliximab for use in people with very severe disease or
people in whom other available biologic agents have failed or cannot be used.
 Others: Offer adalimumab (age ≥4 y), etanercept (≥6 y), or ustekinumab (≥12 y)
to children and young people who fulfill the criteria for biologic therapy.

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.

Medication Summary

Many drugs that affect the rate of skin cell production are used in psoriasis therapy
alone or in combination with light therapy, stress reduction, and climatotherapy.
Adjuncts to treatment include sunshine, moisturizers, and salicylic acid as a scale-
removing agent. Generally, these therapies are used for patients with less than 20% of
body surface area involved, unless the lesions are physically, socially, or economically
disabling.

Treatments for more advanced psoriasis include narrowband ultraviolet B (UVB) light,
psoralen with ultraviolet A (UVA) light retinoids (eg, isotretinoin [Accutane, Claravis],
acitretin [Soriatane]), methotrexate (particularly for arthritis), cyclosporine (Neoral,
Sandimmune), infliximab (Remicade), etanercept (Enbrel), adalimumab (Humira),
apremilast (Otezla), and secukinumab (Cosentyx). Decreased effectiveness of
infliximab or adalimumab in a patient previously well controlled on the medication may
mean that antibodies to the medication are being produced. [54]

In a study of ustekinumab in patients with moderate-to-severe psoriasis, investigators


did not observe an increased trend in dose-related or cumulative toxicity with the
duration of ustekinumab treatment. The investigators also reported rates of adverse
events generally comparable to those of other biologics approved for managing
moderate-to-severe psoriasis. [2] It is approved in two dosages, administered
subcutaneously, with the higher dose given to those weighing 100 kg (220 pounds) or
more. It has been suggested that 91 kg (200 pounds) might be a better cutoff for the
higher dose for optimal control. [3]

Recommendations from a 2013 international consensus report on treatment


optimization and transitioning for moderate-to-severe plaque psoriasis include
methotrexate and cyclosporine, biologic agents, and combination therapy. [6]
The AAD guidelines recommend treatment with methotrexate, cyclosporine, and
acitretin, with consideration of the contraindications and drug interactions noted in the
discussion of each medication below. [5]

Many other medications are used off label for psoriasis. Many of these are drugs
approved initially for rheumatoid arthritis or inflammatory bowel disease but are found to
also have benefits in skin psoriasis. Tofacitinib citrate, a Janus kinase inhibitor, is such
a medication that has shown promise in the treatment of psoriasis. [55] Caution must be
taken any time a medication is used off label because the true risks and benefits may
not yet have been defined for a different patient population than that originally studied.

Topical Corticosteroids

Class Summary

Topical corticosteroids are the mainstay of treatment for mild and limited psoriasis. They
can reduce plaque formation. These agents have anti-inflammatory effects and may
cause profound and varied metabolic activities.

The strength of topical steroid and vehicle are chosen according to the thickness of
plaques and body location. No topical corticosteroids are conclusively superior in
efficacy or adverse effects than others in the same class. Some formulations such as
foams and solutions are easier to use in the scalp than either creams or ointments. A
patient who has been doing well on a topical steroid who begins to have worsening,
especially with itching, should be evaluated for either a concomitant fungal infection or
the development of allergic contact dermatitis to a steroid or vehicle component. Potent
and superpotent corticosteroids generally only need be applied once daily unless the
scale on a plaque is particularly thick. Extended use of very potent steroids should be
avoided when possible in the treatment of genital and inverse psoriasis.

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

 View full drug information

Triamcinolone treats inflammatory dermatosis responsive to steroids. It decreases


inflammation by suppressing the migration of polymorphonuclear leukocytes and
reversing capillary permeability. It has mild potency and is the first drug of choice for
most patients.
Betamethasone topical (Alphatrex, BetaVal, Dermabet)

 View full drug information

Betamethasone treats inflammatory dermatosis responsive to steroids. It decreases


inflammation by suppressing the migration of polymorphonuclear leukocytes and
reversing capillary permeability. It is a potent topical steroid and is the drug of choice if
psoriasis is resistant to milder forms.

Ophthalmic Corticosteroids

Class Summary

Ophthalmic corticosteroids treat conjunctival, corneal, and anterior chamber


inflammation. These agents help control infiltration and delay vascularization. Care must
be taken with long-term use because of concerns about infection with viruses such as
herpes simplex or fungal infections.

Prednisolone acetate ophthalmic (Pred Forte, Pred Mild, Omnipred)

 View full drug information

Prednisolone decreases inflammation by suppressing migration of polymorphonuclear


leukocytes and reversing increased capillary permeability.

In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if


signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be
reduced, but advise patients not to discontinue therapy prematurely.

Dexamethasone ophthalmic (Maxidex, Ozurdex)

 View full drug information

Dexamethasone is used for various allergic and inflammatory diseases. It decreases


inflammation by suppressing migration of polymorphonuclear leukocytes and reducing
capillary permeability.
Coal Tar

Class Summary

Coal tar is an inexpensive treatment that is available over the counter in shampoos,
lotions, creams, or foam for use in widespread areas of involvement. It is particularly
useful in hair-bearing areas. Some recent research has shown the 1% concentration
may be superior in control of lesions to more concentrated preparations. Tar
preparations may be especially useful when combined with topical corticosteroids. This
may be accomplished by applying the products sequentially or, when available,
obtaining them from a compounding pharmacy. Treatment with tar preparations may be
especially useful when combined with topical corticosteroids.

Coal tar 0.5-33% (DHS Tar, Balnetar, Cutar, Polytar, Theraplex T)

 View full drug information

Coal tar is antipruritic and antibacterial and inhibits deregulated epidermal proliferation
and dermal infiltration. It does not injure the normal skin when applied widely, and it
enhances the usefulness of phototherapy. It generally is used as a second-line drug
therapy due to messy application, except for shampoos, which may be used and rinsed
at once.

Keratolytic Agents

Class Summary

Keratolytic agents are used to remove scale, to smooth the skin, and to treat
hyperkeratosis.

Removing the thick scale allows topical corticosteroids and other topical medications to
better reach the target tissues and achieve better results. This is especially important on
the scalp. Many over-the-counter preparations can be used for this, most of which
contain salicylic acid. Lactic acid, ammonium lactate, and urea are other ingredients that
may be applied before or at the same time as other topical medications. Urea
preparations stronger than 30% require a prescription, a variety of creams, lotions, and
foams are available for this. Many “foot creams” contain combinations of keratolytics
and may be applied to any area of the body needing scale removal.

Anthralin is also considered to be in the antipsoriatic therapeutic class.


Anthralin (Dritho-Creme, Zithranol)

 View full drug information

Anthralin reduces the rate of cell proliferation. Its chemically reducing properties may
also upset the oxidative metabolic processes, further reducing epidermal mitosis. It is
not the first or second drug of choice due to irritation problems of normal skin
surrounding lesions and staining of the skin.

Vitamin D Analogs

Class Summary

Vitamin D analogs are used in patients with lesions resistant to topical therapy or with
lesions on the face or exposed areas where thinning of the skin would pose cosmetic
problems. These come as ointments, solutions, and foams. The latter two are especially
useful for scalp treatments.

Calcitriol ointment (Vectical)

 View full drug information

Calcitriol is a topical vitamin D analog similar to calcipotriene but seems to be less


irritating in sensitive areas of skin.

Calcipotriene (Dovonex, Sorilux, Calcitrene)

 View full drug information

Calcipotriene is a synthetic vitamin D-3 analog that regulates skin cell production and
development. It is used in the treatment of moderate plaque psoriasis. This treatment
does not cause long-term skin thinning or systemic effects. Sorilux is a newer foam
version of this medication.
Calcipotriene/betamethasone (Enstilar, Taclonex Ointment, Taclonex Topical
Suspension)

 View full drug information

Calcipotriene is a synthetic vitamin D-3 analog that regulates skin cell production and
development. It inhibits epidermal proliferation, promotes keratinocyte differentiation,
and has immunosuppressive effects on lymphoid cells. Betamethasone is a
corticosteroid that decreases inflammation by suppressing migration of
polymorphonuclear leukocytes and reversing capillary permeability. The combination is
available as a topical ointment, foam, or as a solution that can be applied to the body or
scalp. The products contain calcipotriene 0.005% and betamethasone dipropionate
0.064%.

The combination product is quite expensive and the same results may be obtained by
using a generic corticosteroid sequentially in combination with one of the other vitamin
D analog products.

Topical Retinoids

Class Summary

Aqueous gel formulations are odorless and colorless, and no long-term skin damage
has been noted with topical retinoids. There is also no threat of worsening if the therapy
is withdrawn, as with steroids. These drugs should not be used in women if pregnancy
is a possibility.

Tazarotene (Tazorac Fabior, Avage)

 View full drug information

Tazarotene is a retinoid prodrug that is converted to its active form in the body and
modulates differentiation and proliferation of epithelial tissue and perhaps has anti-
inflammatory and immunomodulatory activities. It may be the drug of choice for those
with facial lesions who are not at risk of pregnancy.

Tazarotene, although topical, is a category X medication. Topical tretinoin is of less use


in psoriatic patients. A strategy that may be tried in patients who experience
unacceptable irritation is to use short contact times. There are several protocols, but the
least irritating is to apply the medication for 15-20 min and then wash off. The total time
on may be increased by 15-20 minutes every few weeks until clinical efficacy or adverse
cutaneous effects are seen. This short-contact method may be especially useful when
one is using it in skin folds but is less effective for the plaque with very thick scale.

Antimetabolites

Class Summary

Antimetabolites inhibit cell growth and proliferation.

Methotrexate (Trexall, Otrexup, Rheumatrex)

 View full drug information

Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to


tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon
groups in the synthesis of nucleotides and thymidylate. Subsequently, methotrexate
interferes with DNA synthesis, repair, and cellular replication. Actively proliferating
tissues are in general more sensitive to this effect of methotrexate.

Immunomodulators

Class Summary

Immunomodulators regulate key factors responsible for inflammatory response.

Tacrolimus topical 0.1% (Protopic)

 View full drug information

Topical tacrolimus has been used in the past for management of refractory atopic
dermatitis. However, multiple studies have shown effectiveness with psoriasis affecting
intertriginous regions as well as the face. Generally, it seems to be effective in thin-
skinned areas. However, it has become somewhat of a second-line agent given other
studies showing topical steroids may be more effective and potential serious disease
association.
Cyclosporine (Sandimmune, Neoral, Gengraf)

 View full drug information

Cyclosporine is an 11-amino acid cyclic peptide and natural product of fungi. It acts on
T-cell replication and activity.

Cyclosporine is a specific modulator of T-cell function and an agent that depresses cell-
mediated immune responses by inhibiting helper T-cell function. Preferential and
reversible inhibition of T lymphocytes in the G0 or G1 phase of cell cycle is suggested.
The drug binds to cyclophilin, an intracellular protein, which, in turn, prevents formation
of interleukin (IL)-2 and the subsequent recruitment of activated T cells.

Cyclosporine has about 30% bioavailability, but there is marked interindividual


variability. It specifically inhibits T-lymphocyte function with minimal activity against B
cells. Maximum suppression of T-lymphocyte proliferation requires that the drug be
present during first 24 h of antigenic exposure.

Cyclosporine suppresses some humoral immunity and, to a greater extent, cell-


mediated immune reactions (eg, delayed hypersensitivity, allograft rejection,
experimental allergic encephalomyelitis, and graft versus host disease) for a variety of
organs.

Cyclosporine is used in extensive disease refractory to other treatments, especially


when used at 5 mg/kg/d. Remission is usually rapid with this therapy; however, skin
lesions tend to recur within days to weeks after treatment is stopped (although patients
do not usually have the severe rebound that patients withdrawing from therapy may
have). Maintenance therapy (3 mg/kg/d) usually is required with lower doses of this
drug.

Tumor Necrosis Factor Inhibitors

Class Summary

These agents neutralize the effects of tumor necrosis factor-α (TNF-α). For
adalimumab, weight-based dosing regimens exist for pediatric-aged patients. For
etanercept, some patients will require twice-weekly dosing of the induction period
indefinitely in order to maintain satisfactory control. Decreased effectiveness of
infliximab or adalimumab in a patient previously well controlled on the medication may
mean that antibodies to the medication are being produced.
Infliximab (Remicade)

 View full drug information

Infliximab is a chimeric antibody that binds both the soluble and transmembrane TNF-α
molecules, thereby neutralizing the effects of TNF-α. It is indicated for chronic severe
(ie, extensive and/or disabling) plaque psoriasis in adults who are candidates for
systemic therapy and when other systemic therapies are medically less appropriate. It is
also indicated to reduce signs and symptoms, and to improve physical function of
patients with psoriatic arthritis. Screen patients for tuberculosis (TB) and hepatitis B, as
reactivation of both illnesses is associated with TNF-α inhibitors.

This drug is delivered by infusion only.

Etanercept (Enbrel, Erelzi, etanercept-szzs)

 View full drug information

Etanercept is a recombinant human TNF-α receptor protein fused with the Fc portion of
IgG1 that binds to soluble and membrane-bound TNF-α, thereby neutralizing the effects
of TNF-α. It is indicated for adults and children aged 4 years and older with moderate-
to-severe psoriasis. It is also indicated for adults with moderate-to-severe psoriatic
arthritis. Screen patients for TB and hepatitis B, as reactivation of both illnesses is
associated with TNF-α inhibitors.

Adalimumab (Humira)

 View full drug information

Adalimumab is a fully human anti–TNF-α monoclonal antibody. It binds specifically to


soluble and membrane-bound TNF-α, thereby neutralizing the effects of TNF-α. It is
used to treat moderate-to-severe psoriasis and moderate-to-severe psoriatic arthritis.
Screen patients for TB and hepatitis B, as reactivation of both illnesses is associated
with TNF-α inhibitors.
Phosphodiesterase-4 Enzyme Inhibitors

Class Summary

The mechanisms by which phosphodiesterase-4 (PED4) inhibitors elicit anti-


inflammatory effects are not completely understood. Unlike biologics that neutralize
inflammatory mediators at the protein level, apremilast modulates mediator production
at the level of mRNA expression.

Apremilast (Otezla)

 View full drug information

Apremilast is a phosphodiesterase-4 inhibitor specific for cAMP, resulting in increased


intracellular cAMP levels. It may affect cytokines and chemokine synthesis, leading to
anti-inflammatory effects. It is indicated for moderate-to-severe plaque psoriasis in
adults who are candidates for phototherapy or systemic therapy.

Interleukin Inhibitors

Class Summary

Interleukins play key roles in the pathogenesis of plaque psoriasis.

Secukinumab (Cosentyx)

 View full drug information

Secukinumab is a human IgG1 monoclonal antibody that selectively binds to and


neutralizes the proinflammatory cytokine IL-17A. 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. Following the initial once-weekly SC dosage
regimen, the drug is given as a maintenance dose once monthly. It is indicated for
moderate-to-severe plaque psoriasis in patients who are candidates for systemic
therapy or phototherapy.
Ixekizumab (Taltz)

 View full drug information

Ixekizumab is a humanized monoclonal IgG4 antibody that targets IL-17A and


neutralizes the proinflammatory effects of IL-17A. It is administered as a SC injection. It
is indicated for adults with moderate-to-severe plaque psoriasis.

Brodalumab (Siliq)

 View full drug information

Brodalumab is a human monoclonal IgG2 antibody that selectively binds to the human
IL-17A receptor and inhibits its interactions with cytokines IL-17A, IL-17F, IL-17C, IL-
17A/F heterodimer, and IL-25. It is indicated for moderate-to-severe plaque psoriasis in
adults who are candidates for systemic therapy or phototherapy and have failed to
respond or have lost response to other systemic therapies.

Ustekinumab (Stelara)

 View full drug information

Ustekinumab is a human monoclonal antibody directed against IL-12 and IL-23, thereby
interfering with T-cell differentiation and activation and subsequent cytokine cascades. It
is indicated for moderate-to-severe plaque psoriasis.

Guselkumab (Tremfya)

 View full drug information

Guselkumab is a human monoclonal IgG1-lambda antibody that selectively binds to the


p19 subunit of 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. It is indicated for adults with moderate-to-
severe plaque psoriasis who are candidates for systemic therapy or phototherapy.

Tildrakizumab (Ilumya, Tildrakizumab-asmn)

 View full drug information

This humanized IgG1/k monoclonal antibody selectively binds to the p19 subunit of IL-
23 and inhibits its interaction with the IL-23 receptor. IL-23 is a natural cytokine
associated with inflammatory and immune responses. Tildrakizumab inhibits the release
of proinflammatory cytokines and chemokines. It is indicated for adults with moderate-
to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.

Ophthalmic agents, Miscellaneous

Class Summary

Artificial tears are used to treat dry eye irritation. Many types of artificial tears are
available over the counter. In mild cases, preserved tears can be used. In severe cases,
only nonpreserved tears should be used. Preserved tears include GenTeal, Refresh
Tears, and Tears Naturale II. Nonpreserved tears include Refresh, Refresh Plus,
OcuCoat, Bion, and Hypo Tears PF.

Artificial tears (Tears Naturale Forte, BionTears, HypoTears, Murine Tears)

 View full drug information

Artificial tears contain the equivalent of 0.9% NaCl and are used to maintain ocular
tonicity. They act to stabilize and thicken precorneal tear film and prolong tear film
breakup time, which occurs with dry eye states.

Injectable Corticosteroids

Class Summary

Intramuscular corticosteroids are not recommended for the management of psoriasis


because of the risk of flare upon withdrawal. On the other hand, isolated plaques may
be injected intralesionally, as may the nail matrix in cases of severe psoriatic nails.
Triamcinolone (Kenalog, Aristospan)

 View full drug information

For inflammatory dermatosis responsive to steroids; decreases inflammation by


suppressing migration of polymorphonuclear leukocytes and reversing capillary
permeability. Many other topical steroids also are available.

Up to 0.4 mL may be injected, after ring block, into the nail bed and matrix to improve
psoriatic dystrophy. Results may be long lasting but more than one treatment may be
required.

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