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psoriasis.

Case 41-3 (Question 2)

EPIDEMIOLOGY

Psoriasis, a chronic, proliferative skin disease, is one of the most common immune-

mediated disorders, occurring in 1.5% to 3% of the population worldwide, with

northern Europeans and Scandinavians affected most.

1–4

It is characterized by welldelineated, thickened erythematous epidermis or dermal plaques covered with a

distinctive silvery scale. Of patients, 75% present with symptoms of psoriasis before

the age of 46 years.

2 A family history of psoriasis is found in nearly half of patients.

At least 36 chromosomal loci have been identified that increase psoriasis

susceptibility.

5–7 Modifiable triggers, such as tobacco and alcohol use, stress,

obesity, skin injury, and hormone changes, also play a major role in disease

expression.

3,8

Pathogenesis

Innate and adaptive immunity are both involved in the initiation and maintenance of

psoriatic plaques. Because the epidermis is the body’s main barrier to environmental

insult, epidermal hyperplasia forms a key component of the innate immune response.

Natural killer cells and natural killer T cells are part of the cutaneous inflammation

in psoriasis.

3,9

Because CD4

+ and CD8

+ T-lymphocytic cells constitute most of the leukocyte

infiltrates found in plaques early in the development of lesions, current evidence

supports an autoimmune mechanism for psoriasis. Cytokines such as interferon-α2 or

interleukin-2 are also found in psoriatic plaques.

10 T cells in the cutaneous infiltrate

are positive for cutaneous lymphocyte–associated antigen, a marker for skin-homing

leukocytes. Pathogenesis also involves

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vascular and inflammatory changes, which precede epidermal changes.

11

Alterations in the dermal vasculature also appear to be a result of angiogenesis, the

development of new blood vessels, similar to a number of other disease processes,

including tumor growth. Many commonly used therapeutic agents for psoriasis have

antiangiogenic activity.

1

The epidermal changes of psoriasis are based on the time required for affected

epidermal cells to travel to the surface and be cast off, which is markedly reduced

(3–4 vs. 26–28 days in normal cells).

12 This sixfold to ninefold transit time decrease

does not allow the normal events of cell maturation and keratinization to take place

and is reflected clinically as diffuse scaling. T cells contribute to this keratinocyte

hyperproliferation through the secretion of various growth factors.

13,14 Memory T

lymphocytes marked with cutaneous lymphocyte–associated antigen, to remember the

anatomic site where they first encountered antigen, migrate to the (epi)dermis by a

number of immunologic and inflammatory triggering mechanisms released from

keratinocytes after minor trauma. On entry into the skin, these T cells complex with

epidermal self-antigens presented by major histocompatibility complex molecules

that confer the risk of psoriasis. The subsequent release of T-cell cytokines results in

further inflammation, the recruitment of additional marked (i.e., with cutaneous

lymphocyte–associated antigen) T cells, and, ultimately, the development of psoriatic

lesions in susceptible persons.

13,14

Prognosis

Similar to those with diabetes, cancer, or heart disease, patients with psoriasis

experience a reduced quality of life related to an impairment of social,

psychological, and physical functioning.

15–17 Although psoriasis is a treatable

disease, there is no known cure. Optimism and encouragement are justified and make

it easier for patients to conscientiously apply sometimes awkward and messy topical

treatments or take medications that have significant adverse effects. The goal of

therapy should be to achieve complete clearing of psoriatic lesions, particularly

during emotionally critical times, such as the commencement of school, puberty, and

the summer months.

Clinical Presentation of Psoriasis

CASE 41-1

QUESTION 1: M.M., a 35-year-old man, presents with complaints of several thick, well-defined

erythematous areas on both his elbows and knees that have silvery scales on them. He complains of itching in

these areas and that the areas bleed when he removes the scales. M.M. states that he has had these lesions for

some time; however, he has used over-the-counter hydrocortisone and some of his friend’s triamcinolone

0.025% cream on them for the itching. He feels that the lesions have gotten worse since he went on vacation in

the Dominican Republic and got “a pretty bad sunburn.” His medical history is noncontributory. His only

medications, besides topical corticosteroids, include a recent course of chloroquine for malaria prophylaxis

during his recent travel. On physical examination, M.M. is also found to have a few scattered, circumscribed,

erythematous, scaly plaques on the flexural surfaces of both arms and legs and a dense scale on his forehead

and scalp. Approximately 4% of his body surface area (BSA) is estimated to be affected with psoriasis. The

rest of M.M.’s physical examination and laboratory results are within normal limits.

Laboratory values and vitalsigns include the following:

BP, 132/78 mm Hg

HR, 64 beats/minute

Sodium, 140 mEq/L

Potassium, 4.3 mEq/L

Blood Urea Nitrogen (BUN), 13 mg/dL

Creatinine, 0.9 mg/dL

What classic signs and symptoms suggestive of psoriasis are demonstrated by M.M.?

Most psoriatic lesions are asymptomatic, but not always. Pruritus, for example, is

noted in 50% of patients, and it can be severe.

18 Patients also report stinging or

burning sensations.

19 The primary psoriatic lesion is a relapsing eruption of scaling

papules that rapidly coalesce or enlarge to form circumscribed, erythematous, scaly

plaques. The scale is adherent and silvery white and may reveal bleeding points

when removed, called the Auspitz sign. Scales can become extremely dense on the

scalp or macerated and dispersed in intertriginous areas.

The development of lesions of active psoriasis at the site of epidermal trauma is

known as the Koebner phenomenon. Scratch marks, sunburn, or surgical wounds may

heal, leaving psoriatic lesions in their place. The elbows, knees, scalp, gluteal cleft,

fingernails, and toenails are favored areas of involvement. Extensor surfaces are

affected more than the flexor surfaces, but the disease usually spares the palms, soles,

and face. Nail beds may show punctate pitting, profuse collections of keratotic

material, yellow-brown discoloration (“oil spot”), or onycholysis (nail plate

separation) in approximately 50% of patients.

20 Psoriatic arthritis is a seronegative

inflammatory arthritis that occurs in approximately 25% of all patients with

psoriasis, with combined features of both rheumatoid arthritis and the seronegative

spondyloarthropathies.

2,18

Most patients (90%) have chronic localized disease (plaque type or psoriasis

vulgaris), but several other presentations exist.

3 The most severe form of the disease

is erythrodermic psoriasis, a condition of acute inflammatory erythema and scales

involving greater than 90% of the BSA. Pustular psoriasis is generally localized to

palms and soles, but there is also a generalized version. Both generalized pustular

psoriasis and erythrodermic psoriasis can be accompanied by systemic symptoms

(i.e., hyperthermia, tachycardia, edema, dehydration, shortness of breath) and can

have life-threatening consequences (i.e., hypovolemia, electrolyte imbalance,

septicemia) if not promptly treated.

21 Lesions of Guttate psoriasis are small, fine,

erythematous scales, usually found on the trunk, arms, or legs, classically after βhemolytic streptococcal pharyngitis. Flexural or inverse psoriasis is shiny and red,

and typically lacks scales and looks more like intertrigo.

2 Of interest, psoriatic skin

is rarely secondarily infected, because of the overexpression of the endogenous

peptides cathelicidins and β-defensins.

20

Systemic disorders that can have a causative association with psoriasis include

type 2 diabetes mellitus, Chron’s disease, metabolic syndrome, depression, and

cardiovascular disease.

2,15–17 This increased risk is thought to be caused by the

presence of endothelial activation, proinflammatory cytokines, and

hyperlipidemia.

2,17,21 Disease severity is also thought to be a factor, because psoriatic

patients with more severe conditions have an increased risk of metabolic, coronary

heart disease or stroke compared with those with milder forms of psoriasis.

15

M.M. presents with many classic signs of psoriasis, including symmetric,

distinctive, chronic, and erythematous plaques covered with silvery scales on the

extensor surfaces of the elbows and knees as well as the flexural surface of his arms

and legs. He also shows scalp involvement, but does not appear to have plaques on

his trunk or nail or systemic involvement. He exhibits the Auspitz sign and evidence

of the Koebner phenomenon because

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his lesions worsened after skin trauma from the sunburn. His report of pruritus is

consistent with the presentation in 50% of patients.

CASE 41-1, QUESTION 2: What are the factors that can precipitate or aggravate psoriasis? What are the

potential causes of M.M.’s psoriatic exacerbation?

A thorough medical history may reveal a cause of exacerbations of psoriatic

lesions. Most patients report that hot weather, sunlight, and humidity help clear

psoriasis, whereas cold weather has an adverse effect on its course. Anxiety or

psychological stress is believed to contribute adversely. Viral or bacterial infections,

especially streptococcal pharyngitis, may precipitate the onset or flare-up of

psoriasis. Cuts, burns, abrasions, injections, and other trauma can also elicit the

development of lesions. Any drug that causes a skin eruption to develop can

exacerbate psoriasis via this response.

Drug-Induced Psoriasis

A number of drugs have been reported to exacerbate preexisting psoriasis, induce

psoriatic lesions on apparently normal skin in patients with psoriasis, or precipitate

psoriasis in persons with or without a family history of psoriasis (Table 41-1).

23

Antimalarial agents, such as chloroquine (taken by M.M.), may have an adverse

effect on the course of psoriasis and can cause exfoliative erythroderma.

24

Hydroxychloroquine, however, has not shared this association (except for one case

report) and usually induces a beneficial response in 75% of patients with psoriatic

arthritis.

24

It is preferred over chloroquine in patients with psoriasis who need

prophylactic treatment for malaria when both are effective against the particular

plasmodium species in the area (see Chapter 81, Parasitic Infections).

24

Lithium also can precipitate psoriasis and contribute to resistance to treatment

through its effects on cell kinetics (increase in circulating neutrophils, accelerated

neutrophil turnover, increased epidermal cell proliferation).

22 Psoriasis is not a

general contraindication, however, to lithium therapy. More intensive psoriasis

treatment can be used if these reactions occur, and lithium must be continued.

22

β-Blockers and some nonsteroidal anti-inflammatory drugs (NSAIDs) also can

precipitate a psoriasiform state.

22 Because both lithium and propranolol inhibit cyclic

adenosine monophosphate (cAMP), cyclic nucleosides may play a role in the onset

and clinical course of psoriasis. Chemotactic substances, including 12-

hydroxyeicosatetraenoic acid and leukotrienes, may accumulate in the epidermis of

some patients taking indomethacin, thereby precipitating psoriasis.

22

When compared with other NSAIDs, indomethacin may selectively inhibit

cyclooxygenase more than lipoxygenase pathways of arachidonic acid metabolism.

As a result, indomethacin may have a more significant adverse psoriatic effect than

other NSAIDs that have been reported to ameliorate psoriasis.

22

Flare-ups of pustular psoriasis also can be precipitated by withdrawal from

systemic corticosteroids or withdrawal from high-potency topical corticosteroids

that are applied under occlusion to large areas.

25 Because of this problem and

because fatalities have been associated with systemic corticosteroid use and

withdrawal, systemic corticosteroids are not routinely used to treat psoriasis.

Chloroquine prophylaxis, a Caribbean sunburn, and triamcinolone tachyphylaxis

probably all contributed to the exacerbation of M.M.’s psoriasis.

Categorization of Psoriasis

CASE 41-1, QUESTION 3: How would you categorize M.M.’s psoriasis?

The Self-Administered Psoriasis Area and Severity Index (SAPASI) is a

validated, structured instrument that can be used for patient assessment of psoriasis

severity and the response to therapy. It closely correlates with the standard clinician

assessment instrument, Psoriasis Area and Severity Index (PASI), which includes

quantification of the percentage of body involvement and severity of lesions.

26,27 A

PASI of 75 (a ≥75% decrease in PASI score) at 3 months from baseline has become

the most prominent marker to assess systemic agent efficacy (see

http://escholarship.org/uc/item/18w9j736, which is Dermatol Online J.

2004;10(2):7, for a good reference to teach someone the PASI and SAPASI).

28

Table 41-1

Drugs Reported to Induce Psoriasis

Anesthetics Procaine

Antimicrobial agents Amoxicillin, ampicillin, imiquimod, penicillins, sulfonamides, terbinafine,

tetracyclines, vancomycin, voriconazole

Anti-inflammatory drugs Corticosteroids (after withdrawal), NSAIDs (indomethacin, salicylates),

mesalamine

Antimalarial agents Chloroquine, hydroxychloroquine

Cardiovascular drugs Acetazolamide, amiodarone, angiotensin-converting enzyme inhibitors

(enalapril, lisinopril), β-blockers (atenolol, metoprolol, propranolol, timolol),

calcium channel blockers (dihydropyridines, diltiazem, verapamil), clonidine,

digoxin, gemfibrozil, quinidine

H2

-antagonists Cimetidine, ranitidine

Hormones Oxandrolone, progesterone

Opioid analgesics Morphine

Psychotropics and neurologic

agents

Lithium carbonate, venlafaxine, fluoxetine, carbamazepine, olanzapine,

gabapentin, oxcarbazepine, tigabine, valproic acid, zaleplon

Miscellaneous Potassium iodide, mercury, α-interferon, β-interferons, granulocytemacrophage colony-stimulating factor (GM-CSF)

NSAIDs, nonsteroidal anti-inflammatory drugs.

Source: Kim GK, Del Rosso JQ. Drug-provoked psoriasis: is it drug induced or drug

aggravated? J Clin Aesthet Dermatol. 2010;3:32–38; Basavaraj KH et al. The role of

drugs in the induction and/or exacerbation of psoriasis. Int J Dermatol.

2010;49:1351; Facts & Comparisons eAnswers. Accessed August 21, 2015, with

permission.

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The National Psoriasis Foundation has released a clinical consensus statement on

the classification of severity of disease. Rather than using a mild (less than 5% BSA

affected) to moderate (5%–10%) to severe (greater than 10% BSA affected)

classification system, the statement recommends two categories for patients: those

who are candidates for topical therapy (less than 5% of BSA affected) and those who

are candidates for systemic or phototherapy (more than 5% of BSA affected).

27,28

M.M. would be categorized as having mild psoriasis and is a candidate for topical

therapy because less than 5% of his BSA is currently affected by psoriasis.

TREATMENT OF MILD PSORIASIS

Many topical and systemic therapeutic agents are available, varying from simple

topical emollients to systemic, highly potent immunosuppressant drugs for more

recalcitrant conditions. Often, treatment modalities are chosen on the basis of disease

severity, cost, convenience, and patient response. Patients with mild disease can

generally be treated with topical therapy (Table 41-2). Patients with psoriasis

covering more than 5% of the body require more specialized systemic or

phototherapy treatment programs (Table 41-3). Nonpharmacologic treatment is also

very important and can range from spa therapy to support groups.

Initial Therapy

NONPHARMACOLOGIC MODALITIES

CASE 41-1, QUESTION 4: What role can emotional support play in the comprehensive management of

M.M.’s psoriasis?

Psoriasis is often more emotionally or psychologically disturbing than is

recognized, and it may cause a reluctance from patients to participate in sports and

other outdoor activities that may expose their skin to sunlight. Although exposure to

sunlight helps most patients with psoriasis, there is an unwillingness to sunbathe if

the lesions can be seen. Furthermore, if the psoriatic lesions become pruritic and are

scratched, there can be further deterioration at the site. Many patients alter their

lifestyles or use nontraditional medications and modalities, often in desperation.

Emotional support should begin with explanation of the psoriatic condition. M.M.

needs to be reassured that many other people have the same condition, that the

disorder is not contagious or fatal, and that it can be controlled, although no cure

exists.

29 Patients usually are comforted in the knowledge that a wide range of

treatments are available. Psychological encouragement and support are justified and

make it easier for the patient to conscientiously apply messy topical treatments or to

take toxic medications.

Table 41-2

Topical Agents for the Treatment of Psoriasis (Mild to Moderate; <5%Body

Surface Area Involvement)

Treatment Modality Advantages Disadvantages

Emollients Basic adjunct for all treatments; safe,

inexpensive, reduces scaling, itching,

and related discomfort

Provide minimal relief alone

Keratolytics (salicylic acid, urea,

α-hydroxy acids [i.e., glycolic

and lactic acids])

Reduce hyperkeratosis; enable other

topical modalities to better penetrate;

inexpensive

Provide minimal relief individually;

nonspecific; salicylism (tinnitus,

nausea, vomiting) with salicylic acid if

applied extensively

Topical corticosteroids Rapid response; control inflammation

and itching; best for intertriginous

areas and face; convenient, not

messy; mainstay topical treatment

modality for psoriasis

Temporary relief; less effective with

continued use (tachyphylaxis occurs);

withdrawal can produce flare-ups;

atrophy, telangiectasia, and striae with

continued use after skin returns to

normalized state; expensive; adrenal

suppression possible

Coal tar Particularly effective for “flaky” scalp

lesions; newer preparations are more

cosmetically appealing; efficacy

enhanced in combination with UVB

(i.e., Goeckerman regimen)

Effective only for mild psoriasis or

scalp psoriasis; inconvenient with

difficult application; stains clothing

and bedding, not skin; strong smelling;

folliculitis and contact allergy

(bronchospasm in atopic patient with

asthma after inhalation of vapor);

carcinogenicity in animals

Anthralin Effective for widespread, refractory

plaques; produces long remissions;

short, concentrated programs

preferred; enhanced efficacy in

combination with UVB (i.e., Ingram

Purple-brown staining (skin, clothing,

and bath fixtures); irritating to normal

skin and flexures; careful application

is required; can precipitate

generalized psoriasis

regimen) Calcipotriene and calcitriol As effective as topical corticosteroids,

although slower onset, without longterm corticosteroid adverse effects;

convenient, well tolerated

Slow onset; expensive; potential

effects on bone metabolism

(hypercalcemia); irritant dermatitis on

face and intertriginous areas;

contraindicated during pregnancy

Tazarotene Extended response; convenient

(applied once daily, in gel

formulation); maintenance therapy;

effective on scalp and face; used in

combination with topical

corticosteroids

Slow onset; local irritation and

pruritus; teratogenic (adequate

contraception is required)

Ultraviolet B (UVB) Effective as maintenance therapy;

eliminates problems of topical

corticosteroids

Expensive; office-based therapy;

sunburn (exacerbates psoriasis);

photoaging; skin cancers

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Table 41-3

Agents for the Treatment of Severe Psoriasis (>5%Body Surface Area

Involvement)

Treatment Modality Advantages Disadvantages

Psoralens plus UVA (PUVA) 80% efficacy; “suntan” effect is

cosmetically desirable

Time-consuming; expensive, officebased therapy (restrictive); sunburn

(exacerbates psoriasis); photoaging;

both nonmelanoma skin cancer and

melanoma; contraindicated during

pregnancy and lactation

Acitretin Not as effective as other systemic

agents; efficacy enhanced if given

with PUVA or UVB (i.e., RePUVA

or ReUVB); less hepatotoxic than

methotrexate

Teratogenic (contraception required);

contraindicated with liver or renal

dysfunction, drug or alcohol abuse,

hypertriglyceridemia, hypervitaminosis

A

Methotrexate Effective for both skin lesions and

arthritis, as well as psoriatic nail

disease

Hepatotoxicity (liver biopsy may be

indicated); bone marrow toxicity; folic

acid protects against stomatitis (but

not against hepatic or pulmonary

toxicity); drug interactions;

contraindicated during pregnancy and

lactation, drug or alcohol abuse; use

with caution during acute infections

Cyclosporine Toxicities and short-lived remissions;

used in patients with extensive disease

who are unresponsive to other agents;

however, given changing

pathophysiology and increasing

experience at lower dosages,

increasing role in rotational therapy to

Renal impairment; suppressive

therapy (relapse occurs when

discontinued); increased risk of skin

cancer, lymphomas, and solid tumors;

phototoxic; contraindicated during

pregnancy and lactation, and with

hypertension, hyperuricemia,

induce remissions hyperkalemia, acute infections

Immunomodulators

(etanercept, infliximab,

adalimumab, golimumab,

secukinumab, ixekizumab)

Specific, targeted therapy; effective

for both moderate-to-severe skin

lesions and arthritis; maintains

remission

Expensive; parenteral therapy (often

administered in an office-based

practice); long-term safety unknown;

increased risk of serious infections

PUVA, psoralens plus ultraviolet A light; RePUVA, retinoid-PUVA; UVA, ultraviolet A; UVB, ultraviolet B.

TOPICAL CORTICOSTEROIDS

CASE 41-1, QUESTION 5: What topical corticosteroid therapy is appropriate for M.M.?

Topical corticosteroids, the most widely prescribed treatment for psoriasis, are

effective in the treatment of psoriasis because of their anti-inflammatory, antimitotic,

immunosuppressant, and antipruritic properties.

25,30,31 These properties are explained

by a reduction in phospholipase A2

, DNA synthesis, and epidermal mitotic activity,

as well as their vasoconstrictive actions. They provide prompt relief, and patients

find them convenient and acceptable. Mild-strength topical products or intermediatestrength products, for limited periods, can be used on facial lesions or intertriginous

areas, or for maintenance therapy.

32 However, topical corticosteroids can, in a

process called tachyphylaxis, also become less effective with continued use, and

long-term use after the skin has returned to a normalized state leads to typical

corticosteroid adverse effects (atrophy, telangiectasia, and striae). Thin-skinned

areas (i.e., facial and intertriginous) are particularly susceptible.

33

Psoriasis is generally a relatively corticosteroid-resistant disease; therefore, the

more potent corticosteroids are frequently necessary, often with occlusion (e.g.,

plastic food wrap on top of the topical corticosteroid-treated area) (see Table 39-8

i n Chapter 39, Dermatotherapy and Drug-Induced Skin Disorders, for a listing of

topical corticosteroids by potency). Less-potent agents are more appropriate in

intertriginous areas, on the face, and for maintenance. Potent fluorinated

corticosteroid preparations should be used cautiously and only for short periods on

the face and flexures, if at all. Potent topical corticosteroids may clear psoriasis in

25% of patients in 3 to 4 weeks, with 75% clearing in 50% of treated patients.

34

Intermittent dosing or “pulse therapy” with several weeks between successive

courses appears to yield the best long-term results and minimizes tachyphylaxis and

adverse effects. An additional drawback of chronic corticosteroid therapy is an

associated acute flare-up of psoriasis when corticosteroid therapy is terminated.

35

Continuous application for more than 3 to 4 weeks should be discouraged in patients

with psoriasis, and systemic corticosteroids have no place in therapy.

33,34 Topical

corticosteroids occasionally can cause a reversible suppression of the hypothalamic–

pituitary–adrenal (HPA) axis, as indicated by a decrease in the morning plasma

cortisol level.

33 For anything more extensive than mild disease and short duration of

therapy, topical corticosteroids are best used in an adjunctive role. During a flare-up,

corticosteroids help reduce inflammation, redness, and irritation and prepare the

involved area for initiation of other potentially irritating, but more appropriate,

maintenance topical treatments (e.g., coal tar, anthralin, calcipotriene, or tazarotene).

A short course of a potent topical corticosteroid is appropriate for this flare-up of

erythematous plaque psoriasis in M.M. This will help reduce inflammation, redness,

and irritation before possible initiation of more appropriate chronic topical

treatments, such as calcipotriene, coal tar, or anthralin with ultraviolet B (UVB).

Topical corticosteroids also may continue to be useful for M.M.

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on the face and flexures, where the alternative topical agents are poorly tolerated.

His scalp psoriasis can be treated with corticosteroid preparations in gels, lotions,

or aerosol sprays. This will allow for a more effective treatment of scaling and

pruritus using an agent such as coal tar shampoo lathered into the scalp for 5 to 10

minutes, then rinsed out.

The response to once- or twice-daily corticosteroid application is as effective as

or better than that observed with more frequent regimens (owing to a corticosteroid

reservoir effect) and is much less expensive. M.M. should apply a topical

corticosteroid preparation after a bath, at bedtime with occlusion, and possibly again

during the day without occlusion. As the lesions subside, occlusion should be

decreased or omitted, emollient use should increase, and the corticosteroid potency

should decrease. After lesions have flattened, the topical corticosteroid products can

be continued intermittently (e.g., 1–2 weeks on, 1–2 weeks off; or on alternate days

[e.g., days 1, 3, 5, and 7]).

ALTERNATIVE TOPICAL TREATMENTS

CASE 41-1, QUESTION 6: M.M.’s acute psoriasis flare-up has responded well to a short course of topical

corticosteroid. What alternative topical therapeutic regimens are available for patients such as M.M. who have

localized or mild disease?

Effective alternative topical therapies available for patients with localized, mild

psoriasis include crude coal tar, anthralin, calcipotriene, calcitriol, and tazarotene.

31

Although anthralin has irritating properties and both coal tar and anthralin generally

stain clothing and skin and are somewhat inconvenient to apply, their efficacy is well

established and may be an option to consider for initial management. Tachyphylaxis

does not occur with chronic use of any of these alternative agents. Once the

inflammation and erythema have lessened with corticosteroid use or when a twicedaily, high-potency corticosteroid regimen along with bedtime application of coal tar

is ineffective, calcipotriene ointment applied twice daily or tazarotene gel applied

once daily is effective in treating flare-ups and maintaining remission. Ointment

vehicles are favored because they help moisturize the plaques (in contrast to creams,

which dry the plaques further). Also, moisturizers or emollients are often helpful for

psoriasis.

31

Coal Tar

Crude coal tar is a complex mixture of thousands of hydrocarbon compounds.

31,36

It is

a time-honored modality for treating psoriasis. It affects psoriasis by enzyme

inhibition and antimitotic action (antiproliferative and anti-inflammatory).

36 The

efficacy of the combination of tar and UVB light (i.e., Goeckerman regimen) led to its

increased popularity beginning in the 1920s. Tar preparations of 2% to 10% are

processed as creams, ointments, lotions, gels, oils, shampoos, and coal tar solution.

Newer purified preparations, using refined coal tar, are less messy and more

cosmetically acceptable, but perhaps not as effective.

36 Tar may be helpful for

patients with mild-to-moderate disease, and tar shampoos are useful for psoriasis of

the scalp. The potential severity of adverse drug effects from topical tar products is

less than that from anthralin and much less than that from topical corticosteroids.

Because tar, in every form, is messy, stains the skin, has an odor, and is low potency

compared with anthralin, it has been relegated to second-line therapy for most

patients, despite its moderate price and newer, more cosmetically appealing

formulations.

33,37

Tar preparations generally are used once or twice daily, and a bedtime application

(as a shampoo or cream overnight) is particularly useful in psoriasis of the scalp.

Patients should be warned about the staining properties of tar on clothing and

bedding. Other adverse effects include photosensitivity, acneiform eruptions,

folliculitis, and irritation dermatitis. Care should be taken to avoid use of tar on the

face, flexures, and genitalia and with inflammatory psoriasis because of tar’s irritant

properties.

The polyaromatic hydrocarbons contained in coal tar may be metabolized to active

carcinogens by epidermal microsomal enzymes. The incidence of hyperkeratotic

lesions, including squamous cell carcinoma, is increased after prolonged industrial

exposure to tar; however, extensive reviews of patients who have used tar

preparations in psoriasis have not revealed an increased risk of carcinom