General information of psoriasis in Western Medicine

General information of psoriasis in Western Medicine1.1Definition of psoriasisPsoriasis is a chronic, inflammatory and systemic disease that manifests most commonly as well-circumscribed, erythematous papules and plaques on the skin that are covered with silvery scales. Usually the skin lesions are pruritic and painful with adherent thick scales, removal of these scales may reveal pinpoint bleeding. The disease is a chronic recurring condition that varies in severity from minor localised patches to complete body coverage. Nails and joints can also be affected by psoriasis (1).1.2Pathology and pathogenesis of psoriasisThe etiology and pathogenesis of psoriasis has not been completely defined but it involves immune stimulation of epidermal keratinocytes. It involves a complex immunological and inflammatory reaction (1). The pathogenesis of psoriasis has a large hereditary component. At least eight chromosomal loci have been identified for which statistically significant evidence for linkage to psoriasis has been observed (these loci are known as psoriasis susceptibility (PSORS) 1 to 8) (1). Of these chromosomal loci, the human leukocyte antigen (HLA-Cw6 allele/ HLA-Cw0602–Cw0613), also known as PSORS1, is the key susceptibility gene for psoriasis (2). In addition to genetic factors, environmental factors including infection, smoking, medications (e.g. beta blockers, nonsteroidal anti-inflammatory drugs (NSAIDs ), antimalarials, terbinafine, calcium channel blockers, lipid-lowering drugs, etc), skin injury (Koebn er’s phenomenon) and stress are thought to evoke an inflammatory response and subsequent hyperproliferation of keratinocytes, resulting in psoriasis (1, 3).The development of psoriasis is thought to involves the following process:∙T-cells activate and migrate into the skin after elements of the innate immune system are activated (keratinocytes and dendritic cells) (3, 4);∙Functional T-cells including type 1 helper T cells (Th1) and type 17 helper T cells (Th17) grow under the influence of cytokines such as interleukin 12 (IL-12) and interleukin 23 (IL-23) (3, 4);∙Pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α), IL-17 and IL-22 are secreted by Th1 and Th17 cells promoting the inflammatory process in psoriasis (3, 4);∙Local skin cells including endothelial cells, fibroblasts, and keratinocytes enhance the cutaneous immune response through expression of adhesion molecules and other mediators (3, 4).Overall, psoriasis is an immune-mediated organ-specific (skin, and/or joint) inflammatory disease in which intralesional inflammation primes basal stem keratinocytes to hyperproliferate and perpetuate the disease process (3, 4).1.3Epidemiology of psoriasis1.3.1 Prevalence of psoriasis in global general populationAlthough psoriasis occurs worldwide, its prevalence varies considerably (5). It is reported that the average global prevalence of psoriasis is approximately 3%–4%. About 15%-30% of psoriasis sufferers have the sequelae ‘psoriatic arthritis’, equating to approximately 0.5%–1% of the total population (6). Table (chapter 1-1) presents the prevalence data reported in recent surveys.Table (chapter 1-1) Prevalence of psoriasis by country1.3.2 Factors impacting on the prevalence of psoriasisThe reported prevalence surveys differ in many regards, namely geographical origin of the study, definition of prevalence on time point, period, and lifetime of psoriasis, sampling methods, and whether it is self-reported or diagnosis confirmed by physician. Most of these studies are based on self-reported diagnosis, which may leave mild cases of psoriasis, e.g. nail disease, undiagnosed. Moreover, the elusive aetiology of skin diseases and the lack of precise classification criteria for psoriatic arthritis may also lead to misdiagnosis (6).Geographic and ethnic factors also contribute to differences in psoriasis prevalence. For instance, the prevalence in cooler regions is higher than that of other regions (15). In addition, lower prevalence is observed among African Americans (1.3%), compared with the Caucasian American population (2.5%) (13).Multi-factorial components such as physical environment, genetic factors, gender, age and behavioural patterns play a role in the progression of psoriasis (15).It has been suggested that the onset of psoriasis occurs at a younger age in female patients compared with males, which results in a higher prevalence in young female patients (16). Furthermore, the mean age of onset for the first presentation of psoriasis is between 15–20 years, with a second peak often occurring between 55–60 years, and then a significant decline after the age of 70 years, irrespective of gender (16).1.3.3 Risk factors of psoriasisThe risk factors of psoriasis are not well defined. However, obesity is believed to be associated with psoriasis as patients have a higher body mass index compared with the non-psoriatic population (17). Smoking is likely to play a role in the onset of psoriasis (18) and alcohol may influence the progression of the disease (19). Stress is an important trigger factor and may influence the development of the condition (20). Furthermore, some medications may be associated with the onset or exacerbation of psoriasis, including antimalarial medications, NSAIDs, β-blockers, lithium salts and withdrawal from steroids (21). Bacterial infections may also trigger or exacerbate psoriasis (21). Conversely, the consumption of fruit and vegetables, carrots, tomatoes and β-carotene can decrease the risk of psoriasis (22).1.3.4 Impact of psoriasis1.3.4.1 Quality of lifePsoriasis itself is not a life-threating condition however, it has a significant impact on the sufferers’ quality of life. The psychological comorbidities of psoriasis can significantly impair a patients’ q uality of life (23-25). One study compared quality of life in people with psoriasis with people who have other diseases, and found that the quality of life of patients with psoriasis was more severe than that of patients with diabetes, coronary heart disease and cancer (26). Besides the patient's appearance, the amount of time required to treat extensive skin or scalp lesions and to maintain clothing and bedding adversely affects quality of life as well. In addition, arthritic psoriasis can also result in increasing and debilitating joint pain and stiffness and impaired movement (27) .1.3.4.2 Economic burdenGenerally, the cost of disease consists of direct costs including diagnostic procedures, therapies and hospital admissions and indirect costs including work absenteeism, early retirement, and unemployment. The cost of psoriasis is considerable because of its long-term duration. Studies in Germany suggested that the average annual costs of mild psoriasis vulgaris per patient ranged from 500 € to 2,000€ and for severe disease from 4,000 € to10, 000 € (28, 29). The indirect cost was estimated to be about 1,600 € per person per annum (29). A survey investigating patients with psoriasis in the United Kingdom indicated that an average psoriasis patient was absent from work for 26 days a year. In America, psoriasis costs US$11.3 billion in health care annually (when calculated at 2% prevalence) and the loss in productivity from psoriasis is around US$16.5 billion per year (30).1.4Diagnosis of psoriasis1.4.1Types of psoriasisPsoriasis is classified into seven categories:1.Plaque psoriasis (psoriasis vulgaris)Plaque psoriasis is the most common type of psoriasis, observed in approximately 80% to 90% of patients (1). Plaque psoriasis appears as sharply marginated, erythematous patches or plaques with a characteristic silvery-white micaceous scale (31). The plaques are round or oval in shape and are typically located on the scalp, trunk, buttocks and limbs, especially on extensor surfaces such as the elbows and knees (1).2.Guttate psoriasisTypical manifestation is dew-drop-like, 1 to 15 mm, salmon-pink papules, usually with a fine scale. It is found primarily on the trunk and the proximal extremities. A history of upper respiratory infection with group A beta-hemolytic streptococci often precedes guttate psoriasis. The disease is most common during childhood or adolescence and can transition into psoriasis vulgaris (1, 3).3.Inverse psoriasisInverse psoriasis commonly appears in the inframammary and abdominal folds, groin, axillae, and genitalia. The lesions appear as erythematous plaques with small scales (1, 3).4.Nail diseaseThe characteristics of nail psoriasis include pitting, onycholysis, subungual hyperkeratosis, and the oil-drop sign (a translucent discolouration in the nail bed that resembles a drop of oil beneath the nail plate). Nail psoriasis usually affects nails on the hands more often than the feet. It is seen in 90% of patients with psoriatic arthritis (1).5.Psoriatic arthritisPsoriatic arthritis is an inflammatory seronegative spondyloarthropathy associated with psoriasis. The characteristics of psoriatic arthritis are stiffness, pain, swelling, and tenderness of the joints and surrounding ligaments and tendons (dactylitis and enthesitis). The severity of the arthritis usually does not correlate with the skin disease. Nail damage is very common in psoriatic arthritis. The radiographic features of psoriatic arthritis mainly involve joint erosion, joint space narrowing, and bony proliferation (32).6.Pustular psoriasisPustular psoriasis consists of generalised and localised types. Generalised pustular psoriasis shows widespread pustules often on an erythematous background. If the pustules combine to form one mass and are accompanied by fever and toxinemia , it is known as psoriasis pustulosa generalisata (von Zumbusch pustular psoriasis). Localised pustular psoriasis presents as pustules on the palms of hands and/or soles of the feet (1, 3).7.Erythrodermic psoriasisChronic plaque psoriasis may develop in to erythrodermic psoriasis. The patients’ entire body surface area may be covered with erythema accompanied by varying degrees of scaling. The dysfunction of erythrodermic skin might lead to hypothermia and dehydration (1).This monograph will focus on psoriasis vulgaris only.1.4.2Symptom assessmentThe diagnosis of plaque psoriasis (psoriasis vulgaris) is based on typical lesion morphology and clinical history (3, 32). The Auspitz sign (bleeding that occurs after psoriasis scales have been removed) is regarded as the key to diagnosing psoriasis, comprising of 1) candle-wax scales; 2) punctate bleeding when the covering skin is removed; and 3) pinpoint bleeding (3). Identifying the time of onset of lesions, possible triggers, related symptoms (i.e. itch, pain, sensitivity, irritation), and family history are essential to informing the diagnosis (32). Guttate psoriasis describes the rapid development of multiple small papules of psoriasis over wide areas of the body. Pustular psoriasis is rare and is characterised by the development of multiple sterile non-follicular pustules with plaques of psoriasis on red tender skin. This may occur acutely and be associated with fever. In psoriatic arthritis, patients often present with a mixture of subtypes and the pattern of disease may vary over time. The most frequent presentation is polyarthritis, followed by oligoarthritis. Other common features of psoriatic arthritis include enthesitis (inflammation at the tendon/bone interface), tenosynovitis and dactylitis. The presence of psoriatic plaques or nail psoriasis helps to differentiate psoriatic arthritis from other types of arthritis (such as rheumatoid arthritis or osteoarthritis). Psoriatic arthritis is often undiagnosed. All patients suspected as having psoriatic arthritis should be assessed by a rheumatologist so that an early diagnosis can be made and joint damage can be reduced (3).1.4.3Diagnostic assessmentThe diagnosis of psoriasis vulgaris is based almost exclusively on the clinical appearance of the lesion. In some cases, histological examination of biopsies taken from the border of representative lesions is needed to confirm the diagnosis (3, 33).1.4.4Evaluation of psoriasis symptom severityTo some extent, evaluating the severity is more complicated than diagnosing psoriasis. Various outcome measures are used to evaluate psoriasis symptom severity. The Psoriasis Area and Severity Index (PASI), Physicians Global Assessment (PGA), Body Surface Area (BSA) and the Dermatology Life Quality Index (DLQI) are most commonly used (1, 3).The PASI is a tool to assess the overall psoriasis severity based on lesion area, erythema, induration, and scaling (34). PASI estimates disease severity by assigning numerical values to qualitative assessments of redness, scale and thickness of psoriatic plaques at individual body sites, as well as estimates of the affected body surface area. It is a non-linear measure (range 0–72) and scores of 10 or more have been shown to correlate with a number of indicators of severe disease such as needing hospital admission or use of systemic therapy (33). However, there are problems associated with the PASI in that it is non-linear, lacks sensitivity to change when body surface area <10% and the three features (erythema, scale, induration) are co-dependent. It has not been validated in children where assessments for body surface area may be inaccurate and in addition it is limited to plaque-type disease (33). The DLQI is primarily used to determine health-related quality of life (35). The combination of PASI and DLQI are applied to evaluate the effectiveness of treatment (3). PGA is an average assessment of all psoriatic lesions, regardless of quantifying BSA or evaluating individual lesion locations (36). Clinically, dermatologists often combine objective assessment of lesion location, thickness, symptoms, presence or absence of psoriatic arthritis with the subjective assessment of the physical, financial and emotional impact of the disease on the patient’s quality of life to assess the disease severity (1).1.4.5Classification of psoriasis stagesThere are three main stages of psoriasis (reference needed here):∙Progressive stageIn the progressive stage new psoriatic lesions appear, which merge with one another and form plaques of different forms and sizes and the colour of the lesions is more intense. The centre of the plaque is often covered with scale, but the surrounding rim is often red and free from the scale. The skin of people with psoriasis in the progressive stage can be hypersensitive. The Koebner's phenomena is present - the appearance of new lesions on the location of a skin trauma (scratches, bites, pricks, cuts, burns, friction etc). In the progressive stage one should not use irritating therapeutic means, frequent baths, or even ultraviolet light as they can cause flare-ups and even the development of psoriatic erythroderma.∙Stationary stageStationary stage usually begins at 1–4 weeks after the progressive stage. In the stationary stage new lesions do not appear, the red rim around the plaques disappears and the lesions become completely covered with silvery white scales which indicate the curtailment of their further growth.∙Regressive stageIn the regressive stage, the infiltration, redness and peeling of psoriatic plaques decrease. Around the lesions it is possible to see a narrow pale rim of pseudo-atrophy - tender 2–7 mm folding. The elements become thinner and are freed from the scales and gradually dissipate leaving only the sections of a temporary hyper-pigmentation (darker colour). Previously plaqued skin areas become hypo-pigmented and turn pale in colour. This stage may completely clear the skin from psoriasis or sometimes only leave the on-duty plaques on the elbows and knees.1.4.6Classification of psoriasis severityA classification of psoriasis severity should take into account: 1) the body surface area affected by psoriasis; 2) the intensity of local signs and symptoms (redness, thickness and scaling); 3) response to previous treatments, if any; 4) length of time the individual has had the disease; 5) degree to which the psoriasis causes disability, and 6) impact of the disease on theindividual’s quality of life. There is still no widely accepted definition of what represents mild, moderate or severe psoria sis, but the following criteria outlines how the disease is often classified in practice (37):∙Mild to moderate psoriasis: Good control of lesions with topical therapies alone; <10% of body affected;∙Moderate psoriasis: Topical therapy still possible to control the disease; >10% of body affected;∙Moderate to severe psoriasis: Topical therapies fail to control the disease; >10% of body affected. Very thick lesions located in ‘difficult-to-treat’ regions, such as the palms and soles.∙Severe psoriasis: Systemic treatments are required to control the disease; >20% of body affected. Very intense local signs with very thick lesions and >10% of body affected may also be considered as severe.1.4.7Differential diagnosisThe clinical diagnosis of psoriasis is relatively easy, especially when the lesions consist of erythematous, silvery white scales and indurated plaques that are sharply demarcated and distributed symmetrically on the extensor surfaces of limbs, the lower back and the scalp. Differential diagnosis of plaque psoriasis (psoriasis vulgaris) should focus on nummular eczema, tinea, mycosis fungoides and pityriasis rosea. Predilection sites and the nails’ appearance may aid diagnosis. S ometimes a skin biopsy may be useful to confirm the diagnosis (3).1.5Co-morbidities of psoriasis1.5.1 Medical co-morbiditiesAlthough psoriasis is thought to be a disease solely affecting the skin and joints, comorbidities may be associated with this disease and recent evidence suggests an increased overall risk of mortality in patients with severe psoriasis (1). Cardiovascular diseasePatients with psoriasis have an increased risk of cardiovascular disease. Several factors are believed to contribute to the increased risk for cardiovascular disease in psoriasis patients: including the fact that psoriasis is more likely seen in overweight people, and those that have diabetes, hypertension, and an atherogenic lipoprotein profile (15, 18, 22, 38-40). The incidence of myocardial infarction in patients with psoriasis is higher than the average incidence (38).Metabolic syndromeMetabolic syndrome manifests as obesity, impaired glucose regulation, hypertriglyceridemia, reduced high-density lipoprotein, and hypertension. The prevalence of metabolic syndrome is higher in psoriasis patients, which leads to increased risk of developing cardiovascular morbidity and mortality (1, 41).Autoimmune diseasePeople with psoriasis have a higher likelihood of developing other immune-related diseases, which have been attributed to shared or closely linked genetic susceptibility traits (1). These include inflammatory diseases, predominately Crohn’s disease and ulcerative colitis (42). A possible link between multiple sclerosis (MS) and psoriasis has also been suggested as psoriasis is seen more commonly in families of patients with MS (43).CancerSeveral studies have investigated the risk of cancer in patients with psoriasis. A study demonstrated that psoriasis patients have an increased risk of developing cutaneous T-cell lymphoma or Hodgkin’s lymphoma (44). It has also been reported that the occurrence of cutaneous squamous cell carcinoma increases in Caucasians using oral methoxsalen (psoralen) plus ultraviolet A radiation (PUVA) to treat psoriasis (45, 46).1.5.2 Psychiatric/psychological comorbiditiesPsoriasis can have a substantial psychological and emotional impact on an individual, which is not always related to the extent of skin disease. Patients with psoriasis may experience shame and embarrassment because of their appearance (24). The disfigured appearance can lead to difficulties in work and social activities due to discrimination (23, 24). Psoriasis patients tend to be anxious about the effectiveness of treatment and potential for exacerbation of the disease (23, 24). Psoriasis leads to a lack of self-esteem and is related to increased prevalence of mood disorders, including depression. Depression may be severe enough that some patients will contemplate suicide (23, 24). The reported active suicidal ideation among psoriasis patients is 5.6–7.2% (47).1.6Management of psoriasisFor the treatment of psoriasis, the complete absence of cutaneous symptoms is not achievable in all patients. In recent years, clinical studies have used PASI 75 as the goal of psoriasis therapies, which means a 75 % reduction from baseline PASI score. In most studies, the primary endpoint for achieving the targeted PASI 75 is at 10–16 weeks of the therapy. Therefore, PASI 75 seems a reasonable goal of therapy at the end of induction therapy, while PASI 50 (a 50 % reduction of PASI score) is considered as the minimum target. In regard to quality of life, the goal of psoriasis therapy is to achieve a DLQI score of 0 or 1, meaning that the patient no longer experiences any impairment of quality of life due to skin symptoms. A DLQI score of less than 5 can be taken as the minimum target. It is suggested that if the minimum target is not reached within a given amount of time, the therapy must be modified (3). An overview of evaluated treatment options for chronic plaque psoriasis is shown in Figure (chapter 1-1).1.6.1 Pharmacologic treatments for psoriasis1.6.1.1 Systemic treatments∙Cyclosporine is a neutral, strongly hydrophobic, cyclical peptide composed of 11 amino acids. Since the early 1990s, the use of cyclosporine in the treatment of plaque psoriasis has become an established method. Reportedadverse effects of cyclosporine include renal effects, liver/gastrointestinal tract damage (3, 49);∙Fumaric acid esters are proved to be effective in systemic therapy of severe psoriasis vulgaris. Reported undesirable adverse effects of fumaric acid esters are gastrointestinal tract symptoms, leukocytopenia,lymphocytopenia, and eosinophilia (3, 49);∙Methotrexate has been approved for the treatment of severe psoriasis vulgaris. It is primarily used for severe, treatment-refractory chronic plaque psoriasis as well as pustular psoriasis and erythrodermic psoriasis. Livertoxicity is the most common adverse effect limiting the use of methotrexate (3, 49);∙Retinoids are vitamin A derivatives which have been used for the treatment of psoriasis vulgaris since the 1970s.Cheilitis is the most commonly reported side effect. The risk of birth defects limits the use of this therapy (3, 49);∙Azathioprine is approved for use in renal transplantation and rheumatoid arthritis and also has been used for many years in the treatment of the autoimmune blistering disease and atopic dermatitis. Adverse effects of azathioprinemay include leukopenia, anemia, thrombocytopenia, or pancytopenia (49);∙Hydroxyurea is an antimetabolite used in the treatment of certain cancers and hematologic conditions. It has been used in the treatment of psoriasis for more than 30 years and is thought to work by inhibiting DNA replication. The major adverse effects of hydroxyurea are bone-marrow toxicity causing leukopenia, anemia, thrombocytopenia, or pancytopenia (49);∙Leflunomide is a disease-modifying antirheumatic medication that inhibits de novo pyrimidine synthesis. It is approved for the treatment of rheumatoid arthritis, and has more recently been studied for the treatment ofpsoriatic arthritis and psoriasis vulgaris. Potential toxicities caused by leflunomide are predominantlygastrointestinal irritation, but also include elevated liver enzymes, leukopenia, drug eruption, headaches, increased risk of infections, and teratogenicity (49);∙Mycophenolate mofetil is an immunosuppressive agent approved for prophylaxis or organ rejection in patients with transplantation, but was originally used to treat psoriasis in the 1970s. Mycophenolate mofetil is associatedwith a relatively high incidence of gastrointestinal and infectious adverse effects (49);∙Sulfasalazine is used to treat inflammatory bowel disease and, occasionally, rheumatoid arthritis. It is thought to act as an anti-inflammatory agent. Adverse effects caused by sulfasalazine such as gastrointestinal intolerance,malaise, headache and arthralgia are generally not serious in nature but occur in almost 60% of patients (49);∙Tacrolimus is a macrolide antibiotic, a metabolite of the fungus Streptomyces tsukubaensis, that is indicated for prophylaxis of organ transplant rejection. It has been approved in a topical formulation for the treatment of atopic dermatitis and has been successfully used for the treatment of inverse psoriasis. Side effects of tacrolimus typically include hypertension, diabetes mellitus, nephrotoxicity, neurotoxicity and gastrointestinal irritation (49);∙6-thioguanine is the natural metabolite of azathioprine but it appears to be more effective than its parent compound.It has been used extensively in the treatment of acute myelogenous leukaemia and for inflammatory bowel disease, as well as for psoriasis. The mechanism of action of 6-thioguanine is the inhibition of purine synthesis.Bone-marrow suppression is the most frequent side effect (49).1.6.1.2 Biologics1.6.1.2.1 TNF inhibitors for the treatment of psoriasis∙Adalimumab is a fully human therapeutic monoclonal antibody. It has been used in adults with moderate to severe plaque psoriasis and moderate to severe psoriatic arthritis who did not tolerate or failed to respond to systemictherapies, or who have contraindications to those therapies. Adalimumab is administered by subcutaneous injection.Moderately painful injection site reactions are commonly reported side effects of Adalimumab (1, 3);∙Etancercept is a TNF-α antagonist. It has bee n used successfully in the treatment of rheumatoid arthritis, psoriatic arthritis and other forms of arthritis. Etancercept is recommended to be used for moderate to severe psoriasis andmoderate to severe psoriatic arthritis. A maximum course of 24 weeks is suggested. Mildly pruritic injection sitereactions may occur (1, 3);∙Infliximab is a chimeric monoclonal antibody against TNF-α. It belongs to the group of selective immunosuppressants. In dermatological disease, infliximab is approved for use in adults with moderate to severeplaque psoriasis and in patients with active and progressive psoriatic arthritis. Commonly reported adverse effects are infections, infusion reactions, and hepatosplenic T-cell lymphoma (1, 3);∙Ustekinumab is a recombinant completely human IgG1k antibody. Ustekinumab has been used in adults with moderate to severe plaque psoriasis. It is given as a subcutaneous injection in the abdomen or thigh. Infections,headache and arthralgia are commonly reported adverse effects of ustekinumab (3);1.6.1.2.2 T-cell inhibitors for the treatment of psoriasis∙Alefacept is a recombinant dimeric fusion protein that consists of the extracellular CD2-binding protein of lymphocyte function-associated antigen (LEA)-3 linked to the Fc portion of human IgG1. It has been used for the treatment of adult psoriasis patients who are candidates for systemic agents or phototherapy. Alefacept mightcause reduction of CD4 T-lymphocyte count (1);∙Efalizumab is a recombinant humanised monoclonal IgG1 antibody directed against the CD11a subunit of LFA-1 that blocks LFA-1 mediated T-cell adhesion. It has been used for the treatment of adult psoriasis patients who are candidates for systemic agents or phototherapy. Dose related headache, fever, nausea, and vomiting have beenreported after initial dosing of efalizumab (1).1.6.1.3 Topical therapies∙Calcineurin inhibitors are approved for the treatment of atopic dermatitis and also have shown effectiveness for the treatment of psoriasis vulgaris. The most common undesirable adverse effects are a burning sensation and pruritus at the application site immediately after applying the drug (3, 48);∙Dithranol/Anthralin was the most common topical therapy for psoriasis in Europe until the 1980s. Dithranol now is primarily used for inpatient care of patients with psoriasis vulgaris. The most common side effects are redness and burning involving the lesion site and the surrounding skin (3, 48);∙Corticosteriods have strong anti-inflammatory effects and therefore have been used for general inflammatory, allergic or pruritic skin symptoms rather than for specific treatment of individual skin disease. They can be applied topically with different forms such as cream, lotion, ointment, foam or spray. Undesired adverse effects includelocal skin symptoms, potential for systemic absorption and adrenal suppression with long-term usage on a largearea of the skin (3, 48);∙Coal tar is a distillation product from coal with a large number of different ingredients, of which 400 have been characterised, including benzols, naphthalene and phenols. Coal tar is included in antipsoriatics, antiseptics, andantipruriginous therapies. Complaints of the permanent brown/black stains on clothing and the unpleasant odour of the preparation make it difficult to use coal tar as a psoriasis treatment (3, 48);。