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Tags : non-infectious, chronic, autoimmune, inflammatory,skin disorder, exacerbations, remissions, thickened, erythematous silvery scaling plaques

Published on : Sep 01, 2020 | Views : 6040 | Downloads : 50

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WHAT IS PSORIASIS It is a common non-infectious, chronic autoimmune inflammatory skin disorder characterized by recurrent exacerbations and remissions of thickened, erythematous silvery scaling plaques. EPIDEMIOLOGY It is universal in occurrence; occurs in all racial groups but is most prevalent in whites. Equally common in males and females. Two epidemiological patterns: Type 1 has an onset between 20 and 30 years, with a familial history of psoriasis and an increased prevalence of HLA group Cw6. Type 2 has an onset between 50 and 60 years, when familial history and HLA group Cw6 is not so prominent. Although rarely life-threatening, it has an adverse physical and emotional impact on quality of life. 2
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ETIOLOGY Complex and multifactorial disease ENVIRONMENTAL FACTORS: Climate- cold weather worsens psoriasis in 90% patients; whereas warm seasons improve it in 80% patients. Stress, emotions (anxiety). Alcohol Smoking Infection- common precipitating factor; beta haemolytic streptococcal throat infections precede guttate psoriasis. Trauma- includes rubbing, venipuncture, bites, surgery, mechanical pressure; developing psoriatic lesions at the site of injury on normal appearing skin (Koebner response) Drugs- Lithium carbonate, alpha-adrenergic blockers, some antimalarial agents,NSAIDS and tetracyclines. 3
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GENETIC FACTORS: Genetically complex with a large familial component; involves a large number of genes. Monozygotic twins have a higher concordance for psoriasis than dizygotic twins. susceptibility genes play an important role in the pathogenesis of early onset psoriasis with no predilection for gender. A number of genetic loci have been identified by genome-wide linkage scans and several loci have been replicated: PSORS1 on chromosome 6p, within major histocompatibility complex, contributes for 30% to 50% psoriasis. PSORS2 on chromosome 17q. PSORS3 in the SLC12A8 gene. PSORS4 on chromosome 1q (involved in terminal differentiation of keratinocytes). 4
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Studies of histocompatibility antigens in psoriatic patients indicate statistically significant associations on the B, C, and D loci, more specifically, human leukocyte antigen (HLA) B13, HLA-B17, and HLA-B37.2. A significant association occurs with HLA-Cw6 indicates 9 to 15 times more tendency of developing psoriasis than normal. Evidently “early onset” psoriasis susceptibility locus exists at 9q33-9q34. Identification of multiple loci indicates that psoriasis is a genetically heterogeneous disease with different genetic causes and a strong candidate gene for sequencing remains to be identified. 5
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PATHOPHYSIOLOGY IMMUNOLOGIC MECHANISMS: Involves cell-mediated immune mechanisms in which central role for activated T cells has been demonstrated by response to drugs that block T-cell activation, migration, or cytokine secretion in psoriasis. Cutaneous inflammatory T-cell mediated immune activation requires two signals: The “first signal” is the interaction of the T-cell receptor with antigen presented by the APC (dendritic cells, macrophages) The “second signal,” also called costimulation, is mediated through various surface interactions. Migration of activated T cells from lymph nodes and the circulation into epidermis of skin forming psoriatic lesions, mediated by selectins, integrins, and other adhesion molecules. Secretion of various cytokines by activated Tcells in skin, that bind to very specific receptors on the cell surface, influencing keratinocytes and other cells inducing the pathologic changes of psoriasis. The cytokine profile in psoriasis is known as a T-helper cell type 1 6
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(TH1) response which produces primarily interferon-© (INF-©), tumor necrosis factor-alpha and interleukin (IL)-2. Other local cells, including keratinocytes, dendritic cells, and local neutrophils, are induced to produce other cytokines, including TNF-alpha, IL-23, IL-20, transforming growth factor-alpha, amphiregulin, IL-1, IL-6, and IL-8, which are believed to be important in the pathophysiology of psoriasis and represent possible targets of biologic therapies. DEFECTS IN THE EPIDERMAL CELL CYCLE: The pathogenic T-cell production and activation leads to sevenfold faster proliferation of psoriatic epidermal cells than normal. The germinative cell population increases and duration of the epidermal cell cycle is nearly eight times faster than normal skin. Lesion-free skin is generally involved because epidermal proliferation is elevated in apparently normal skin of psoriatic patients 7
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TYPES 8
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CLINICAL PRESENTATION General: Nonmalignant, hyper proliferative epidermal cell disorder resulting in accumulated, immature, excessively thickened skin that is manifested as plaques. Symptoms ■ Psoriatic lesions are relatively asymptomatic; however, pruritis is seen in 25% of patients. ■ Severe, widespread psoriasis- exfoliative dermatitis with fever and chills. ■ Psoriatic arthritis- both psoriatic lesions and inflammatory arthritis-like symptoms occur. ■ Classic symptoms-distal interphalangeal joints and adjacent nails, knees, elbows, wrists and ankles are involved. Signs ■ Psoriatic lesions are characterized by sharply demarcated, erythematous papules and plaques often covered with silver-white scales. 10
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Initial lesions are small papules that enlarge over time and coalesce into plaques, sometimes as serpiginous or geographic forms. If the covering scale is removed, a salmon-pink to erythematous lesion is exposed,perhaps with punctate bleeding from prominent dermal capillaries (Auspitz sign). ■ Psoriatic lesions vary in appearance depending on the anatomic site and the variant of psoriasis. psoriasis vulgaris is the most common type.. Scalp involvement can vary from diffuse scaling on an erythematous scalp to thickened plaques with exudation, microabscesses and fissures. Trunk, back, arm, and leg lesions can appear as generalized, scattered, discrete, guttate (resembling drops or spots), or large plaques. Palms, soles, face, and genitalia can be commonly involved. Affected nails often are pitted with subungual keratotic material. Yellowing under the nail plate also can be seen. Laboratory Tests: Skin biopsy of lesional skin is useful in confirming the diagnosis. Other Diagnostic Tests: None 11
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TREATMENT GOALS: Skin normalization. Reduction or clearing of erythema, papules, plaques and scales. Reduction or clearing of skin signs as a treatment objective leads to normalized cosmesis Improvement in quality of life. To achieve resolution and partial clearing of lesions using regimens with decreased toxicity and increased patient acceptability. The psoriasis area and severity index (PASI) serves as a uniform method to determine the extent of body surface area affected, along with the degree of erythema, induration, and scaling. Mild psoriasis has PASI score of less than 12, moderate is PASI -12 to 18, and severe psoriasis is PASI greater than 18. GENERAL APPROACH TO TREATMENT: Pharmacotherapy is effective in clinically controlling psoriasis. It is lifelong relapsing and remitting disease, so therapy should be selected with careful consideration (extent and site of disease, age, concurrent associated diseases) of long-term adverse effects. 12
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KERATOLYTICS Keratolytics are used to remove scale, smoothen skin and decrease hyperkeratosis. salicylic acid is one of the most commonly used. MOA: Disruption in corneocyte-to-corneocyte cohesion in the abnormal horny layer of psoriatic skin (at anatomic sites where thick scales are present). It enhances penetration and efficacy of corticosteroids. 13 Adverse effects: salicylism, with symptoms of nausea, vomiting, tinnitus, and hyperventilation. Salicylate poisoning in small children Fatal cases of percutaneous salicylate intoxication Available as gel or lotion, is usually applied BID or TID in concentrations of 2% to 10%.
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NONPHARMACOLOGIC THERAPY Emollients Used during therapy-free periods to minimize skin dryness that can lead to early recurrence. MOA: Hydrate stratum corneum (swell and flattens the surface contour). Minimize cutaneous transepidermal water loss (evaporation). Effective as moisturizers decreasing binding forces within the horny layer, enhance desquamation and eliminate scaling. Increase pliability of the skin Possess antipruritic activity and mild vasoconstrictor activity. 14 Available as lotions, creams, ointments; applied several times per day (about four times per day). Adverse effects: folliculitis and allergic or irritant contact dermatitis.
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Balneotherapy Balneotherapy (and climatotherapy) is a therapeutic approach consisting of bathing in salt waters, often combined with natural exposure to the sun. Certain areas around the world like the Dead Sea (salt filled, located below sea level), Kangal hot spring in Turkey and the Blue Lagoon in Iceland are also notable salt-containing waters. MOA: Enhance exposure to a natural ultraviolet A (UVA) light source The mixture of salts reduce activated T cells in skin and are remittive for psoriasis. Adverse effects: Reduction in serum manganese and lithium levels is significant after bathing with Dead Sea salt. 15
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PHARMACOLOGIC THERAPY Topical treatment for mild to moderate psoriasis Corticosteroids Vitamin D analogues Tazarotene Coal tar Anthralin Topical calcineurin inhibitors Systemic treatment for moderate to severe psoriasis Biologic agents Mycophenolate mofetil Sulfasalazine 6-thioguanine Hydroxyurea Tazarotene Cyclosporine Acitretin Tacrolimus Pimecrolimus Methotrexate Combination, rotational, and sequential therapy Phototherapy: Ultraviolet B Light, PUVA Therapy and Excimer Laser Phototherapy 16
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Topical Therapy: First-Line Agents Corticosteroids Topical corticosteroids are the most widely used agents to decrease erythema, scaling, and pruritis. Topical vasoconstricting potencies of corticosteroids are ranked by the Stoughton-Cornell classification in seven classes: Class I: Very high-potency (alternatives to systemic adrenocorticoid therapy). Include products such as clobetasol propionate, halobetasol propionate, and betamethasone dipropionate (optimized vehicle). Used for thick, chronic psoriatic plaques, on relatively small body surface areas for finite periods of time (as short as possible). Class VII: Lowest level of vasoconstricting potency (e.g., hydrocortisone 1%). Weak antiinflammatory effect and are safest for long-term application on the face and intertriginous areas, in infants and young children, and with occlusion when necessary and appropriate. 17
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Intermediate classes: Medium vasoconstricting potency Used in moderate inflammatory dermatoses. Used on the face and intertriginous areas for limited periods of time. MOA: Topical corticosteroids appear to inhibit phospholipase A, thus reduce levels of arachidonic acid, prostaglandins and leukotrienes in skin. They bind to steroid receptors in skin and inhibit synthesis and mitosis of DNA in epidermal cells thus decrease epidermal proliferation. Adverse effects: 18
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Topical corticosteroids are available in ointments, creams, lotions, gels, sprays, shampoos, and mousses. Applied 2 to 4 times daily during long-term therapy. Vitamin D Analogues Vitamin D is an important in cellular and systemic calcium metabolism Inhibits keratinocyte differentiation and proliferation (treatment of hyperkeratotic skin disease). Provide antiinflammatory benefits by inducing a shift toward TH2 cytokine expression, with a decrease in IL-2, IL-6, IL-8, INF-γ, and granulocyte-macrophage colony-stimulating factor. Induces inhibition of nuclear factor kappa B (NF-κB) protein in lymphocytes and nuclear factor of activated T cells leading to a reduced transcription of IL-2. vitamin D cause hypercalcemia hence analogues were developed to reduce effect on calcium homeostasis. 19
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Calcipotriene MOA: Vitamin D analogue, binds to vitamin D receptors as it does, but is 100 times less active on systemic calcium metabolism because of its rapid local metabolism. On average, improvement is seen within 2 weeks of treatment in approximately 70% of patients demonstrating marked improvement after 8 weeks of therapy. 20 Adverse effects: Lesional and perilesional irritation (10% of treated patients) Mild burning and stinging. Irritant contact dermatitis on the face. Available in a 0.005% concentration as a cream, ointment and solution; applied one to two times per day (NMT100 g/wk).
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Tacalcitol (1α, 24-dihydroxyvitamin D3) Biologically active hormone derived from vitamin D. Adverse effects: Local, transient, mild irritation. Tazarotene It is a synthetic retinoid, is a prodrug, hydrolyzed to its active metabolite, tazarotenic acid and exerts its pharmacologic activity. MOA: It modulates keratinocyte proliferation and differentiation and is effective for the treatment of mild to moderate plaque psoriasis. Reduction of plaque elevation, scaling, and erythema, for both the gel and cream formulations. 21 calcitriol (1,25-dihydroxyvitamin D3) Used in the treatment of mild to moderate plaque psoriasis, effective in improving or clearing psoriatic plaques. A 0.03% formulation showed clearance or considerable improvement in 89% of patients.
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Adverse effects: Mild to moderate pruritus, burning, stinging, or erythema (dose- and frequency-related). Often used in combination with topical corticosteroids to decrease the incidence of local adverse events and to increase efficacy. Application of the gel to eczematous skin or to more than 20% of body surface area is not recommended because this can lead to extensive systemic absorption. Tazarotene is available as a 0.05 or 0.1% gel and cream; applied once a day, usually in the evening. 22
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Topical Therapy: Second-Line Agents Coal Tar Antipsoriatic therapy includes the use of coal tar which is more efficient than shale tar, or wood tar. It contains numerous hydrocarbon compounds formed from distillation of bituminous coal. MOA: When applied to normal skin, stimulates transient epidermal hyperplasia followed by a cytostatic effect with epidermal thinning. Ultraviolet B (UVB) light–activated topical coal tar forms photo adducts with epidermal DNA, thereby inhibiting DNA synthesis, downregulating epidermal proliferation rate (approaches to normal rate) and leads to reduction in plaque elevation. Disadvantages: Burdensome Time-consuming Causes local irritation Unpleasant odour 23
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Staining of skin and clothing Increased sensitivity to ultraviolet light, including the sun Risk of carcinogenicity is low; however, there are cases of nonmelanoma skin cancers in patients chronically exposed to tar and UV light. Coal tar preparations of 2% to 5% are available in lotions, creams, gels, shampoos, ointments, solutions and also used in bath water Applied in the evening and allowed to remain in skin contact through the night. 24 Anthralin Anthralin, an anthrone derivative of chrysarobin, introduced as dithranol which is efficient in Chronic plaque-type and guttate psoriasis than other variants. Topical anthralin, with UV light, is long established as an effective treatment.
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MOA: It possesses antiproliferative activity on human keratinocytes, inhibiting DNA synthesis by intercalation between DNA strands. It induces NF-κB in murine keratinocytes, which is involved in the transcription of proinflammatory cytokines such as IL-6, IL-8, and TNF-α (irritant properties of anthralin). Anthralin-generated free radicals produce both antipsoriatic effects and irritation. Applied only to affected areas of skin because contact with uninvolved skin can result in excessive and unwanted irritation and staining. Staining of affected plaques is a positive response sign because cell turnover has been slowed enough to take up the stain. Adverse effects: Inflammation, irritation, and staining of skin and clothing (via oxidation and binding to keratins). Classic anthralin therapy starts with low concentrations (0.1% to 0.25%) and gradually proceeds to higher concentrations (0.5% to 1%). 25
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Liposomal-based anthralin 0.5% gel can be used for short contact therapy (10–20 minutes) and reduce staining of skin and irritation. Available as stiff paste bases (provide adherence to plaques), cream and ointment. Usually it is applied in the evening and allowed to remain overnight. Topical Calcineurin Inhibitors (TCIs) Pimecrolimus and tacrolimus: calcineurin inhibitors exerting a local immuno-modulating effect that can serve to normalize hyperproliferation of epidermis. As topical agents, they are approved for the treatment of atopic dermatitis. They do not cause skin atrophy. Clinical studies have shown efficacy on facial and intertriginous psoriasis. 26
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Sirolimus: An immunosuppressive drug (not commercially available) similar in structure to tacrolimus, however it does not inhibit calcineurin. MOA: Inhibits a central kinase that transduces signals from the IL-2 receptor, thus inhibiting T-cell stimulation by IL-2. Clinical studies have shown that topical sirolimus sufficiently crosses the stratum corneum/epidermis and is therefore effective in psoriasis. Systemic Therapy: First-Line Agents Biologic Therapy The field of biologic therapy is expanding rapidly as a result of advances in recombinant DNA technology, microbiology, and immunology. In dermatology, biologic therapies—primarily immunomodulating agents designed to alter immune responses—are the basis for treatment of cutaneous diseases such as psoriasis and atopic dermatitis. 27
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These agents, produced in vitro through rDNA technology, fall into three categories: recombinant human cytokines, (2) humanized monoclonal antibodies, (3) molecular receptors that can bind target molecules. The biologic agents currently FDA approved for the treatment of moderate to severe psoriasis are infliximab, etanercept, alefacept, and efalizumab. One agent, adalimumab, is currently FDA approved for the treatment of psoriatic arthritis but not yet approved for psoriasis. In psoriasis, biologic agents typically act through one or more of the following mechanisms: (1) elimination of activated T cells, (2) inhibition of T-cell activation, (3) interference with T-cell trafficking to the skin, (4) neutralization of the effects of TH1-type cytokines, (5) induction of immune deviation by introducing TH2-type cytokines. 28
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Tumor Necrosis Factor Inhibitors Infliximab MOA:It is a chimeric monoclonal antibody (IgG1) directed against TNF-α. It binds with high affinity soluble and transmembranous forms of TNF-α and inhibits binding of TNF-α with its receptors. TNF-α plays an important role in the pathogenesis of psoriasis. Increased amounts of TNF-α have been found in psoriatic lesions, stimulating synthesis of numerous cytokines and inducting expression of intracellular adhesion molecules on endothelial cells and keratinocytes. Indications: Treatment of rheumatoid arthritis, Crohn disease, psoriatic arthritis and also in adults with chronic severe plaque psoriasis. Adverse effects: Headaches Fever Chills Fatigue 29
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Diarrhoea Pharyngitis Upper respiratory and urinary tract infections Hypersensitivity reactions (urticaria, dyspnoea, and hypotension). Infections and lymphoproliferative disorders. Dose: Administered in three doses at weeks 0, 2, and 6, of 5 mg/kg or 10 mg/kg by slow intravenous infusion. Etanercept It is another TNF-α blocker which is genetically engineered fusion protein that combines the extracellular domain of the TNF-α receptor with the crystallizable fragment (Fc) region of human IgG1. MOA: It binds free and membrane-bound TNF-α, competitively interfering the interaction of TNF-α with cellbound receptors and inhibits its effects on target cells. 30
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Unlike the chimeric infliximab, etanercept is fully humanized, thereby minimizing the risk of immunogenicity. Indications: subcutaneous treatment of rheumatoid arthritis, psoriatic arthritis and psoriasis. Adverse effects: Local reaction at the injection site (20% of patients) Respiratory tract and gastrointestinal infections Abdominal pain Nausea and vomiting Headaches Rash Serious infections (including tuberculosis) and malignancies are rarely observed. Dose: 50 mg SQ twice a week. 31
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Adalimumab MOA: It is a human IgG1 monoclonal TNF-α antibody. Inactivates the proinflammatory cytokine TNF-α. Indications: Treatment of rheumatoid arthritis, psoriatic arthritis and is undergoing trials for psoriasis. Adverse events: Rhinitis Upper respiratory tract infections Nausea Flu-like syndrome Headache Injection site reactions Malignancy, in particular lymphoma Infections- tuberculosis, histoplasmosis, pneumococcus, and listeria Adverse neurologic effects causing demyelinating disease. Dose: 40 mg every other week or every week. 32
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T-Cell Activation Inhibitors 33
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Systemic Therapy: Second-Line Agents 34
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Combination, Rotational and Sequential Therapy Combination therapy of systemic agents with other modalities can enhance therapeutic benefit, reduce dose of the combination and result in lower toxicity as monotherapy with a systemic agent does not provide optimal outcomes. Combinations include: • Acitretin + UVB light • Acitretin + PUVA (UVA combined with psoralen, usually methoxsalen) • Methotrexate + UVB light • PUVA + UVB light • Methotrexate + cyclosporine Rotational therapy is the use of biologic agents with combination therapy. Patients receive a biologic regimen for a limited period of time and then switched to a nonbiologic regimen, continuing on a rotational basis, to minimize cumulative drug toxicity. 38
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Sequential therapy is another treatment strategy designed to optimize therapeutic outcome. It involves rapid clearing of psoriasis with aggressive therapy using cyclosporine, followed by a transitional period in which a safer long-term drug such as maximal dosing acitretin is introduced. Subsequently, a maintenance period with acitretin in lower doses, or if necessary, acitretin in combination with UVB or PUVA, can be continued. Topical sequential therapy can involve the use of a class I corticosteroid (very high potency) and calcipotriene in three different phases to attain rapid clearing of psoriatic lesions while minimizing side effects. 39
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Phototherapy Ultraviolet B Light Therapy: Ultraviolet radiation has been the main stay of outpatient management of those with moderate to severe psoriasis for centuries. Goeckerman therapy: UVB+Coaltar ointment Ingram therapy: UVB + Anthralin Development of a UVB narrowband (NB) light source (produced by Philips TL01 lamp) 40 delivered 2-5 times a week, in which 83% of the UVB emission is at 310 to 313 nm, is the most effective wavelength of UVB for treatment of psoriasis. Numerous topical (emollients,calcipotriene,topical retinoids) and systemic psoriatic therapies (methotrexate,retinoids) used adjunctively to hasten and improve the response to UVB phototherapy. Adverse effects: Burning (short term) and increased skin cancers (long term).
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It is an important treatment consideration for patients with moderate to severe psoriasis and unresponsive to conventional topical and systemic therapies. MOA OF UVB AND PUVA: It is an immunomodulatory mechanism having antiproliferative, antiinflammatory, and immunosuppressive effects. Phototherapy with UVB also induces T-cell apoptosis. In PUVA therapy, psoralens (natural photosensitisers) upon oral or topical administration, intercalate with two DNA strands and upon excitation with UVA, photons cross link the DNA strands. Systemic PUVA: Oral ingestion of a potent photosensitizer such as methoxsalen (8- methoxypsoralen) at a constant dose (0.6 to 0.8 mg/kg) (approximately 2 hours before UVA exposure) and variable doses of UVA, depending on patient skin phototype and history of previous response to UV radiation. 41 Photochemotherapy with oral methoxypsoralen and Ultraviolet A light [PUVA]:
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It is performed two or three times a week. In most patients, control and partial clearing occurs by the twenty-fifth treatment. Topical PUVA: In this therapy photosensitizer (methoxsalen) is topically delivered to the skin by addition to bath water (bath PUVA) or as a topical cream (PUVA cream). Advantages: Less carcinogenic potential, minimal risk of systemic effects; overall reduction of UVA dose to one-fourth that required with conventional PUVA; a relative risk reduction of nonmelanoma skin cancer. Adverse effects: Oral psoralen: Nausea, dizziness, headache. Psoralen + UVA: Long-term adverse effects like actinic skin damage, solar elastosis, dry and wrinkled skin, hyperpigmentation or hypopigmentation and increased risk of skin cancers (squamous cell carcinoma and melanoma). 42
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Excimer Laser Phototherapy Most laser therapy has been ineffective, limited to individualised, isolated plaques with variable results. Whereas the excimer laser, which generates a high-energy 308-nm UVB wavelength is effective at clearing psoriasis and inducing moderately prolonged remissions. EVALUATION OF THERAPEUTIC OUTCOMES For most pharmacotherapeutic approaches to psoriasis the percent reduction in PASI is 75% score after 3 months treatment. Descending order of efficacy: tar + light > cyclosporine > infliximab > PUVA > methotrexate > adalimumab > acitretin > etanercept > efalizumab > alefacept Advantages: Successfully treat psoriatic plaques with fewer treatments Smaller UV radiation dose Lower risk of carcinogenicity and photoaging. 43
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REFERENCES Pharmacotherapy A Pathophysiologic Approach : Joseph T.Dipiro;Dermatologic disorders;Psoriasis; seventh edition; 1603-1615. Davidsons-principles and practice of medicine: Brain R.Walker; Skin disease; Psoriasisand other erythematous scaly eruptions;1260-1264. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001470/ Pharmacology and pharmacotherapeutics: Satoskar.R.S; Drugs used in common skin and eye disorders; Drug therapy of psoriasis;Twenty first edition; 1009-1012. www.dermatology.about.com/od/psoriasisbasics/a/psorcause.htm 44