INTRODUCTION:

Psoriasis is a proliferative disorder of the skin with the repeating events of inflammation and hyperkeratosis; it is characterized by periodic recycling of red and sharp scaly skin plaques. Psoriasis is classify as into plaque, chronic, guttate, erythroderma and pustular. From all the above types, plaque psoriasis is the major one. The etiology of psoriasis is multi-factorial that is the union of both environmental, as well as a genetic factor triggering the immune histological changes. However, the main cause of psoriasis is still unknown^1,2.

The percentage of body affected by the psoriatic plaques is studied as mild psoriasis (<2%), moderate psoriasis (210%), and sever (>10%), it may vary from patient to patients. In the recent research, patients suffering from psoriasis may also express their feeling of consciousness, helplessness, anger, frustration and embarrassment and which is followed by low confidence, poor self-visualize the absence of self-assurance, and huge low feeling of prosperity.

Psoriasis is associated with diseases like diabetes, cardiovascular diseases, hypertension, and hypercholesterolemia. The connection between psoriasis with a cardiometabolic disorder like hypertension, obesity, and chronic kidney disease were reported, and has been confirmed via inspection in pediatric patients. World health organization (WHO) says that psoriasis is the most suffering autoimmune diseases in the US. According to world psoriasis day, around 2-3% worldwide and 125 million people are suffering from psoriasis. According to study in the US, 7.5million (2.2%) of the American population are suffering from psoriasis. Prevalence of psoriasis in Africa resident American’s is 1-3% when compared with 2.5% of Caucasians.

The prevalence study states that psoriasis in adults ranging from 0.91 to 8.5% and same in case of the children, which is 0-2.1%. Prevalence data of psoriasis in India is obtained from studies carried out in the hospitals and studies conducted in medical colleges of north India such as Calcutta, Patna, Lucknow, New Delhi, and Amritsar. The total incidence of dermatological patients was ranging from 0.44 - 2.22% and the prevalence of psoriasis was 1.02%, due to the different climatic conditions, food habitat, lifestyle, and genetic difference, etc. In Amritsar, the incidence of psoriasis was found to be 2.2% compared to eastern India. Later, the study was conducted on a large number of patients, and the occurrence of psoriasis among dermatology patients was observed to be 2.8% in both male and females^3,4.

Pathogenesis of Psoriasis:

The mechanism involves in the treatment of psoriasis is still unknown. Pathologicprocess of psoriasis is defined into three stages.

T-lymphocyte Activation:

It describe as the role of Antigen-presenting cell (APC’s) which is located in dermis and epidermis to identify and interact with an unidentified antigen.

Figure 1: Mechanism of Psoriasis

Psoriasis is an immune mediated inflammatory disease with unknown etiology that may be associated with the defect in proliferation and differentiation of keratinocytes associated with inflammatory cell infiltration particularly consisting T‑lymphocytes, macrophages, and neutrophils. Psoriasis affects 1–3% of the adult population with various extra cutaneous manifestations. The psoriasis affected patients have ocular manifestations that are characterized by hyperproliferation of keratinocytes with abnormal differentiation along with infiltration of inflammatory cells mainly activated T cells in the epidermis and papillary part of dermis. Ocular lesions are more common in males, and they often occur during psoriasis exacerbations. The study of an author found that only one ophthalmic abnormality out of 67% patients with psoriasis, whereas 20% had more than one abnormality. The present figures seem to be higher as postulated by the authors than would be expected; this could be verified only in presence of a control group or population based data for comparison. Various clinical findings associated with psoriatic eye include conjunctivitis, dry eye, episcleritis, and uveitis. Lambert and Wright in 1976 noted the presence of ocular inflammation with psoriatic arthritis, conjunctivitis iritis in patients suffering from psoriasis^5,6.

Epidemiology:

Although psoriasis occurs worldwide, As, High rates of psoriasis have been reported in people of the Faroe islands, where one study found 2.8% of the population to be affected and in USA, approximately 2% of the population is affected. Psoriasis is low in certain ethnic groups such as the Japanese, and may be absent in aboriginal Australians and Indians from South America. Psoriasis can occur at any age and has been reported at birth or in older people of advanced age. Accurate determination of the age of onset of psoriasis is still a problem, as in studies it typically rely on a patient’s recall of the onset of lesions or determine the onset from the physician’s diagnosis. A bimodal age of onset has been recognised in several large studies. The mean age of onset for the first occurrence of psoriasis can range from 15 to 20 years of age, with a second peak occurring at 55–60 year. Henseler and Christophers examined a series of 2147 patients and reported two clinical occurrence of psoriasis, type I and II, distinguished by a bimodal age at onset. As Type 1 begins on or before age 40 years; Type II begins after the age of 40 years. Type I disease accounts for more than 75% of cases. Patients with early onset, or type I psoriasis, tended to have more relatives affected and more severe disease than patients who have a later onset of disease or type II psoriasis.

In addition, strong associations have also been reported with human leucocyte antigen (HLA)-Cw6 in patients with early onset, compared with later onset of psoriasis. The course and progress of psoriasis is still unpredictable. In one study, 39% of patients reported complete remission of disease for between one and 54 years. Higher figures have been reported in Japan^7,8.

Types of Psoriasis:

The various types of psoriasis should be enlisted in Table 1:

Table 1: Classifications of Psoriasis with their Characterstics

S. No	Types	Characteristics
1	Plaque psoriasis	Dry scaling patches
2	Guttate psoriasis	Drop-like dots, occurs after streptococcal or viral infections
3	Erythrodermic psoriasis	Exfoliation of fine scales, widespread, often accompanied by severe itching and pain
4	Pustular psoriasis	Pus-like blisters, noninfectious, fluid contains white blood cells
5	Nail psoriasis	Seen on toenails and fingernails, starts as numerous pits, at times progresses to yellowing, crumbly, and thickened nail; may slough
6	Scalp psoriasis	Plaque-type lesion
7	Inverse psoriasis	Smooth, inflamed lesions, mostly of flexural surfaces (e.g., the armpits)

Pathogenesis of Psoriasis:^9,10

The pathogenesis of psoriasis can be explained by considering the roles of the immune system, inflammatory pathway, and genetic factors. Psoriasis is an immune mediated skin disease with the involvement of the innate and acquired immune system, activation of the inflammatory pathway, and expression of alleles in the genes.

Role of Immune System and Inflammatory Pathway:

Events in Innate Immunity:

When an external stimulus such as trauma, stress, or infection occurs on the skin barrier i.e. stratum corneum, the effector cells such as neutrophils, plasmacytoid dendritic cells (DCs), and myeloid dendritic cells (CD 11C+ DCs) present in the keratinocytes are activated. The activated keratinocytes release several cytokines and chemokines especially interleukin-8 (IL-8), chemokine (C-X-C) motif ligand 1 (CXCL), and some proteins such as S100A7/A8/A9 which create an environment for the neutrophil migration into the epidermal lesional site. On activation, tumor necrosis factor-α (TNF-α), myeloid dendritic cells release interleukin-23, plasmacytoid DCs release interferon-α (IL-α) interleukin-20, and inducible nitric oxide synthase (iNOS)^9,10.

Events in Acquired Immunity:

T lymphocytes, mainly T-helper(Th) cells, are involved in the hyperproliferation of the cells which are mediated by various cytokines such as interferon-γ (IFN-γ) and TNF-α from Th-1 cells, interleukin-17A (IL-17A) and interleukin- 17 F (IL-17F) from Th-17 cells, and interleukin-22 (IL-22) from Th-22 cells. The peripheral blood monocytic cells are more abundant in the suprabasal keratinocytes. The characteristic feature of this cell is the presence of CCR6, a chemokine receptor with CCL20 ligand. In normal physiological conditions, the level of CCL20 expressed in epidermal keratinocytes and dermal endothelial cells seems to be low but its level is raised in the psoriatic condition by stimulation of the pro-inflammatory cytokines such as TNF-α, IL-1α, IL-17, and IFN-γ. The CCL 20 expressed in the epidermis may recruit more of the CCR6 T cell into the inflamed epidermis which enhances the release of IL-17. Hence, the level of CCR6 is elevated both in the skin and blood of the psoriatic patient^11,12.

Role of Genes and Transcription Factors:

Genetic factors play a crucial role in the pathogenesis of psoriasis which has been well studied by the Genome-Wide Association Studies (GWAS). The genome and immune response are strongly associated with disease development. More than 1300 genes are expressed in psoriatic lesions which are regulated by transcription factors that belong to the STAT family of which STAT-1, STAT-3, and NF-κ Btranscription factors are more prominent. The activity of STAT1 is regulated by TNF-α, IL-1, IFNs, IL-20, IL-22, and NF- κ B. The activated transcription factors amplify inflammatory cells which further synthesize inflammatory T cells, keratinocytes growth factor (KGF), keratinocytes derived cytokines (platelet-derived growth factor, activate pattern recognition receptors (Toll-like receptors, C-type lectin receptors), heat shock proteins, vascular endothelial growth factor (VEGF), which are the key mediators regulated in hyperproliferation of the cells. The increased level of VEGF contributes towards the angiogenesis, dilatation, and high endothelial venule formation in the psoriatic lesion. The genetic contribution to psoriasis is complex and is influenced by environmental and immune factors. More than 10 susceptible loci are identified of which the common gene is PSOR1 with HLA‑Cw*0602allele. Based on the presence or absence of this allele, psoriasis is classified into two types^11,12.

a) HLA‑Cw*0602 positive (Type I):

It is early-onset psoriasis that occurs before 40 years of age. It is inherited from the parents and the condition is very aggressive. It accounts for approximately 75% of patients.

b) HLA‑Cw*0602 negative (Type II):

It is late-onset psoriasis acquired after 40 years of age mostly between 55-60 years. Most of them presented stable psoriasis with nail involvement and it is not inherited.

The most exclusively associated alleles in psoriatic arthritis are HLA-B (B*08, B*027, B*38, and Bw4). B*027 has been recognized as the risk factor for the spondylitic form of psoriatic arthritis. More specifically, risk genes organic cation/carnitine transporter 2 (OCTN2)/SLC 22A5, and Protein Tyrosine Phosphates Non-Receptor 22 (PTPN22) are associated with psoriatic arthritis development and not with psoriasis. Any external stimulus can trigger polymorphism in the alleles of the cytokines which may alter the release of corresponding cytokines. The single nucleotide polymorphism is expressed for cytokines such as TNF-α (rs 1800629 and rs 361525), IL-23 (rs11209026), and IL-12B (rs3212227). The pro-inflammatory cytokine TNF-α cells plays a key role in the pathogenesis of psoriasis. Polymorphism in the TNF-α gene (rs 1800629 and rs 361525) may alter the release of its cytokine in healthy subjects. The pro-inflammatory cytokines are over expressed in the psoriatic lesions. Based on the pharmacogenetic changes, the treatment can be carefully chosen. The use of anti-TNF drugs (etanercept, infliximab, and adalimumab) is preferred for over expression of TNF-α gene.

The mode of inheritance of psoriasis can be due to genetic, epigenetic, or environmental triggers:

1. Genetic:

In genetic the familial investigation, epidemiological investigation among the population, by involving with Human Leukocyte Antigens (HLA) would be susceptible. Also the major histocompatibility complex (MHC) account for the genetic background. The pattern of inheritance can be autosomal dominant and autosomal recessive. Further investigation of the psoriatic susceptibility loci can be performed with the help of gene mapping methods including linkage analysis and allele sharing method. The linkage method helped in mapping psoriasis susceptibility loci. The allele sharing method helps in analyzing the HLA alleles which are responsible for the pathogenesis of psoriasis.

2. Epigenetic:

In addition to genetic factors, epigenetic modifications such as DNA methylation play a major role in pathogenesis of the psoriasis. The aberrant DNA methylation occurs in the PSOR region due to over expression of DNA methyltransferase 1 in the skin tissues and peripheral blood mononuclear cells which thereby significantly affect the expression of pathogenic genes. This is the major reason for the histopathologically changes in the keratinocytes. The reversal of methylation can be done with methotrexate therapy.

3. Environmental triggers:

Apart from the genetic and epigenetic factors, some of the environmental risk factors such as UV exposure, diet, medication, intake of alcohol, and smoking have a negative impact on the psoriasis condition. These factors can cause genetic polymorphism or epigenetic changes triggering the release of cytokines such as tissue necrosis factor and interleukins which activate the immune system and exacerbate the psoriatic condition^13,14.

Pharmacotherapy:

The selection of therapy is mainly based on patient preferences which are influenced by the sociodemographic (age, sex, and marital status) and socioeconomic (income and employment) characteristics as well as the severity index of the affected area (body surface area). The drug selection is based on the age, weight, disease phenotype, and patient category, which may include children (less than 14 years of age), adolescents, pregnant women, and patients with other comorbidities. In the case of pregnant women, the selection of the drug requires utmost care due to adverse effects such as teratogenicity. In pediatric patients, the medications are recommended based on the type of psoriasis as well as age. In the case of recommendation of vitamin D analogues, it is advised to apply in children above the age of 6 years due to the negligible risk of hypocalcaemia^15,16.

Conventional Treatment of Psoriasis:

Conventional treatment of psoriasis is based on the degree of severity. Mild and limited psoriasis treatment includes topical Corticosteroids, Anthralin, Tars, Tazarotene (a retinoid), Calcipotriene (a vitamin D3 analog), and Phototherapy. Narrow-band UVB is less effective but safer than psoralen plus ultraviolet A (PUVA), which carries with it an increased risk of skin cancer.

Sun exposure is another form of phototherapy. UV exposure reduces antigen presenting and affects cell signaling, favoring development of T-helper (Th2) immune responses. Antigen-presenting Langerhans cells are decreased in both number and function. A topical combination of Calcipotriene and Beta Methasone have shown greater efficacy in severe psoriasis than monotherapy with either alone. Patient compliance must be considered when developing a treatment plan. The use of less messy topical solution and foam preparations of topical Calcipotriene and Corticosteroids (compared to ointments and creams) can improve compliance. Systemic treatment of severe psoriasis usually involves the use of Oral Retinoids, Cyclosporine, Methotrexate and biological agents that can significantly impact other body systems.

This can be improved with the implementation of advanced technology in developing the drug delivery system. The treatment started with the application of emollients and now progressing with biologics formed by recombinant DNA technology. The benchmark for selection of treatment route is related to the severity of the disease. For mild to moderate conditions, topical route is preferred and for moderate to severe condition oral or biologics.^17,18

Topical Therapy:

The treatment of skin diseases prefers the use of topical therapy such as cream, gel, ointment, etc. This can provide intimate contact with the affected area, which ensures more effectiveness and bypasses systemic adverse effects. The following drugs are used in the treatment of psoriasis.

· Tar Preparation (Coal Tar):

It was routinely used as a dressing regimen along with UV-B therapy. The combination of coal tar preparation along with juniper tar was reported to form an adduct with DNA through covalent bonding. This was found to be carcinogenic and its use is diminished nowadays.

· Emollients and Moisturizers:

Petroleum jelly and liquid paraffin which can provide protective action, prevent microbial invasion, and reduce transepidermal water loss.

· Anthralin (Dithranol):

This is very effective in case of localized plaque psoriasis and scalp psoriasis. But its use is declining due to its staining property and occurrence of skin irritation due to its high dose. Mostly it is applied at night time to the site at a concentration of more than 1% w/w and this is considered as short contact anthralin therapy (SCAT).

· Non-Steroidal Anti-inflammatory Drugs:

Under this category, mostly used is salicylic acid which has keratolytic and anti-inflammatory action. It can be used as monotherapy with a concentration of 2% -10%. An intercellular binding of salicylic acid with corneocytes occurs resulting in desquamation, swelling, hydration, and softening of stratum corneum. This helps in the removal of excessive stratum corneum layers.

· Retinoids:

Tazarotene is the first synthetically developed Vitamin A derivative. It is a prodrug converted to tazarotenic acid on esterase hydrolysis. The active form will bind to the retinoic acid receptor (RAR-β/γ), which involve in the gene expression modification. This will down-regulate the inflammatory markers and normalize the abnormal keratinocyte proliferation and differentiation. It is used in maintenance therapy of stable plaque psoriasis. Localized skin irritation is the only reported side effect that can be neglected by using a combination of topical corticosteroids.

· Corticosteroids:

Topical corticosteroids were considered as the gold standard for psoriasis treatment until the introduction of newer corticosteroid binds to the glucocorticoid receptors in the cytoplasm. Upon activation, this complex moves into the nucleus and binds to DNA which results in transcriptional changes in mRNA and stimulates lipocortin. The formation of lipocortin inhibits the phospholipase A2 activity and inhibits mRNA responsible for IL-1 formation. These events exert anti-inflammatory, immunosuppressant, antiproliferative action, and anti-mitogenic effects.

The selection of a steroidal drug is based on the severity of the condition and potency of steroids. The main side effects of corticosteroids on the epidermis are photosensitivity, atrophy, loss of skin barrier, and hypo or hyper pigmentation and on the dermis are delayed wound healing, telangiectasias, and ulceration. The most serious impact of corticosteroid usage is the increased susceptibility to infections and also the rebound flares on withdrawal of the therapy^19,20,21.

· Vitamin D Analogues:

Calcipotriene, Calcitriol, and Tacalcitol are the synthetic Vitamin D analogues mostly used in conjugation with corticosteroids to reduce its hypercalcemic side effects and to enhance efficacy. The antipsoriatic activity is exerted by hindering the production of S100 proteins especially psoriasis (S100A7) and koebnerisin (S100A15), thereby Th-17 mediated release of cytokine from keratinocytes is reduced.

· Pyrimidine Antagonist:

5-Fluorouracil (5-FU), an antimetabolite, inhibits the synthesis of DNA and processing of RNA which leads to diminished epidermal proliferation. It is the mostly applied topical aid to localize in resistant plaque psoriasis. This contributes towards rapid epithelialization and prolonged relapse period. The burning sensation and pain reduce its use^21,22.

· Radiation Therapy:

Phototherapy is widely used in the treatment of stable psoriatic lesions. A variety of light/laser sources are introduced for the treatment but most commonly used is ultraviolet radiation.

In Table 2 the overview of currently applied (and widely approved) treatments of psoriasis is given. All of these treatments may be used alone or in combination with one another^23,24.

Table 2: An overview of currently applied (and widely approved) treatments of psoriasis

S. No	Treatment options
S. No	Topical	Photo (chemo) therapy	Systemic
1	Corticosteroids	Broadband UVB (290-320 nm)	Methotrexate
2	Dithranol	Narrowband UVB (311 nm)	Cyclosporine A
3	Tar	PUVA (320-400 nm)	Acitrein
4	Tazarotene	Excimer laser (308)	Fumaric acid
5	Vitamin D Analogues	-	Biologicals

Oral Therapy:

Chemotherapy and Immuno-suppressants:

Folic Acid Antagonist:

Methotrexate (MTX) exerts antiproliferative and immunosuppressive action by inhibiting the deoxyribonucleic acid synthesis in the proliferated epidermal cells. It is administered orally, topically, and parenterally (subcutaneously, dermally, and intramuscularly). Now it is considered as “the gold standard” for psoriasis treatment. The routine monitoring of its pharmacokinetic profile in the systemically treated patient is essential as it is more prone to Nephrotoxicity, and hepatotoxicity. Along with treatment, it is required to supplement with folic acid as it is a folic acid antagonist. The recommended dosing regimen starts with the initial dose of 5-15 mg/week and maintenance dose of 5-22.5mg/week^25,26.

Calcineurin Inhibitor:

Cyclosporine interferes in T cell-dependent as well as independent activities. It is involved in the early stage of T cell activation where it inhibits the calcineurin-dependent dephosphorylation and nuclear factor activated transcription process. This inhibition interferes in interleukin-2 production. The dose of cyclosporine is 2-5 mg/kg body weight per day. The reported side effects are nephrotoxicity, hypertension, and high relapse on cessation of therapy that leads to the limited usage of the drug^27,28.

Retinoids:

Acitretin:

It is a second-generation retinoid used in severe psoriasis. It binds to RAR-α, β, γ to down-regulate the release of cytokines and normalizes the keratinocyte proliferation and differentiation. The drug is not an immunosuppressant hence it can be employed for long term treatment. It can be used alone or in the combination with Psoralen ultraviolet A (PUVA) or ultraviolet-B (UV-B) phototherapy to enhance efficacy. Alopecia, cheilitis, elevation in cholesterol level and dryness of the mucous membrane, are some of the common side effects associated. It is contraindicated in women due to its teratogenicity^29,30.

Phosphodiesterase 4 (PDE 4) Inhibitors:

Apremilast (Otezla) is an orally administered PDE 4 inhibitor that enhances the cAMP level and expresses pro-inflammatory and anti-inflammatory mediator which in turn decrease iNOS, TNF-α, IL-23, and IL-10.

Alternative Systems of Medicine (ASM):

The alternative systems of medicine are ancient therapy with a holistic approach for the wellness of the patient. It mainly comprises Ayurveda, Yoga and Naturopathy, Unani, Siddha, and Homeopathy. All these systems of medicine use herbal products and inorganic salts for treatment with special focus on the restricted diet thereby reducing the side effects^31,32.

Ayurvedic System of Medicine:

The Ayurvedic treatment provides many external and internal medications or practices of Panchakarma procedures. In some patients, leech therapy is also recommended. Some of the marketed Ayurvedic products by the leading Ayurvedic outsource mainly Kottakkal Arya Vaidhya Sala, Oushadhi, and Himalaya are mentioned here. The main products of Kottakkal Arya Vaidya Sala are the Ayyappala coconut skin oil. This is also a blood detoxifier. The ingredients in these formulations have shown anti-bacterial, antipruritic, anti-fungal, antioxidant, astringent, and moisturizing properties that help in fighting against psoriasis. The key ingredients in the formulation are Turmeric and Neem.

Yoga and Naturopathy:

Yoga mainly focuses on deep breathing exercises which helps in detoxification of the body, stress buster, immunity booster, maintaining body pH, aid in digestion, weight loss, and blood purification. The basic principle behind this is the elimination of toxin and enhances oxygen supply to overall organs. It is mainly focused on the diet and the condition is treated with freshly extracted juice of carrot, cucumber, and grapes for a week. This therapy is more effective along with filtered sun rays^33,34.

Unani System of Therapy:

Unani is a Greek system of medicine and the treatment principle is to normalize the humor of the body (blood/lymph and hormones). The therapy focuses on the purification of the blood and normalization of skin cell function by improving the immunity and cytokine regulation. For topical therapy, a paste containing sulfur, borax, camphor, and sesame oil is applied to the lesion. Both oral and topical formulations are given to the patients and they experienced marked improvement in the lesion. The continuous treatment for a month reported almost complete clearance of the skin lesions^35,36.

Siddha System of Therapy:

Siddha is one of the oldest traditional systems of medicine originated in South India (Tamil Nadu). This system of therapy is based on 5 basis properties- suvai, gunam, veeryam, pirivu, and mahimai. The National Institute of Siddha, Chennai recognized the treatment for psoriasis (Kalajagapadai) with a composition of herbo mineral formulation named “Gandhaga Mezhugu, Vetipalai thailam or 777 oil is a topical formulation prepared from the leaves of Wrightia tinctoria containing coconut oil as the vehicle. The process of preparation is called“Sooriyapudam”. Some modification is done in the process with the bark of the same plant since it has proteolytic enzyme activity^37,38.

Homeopathy System of Medicine:

Homeopathy is the natural way of treatment with a high dilution of the natural substance. Each individual’s mind, body, spirit, and emotion are considered for the appropriate selection of medicine for the management and prevention of disease. Based on the type of psoriasis and patient’s psychology, medicines are prescribed. Scalp psoriasis can be treated with Lycopodium C200 (diluted to 200 times) potency along with hydrating cream^39,40.

Miscellaneous Therapy:

Essential Oils:

The essential oil is being commonly used in aromatherapy and for inhalation therapy. But it can also be used as a complementary (second line) therapy for psoriasis. Mostly these oils provide soothing effect with some therapeutic activities^41,42,43.

Tea Tree Oil (TTO):

TTO is obtained by steam distillation of the leaves and terminal branchlets of Melaleuca alternifolia (Myrtaceae). It contains terpinen-4-ol which has potent anti-inflammatory properties. It prevents infection of the affected area, stimulates the immune system, and supports to maintain healthy skin. It also exerts antibacterial, antifungal, antiviral, and antipsoriatic activities^44,45,46.

Lavender Oil:

It is obtained by the steam distillation of flowers of Lavendula angustifolia belonging to the Lamiaceae family. The major component includes linalyl acetate and linalool. The essential oil shows rapid absorption through the skin showing antibacterial, antifungal, and cytotoxic effects. The cytotoxic effect can be used in psoriasis treatment^47,48,49,50.

Conclusion and Future Perspectives in Psoriasis Therapy:

Although there are several systemic treatments for patients with moderate to severe psoriasis, they don’t fully meet the need of patients. The toxicity, inefficacy and often inconvenience of current conventional treatments, in addition to the impaired quality of life in psoriasis patients lead to new therapeutics options. With the growing knowledge and understanding of the pathogenesis of psoriasis, more specific immunomodulating therapies are being developed, the so-called ‘biologic response modifiers’ or ‘biologics’. These custom-made, protein-like molecules can target specific parts of the activated immune system in psoriasis, e.g. activation, co-stimulation, or proliferation of T cells, their trafficking into the skin, or effector cytokines. Since 1989 several biological therapies have been tested for psoriasis and in January 2003 Alefacept (Amevive®), anti-CD2, was the first biological therapies that was approved by the US Food and Drugs Administration (FDA).

Current concepts to treat psoriasis are phototherapies, pharmacotherapies, novel drug delivery systems, and the traditional system of medicines as well as marine sources. Since the disease involves multiple pathological mechanisms, a single treatment may not be effective. Hence, there is a need to understand the best combination of therapies that can provide better relief to patients. It is a well-known fact that treatment with corticosteroids and radiation therapy provides better relief. However, they are also associated with severe side effects. Novel drug delivery systems have found success to treat the disease but poor drug loading, toxicity, and stability issues became the major impediments in their successful positioning. One needs to focus on the development of safe and stable advanced drug delivery systems. Psoriasis requires long-term treatment; hence, safe and effective therapies that can overcome the associated side effects of radiation and pharmacotherapy’s should be prioritized. One such approach could be the development of a novel targeted delivery system using a combination of synthetic and herbal drugs and simultaneously applying the principle of any of the traditional methods for effective treatment of psoriasis.

ACKNOWLEDGEMENT:

The authors are grateful to the authorities of Laureate Institute of Pharmacy, Kathog Jawalaji for the facilities.

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Received on 26.05.2021 Modified on 03.11.2021

Asian J. Pharm. Res. 2022; 12(1):76-83.

DOI: 10.52711/2231-5691.2022.00012