INTRODUCTION:

The term psoriasis etymologically arises from Greek ψωρίασις (psōriāsis), expressing a state of pruritus, formed via ψώρα (psōra; signifying "itch" or "scabies") and -iasis (denoting diseased process).^1,2Psoriasis qualifies as a persistent immune-driven dermatosis characterized by markedly elevated keratinocyte proliferation rates, which generate distinctly circumscribed erythematous plaques adorned with characteristic silvery-white scales. Psoriasis underwent initial nosological differentiation within ancient Roman medical treatises by Cornelius Celsus, followed by taxonomic classification by English dermatologist Thomas Willan; Thomas Bateman discerned potential associations between psoriatic eruptions and arthritic symptomatology circa 1813. Historical pharmacotherapeutics comprised suboptimally efficacious, overtly toxic modalities, including 18th–19th century arsenicals (e.g., Fowler's vesicant solution), mercurial agents, sulfur/iodine/phenol topicals—underpinned by erroneous infectious postulates—yielding to coal tar–phototherapeutic regimens around 1900 and parenteral gold salts for psoriatic arthropathy mirroring rheumatoid paradigms, now obsolete in favor of modern topicals and systemics.³ Psoriasis significantly impairs emotional, psychological, and social functioning, with ~30% onset before age 18. This T cell-driven chronic immune-mediated inflammatory dermatosis may respond to plasmapheresis, which modulates triggers (age, stress, hormones, trauma, inflammation) with sustained, safe, non-toxic effects^.4These pathological skin manifestations predominantly localize to the scalp, extensor surfaces of the upper and lower limbs, palmar aspects of the hands, and sacral regions of the lower back, with clinical debut most frequently observed during the early adult phase of life and accompanied by a conspicuous pattern of familial aggregation that underscores its heritable component.⁵On a global scale, the condition imposes a heavy disease burden upon approximately 125million affected individuals, wherein epidemiological prevalence exhibits considerable oscillation ranging from less than 1% in certain low-incidence cohorts to exceeding 8% in high-prevalence populations, reflecting diverse genetic, environmental, and socioeconomic influence spectrum of clinical variants extends across plaque-dominant presentations (accounting for the majority of cases), guttate eruptions resembling small droplets, flexural or inverse involvement in intertriginous areas, pustular subtypes with sterile pus-filled lesions, and severe erythrodermic forms encompassing widespread cutaneous involvement, collectively precipitating profound somatic distress through pruritus and pain, substantial affective and emotional loading via stigma and self-image disruption, as well as a measurable decrement in overall life quality metrics encompassing vocational, relational, and recreational domains.⁶The underlying pathophysiology integrates intrinsic genotypic risk architectures with a repertoire of precipitating environmental factors—including acute psychological stress, opportunistic microbial pathogens such as streptococci, and localized cutaneous trauma via the Koebner phenomenon. Resident epidermal keratinocytes serve as sentinel responders by dispatching a cascade of proinflammatory cytokines, which in turn prime and mobilize dendritic cell activation within the skin microenvironment while skewing adaptive immunity toward pathogenic Th1 and Th17 lymphocyte effector profiles. This amplification is rigidly enforced by a triad of master cytokines—interferon-gamma (IFN-γ), interleukin-17 (IL-17), and interleukin-22 (IL-22)—that collectively impose inflammatory perpetuity through autocrine and paracrine signaling loops, culminating in unchecked epidermal hyperplasia and the architectural derangements emblematic of psoriatic lesions.⁷The systemic scope of psoriasis extends its inflammatory footprint well beyond dermatologic confines, forging robust epidemiological links with psoriatic arthropathy manifesting as enthesitis and dactylitis, metabolic derangements inclusive of insulin resistance and dyslipidemia, macrovascular vasculopathy predisposing to ischemic events, and a spectrum of psychopathologic conditions ranging from major depressive disorder to anxiety syndromes these associations are further amplified by convergent pathological amplifiers such as dysregulated oxidant-antioxidant homeostasis, dynamic fluxes in enteric microbiota composition altering immune homeostasis, and adaptive epigenome shifts that reprogram transcriptional landscapes in susceptible cells.⁸ This study analyzed treatment-related changes in Psoriasis Area and Severity Index (PASI) scores and serum transaminase levels—aspartate aminotransferase (AST) and alanine aminotransferase (ALT)—in patients with psoriasis vulgaris attending the Dermatology and Venereology clinics at Dr. Soetomo General Academic Hospital.⁹ Psoriasis links strongly to HLA-C*06:02, which boosts T-cell responses, causing keratinocyte hyperproliferation and plaques via cytokines like TNF-α; TNF inhibitors effectively treat it regardless of genotype.¹⁰

Therapeutic frameworks have evolved to hone sophisticated immunomodulation paradigms tailored for maximal remission durability and minimal relapse rates particularly promising are phytocomplexes harnessing bioactive polyphenolics from select botanicals for broad-spectrum anti-inflammatory action, nanovehicles engineered for site-specific pharmacodelivery enhancing penetration and retention within psoriatic strata, alongside adjuvant modalities that synergistically assure comprehensive inflammation abatement, optimized epidermal barrier reconstitution, and sustained therapeutic equity through economically viable, patient-centric protocols suitable for indefinite application.¹¹

Epidermiology:

Psoriasis exhibits comparable prevalence across sexes, affecting males and females at similar rates overall however, women and patients with familial predisposition display earlier age of symptom emergence. Onset age follows a bimodal pattern, with peaks for males at 30–39 and 60–69 years, while females typically present ~10 years earlier. Worldwide, it impacts ~60 million individuals, marked by wide regional variation from 0.05% in Taiwan to ~1.88% in Australia.Higher rates align with high-income countries and populations with older median ages. In the UK, population prevalence approximates 1.52%.¹²

Etiology:

The precise etiology of psoriasis remains elusive; nonetheless, accumulating evidence implicates a confluence of genetic susceptibility and aberrant immune responses as central drivers of pathogenesis. Multifactorial exogenous and endogenous precipitants further modulate disease initiation and exacerbation. Key etiological and triggering elements encompass chest infections, or common viruses like colds and flu that provoke flares.¹³

1. Genetic Factors:

Although definitive genetic linkages await full elucidation, genomic investigations have delineated at least 25 risk-conferring mutations, per data from the National Psoriasis Foundation. Targeted linkage analyses have moreover identified 15 susceptibility loci designated PSORS1 through PSORS15.Sporadic cases arise de novo without familial antecedents conversely, a positive family history confers dose-dependent elevated risk for disease manifestation.¹⁴

2. Psoriasis Triggers:

Stress activates cytokines causing flares. Alcohol impairs drug efficacy. Smoking worsens pustular forms. Fatty foods or dairy trigger symptoms. Obesity increases severity via fat-cell inflammation.¹⁵

3. Drug-Induced Psoriasis Exacerbation:

Certain therapeutics precipitate de novo or aggravate preexisting psoriatic lesions, including beta-blockers (propranolol, atenolol), lithium, antimalarials (chloroquine), interferons (alpha/beta), ACE inhibitors, NSAIDs, tetracyclines, and terbinafine.

4. Environmental Influences Ambient factors profoundly shape psoriasis initiation and progression:

Wintry settings commonly provoke eruptions, heightened by parched air, minimal outdoor sunlight, and balmy heated interiors, whereas natural solar rays benefit select patients by tempering immune responses yet inflame patches among those with elevated light sensitivity.

5. Other Psoriasis Triggers:

Hormone variations in females around puberty or menopause frequently initiate or heighten outbreaks, while lactation-related prolactin can further irritate skin patches. Physical damage such as scrapes, bites, burns, sunburn, itching, bruises, or surgical sites often awakens immune activity, spurring lesions through the Koebner response. HIV status elevates psoriasis likelihood strep often sparks guttate form among youth, alongside ear issues, throat inflammation, chest infections or common viruses like colds and flu that provoke flares.¹⁶

Pathogenesis of Psoriasis:

Psoriasis constitutes a persistent immune-driven skin disorder featuring hyperproliferative keratinocytes and defective maturation, resulting from multifaceted immune-epidermal crosstalk that incorporates T lymphocytes, dendritic cells, macrophages, cytokines, alongside VEGF and KGF to elicit inflammatory cascades and epidermal acanthosis. Fundamental Pathways.

· T Lymphocytes: CD4+ helper and CD8+ effector populations activate through APC engagement, secreting lymphokines to induce dermal edema and keratinocyte overgrowth.

· Dendritic Cells: Mature CD83-expressing forms in plaques intensify T-cell responses and proinflammatory signaling.

· Keratinocytes: Basal-layer mitoses accelerate to 1.5-day cycles (normal: 28 days), yielding marked epidermal hyperplasia across strata.

· Neovascularization: Keratinocyte-sourced VEGF/IL-6 drives endothelial expansion and pericyte-stabilized vessel formation for leukocyte recruitment.

· Cytokine Imbalance: IL-1/6/8/12, TNF-α, IFN-γ stimulate proliferation, neutrophil influx, Th1 skewing, and persistent inflammatory states.

· Apoptotic Evasion: Overexpressed p53 and sustained Bcl-2 in basal keratinocytes resist programmed cell death.¹⁷

Classification of Psoriasis:

Clinical features and epidemiology psoriasis manifests in multiple subtypes, each with unique clinical presentations, etiologic factors, and long-term outcomes. This section outlines major forms per current dermatologic consensus.

1. Guttate Variant: This acute subtype involves abrupt onset of numerous small (<1 cm) scaly erythematous lesions resembling teardrops, chiefly in pediatric and young adult populations. Group A β-hemolytic streptococcal tonsillitis frequently precedes flares. Resolution without intervention is common, though ~33% evolve into persistent plaque-type psoriasis.

2. Inverse Psoriasis (Flexural Psoriasis): Flexural psoriasis occurs in skin-fold zones like armpits, groin creases, under-breast areas, and around the anus, marked by clear-cut red patches or plaques with little scaling from moisture, sometimes showing mild surface softening.¹⁸

3. Pustular Variant: Marked by sterile pustules atop inflamed skin, this uncommon severe form appears as focal or diffuse disease. Focal types include palmoplantar pustulosis and acrodermatitis continua of Hallopeau. Diffuse pustular psoriasis presents with rapid-onset erythroderma, postulation, fever, fatigue, and elevated white cell count.¹⁹

4. Erythrodermic Variant: Characterized by near-total (>90%) cutaneous erythema and shedding, this subtype may debut independently or complicate prior psoriasis. It triggers systemic issues like pyrexia, fluid loss, and metabolic disturbances, demanding inpatient management.

5. Psoriatic Arthropathy: An autoinflammatory seronegative arthritis linked to psoriasis (prevalence 20-30%), it preferentially strikes distal finger or toe joints alongside possible spinal or tendon involvement, causing tenderness, effusion, and limited mobility.²⁰

6. Chronic Plaque Variant: Dominant in 80-90% of patients, it displays discrete red plaques capped by white scales at extensor sites (e.g., elbows, knees, scalp, sacrum). Itch disrupts well-being.

7. Scalp involvement: Seen in ~80% of cases, scalp lesions resist therapy due to hair interference, provoking itch, soreness, and emotional strain. Interventions must address usability and appearance.²¹

8. Nail Involvement: Present in up to 50% of individuals, it produces pitting, separation, striations, and yellow-brown hues. Associated with arthropathy, it responds poorly to locals, favoring systemics or biologics. ²²

Clinical Manifestations of Psoriasis:

Psoriasis is a chronic inflammatory skin disorder with variable clinical manifestations. It most commonly presents as well-defined erythematous plaques covered with silvery-white scales. These lesions are frequently associated with pruritus, buming sensation, pain, fissuring, or bleeding and typically involve the elbows, knees, scalp, trunk, palms, and soles. Nail involvement is commonly observed and may manifest as nail pitting, thickening, discoloration, onycholysis, or dystrophic changes. Scalp psoriasis usually presents as adherent scaly plaques on the scalp and may extend beyond the hairline. In some individuals, psoriasis may also involve the joints, leading to psoriatic arthritis characterized by joint pain, stiffness, and swelling Overall, the common clinical features of psoriasis include erythematous scaly plaques, dry and cracked skin prone to bleeding, and characteristic nail abnormalities.²³

Diagnosis of Psoriasis:

A. Clinical Assessment:

Psoriasis diagnosis hinges chiefly on clinical inspection, integrating patient history with hallmark lesional morphology. Evaluation proceeds via unaided visual scrutiny or dermoscopic augmentation. Dermoscopy exploits optical phenomena incident illumination interacts with cutaneous strata through reflection, refraction, diffraction, and selective absorbance. Magnified analysis of emergent light unmasks adnexal and dermal microstructures. Immersion media minimize specular glare, optimizing subsurface visualization.²⁴

B. Skin Sampling:

If visual checks leave doubts, a tissue sample goes under the microscope via punch method (small circular cutter grabs deep skin column, 3-6 mm across), shave approach or cut-out technique (knife removes full sore plus some edge). Key signs include layered skin buildup, scales holding old cell bits, tiny pus clumps, flattened peaks over skin bumps, and bushy vessels below.

C. Psoriasis Area and Severity Index (PASI):

provides a validated, quantitative metric for evaluating psoriatic burden, stratifying the body surface into four anatomic zones: head/neck (scalp inclusive, 10% area weighting),upper limbs (arm 20%), trunk (thorax 30%), and lower limbs (legs 40%). Severity scoring per region integrates erythema, induration, desquamation (0-4 scale each) multiplied by affected area percentage (0-6 bands), yielding a composite score from 0 (clear) to 72 (maximal disease).

D. Dermatology Life Quality Index (DLQI):

serves as a validated instrument to gauge psoriasis-induced detriment to health-related quality of life, comprising a 10-question self-report survey with tick-box responses on a 0-3 ordinal scale (aggregate 0-30 elevated values reflect worsening impairment). Evaluated constructs include somatic sensations/emotions (questions 1-2), vocational/scholastic function (7), customary endeavors (3-4, 6), relational dynamics (8-9), and therapeutic encumbrance (10), alongside perceptual burden of visible dermatoses. Minimal clinically meaningful change approximates 4 points scores exceeding 10 denote severe lifestyle disruption.²⁵

Management of Psoriasis:

Psoriasis Management Paradigm Incurable yet tractable, psoriasis engages risk-stratified pharmacodynamics mild-moderate cutaneous confines inaugurate topical monotherapy under primary oversight, mandating dermatologic triage for therapeutic nonresponse or areal extensiveness.

a) Topical Therapy: Corticosteroids buttress inaugural intervention, expediting cytokine abatement via tiered potencies and vehicles, potentiated by salicylic acid keratolysis (3-6%) albeit tempered by atrophic rebound, tolerance, and endocrine perturbation risks concurrently, vitamin D agonists (calcipotriol) rectify proliferative dysregulation and immunomodulation, rivaling glucocorticoid efficacy per meta-analyses with irritancy as principal limitation.²⁶

b) Phototherapy: Phototherapy in Psoriasis Narrow band UVB irradiation (311-313 nm) constitutes the preferred first-line photo biologic intervention for moderate-to-severe plaque psoriasis, achieving PASI75 responses in 60-80% of patients through T-cell apoptosis, keratinocyte cytostasis, and immunomodulation, with established safety across pediatric, pregnant, and systemic-contraindicated cohorts despite necessitating 2-3 sessions weekly.Targeted 308-nm excimer laser therapy excels for localized refractory lesions (scalp, ears, eyelids, flexures) yielding durable remissions, while psoralen-ultraviolet A (PUVA) therapy reserved post-NB-UVB failure attains 75-80% PASI reduction at expense of acute photo toxicity, pigmentary sequelae, nausea, and protracted non melanoma skin cancer risk.²⁷

c) Systemic therapy: Acitretin, a second-generation retinoid, serves pustular and erythrodermic psoriasis either as monotherapy or adjunctive therapy, though mucocutaneous desiccation, dyslipidemia, and teratogenicity necessitate rigorous contraception protocols and hepatic surveillance cyclosporine, a calcineurin inhibitor, induces rapid PASI75 responses within 2-4 weeks but incurs cumulative nephrotoxicity, hypertension, hypertriglyceridemia, and oncogenicity precluding prolonged administration.²⁸

d) Biologic Therapy: Anti-TNF-α (infliximab, adalimumab), anti-IL-17 (secukinumab, ixekizumab), anti-IL-23 (guselkumab, risankizumab), and anti-IL-12/23 (ustekinumab) disrupt canonical inflammatory cascades, attaining PASI90 clearance in 70-90% of conventional failures with unprecedented DLQI improvements and favorable long-term safety.²⁹

e) Nano carrier Systems in Psoriasis:

Pharmacotherapy Nanotechnology optimizes psoriasis treatment via precision drug targeting, cutaneous reservoir formation, and sustained pharmacodynamics surpassing traditional dermal pharmacokinetics.

1. Lipid Matrix Carriers:

Physiologic lipid architectures (100-1000nm) accommodate polar or nonpolar therapeutics, enhance corneum permeation, and limit systemic biodistribution relative to polymeric alternatives, favoring dermal or transdermal applications.

a) Solid lipid Nanoparticles (SLNs): Matrix-type constructs featuring solidified lipid cores stabilized by emulsifiers enable prolonged elution, oxidative protection, and manufacturing scalability through hot homogenization. Lipophilic drug preference prevails, tempered by lattice imperfections restricting payload capacity and inducing polymorphic transitions.

b) Liposomes: Concentric amphiphilic bilayers (50-1000nm) generate aqueous compartments via ethanol injection, pro liposome hydration, with post-processing extrusion. Endogenous composition confers tolerability, offset by peroxidation liability, osmotic instability, and manufacturing overhead surface-modified iterations facilitate nucleic acid condensation and prolonged circulation.

c) Niosomes: Vesicular assemblies of nonionic surfactants cholesterol provide cost-effective liposomal alternatives with enhanced bilayer integrity. HLB 4-8 C16-18 saturated chains optimize formation via thin-film hydration, yielding biocompatible nongeotoxic carriers with superior entrapment efficiency.

d) Ethosomes: Phospholipid vesicles incorporating 20-50% ethanol generate soft deformable carriers facilitating stratum corneum permeation ethanol-mediated corneum fluidization enables intercellular fusion and deep dermal drug depot formation. Synthesized through cold or hot hydration or reverse-phase evaporation.

e) Transfersomes: Phospholipid bilayers edge-activated by single-chain surfactants (Tween/Span 80, sodium cholate) confer ultradeformability adaptive elasticity navigates corneum constrictions while edge activators destabilize intercellular lipids, achieving superior transdermal flux versus conventional liposomes.

f) Nanoemulsions: Thermodynamically stable submicron dispersions (20-200nm) of oil or water phases stabilized by nonionic surfactants/co-surfactants solubilize lipophilic actives within oil cores for topical spray or gel or foam delivery, mimicking micellar architecture.³⁰

2. Polymer-Based Nanocarriers:

Polymeric Systems Synthetic or natural polymer colloids preferentially localize within viable dermis versus systemic absorption characteristic of lipid carriers, optimizing topical psoriasis pharmacodynamics. Configurations encompass micelles, dendrimers, nanospheres, and nanocapsules.

a) Polymeric Micelles: Amphiphilic co-polymer self-assembly yields core-shell nanoparticles (<100nm) with lipophilic cores solubilizing hydrophobic actives (tacrolimus, silibinin) and hydrophilic coronas conferring aqueous stability pH or thermosensitive variants enable stimulus-responsive transdermal elution with superior dermal retention versus commercial semisolid preparations.

b) Dendrimers: Monodisperse, radially symmetric arborescent polymers (2-10nm) feature multivalent surface functionalities enabling covalent or adsorptive drug conjugation poly(propyleneimine) (PPI) and poly(amidoamine) (PAMAM) G3-G4 dendrimers augment 8-methoxypsoralen flux and siRNA-mediated TNF-α silencing, effecting cytokine suppression and lesional amelioration.

c) Nanocapsules: Reservoir-type vesicles encapsulate therapeutics within polymeric envelopes, conferring photostabilization (tretinoin), irritancy mitigation (dithranol), and protracted release (dexamethasone) for sustained dermal anti-inflammatory action.³¹

CONCLUSION:

Psoriasis embodies a complex immune dysregulation syndrome wherein traditional palliative interventions fail to confer sustained remission. Persistent recurrence rates and multidimensional patient burden highlight persistent therapeutic gaps despite biologic and nanotechnologic advances that enable pathway-selective immunomodulation and optimized cutaneous pharmacokinetics. Convergence of pharmacogenomics, targeted nanocarriers, and patient-reported outcomes promises transformation from episodic control to individualized, relapse-preventive disease modification with concomitant psychosocial amelioration.

Future Directions in Psoriasis:

1. Advanced Delivery Platforms: Nanostructured systems solid lipid nanoparticles, polymeric micelles, dissolvable microneedles engineer enhanced dermal retention, zero-order kinetics, and localized pharmacodynamics, circumventing systemic exposure.

2. Integrated Care Models: Digital phenotyping (teledermatology, AI-PASI scoring, adherence algorithms) coupled with multidisciplinary psychosocial support addresses the biopsychosocial disease continuum.

3. Precision Remission Endotypes: Molecular stratification (IL-23R genotypes, cytokine endotyping) guiding nano carrier selection portends era of personalized, long-term clearance versus reactive flare management.

4. Medicated nail lacquers augment systemic therapies for severe onychopathies. Novel formulations use enhancers like serratiopeptidase and thioglycolic acid for targeted nail bed delivery. Studies optimize in vitro/in vivo models to profile ADME and nail pH effects on transungual permeation.

REFERENCE:

1. Singh N, Sondhi S, Jindal S, Pandit V, Ashawat MS. Treatment and management for patients with mild to severe psoriasis: a review. J Clin Aesthet Dermatol. 2023; 16(1): 45-52.

2. Ingawale R, Adsul AV, Chavan P, Kale G. Protecting Psoriasis: A Comprehensive Review of Sunscreen. J Pharm Res. 2024; 12(3): 45-60.

3. Unissa R, Kumar PM, Sunil G. Psoriasis: A Comprehensive Review. J Pharm Sci. 2024; 15(2): 123-145.

4. Sharma MC, Sharma M. Novel applications of Cold Atmospheric Plasma for the treatment of Plaque Psoriasis. J Pharm Sci Tech. 2025; 18(4): 78-92.

5. Yunita I, Hidayati AN, Lis Ervianti MY, Damayanti B, Sylvia S. Retrospective assessment of methotrexate efficacy on psoriasis severity and hepatic transaminase elevations in psoriasis vulgaris patients. J Dermatol Venereol Indonesia. 2026; 18(1): 15–22.

6. Hari G, Prabhu A, Kalakota C, Johnson J, Mansoor K, Shenoy RR, Pai KSR, Nandakumar K. Development and pharmacological assessment of dehydrozingerone gel formulation on imiquimod-induced psoriasis in mice. Res J Pharm Technol. 2022; 15(10): 4469-72.

7. Rahman M, Yashika, Kaur M, Anurag, et al. A review on psoriasis. Maharishi Markandeshwar (Deemed to be University), Mullana, Ambala, Haryana, India. 2025:1-1

8. Wadher K, Dabre S, Gaidhane A, et al. Evaluation of antipsoriatic activity of gel containing Pongamia pinnata extract on Imiquimod-induced psoriasis. Clin Phytoscience. 2021; 7: 20

9. Agrawal A. Kulkarni GT, Lakshmayya. Topical application of aerial portion of Acalypha indica Linn ameliorates. psoriasis in rodents: Evidences from in vivo and in silico studies. J Ethnopharmacol. 2023: 116685

10. Srivastava AK, Nagar HK, Chandel HS, et al. Antipsoriatic activity of ethanolic extract of Woodfordia fruticosa (L.) Kurz flowers in a novel in vivo screening model. Indian J Pharmacol. 2016; 48(5): 531-6.

11. Zhang Y. Wang Q. San S, et al. The therapeutic effect of glycyrrhizic acid compound ointment on imiquimod induced psoriasis-like disease in Mice. PLoS One. 2023:18(8): e0290617

12. Shah NV, Maheshwari RA, Sailor GU, et al. Javia AR A review on etiology, types and treatment of psoriasis Pharmacology online 2010: 1: 159-79

13. Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021; 397(10281): 1301-15.

14. Sondhi S, Singh N, Jindal S. Natural remedies used in the treatment of psoriasis: a short review. Asian J Pharm Res. 2021; 11(1): 43-5.

15. Kakade KV, Khaire RD. A review on psoriasis. Int J Technol. 2022; 12(2): 47-52.

16. Rendon A. Schakel K. Psoriasis pathogenesis and treatment. Int J Mol Sci. 2019, 20(6): 1475

17. Michalek IM, Loring B, John SM. Global report on psoriasis. Geneva.World Health Organization, 2016.

18. Gori P, Desai C. A case study on homeopathic management of psoriasis: an alternative treatment approach. Asian J Pharm Res. 2025; 15(1): 1-5.

19. Kimmel GW, Lebwohl M. Psoriasis: Overview and Diagnosis. In: Bhutani T, Liao W, Nakamura M, editors. Evidence-Based Psoriasis. Cham: Springer, 2018. p. 1-16.

20. Sharma S, Sharma R, Goyal K, Jindal S. Potential of herbal treatment of Psoriasis: A Laconic Review. Asian J Res Pharm Sci. 2021; 11(1): 51-7.

21. Brannon HL. Psoriasis: Causes and risk factors, very well Health: 2024 Nov 14 [cited 2025 Oct 12]

22. Nischal KC, Khopkar U. Dermoscope. Indian J Dermatol Venereol Leprol 2005: 71: 300-3.

23. Gharge R, Phadtare S, Shinde S, et al. Psoriasis: Causes, diagnosis and management. World J Pharm Res. 2021; 10(14): 1393-1406.

24. Kim WB, Jerome D, Yeung J. Diagnosis and management of psoriasis. Can Fam Physician. 2017; 63(4): 278-285.

25. Riojas ME. Psoriasis treatment: a literature review. Int J. Res. Dermatol. 2023 Sep; 9(5): 314-317.

26. Sakthi Priyadarsini S, Vani PB, Kumar PR. A comparative review on conventional and traditional medicine in the treatment of psoriasis. Res J Pharm Technol. 2020; 13(11): 5642-6.

27. Raharja A, Mahil SK, Barker JN. Psoriasis: a brief overview. Clin Med (Lond). 2021 May 21; 3: 170-3.

28. Zhu B, Jing M, Yu Q, et al. Treatments in psoriasis: from standard pharmacotherapy to nanotechnology therapy. Adv Dermatol Allergol. 2022; 39(3): 460-71.

29. Nordin UUM, Ahmad N, Salim N, et al. Lipid-based nanoparticles for psoriasis treatment: a review on conventional treatments, recent works, and future prospects. RSC Adv. 2021; 11(46): 29080-29101.

30. Zhang M, Hong S, Sun X, et al. Exploration of and insights into advanced topical nanocarrier systems for the treatment of psoriasis. Front Med. 2022 Dec 15; 9: 1017126

31. Bodnár K, Feher P, Ujhelyi Z, et al. Recent approaches for the topical treatment of psoriasis using nanoparticles. Pharmaceutics. 2024; 16(4): 449.

Received on 19.01.2026 Revised on 26.02.2026

Accepted on 25.03.2026 Published on 10.07.2026

Available online from July 14, 2026

Res.J. Pharmacology and Pharmacodynamics.2026;18(3):265-270.

DOI: 10.52711/2321-5836.2026.00035

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.