All About Psoriasis

Scales typically develop on joints, such as elbows and knees. However, they may develop anywhere on your body, including the:

• hands
• feet
• neck
• scalp
• face

Less common types of psoriasis affect the:

• nails
• mouth
• area around the genitals

It’s commonly associated with several other conditions, including:

• type 2 diabetes
• inflammatory bowel disease
• heart disease
• psoriatic arthritis
• anxiety
• depression

Psoriasis manifests in various forms, each presenting distinct clinical features. The most prevalent type is chronic plaque psoriasis, also known as psoriasis vulgaris . This form is typically recognized by sharply defined, salmon-red plaques covered with silvery scales, commonly appearing on the extensor surfaces of the limbs, such as elbows and knees, and on the scalp . While this classical presentation is widely known, the disease can exhibit numerous morphological variants .

Other types of psoriasis include:

• Guttate Psoriasis: This type is characterized by small, distinct, drop-like lesions. It often appears suddenly, frequently after a streptococcal infection .
• Inverse Psoriasis (Flexural Psoriasis): This form affects skin folds, such as the armpits, groin, under the breasts, and around the genitals. The lesions are typically smooth, red, and inflamed, often lacking the characteristic scaling due to moisture in these areas .
• Pustular Psoriasis: This is a less common but more severe form, marked by widespread red skin covered with small, non-infectious pus-filled bumps (pustules). It can be generalized or localized, for example, to the palms and soles (palmoplantar pustulosis) . Palmoplantar psoriasis, in general, can present with predominantly hyperkeratotic lesions, pustular lesions, or a combination thereof .
• Erythrodermic Psoriasis: This is a rare, severe, and potentially life-threatening form that affects almost the entire body surface. It causes widespread redness, peeling skin, and intense itching or burning .
• Psoriatic Arthritis (PsA): While primarily a skin condition, psoriasis can also affect the joints, leading to psoriatic arthritis. This condition causes joint pain, stiffness, and swelling, which can occur in any joint in the body. It is considered the most well-known non-cutaneous condition associated with psoriasis . Joint involvement can significantly impact the quality of life .

The clinical presentation of psoriasis can be influenced by various endogenous and environmental factors, leading to diverse manifestations . Misdiagnosis of atypical psoriasis forms is not uncommon and can result in suboptimal prognostic assessments and therapeutic approaches .

The symptoms of psoriasis primarily involve characteristic skin lesions, though systemic manifestations are also common. The most distinctive feature is the presence of sharply demarcated, salmon-red plaques, typically covered by silvery, adherent scales . These lesions frequently appear on extensor surfaces, such as the elbows and knees, as well as on the scalp and lower back . However, psoriasis can affect any part of the body, including nails, palms, and soles, and flexural areas .

Beyond the visible plaques, individuals with psoriasis frequently report subjective sensory skin symptoms. A study revealed that 42.6% of patients reported skin pain, while 36.7% experienced skin discomfort . The average intensity for pain was 4.4 on a 0-10 numeric rating scale, and for discomfort, it was 3.5 . Common qualities of these symptoms included an unpleasant sensation, surface sensitivity, itchiness, and a hot or burning feeling . The presence and severity of these skin symptoms are often correlated with the overall severity of psoriasis .

Other symptoms include:

• Nail Changes: Psoriasis can affect the nails, leading to pitting, discoloration, thickening, crumbling, or separation from the nail bed. Nail involvement is significantly associated with more severe forms of the disease .
• Scalp Involvement: Psoriasis on the scalp can range from mild scaling to thick, crusted plaques, sometimes extending beyond the hairline. This can lead to significant discomfort and aesthetic concerns .
• Joint Pain and Stiffness: For individuals with psoriatic arthritis, joint symptoms are prominent. These can include pain, swelling, and stiffness in the affected joints, which may vary in severity and location . The disease can affect peripheral joints, the spine, or both . Studies have indicated that skin-targeted overexpression of certain proteases, such as Kallikrein-related peptidase 6 (KLK6), can cause severe psoriasiform dermatitis accompanied by debilitating psoriatic arthritis-like joint disease .
• Fatigue: Chronic inflammation associated with psoriasis can contribute to persistent fatigue, impacting daily activities and overall quality of life .

The impact of these symptoms on an individual’s quality of life can be substantial. Sleep disruption, for instance, is a frequently reported consequence of severe itching and discomfort .

Psoriasis is a complex immune-mediated disorder with a multifactorial etiology involving genetic predisposition, immunological dysregulation, and environmental factors. Although its precise cause remains under investigation, significant progress has been made in understanding the underlying mechanisms.

The condition is recognized as a genetic disorder, inherited in an autosomal dominant pattern, albeit with impaired penetrance, which accounts for its non-manifestation in every generation. Genetic susceptibility is particularly linked to the HLA-C*06:02 risk allele. However, the development of psoriasis is not solely determined by genetics; it represents a reaction of the skin to various agents in genetically predisposed individuals.

Immunological mechanisms are central to psoriasis pathogenesis. The disease involves a dysregulation of the immune system, particularly T-cell-mediated immunity. Key cytokines, such as interleukin-17 (IL-17) and interleukin-23 (IL-23), are identified as central drivers of the inflammatory process. These cytokines, along with oncostatin M (OSM), tumor necrosis factor-alpha (TNF-α), and interleukin-1 alpha (IL-1α), are potent inducers of cutaneous inflammation. They synergistically enhance the production of chemokines like CXCL8 and antimicrobial peptides such as β-defensin 2 (BD2), contributing to the inflammatory milieu. For instance, OSM overexpression in the skin induces epidermal thickening and keratinocyte proliferation, alongside increased expression of S100A8/9 and various chemokines, resulting in neutrophil and macrophage infiltration.

The innate immune system also plays a role in driving the autoimmune cascade. For example, activation of Toll-like receptor 7 (TLR7) can aggravate psoriasis by inducing type I interferon activity. A dynamic interplay exists between immune cells, keratinocytes, and other skin-resident cells, which is crucial for both the initiation and perpetuation of psoriatic changes. Keratinocytes, when stimulated, release cytokines that further activate T cells, establishing a self-perpetuating inflammatory cycle.

Recent investigations also point to the role of cytosolic DNA (cyDNA) in keratinocytes, which may disrupt immune tolerance and foster chronic inflammation in psoriatic lesions. Endogenous reverse transcriptase activities have been shown to generate RNA:DNA duplexes, which subsequently activate the production of Th1-inflammatory cytokines.

Furthermore, research on the gut microbiome suggests a connection with psoriasis. While findings are debated, some reports indicate elevated levels of certain bacterial genera, such as Staphylococcus and Streptococcus, in the skin microbiome of psoriasis patients . Studies in animal models indicate that specific gut bacteria, including Staphylococcus aureus and Streptococcus danieliae, can exacerbate skin inflammation, suggesting a potential feedback loop where skin inflammation influences gut microbiota, which in turn intensifies skin lesions.

Psoriasis is also associated with a range of comorbidities, suggesting common inflammatory mechanisms . These include metabolic derangements, cardiovascular disease, and psoriatic arthritis . For instance, patients with psoriasis exhibit an increased risk of cardiovascular disease, characterized by impaired insulin sensitivity, carotid intima-media thickening, and endothelial dysfunction . Even mild to moderate psoriasis is associated with increased carotid intima-media thickness (IMT) and impaired flow-mediated dilation (FMD), alongside elevated levels of oxidative stress markers . Atheroma plaques and metabolic syndrome are also more prevalent in psoriatic patients compared to controls.

The onset or exacerbation of psoriasis symptoms can be influenced by a variety of triggers, acting on an individual with genetic susceptibility. These factors can be broadly categorized as environmental, infectious, pharmacological, and psychological.

Environmental Triggers

• Physical Trauma (Koebner Phenomenon): Injury to the skin, such as cuts, scrapes, burns, or even severe sunburn, can induce psoriatic lesions in previously unaffected areas. This phenomenon underscores the skin’s heightened reactivity in predisposed individuals.
• Climate: Exposure to hot and sunny climates has been observed to lead to the spontaneous disappearance of psoriasis in some instances. Conversely, cold, dry weather may contribute to flare-ups.
• Smoking and Alcohol Consumption: These lifestyle factors are recognized environmental triggers. Smoking, in particular, has been identified as a significant predictor for the development of psoriasiform skin lesions, especially in patients undergoing anti-TNF-α therapy.
• Obesity: Increased body mass index (BMI) is also considered a predictor for psoriasiform lesions. Obesity is frequently associated with psoriasis and its comorbidities, including metabolic syndrome.

Infectious Triggers

• Streptococcal Infections: Particularly in children and young adults, streptococcal infections (e.g., strep throat) are a common trigger for guttate psoriasis. The onset often occurs a few weeks after such an infection.
• Skin Microbiome: Changes in the skin’s microbial environment, including elevated levels of Staphylococcus and Streptococcus, have been observed in psoriatic patients. Immunity to commensal skin fungi can also aggravate inflammation, with enhanced pathology linked to IL-17-producing lymphocytes and neutrophil extracellular traps.

Pharmacological Triggers

Certain medications can induce or worsen psoriasis. Examples include beta-blockers, lithium, antimalarials, and non-steroidal anti-inflammatory drugs (NSAIDs). Of particular note, tumor necrosis factor-alpha (TNF-α) inhibitors, widely used in various inflammatory conditions including inflammatory bowel disease (IBD) and psoriasis itself, can paradoxically induce psoriasiform eruptions in a small percentage of patients (around 4.8%). These drug-induced lesions are characterized by infiltrates of Th17 and Th1 cells.

Psychological Triggers

Stress is a well-documented trigger for psoriasis flare-ups. Emotional disturbances and psychological stress can influence the immune system, potentially exacerbating inflammatory responses. The concept of psoriasis as a “disease of adaptation” suggests that it can be a morbid reaction to various forms of stress, including physical and mental fatigue.

The diagnosis of psoriasis is primarily established through clinical examination, relying on the characteristic appearance and distribution of skin lesions . In many instances, the typical features of chronic plaque psoriasis—such as sharply defined, salmon-red plaques with silvery scales—are sufficient for a confident diagnosis . However, diagnostic challenges may arise in cases presenting with atypical features or when lesions are localized to specific, less common sites .

A thorough medical history is crucial, including questions about family history of psoriasis, as it is a genetic condition . Information regarding the onset, duration, and progression of symptoms, as well as any prior treatments and their efficacy, assists in forming a comprehensive understanding of the patient’s condition. The presence of joint pain or swelling should also be evaluated to assess for concomitant psoriatic arthritis.

In situations where the clinical presentation is ambiguous, a skin biopsy may be performed to confirm the diagnosis or to differentiate psoriasis from other dermatological conditions that may have similar appearances. Histopathological examination reveals characteristic changes, including epidermal hyperplasia, parakeratosis, and inflammatory infiltrates within the dermis .

Beyond visual inspection and biopsy, advanced imaging techniques are emerging as tools to identify systemic inflammation associated with psoriasis, particularly in relation to its comorbidities. For example, -fluorodeoxyglucose positron emission tomography-computed tomography (FDG-PET/CT) can detect and quantify systemic inflammation . This technique can identify foci of inflammation in various tissues beyond the skin, including the liver, joints, tendons, and aorta . Increased vascular inflammation in the aorta and hepatic inflammation have been observed in patients with psoriasis through FDG-PET/CT, even after adjusting for traditional cardiovascular risk factors.

Given the strong association of psoriasis with cardiovascular disease and metabolic syndrome, screening for these conditions is often recommended as part of the diagnostic and management process . This may involve assessing metabolic syndrome criteria and performing carotid ultrasound to detect early signs of atheroma plaque formation . Biomarkers such as the neutrophil to lymphocyte ratio (NLR) and C-reactive protein (CRP) have also been identified as independent predictors of psoriasis severity, offering additional insights into the inflammatory burden.

Psoriasis, a chronic condition, currently has no definitive cure; however, a wide array of treatments exists to manage symptoms, minimize physical and psychological burden, and improve quality of life . Treatment approaches are often personalized, considering disease severity, specific presentation, comorbidities, and patient preferences.

Topical Therapies

For mild to moderate psoriasis, topical treatments are frequently the first line of therapy. These include corticosteroids, vitamin D analogues, retinoids, and coal tar. While ointments can help reduce scaling , their efficacy varies. Emerging topical agents, such as a water-soluble extract from hardy kiwifruit (PG102), have demonstrated anti-inflammatory effects by suppressing hyperproliferation and downregulating inflammatory mediators through NF-κB and STAT inhibition . Similarly, the antimicrobial peptide RIS-1/psoriasin (S100A7) has shown promise, with its expression upregulated in inflammatory skin diseases and increased by retinoids, suggesting potential for epithelial-targeted anti-inflammatory treatments .

Phototherapy

Phototherapy, using controlled exposure to ultraviolet (UV) light, is an effective option for moderate to severe psoriasis. Common forms include narrowband ultraviolet B (UVB) and psoralen plus ultraviolet A (PUVA) . Phototherapy works by suppressing the immune response in the skin and slowing down the rapid growth of skin cells. While generally effective, some forms, like PUVA, may have cardiac side effects .

Systemic Therapies

For more severe or widespread psoriasis, systemic medications are employed. These include conventional systemic agents and advanced biologic therapies.

Conventional Systemic Agents

These older medications work throughout the body and include methotrexate, cyclosporine, and oral retinoids. While effective, they are associated with various side effects and require careful monitoring . Cyclosporine has shown beneficial immunological effects, suggesting an autoimmune component to psoriasis . However, it can elevate serum lipid levels and blood pressure . Similarly, systemic retinoids can cause severe dyslipidemia .

Biologic Therapies

Biological agents represent a significant advancement in the management of severe chronic plaque psoriasis, revolutionizing care . These therapies target specific components of the immune system involved in psoriasis pathogenesis. Key targets include TNF-α, IL-17, IL-23, and IL-12/IL-23 . For instance, anti-IL-12/IL-23 p40 antibody (ustekinumab) has shown high efficacy in treating psoriasiform lesions, even those induced by anti-TNF-α therapy . At present, a substantial proportion of patients with moderate to severe psoriasis are treated with biologic agents .

Emerging and Adjunctive Therapies

• Mesenchymal Stem Cell (MSC) Therapies: MSCs and their derived exosomes (hucMSCs-Exo) demonstrate immunomodulatory and anti-inflammatory properties . Studies show hucMSCs-Exo can suppress epidermal proliferation and reduce Psoriasis Area and Severity Index (PASI) scores in models, along with reducing inflammatory cytokines like IL-17 and IL-23 .
• Targeting Histamine Receptors: Histamine H4 receptor (H4R) agonists, such as 4-methylhistamine, have shown promise in ameliorating psoriasis-like inflammation in models by reducing Th1 cytokines and increasing regulatory T cells .
• Modulating Immune Checkpoints: The enzyme indoleamine 2,3-dioxygenase 2 (IDO2) may play a role in suppressing skin inflammation, suggesting that enhancing IDO2 activity could be a therapeutic avenue .
• PAR1 Antagonists: Given the role of Kallikrein-related peptidase 6 (KLK6) and protease-activated receptor 1 (PAR1) in promoting psoriasis and psoriatic arthritis, PAR1 antagonists are being explored as cytokine-independent therapeutic targets .
• Acupuncture: Acupuncture-related techniques, including acupuncture needling, electroacupuncture, and fire acupuncture, have demonstrated benefits in reducing psoriasis-like skin lesions in models. Electroacupuncture, in particular, showed superior effects by reducing epidermal thickness, inhibiting keratinocyte proliferation, and decreasing inflammatory cytokines .
• Chinese Herbal Medicine (CHM): Formulations like ‘Psoriasis 1’ have been observed to suppress inflammatory responses by modulating signaling pathways such as NF-κB and STAT .

The management strategy often involves a stepwise approach, starting with less intensive therapies and escalating to systemic or biologic agents if the condition is severe or unresponsive.

Dietary considerations for individuals with psoriasis are increasingly recognized as a complementary aspect of overall management, primarily focusing on reducing systemic inflammation and addressing associated comorbidities. While no specific diet offers a universal cure for psoriasis, certain nutritional approaches may help alleviate symptoms and improve general health.

Anti-Inflammatory Diets

Given that psoriasis is an inflammatory condition, adopting a diet rich in anti-inflammatory components is often recommended. This typically involves:

• Increased Intake of Fruits and Vegetables: These foods are abundant in antioxidants and phytochemicals that can help combat oxidative stress and inflammation .
• Omega-3 Fatty Acids: Found in fatty fish (salmon, mackerel, sardines), flaxseeds, and walnuts, omega-3s possess potent anti-inflammatory properties that may help modulate the immune response .
• Whole Grains: Opting for whole grains over refined carbohydrates can help reduce systemic inflammation and support gut health.
• Lean Proteins: Sources like poultry, legumes, and lean cuts of meat are generally preferred.

Addressing Comorbidities and Lifestyle Factors

Psoriasis is strongly linked with metabolic comorbidities, including obesity, hypertension, dyslipidemia, and diabetes mellitus . Dietary modifications can play a crucial role in managing these associated conditions:

• Weight Management: Obesity is a known trigger for psoriasis flare-ups and is associated with increased disease severity . A balanced diet that supports healthy weight management can reduce the overall inflammatory burden. Individuals should be mindful of their actual food intake, as underestimation can occur .
• Reducing Saturated and Trans Fats: Limiting intake of unhealthy fats found in processed foods and red meats can help improve lipid profiles and cardiovascular health, which is particularly relevant given the increased cardiovascular risk in psoriatic patients .
• Moderating Alcohol Consumption: Alcohol is a known environmental trigger for psoriasis exacerbations . Reducing or eliminating alcohol intake can be beneficial.

Gut Microbiome and Probiotics

The relationship between the gut microbiome and psoriasis is an area of active research. Evidence suggests a potential link between psoriasis and an imbalanced gut microbiome . Some studies have indicated that specific gut bacteria, such as Staphylococcus aureus and Streptococcus danieliae, can worsen skin inflammation .

Modulating the gut microbiota through dietary interventions, including the use of probiotics, has shown promise. A study involving psoriatic patients demonstrated that probiotic supplementation significantly improved quality of life and disease severity (measured by PASI scores). This was accompanied by reductions in low-density lipoprotein (LDL), total cholesterol (TC), lipopolysaccharides (LPS), high-sensitivity C-reactive protein (hs-CRP), and interleukin-1 beta (IL-1β) levels . These findings suggest that addressing gut dysbiosis could be a future treatment avenue for inflammatory skin diseases .

While a “psoriasis diet” does not exist, a balanced, anti-inflammatory dietary pattern that supports overall health and addresses metabolic comorbidities can contribute positively to managing the condition.

Living with psoriasis extends beyond managing physical symptoms; it encompasses significant psychological, social, and systemic challenges that influence an individual’s quality of life. The chronic and often visible nature of the disease can impose a substantial burden, leading to distress and affecting various aspects of daily living .

Psychological and Social Impact

Psoriasis is frequently associated with psychological comorbidities, including depression and anxiety . Psychiatric comorbidity has been identified as the strongest predictor of a diminished quality of life in individuals with moderate to severe psoriasis . The visible lesions can lead to social stigma, impacting self-esteem, relationships, and participation in social activities . Furthermore, the chronic discomfort, including pain and itching, can severely disrupt sleep and overall well-being .

Stress is a known trigger for psoriasis exacerbations, creating a challenging cycle where the disease causes stress, which in turn worsens symptoms . Managing stress through coping mechanisms, mindfulness, or professional support can therefore be an important component of living with psoriasis.

Systemic Health Considerations

Beyond the skin, psoriasis is a systemic immune-mediated disease associated with an increased prevalence of extracutaneous conditions and, in severe cases, elevated mortality rates . These associated conditions, or comorbidities, stem from shared inflammatory mechanisms and include:

• Psoriatic Arthritis (PsA): Affecting a significant portion of individuals with psoriasis, PsA causes joint pain, stiffness, and swelling, which can lead to functional impairment and reduced mobility .
• Cardiometabolic Syndrome: This cluster of conditions, including obesity, hypertension, dyslipidemia, and type 2 diabetes, is notably more prevalent in psoriatic patients . Even patients with mild to moderate psoriasis exhibit signs of increased cardiovascular risk, such as elevated carotid intima-media thickness and impaired endothelial function .
• Inflammatory Bowel Disease (IBD): Psoriasis and IBD, particularly Crohn’s disease, are associated due to shared genetic predispositions and common immunological pathways .
• Other Conditions: Psoriasis has also been linked to an increased risk of certain cancers and other autoimmune conditions .

Given these associations, managing psoriasis often involves a multidisciplinary approach that includes monitoring for and addressing these comorbidities. Lifestyle modifications, such as maintaining a healthy weight, avoiding smoking, and limiting alcohol, are significant in reducing the overall health burden .

Practical Strategies for Daily Living

Effective management strategies can significantly enhance the quality of life for individuals with psoriasis:

• Adherence to Treatment: Consistent application of topical treatments, regular phototherapy sessions, or adherence to systemic medication regimens is paramount for controlling flare-ups and minimizing disease progression.
• Skin Care Routine: Regular moisturizing, gentle cleansing, and avoidance of harsh soaps can help maintain skin barrier function and reduce dryness and irritation.
• Support Networks: Connecting with support groups or seeking psychological counseling can provide emotional relief and practical advice for coping with the challenges of psoriasis .
• Personalized Approach: Healthcare providers should aim for a personalized treatment strategy that integrates medical therapies with lifestyle modifications, tailored to the individual’s specific needs and disease presentation .

Psoriasis is a prevalent chronic skin condition with a notable global distribution, impacting a significant portion of the population. Understanding its statistical profile provides insight into its societal burden and demographic patterns.

Prevalence and Incidence

• Global Prevalence: Psoriasis affects approximately 1% to 3% of the world’s population . In Western populations, estimates suggest a prevalence of about 2% . For instance, in Germany, the one-year prevalence was reported as 2.53% in 2005 among continuously insured individuals . Across Italy, 2.9% of the population reported suffering from psoriasis, with regional variations from 0.8% to 4.5% .
• Gender Distribution: Psoriasis affects males and females with roughly equal frequency .
• Age of Onset: While psoriasis can appear at any age, the majority of individuals experience their first episode before the age of 40 . It is uncommon before the age of 10 years . Some studies indicate a bimodal distribution, with peaks occurring between 16-22 years and later between 57-60 years . Notably, population-based studies suggest an earlier age of onset in females compared to males .
• Juvenile Psoriasis: The prevalence rate in children younger than 18 years was 0.71%, increasing linearly from 0.12% at age 1 to 1.2% at age 18 .

Disease Severity and Characteristics

• Severity Distribution: Among patients with palmoplantar psoriasis, a study found that 18% had mild disease, 48% moderate, and 34% severe involvement .
• Comorbidity Rates: Psoriasis is associated with several important medical conditions .
  • Psoriatic Arthritis (PsA): This is the most common non-cutaneous comorbidity .
  • Cardiovascular Risk Factors: Patients with psoriasis are more susceptible to cardiovascular risk factors, including hypertension, obesity, dyslipidemia, and smoking, compared to the general population . Severe psoriasis has been linked to an approximately 60% increased risk of cardiovascular mortality, particularly in younger patients (under 60 years) .
  • Metabolic Syndrome: This condition is diagnosed in a significantly higher proportion of psoriatic patients. A study reported metabolic syndrome in 40.3% of psoriatic patients versus 13.1% of controls .
  • Psychiatric Conditions: Depression and anxiety are commonly associated with psoriasis, with psychiatric comorbidity being a strong predictor of reduced quality of life .
  • Juvenile Comorbidities: In individuals under 20 years with psoriasis, the overall rate of comorbidity was twice as high as in those without psoriasis. This included increased rates of hyperlipidemia, obesity, hypertension, diabetes mellitus, Crohn’s disease, and rheumatoid arthritis .

Treatment Patterns

Treatment patterns have evolved, particularly with the advent of biologic agents. In the five years leading up to a 2009 study, 68% of patients with moderate to severe psoriasis had received conventional systemic treatments, 39.1% biologic agents, and 22.3% phototherapy . At the time of the study, 57.5% were being treated with biologic agents, 32.6% with conventional systemic treatments, and 11% with phototherapy . This indicates a shift towards newer, targeted therapies for more severe disease presentations.

Impact on Quality of Life

The severity of psoriasis is significantly associated with a marked impact on quality of life . Subjective skin symptoms such as pain and discomfort are common, with 42.6% reporting pain and 36.7% reporting discomfort. These symptoms can significantly affect daily functions, with sleep being particularly impacted.

Psoriasis is a pervasive, chronic inflammatory skin condition affecting a substantial global population, estimated at 1% to 3% . Recognized as an immune-mediated disorder, it extends beyond cutaneous manifestations to encompass a range of significant comorbidities, including psoriatic arthritis, depression, and cardiometabolic syndrome .

The disease presents primarily as sharply defined, salmon-red plaques with silvery scales, commonly on extensor surfaces, though clinical presentations vary widely across different types such as guttate, inverse, pustular, and erythrodermic psoriasis . Patients frequently experience discomfort, pain, and itching, which profoundly affect their quality of life, including sleep .

Psoriasis arises from a complex interplay of genetic predisposition, particularly involving the HLA-C*06:02 allele, and dysregulated immunological pathways . Key cytokines, including IL-17 and IL-23, are central to the inflammatory cascade, driving keratinocyte proliferation and immune cell infiltration . Environmental factors such as streptococcal infections, stress, smoking, obesity, and certain medications can trigger or exacerbate the condition . Diagnosis primarily relies on clinical features, but in ambiguous cases, skin biopsies and advanced imaging like FDG-PET/CT can provide further diagnostic clarity and assess systemic inflammation .

While a cure remains elusive, management strategies aim to minimize disease impact. These range from topical treatments and phototherapy to systemic agents and, increasingly, highly effective biologic therapies that target specific inflammatory pathways.