Psoriasis (All Types)
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Psoriasis (All Types)
Psoriasis is a chronic autoimmune skin disease that causes rapid skin cell growth, leading to thick, scaly patches on the skin's surface. It occurs when the immune system mistakenly attacks healthy skin cells, triggering inflammation and accelerating the normal skin cell lifecycle from 28 days to just 3-4 days. While plaque psoriasis is the most common form (affecting 80-90% of patients), the condition manifests in multiple types including guttate, inverse, pustular, and erythrodermic psoriasis, each with distinct characteristics and severity levels.
Recognizing Psoriasis (All Types)
Common symptoms and warning signs to look for
Thick, red patches covered with silvery-white scales - the hallmark of plaque psoriasis
Small, drop-shaped spots that appear suddenly after an infection (guttate psoriasis)
Smooth, shiny red patches in skin folds like armpits and groin (inverse psoriasis)
Painful, pus-filled blisters surrounded by red skin (pustular psoriasis)
Severe, widespread redness covering most of the body with intense burning (erythrodermic psoriasis)
Pitted, discolored, or separating nails that may crumble or fall off
What a Healthy System Looks Like
In healthy skin, keratinocytes (skin cells) follow a precisely regulated 28-day lifecycle: basal cells in the stratum basale divide and gradually migrate upward through the stratum spinosum and stratum granulosum, undergoing terminal differentiation. During this journey, cells flatten, produce keratin, and eventually form the protective stratum corneum where they are shed imperceptibly. This process maintains epidermal homeostasis with approximately 3.5 billion cells turning over daily in perfect balance. The skin barrier prevents water loss while blocking pathogens and irritants. Resident immune cells including Langerhans cells and dermal dendrocytes maintain surveillance without triggering inflammation. Blood vessels in the papillary dermis provide nutrients without abnormal dilation. The dermal-epidermal junction remains intact, and the skin microbiome maintains a healthy balance of beneficial organisms.
How the Condition Develops
Understanding the biological mechanisms
Psoriasis pathophysiology involves a complex interplay of genetic, immunologic, and environmental factors creating a self-sustaining inflammatory loop: (1) Genetic predisposition - HLA-C*06:02 and other susceptibility loci (PSORS1-9) create baseline risk; (2) Immune dysregulation - Dendritic cells become activated by triggers (stress, infection, trauma) and produce IL-23, which stimulates and expands Th17 cells; (3) Cytokine cascade - Th17 cells release IL-17A, IL-17F, IL-22, and TNF-alpha, driving keratinocyte hyperproliferation and recruitment of neutrophils; (4) Accelerated turnover - Normal 28-day keratinocyte lifecycle compresses to 3-4 days, causing acanthosis (epidermal thickening), parakeratosis (retained nuclei in stratum corneum), and characteristic scale formation; (5) Angiogenesis - VEGF and angiopoietins promote tortuous, dilated blood vessels in dermal papillae, creating plaque erythema; (6) Neutrophil infiltration - Collections form Munro microabscesses in the stratum corneum and spongiform pustules of Kogoj in pustular variants; (7) Type-specific variations - Guttate psoriasis shows prominent neutrophilic infiltration post-streptococcal infection; inverse psoriasis lacks scale due to moisture in intertriginous areas; pustular psoriasis features prominent IL-36 pathway activation; erythrodermic psoriasis represents massive cytokine storm with generalized vasodilation; (8) Systemic inflammation - Elevated inflammatory mediators circulate systemically, explaining cardiovascular comorbidities and psoriatic arthritis in 30% of patients.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| TNF-Alpha (Tumor Necrosis Factor-alpha) | <8 pg/mL | <4 pg/mL | Primary inflammatory cytokine elevated across all psoriasis types; central mediator of inflammation and keratinocyte activation; target of adalimumab, infliximab, etanercept |
| IL-17A (Interleukin-17A) | <5 pg/mL | <2 pg/mL | Master cytokine driving keratinocyte hyperproliferation; elevated in all psoriasis types; target of secukinumab, ixekizumab, brodalumab; correlates with PASI score |
| IL-23 (Interleukin-23) | <10 pg/mL | <5 pg/mL | Th17 cell survival and expansion factor; elevated in chronic plaque and pustular psoriasis; target of guselkumab, tildrakizumab, risankizumab |
| IL-36 (Interleukin-36) | <20 pg/mL | <10 pg/mL | Particularly elevated in pustular psoriasis (GPP); drives neutrophilic inflammation; target of spesolimab for generalized pustular psoriasis |
| CRP (C-Reactive Protein) | <3 mg/L | <1 mg/L | Non-specific inflammation marker; elevated in moderate-severe disease and erythrodermic psoriasis; cardiovascular risk predictor |
| ESR (Erythrocyte Sedimentation Rate) | <20 mm/hr | <10 mm/hr | Acute phase reactant; elevated in active disease and erythrodermic psoriasis; monitors treatment response |
| Uric Acid | 3.5-7.2 mg/dL | 4.0-6.0 mg/dL | Elevated due to increased nucleic acid turnover from rapid skin cell proliferation; may contribute to gout comorbidity |
| Streptococcal Antibodies (ASO, Anti-DNase B) | <200 IU/mL | <100 IU/mL | Elevated in guttate psoriasis triggered by streptococcal pharyngitis; guides antibiotic therapy |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Predisposition","contribution":"40-60% heritability; HLA-C*06:02 allele present in 60% of early-onset plaque psoriasis and 90% of guttate psoriasis; PSORS1-9 susceptibility loci identified; family history increases risk 3-10x depending on number of affected relatives; first-degree relatives have 10% lifetime risk; twin concordance 65-70%","assessment":"Detailed family history; HLA typing (research setting); genetic counseling for severe familial cases"}
{"cause":"Th17/IL-23 Pathway Dysregulation","contribution":"Core immunologic mechanism across all types; IL-23 drives Th17 expansion and survival; IL-17A/F stimulate keratinocyte proliferation and neutrophil recruitment; IL-22 promotes epidermal hyperplasia; IL-36 prominent in pustular variants; creates self-sustaining inflammatory loop","assessment":"Serum cytokine panels (IL-17, IL-23, IL-22, IL-36); clinical disease severity (PASI, BSA); response to targeted biologics confirms pathway involvement"}
{"cause":"Environmental Triggers","contribution":"30-50% of flare triggers across all types: Stress (psychological and physical), infections (streptococcal pharyngitis triggers guttate; HIV worsens all types), trauma (Koebner phenomenon), medications (beta-blockers, lithium, antimalarials, NSAIDs, systemic steroids), smoking, alcohol, weather changes","assessment":"Detailed trigger history including medication review; symptom diary; infection workup for acute flares; streptococcal testing for guttate onset"}
{"cause":"Immune System Dysfunction","contribution":"Central mechanism; dendritic cell activation, Th1/Th17 polarization, neutrophil infiltration, mast cell activation; impaired regulatory T-cell function; autoantibodies against LL-37/cathelicidin complexes in some patients","assessment":"Immunologic panel; T-cell subset analysis; autoantibody screening; clinical assessment of infection history"}
{"cause":"Metabolic Factors","contribution":"Obesity strongly associated with psoriasis severity; adipose tissue secretes pro-inflammatory adipokines (leptin, resistin); insulin resistance increases inflammation; mechanical stress on skin folds triggers inverse psoriasis; weight loss improves disease severity","assessment":"BMI, waist circumference, body composition; fasting glucose, HbA1c, fasting insulin; lipid panel; metabolic syndrome criteria assessment"}
{"cause":"Microbiome Dysbiosis","contribution":"Altered skin microbiome with reduced diversity; Staphylococcus aureus colonization common; gut microbiome alterations (reduced Firmicutes, increased Bacteroidetes); streptococcal superantigens trigger guttate flares","assessment":"Skin and gut microbiome analysis; bacterial cultures; streptococcal screening"}
{"cause":"Nutritional Deficiencies","contribution":"Vitamin D deficiency common and associated with severity; omega-3 deficiency reduces anti-inflammatory mediators; zinc deficiency impairs wound healing and immune function; antioxidant depletion from chronic inflammation","assessment":"Serum 25-OH vitamin D; omega-3 index; zinc, selenium levels; dietary assessment; antioxidant status"}
{"cause":"Psychological Stress","contribution":"Major trigger for flares and disease onset; activates HPA axis and sympathetic nervous system; increases cortisol and catecholamines; stress-induced scratching worsens disease; depression and anxiety common comorbidities","assessment":"Stress history; Perceived Stress Scale; PHQ-9 for depression; GAD-7 for anxiety; identification of emotional triggers"}
Risks of Inaction
What happens if left untreated
{"complication":"Psoriatic Arthritis Progression","timeline":"Develops in 30% within 5-10 years of skin onset; can precede skin disease in 15%","impact":"Progressive joint destruction with erosions and deformities; irreversible damage if untreated for >6 months; dactylitis and enthesitis cause significant disability; functional impairment affects work and daily activities; increased mortality from cardiovascular complications"}
{"complication":"Cardiovascular Disease","timeline":"Lifetime elevated risk; accelerates with disease duration and severity","impact":"2-3x increased risk of myocardial infarction; 1.5x increased stroke risk; accelerated atherosclerosis from chronic inflammation; increased cardiovascular mortality; patients with severe psoriasis have 3-4 year reduced life expectancy"}
{"complication":"Metabolic Syndrome and Type 2 Diabetes","timeline":"Progressive with disease duration; 50% prevalence in psoriasis patients","impact":"Cluster of insulin resistance, hypertension, dyslipidemia, and obesity; creates vicious cycle worsening psoriasis; 1.5-2x increased diabetes risk; multiplies cardiovascular risk exponentially"}
{"complication":"Psychological Morbidity","timeline":"Chronic, progressive; often begins soon after diagnosis","impact":"Depression 1.5-2x more common; anxiety disorders prevalent; social isolation and relationship strain; unemployment rates 3x higher in severe disease; reduced quality of life comparable to cancer, diabetes, and heart disease; suicide risk elevated"}
{"complication":"Erythrodermic Crisis","timeline":"Can develop acutely from unstable plaque psoriasis or withdrawal of systemic steroids","impact":"Life-threatening emergency with thermoregulatory failure, high-output cardiac failure, protein loss, electrolyte imbalances, and infection risk; mortality 2-5% even with treatment; requires hospitalization"}
{"complication":"Generalized Pustular Psoriasis (GPP) Flares","timeline":"Acute, potentially life-threatening flares","impact":"Fever, leukocytosis, hypocalcemia, dehydration, and potential sepsis; mortality without treatment; requires urgent hospitalization and systemic therapy"}
{"complication":"Ocular Complications","timeline":"Variable; often concurrent with disease flares","impact":"Anterior uveitis (7% lifetime risk), conjunctivitis, blepharitis, keratitis, cataracts; can lead to vision loss if untreated; requires regular ophthalmologic monitoring"}
{"complication":"Nail Destruction","timeline":"Progressive over years; affects 50% of patients","impact":"Functional impairment from pain and deformity; onycholysis and subungual hyperkeratosis cause discomfort; psychosocial impact from visible nail changes; increased risk of secondary infection"}
{"complication":"Reduced Life Expectancy","timeline":"Cumulative lifetime effect of comorbidities","impact":"3-4 year reduced life expectancy in severe psoriasis primarily from cardiovascular disease, metabolic syndrome, and psychological comorbidities; quality-adjusted life years significantly impacted"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"PASI Score Assessment (Psoriasis Area and Severity Index)","purpose":"Standardize disease severity measurement for all types","whatItShows":"Quantifies erythema, induration, scaling on 0-4 scale across four body areas (head, trunk, upper limbs, lower limbs) weighted by body surface area; PASI <3 mild, 3-10 moderate, >10 severe; PASI 75/90/100 response defines treatment success; guides treatment selection and monitoring"}
{"test":"BSA Assessment (Body Surface Area)","purpose":"Quick severity estimation","whatItShows":"Percentage of body surface affected; palm = 1% BSA; <3% mild, 3-10% moderate, >10% severe; correlates with quality of life impact"}
{"test":"DLQI (Dermatology Life Quality Index)","purpose":"Measure disease impact on quality of life","whatItShows":"10-question validated tool assessing symptoms, feelings, daily activities, leisure, work, personal relationships, treatment burden; score 0-1 no effect, 2-5 small, 6-10 moderate, 11-20 very large, 21-30 extremely large effect"}
{"test":"Cytokine Panel (IL-17, IL-23, IL-36, TNF-alpha)","purpose":"Assess inflammatory burden and guide biologic selection","whatItShows":"Elevated Th17-axis cytokines confirm disease activity; IL-36 particularly elevated in pustular psoriasis; helps predict response to specific biologic classes; serial measurements track treatment response"}
{"test":"Cardiovascular Risk Assessment","purpose":"Screen for major comorbidity","whatItShows":"Lipid panel, fasting glucose, HbA1c, blood pressure, BMI, waist circumference; identifies metabolic syndrome; 10-year ASCVD risk calculation; informs holistic treatment planning"}
{"test":"Psoriatic Arthritis Screening (PASE, PEST)","purpose":"Early detection of joint involvement","whatItShows":"Psoriasis Epidemiology Screening Tool (PEST) and Psoriatic Arthritis Screening and Evaluation (PASE) questionnaires; identifies patients needing rheumatology referral; early detection prevents irreversible joint damage"}
{"test":"Rheumatologic Evaluation","purpose":"Confirm PsA diagnosis and assess severity","whatItShows":"Physical exam for enthesitis, dactylitis, synovitis; tender and swollen joint counts; imaging (X-ray, ultrasound, MRI) for erosions and inflammation; CASPAR criteria assessment"}
{"test":"Nail Psoriasis Severity Index (NAPSI)","purpose":"Quantify nail involvement","whatItShows":"Assesses nail matrix (pitting, leukonychia, crumbling) and nail bed (oil drop, onycholysis, hyperkeratosis) across 8 nails; score 0-8 per nail, 0-64 total; monitors treatment response"}
{"test":"Scalp Severity Assessment (PSSI)","purpose":"Quantify scalp involvement","whatItShows":"Psoriasis Scalp Severity Index combines erythema, induration, scaling on scalp specifically; important as scalp psoriasis often persists despite body clearance"}
{"test":"Palmoplantar Severity (PPPASI or PPPGA)","purpose":"Assess palmoplantar involvement","whatItShows":"Palmoplantar PASI or Physician Global Assessment specific to hands/feet; important for functional impairment assessment"}
{"test":"Nutritional Panel","purpose":"Identify modifiable nutritional contributors","whatItShows":"Vitamin D, omega-3 index, zinc, selenium; deficiencies impair immune regulation and barrier function; guides supplementation"}
{"test":"Infectious Workup","purpose":"Identify triggers","whatItShows":"Throat culture for streptococcus (guttate trigger); HIV testing (worsens psoriasis); hepatitis screening (before biologics); TB screening (before biologics)"}
{"test":"Ophthalmologic Screening","purpose":"Detect ocular involvement","whatItShows":"Slit-lamp examination for uveitis; assessment of conjunctivitis, blepharitis; recommended annually or with ocular symptoms"}
{"test":"Liver and Kidney Function","purpose":"Baseline before systemic therapy; detect comorbidities","whatItShows":"CMP including AST, ALT, alkaline phosphatase, bilirubin, creatinine, BUN; identifies NAFLD; monitors medication safety"}
Our Treatment Approach
How we help you overcome Psoriasis (All Types)
Healers Comprehensive Psoriasis Recovery Protocol
Personalized, type-specific treatment approach addressing all psoriasis variants with integrated conventional and functional medicine strategies
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
{"general":["Regular moderate exercise (reduces inflammation, improves mood, supports weight management)","Stress management: meditation, yoga, mindfulness, deep breathing exercises","Adequate sleep: 7-9 hours nightly; consistent sleep schedule","Smoking cessation (critical - smoking worsens psoriasis severity and treatment response)","Limit alcohol consumption (maximum 1-2 drinks weekly; abstinence ideal)","Maintain healthy weight (weight loss of 5-10% can significantly improve psoriasis)"],"skinCare":["Daily moisturizing with thick, fragrance-free emollients (ceramide-based preferred)","Gentle cleansers only; avoid harsh soaps and hot water","Bath oils and colloidal oatmeal baths for soothing","Scale removal: salicylic acid preparations or gentle exfoliation after soaking","Nail care: keep nails short, avoid trauma, moisturize cuticles","Scalp care: medicated shampoos (coal tar, salicylic acid, ketoconazole)","Sun protection: balance vitamin D synthesis with burn prevention"],"triggerAvoidance":["Protect skin from trauma (Koebner phenomenon) - avoid scratches, tight clothing, friction","Manage stress through regular practice of relaxation techniques","Avoid known medication triggers (discuss alternatives with physician)","Treat infections promptly (especially streptococcal)","Maintain stable climate (humidifier in dry environments)"]}
Recovery Timeline
What to expect on your healing journey
{"description":"Treatment response varies by psoriasis type, severity, and chosen therapy","byType":[{"type":"Plaque Psoriasis","initialImprovement":"2-4 weeks - Reduced scaling and plaque thickness, decreased erythema, reduced pruritus","significantChanges":"3-6 months - PASI 75-90 response (75-90% clearance), near-clear skin possible with biologics","maintenancePhase":"6-12 months - Sustained remission, reduced treatment frequency, stable clear skin"},{"type":"Guttate Psoriasis","initialImprovement":"1-2 weeks - If streptococcal trigger treated; spontaneous resolution common within 3-4 months","significantChanges":"2-3 months - Complete resolution in most cases; may evolve to chronic plaque type","maintenancePhase":"Ongoing - Monitor for recurrence; preventive strategies if recurrent"},{"type":"Inverse Psoriasis","initialImprovement":"1-2 weeks - Reduced erythema and discomfort with appropriate topical therapy","significantChanges":"4-8 weeks - Significant clearing; maintenance therapy often required due to location","maintenancePhase":"Ongoing - Intermittent therapy to maintain control in friction-prone areas"},{"type":"Pustular Psoriasis","initialImprovement":"1-2 weeks - With appropriate systemic therapy; hospitalization may be needed for GPP","significantChanges":"1-3 months - Pustule resolution; palmoplantar may require longer treatment","maintenancePhase":"3-6+ months - Maintenance therapy often required; monitor for recurrences"},{"type":"Erythrodermic Psoriasis","initialImprovement":"Days to 1-2 weeks - With urgent hospitalization and systemic therapy","significantChanges":"2-4 weeks - Significant improvement; complete resolution may take 1-2 months","maintenancePhase":"Ongoing - Close monitoring; preventive strategies to avoid recurrence"},{"type":"Nail Psoriasis","initialImprovement":"3-6 months - Fingernails; slow improvement due to growth rate","significantChanges":"6-12 months - Significant improvement; toenails may take 12-18 months","maintenancePhase":"Ongoing - Maintenance often needed; complete normalization may not occur"}],"generalExpectations":["Individual response varies based on adherence, number of root causes, and comorbidities","Biologics generally provide fastest and most complete responses","Nail and scalp psoriasis respond more slowly than skin","Long-term management is typically required for chronic types","Early intervention improves long-term outcomes"]}
Frequently Asked Questions
Common questions from patients
What are the different types of psoriasis and how do they differ?
The five main types of psoriasis are: (1) Plaque psoriasis (80-90% of cases) - thick, red patches with silvery scales on elbows, knees, scalp, and back; (2) Guttate psoriasis - small, drop-shaped spots that appear suddenly, often after strep throat, affecting trunk and limbs; (3) Inverse psoriasis - smooth, shiny red patches in skin folds (armpits, groin) without scale; (4) Pustular psoriasis - pus-filled blisters on red skin, either localized to hands/feet or generalized with fever; (5) Erythrodermic psoriasis - rare, severe form covering most of the body with intense redness and scaling. At Healers Clinic, we identify your specific type to create a targeted treatment plan.
Can psoriasis affect more than just the skin?
Yes, psoriasis is a systemic inflammatory disease, not just a skin condition. Up to 30% of patients develop psoriatic arthritis causing joint pain and damage. Psoriasis increases risk of cardiovascular disease (heart attacks and strokes), type 2 diabetes, metabolic syndrome, inflammatory bowel disease, depression, and anxiety. Some patients experience eye inflammation (uveitis). This is why our comprehensive approach includes screening and management of these associated conditions, not just treating the skin.
What is the most effective treatment for each type of psoriasis?
Treatment depends on type and severity: Plaque psoriasis responds well to topical corticosteroids and vitamin D analogs for mild cases, phototherapy for moderate, and biologics (IL-17, IL-23, or TNF inhibitors) for severe disease. Guttate psoriasis often resolves after treating underlying streptococcal infection and may benefit from phototherapy. Inverse psoriasis requires low-potency steroids or calcineurin inhibitors in skin folds. Pustular psoriasis may need IL-36 inhibitors (for generalized) or acitretin. Erythrodermic psoriasis is a medical emergency requiring hospitalization and systemic therapy. At Healers Clinic, we use advanced testing to select the most appropriate therapy for your specific type.
Is psoriasis hereditary and can it be prevented?
Genetics play a significant role - having one parent with psoriasis increases risk 3-fold, while both parents increase it 10-fold. The HLA-C*06:02 gene is strongly associated, particularly with early-onset and guttate types. However, genetics alone don't determine fate. Environmental triggers like stress, infections (especially streptococcal), skin trauma, certain medications, smoking, and alcohol often precipitate disease in genetically susceptible individuals. While you cannot change your genes, you can reduce risk by: not smoking, limiting alcohol, maintaining healthy weight, managing stress, treating infections promptly, and protecting skin from trauma. Early intervention can modify disease course.
Why does my psoriasis get worse with stress?
Stress is one of the most common psoriasis triggers through multiple mechanisms: (1) Psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis, increasing cortisol and inflammatory cytokines; (2) Stress hormones impair skin barrier function; (3) Neuropeptides released during stress (substance P) directly stimulate inflammation and itching; (4) Stress often leads to poor sleep, unhealthy eating, and reduced self-care; (5) Stress-induced scratching worsens the Koebner phenomenon. Studies show stress management interventions can improve psoriasis severity independent of medical treatment. At Healers Clinic, we incorporate stress reduction as a core component of treatment.
Can psoriasis be cured completely or will I have it forever?
Currently, there is no permanent cure for psoriasis, but it can be effectively controlled to the point of achieving clear or nearly clear skin. Modern biologic therapies have revolutionized treatment - many patients experience 90-100% clearance (PASI 90-100). Some patients achieve long-term remission after years of treatment and can eventually discontinue or reduce therapy. The goal has shifted from 'cure' to 'sustained remission with minimal treatment burden.' Early aggressive treatment may alter the natural disease course, reduce comorbidity risk, and improve long-term outcomes. Research into curative approaches continues.
Medical References
- 1.Greb JE, Goldminz AM, Elder JT, et al. Psoriasis. Nat Rev Dis Primers. 2016;2:16082. doi:10.1038/nrdp.2016.82 - Comprehensive review of psoriasis pathophysiology, types, and treatment.
- 2.Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker J. Psoriasis. Lancet. 2021;397(10273):1301-1315. doi:10.1016/S0140-6736(20)32549-6 - Updated comprehensive review including modern biologic therapies.
- 3.Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496-509. doi:10.1056/NEJMra0804595 - Foundational review of psoriasis immunology.
- 4.Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF Guidelines of Care for the Management and Treatment of Psoriasis with Biologics. J Am Acad Dermatol. 2019;80(4):1029-1072. doi:10.1016/j.jaad.2018.11.057 - Evidence-based guidelines for biologic therapy selection.
- 5.Boehncke WH, Schon MP. Psoriasis. Lancet. 2015;386(9997):983-994. doi:10.1016/S0140-6736(14)61909-7 - Comprehensive clinical overview including all psoriasis types.
- 6.Ritchlin CT, Colbert RA, Gladman DD. Psoriatic Arthritis. N Engl J Med. 2017;376(10):957-970. doi:10.1056/NEJMra1505557 - Detailed review of psoriatic arthritis diagnosis and management.
- 7.Marrakchi S, Guigue P, Renshaw BR, et al. Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis. N Engl J Med. 2011;365(7):620-628. doi:10.1056/NEJMoa1013068 - Landmark study on IL-36 pathway in pustular psoriasis.
- 8.Gisondi P, Fostini AC, Fossà I, et al. Psoriasis and the Metabolic Syndrome. Clinics Dermatol. 2018;36(1):21-28. doi:10.1016/j.clindermatol.2017.09.005 - Review of metabolic comorbidities in psoriasis.
- 9.Kimball AB, Gladman D, Gelfand JM, et al. National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening. J Am Acad Dermatol. 2008;58(6):1031-1042. doi:10.1016/j.jaad.2008.01.006 - Guidelines for comorbidity screening.
- 10.Ford AR, Siegel M, Bagel J, et al. Dietary Recommendations for Adults with Psoriasis or Psoriatic Arthritis from the Medical Board of the National Psoriasis Foundation. JAMA Dermatol. 2018;154(8):934-950. doi:10.1001/jamadermatol.2018.1412 - Evidence-based dietary recommendations.
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Our integrative medicine experts are ready to help you overcome Psoriasis (All Types).