Plaque-type psoriasis

Chronic inflammatory systemic disease which can manifest with erythematous, squamous and infiltrated skin lesions, nail changes and frequently joint involvement.

• Prevalence: 2-3% (Central Europe, USA)
• No gender predominantly affected.

• Genetic factors:
  • Polygenetic disease, at least 40 genetic loci are involved. The strongest risk factor for psoriasis (p value is < 10^-200) is HLA-Cw6
    • HLA-Cw6: PSORS1 (gene locus: 6p21.3)
• Exacerbation by drugs:
  • Lithium
  • Antimalarials
  • NSAIDs
    • Naprofen
    • Diclofenac
    • Indometacin
  • Betablockers, ACE inhibitors (recently cast into doubt by large cohort study)
  • Calcium- channel blockers
  • Rarely systemic glucocorticoids (rebound after discontinuation or even pustular exacerbation)
  • Antibiotics
    • Macrolides
  • Trigger factors :
    • Mechanical factors (Köbner phenomenon)
    • Infections
    • Stress
    • Alcohol and nicotine consumption

• Nail involvement: occurs in approx. 80% of cases
• Joint involvement: occurs in approx. 20% of cases
  • CAVE: this includes patients seen only by rheumatologists

• Sharply demarcated, erythematous, scaling and infiltrated plaques appear particularly on the scalp, on the elbows and knees, on the trunk, the face, the palms of the hands, the soles of the feet, and the nails. In the genital area and other intertriginous regions the lesions can be non-scaly and flat. Patients show both chronically stable plaques and episodic skin lesions.

• Köbner phenomenon: Triggers onset of psoriatic lesions due to mechanical trauma.
• Wax spot phenomenon: Detection of lamellar scaling is possible when scratching, which reveals whitish hyperkeratosis due to hyperparakeratosis .
• Phenomenon of the last cuticle: After scraping off the scales, only thin epidermal layer remains.
• Auspitz phenomenon: Punctate haemorrhages appear as soon as the last epidermal layer has been scraped off, due to injury to the dilated capillaries high in the papillary ends of the stratum papillare of the dermis.

• Seborrhiasis: co-occurrence of psoriasis and seborrhoeic eczema.

• Mucosal changes:
  • On the glans penis, exacerbation may occur due to mechanical stress (Köbner's phenomenon)
  • The oral mucosa is usually only involved in the context of psoriasis pustulosa generalisata.

• Anamnesis
  • Family history
  • Joint pain, enthesis pain
  • Nail changes
  • Improvement with UV exposure?
  • Bacterial infections (tonsillitis, especially in guttate psoriasis)
  • Medications
• Clinical findings
  • Erythematous edge of lesions
  • Silvery scaling
  • Infiltration of plaques
• If necessary, biopsy
  • Distinguishing dermatopathologically between nummular eczema and psoriasis vulgaris is very difficult and not always possible. The clinical findings carry more weight here.
  • Psoriasis palmoplantaris and palmoplantar eczema can also be difficult to distinguish. Here, the determination of NOS2 and CCL27 can be helpful, which is currently an experimental approach.

Most frequent localisation:

Scalp, elbow extensors and knees, sacral, however all skin regions can be affected including the skin folds.

• Hyperparakeratosis
• Neutrophilic granulocytes in the str. spinosum (Kogoj pustule) and in the area of hyperparakeratosis (Munro microabscesses)
• Focal loss of the str. granulosum
• Acanthosis with elongated narrow rete ridges
• Ectatic capillaries
• Papillomatosis
• Perivascular CD4-positive lymphohistiocytic infiltrates

• Psoriatic arthritis
• Coronary heart disease
• Metabolic syndrome
• M. Crohn's disease, ulcerative colitis
• Uveitis
• Depression
• Multiple sclerosis

Moisturizing the skin can reduce or prevent plaques.

Chronic disease, progresses in relapses.

1. Lowes M, Kim J. Faculty of 1000 evaluation for The majority of generalized pustular psoriasis without psoriasis vulgaris is caused by deficiency of interleukin-36 receptor antagonist.  F1000 - Post-publication peer review of the biomedical literature: Faculty of 1000, Ltd.
2. Vollmer S, Menssen A, Trommler P, Schendel D, Prinz JC. T lymphocytes derived from skin lesions of patients with psoriasis vulgaris express a novel cytokine pattern that is distinct from that of T helper type 1 and T helper type 2 cells. European Journal of Immunology 1994;24:2377-82.
3. Altmeyer P, Hartwig R, Matthes U. Das Wirkungs- und Sicherheitsprofil von Fumarsäureestern in der oralen Langzeittherapie bei schwerer therapieresistenter Psoriasis vulgaris. Der Hautarzt 1996;47:190-6.
4. Guenther L, Cambazard F, Van De Kerkhof PCM, et al. Efficacy and safety of a new combination of calcipotriol and betamethasone dipropionate (once or twice daily) compared to calcipotriol (twice daily) in the treatment of psoriasis vulgaris: a randomized, double-blind, vehicle-controlled clinical trial. Br J Dermatol 2002;147:316-23.
5. Gottlieb AB, Masuda S, Ramamurthi R, et al. Pharmacodynamic and pharmacokinetic response to anti-tumor necrosis factor-α monoclonal antibody (infliximab) treatment of moderate to severe psoriasis vulgaris. Journal of the American Academy of Dermatology 2003;48:68-75.
6. Nakamura M, Toyoda M, Morohashi M. Pruritogenic mediators in psoriasis vulgaris: comparative evaluation of itch-associated cutaneous factors. Br J Dermatol 2003;149:718-30.
7. van de Kerkhof PCM, Wasel N, Kragballe K, Cambazard F, Murray S. A Two-Compound Product Containing Calcipotriol and Betamethasone Dipropionate Provides Rapid, Effective Treatment of Psoriasis vulgaris regardless of Baseline Disease Severity. Dermatology 2005;210:294-9.
8. Smith WA, Siegel D, Lyon VB, Holland KE. Psoriasiform eruption and oral ulcerations as adverse effects of topical 5% imiquimod treatment in children: a report of four cases. Pediatr Dermatol 2013;30:e157-60.
9. Nast A, Gisondi P, Ormerod AD, et al. European S3-Guidelines on the systemic treatment of psoriasis vulgaris - Update 2015 - Short version - EDF in cooperation with EADV and IPC. Journal of the European Academy of Dermatology and Venereology 2015;29:2277-94.