eMedicine Specialties > Emergency Medicine > Dermatology

Psoriasis

Author: Richard Gordon Jr, MD, Staff Physician, Department of Emergency Medicine, Detroit Receiving Hospital University Health Center
Coauthor(s): Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Contributor Information and Disclosures

Updated: Apr 10, 2009

Introduction

Background

Psoriasis is a chronic, noncontagious, multisystem, inflammatory disorder. Patients with psoriasis have a genetic predisposition for the illness, which most commonly manifests itself on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glands penis. The joints are also affected by psoriasis in up to 30% of patients with the disease.

Psoriasis has a tendency to wax and wane with flares related to systemic or environmental factors, including life stress events and infection.

Multiple types of psoriasis are identified, with discoid psoriasis, also known as plaque psoriasis, being the most common type. Plaque psoriasis usually presents with plaques on the scalp, trunk, and limbs. These plaques appear as focal, raised, inflamed, edematous lesions covered with silvery white scales.

Plaque psoriasis is raised, roughened, and covere...

Plaque psoriasis is raised, roughened, and covered with white or silver scale with underlying erythema. Contributed by Randy Park, MD.

Plaque psoriasis is raised, roughened, and covere...

Plaque psoriasis is raised, roughened, and covered with white or silver scale with underlying erythema. Contributed by Randy Park, MD.


Pathophysiology

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques. Specifically, there is a large recruitment of T cells to the affected areas. This is supported by histologic examination and immunohistochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions.
 
One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques.1 Ultimately, a ramped up, deregulated inflammatory process ensues with a large production of various cytokines. Interestingly, elevated levels of tumor necrosis factor-alpha (TNF-alpha) specifically are found to correlate with flares of psoriasis.

Many of the clinical features of psoriasis are explained by the large production of proinflammatory mediators (eg, TNF-alpha, interferon-gamma, interleukin 12). Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate, leading to improper cell maturation. Epidermal cell turnover is reduced from 23 days to 3-5 days. Cells that normally lose their nuclei in the stratum granulosum, retain their nuclei, known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions.

Frequency

United States

Between 2% and 2.6% of the US population is affected. Between 150,000 and 260,000 new cases of psoriasis occur annually.

International

Incidence of psoriasis is dependent on the climate and genetic heritage of the population. It is less common in the tropics and in dark-skinned persons.

Mortality/Morbidity

  • Mild psoriasis does not appear to increase risk of death.2
  • Men with severe psoriasis died 3.5 years earlier compared with men without the disease. Women with severe psoriasis died 4.4 years earlier compared with women without the disease.2
  • Psoriasis is associated with cardiovascular disease, smoking, alcohol, metabolic syndrome, lymphoma, depression, suicide, potentially harmful drug and light therapies, and possibly melanoma and nonmelanoma skin cancers.
  • Approximately 1.5 million people with psoriatic arthritis seek medical care each year in the United States.
  • Psoriasis can significantly influence a person’s quality of life. One study suggests that the physical and mental disability experienced with this disease was comparable or in excess of that found in patients with other chronic illnesses such as cancer, arthritis, hypertension, heart disease, diabetes, and depression.3
  • Studies show that psoriasis of the palms and soles tend to have greater impact on the patient’s quality of life compared to those with more extensive psoriatic involvement not involving the palms and soles.4,5

Race

Psoriasis is more common in Caucasians.

Sex

Psoriasis is slightly more common in women than in men.

Age

Approximately 10-15% of new cases begin in children younger than 10 years. The median age at onset is 28 years.

Clinical

History

  • Worsening of a long-term erythematous scaly area
  • Sudden onset of many small areas of scaly redness
  • Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
  • Family history of similar rash
  • Pain
  • Pruritus
  • No fever
  • Vesicles
  • Long-term rash with recent presentation of joint pain

Physical

Findings on physical examination depend on the type of psoriasis.

  • Raised, inflamed lesions covered with a silvery white scale characterize plaque psoriasis. The scale may be scraped away to reveal inflamed skin beneath. This is most common on the extensor surfaces of the knees, elbows, scalp, and trunk.
Plaque psoriasis is most common on the extensor s...

Plaque psoriasis is most common on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.

Plaque psoriasis is most common on the extensor s...

Plaque psoriasis is most common on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.


  • Guttate psoriasis presents as small salmon-pink papules, 1-10 mm in diameter, predominately on the trunk; the lesions may be scaly. It frequently appears suddenly, 2-3 weeks after an upper respiratory infection (URI) with group A beta-hemolytic streptococci.
  • Inverse psoriasis occurs on the flexural surfaces, armpit, groin, under the breast, and in the skin folds. It is characterized by smooth, inflamed lesions without scaling due to the moist nature of the area this type of psoriasis is located in.
  • Pustular psoriasis presents as sterile pustules appearing on the palms and soles or diffusely over the body. Pustular psoriasis may cycle through erythema, pustules, then scaling. The diffuse variant is termed von Zumbush variant, which is accompanied by fever and intense ill feeling in addition to the widespread pustules.
  • Erythrodermic psoriasis presents as generalized erythema, pain, itching, and fine scaling. Erythrodermic psoriasis typically encompasses nearly the entire body surface area. It may be accompanied by fever, chills, hypothermia, and dehydration secondary to the large body surface area involvement.
  • Scalp psoriasis affects approximately 50% of patients. It presents as erythematous raised plaques with silvery white scales on the scalp.
  • Nail psoriasis may cause pits on the nails, which often become thickened and yellowish in color. Nails may separate from the nail bed.
  • Psoriatic arthritis affects approximately 10% of those with skin symptoms. The arthritis is usually in the hands and feet and, occasionally, the large joints. It produces stiffness, pain, and progressive joint damage.
  • Oral psoriasis may present with whitish lesions on the oral mucosa, which may appear to change in severity daily. It may also present as severe cheilosis with extension onto the surrounding skin, crossing the vermillion border.

Causes

  • Psoriatic lesions are caused by an increase in the turnover rate of epidermal cells from the normal 23 days to 3-5 days.
  • The surface of psoriatic lesions often has a layer of dead skin cells that appear as silver scales.
  • Patients with psoriasis have a genetic predisposition for the disease.
    • The gene locus is determined.
    • The triggering event may be unknown in most cases, but it is likely immunologic.
    • The first lesion commonly appears after an upper respiratory infection.
  • Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.
  • Autoimmune function
    • Evidence suggests that psoriasis is an autoimmune disease.
    • Studies show high levels of dermal and circulating TNF-alpha. Treatment with TNF-alpha inhibitors is often successful.
    • Psoriatic lesions are associated with increased activity of T cells in the underlying skin.
    • Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.
  • Superantigens and T cells
    • Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups.
    • Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.
  • Also, of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. 
    • Paradoxical as leading hypothesis on the pathogenesis of psoriasis support T-cell hyperactivity, in addition to the fact that treatments geared to reduce T-cell counts help reduce psoriasis severity. 
    • Possibly explained by decreased CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis.
    • HIV genome may directly drive keratinocyte proliferation.
    • HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

More on Psoriasis

Overview: Psoriasis
Differential Diagnoses & Workup: Psoriasis
Treatment & Medication: Psoriasis
Follow-up: Psoriasis
Multimedia: Psoriasis
References

References

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Further Reading

Keywords

psoriasis, skin itching, itchy skin, scaly skin, psoriasis treatment, psoriasis symptoms, discoid psoriasis, plaque psoriasis, guttate psoriasis, skin disorder, skin lesions, oral psoriasis, nail psoriasis, psoriatic arthritis, scalp psoriasis, erythrodermic psoriasis, pustular psoriasis, inverse psoriasis

Contributor Information and Disclosures

Author

Richard Gordon Jr, MD, Staff Physician, Department of Emergency Medicine, Detroit Receiving Hospital University Health Center
Richard Gordon Jr, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, American Medical Student Association/Foundation, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Adam J Rosh, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Dana A Stearns, MD, Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital
Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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