eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriasis, Guttate

Author: Cary Chisholm, MD, Resident Physician, Department of Pathology, Texas A&M Health Science Center College of Medicine
Coauthor(s): Daniel D Bennett, MD, Assistant Professor, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine; Senior Staff, Department of Dermatology, Scott and White Memorial Hospital
Contributor Information and Disclosures

Updated: Jan 15, 2010

Introduction

Background

Guttate psoriasis is a clinical presentation characterized by a distinctive, acute eruption of small, droplike, 1-10 mm in diameter, salmon-pink papules, usually with a fine scale, as demonstrated in the images below.

The distinctive, acute clinical presentation of a...

The distinctive, acute clinical presentation of an eruption or guttate psoriasis characterized by small, droplike, 1-10 mm in diameter, salmon-pink papules, usually with a fine scale. Courtesy of Hon Pak, MD.

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The distinctive, acute clinical presentation of a...

The distinctive, acute clinical presentation of an eruption or guttate psoriasis characterized by small, droplike, 1-10 mm in diameter, salmon-pink papules, usually with a fine scale. Courtesy of Hon Pak, MD.


 

Guttate psoriasis. Courtesy of Hon Pak, MD.

Guttate psoriasis. Courtesy of Hon Pak, MD.

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Guttate psoriasis. Courtesy of Hon Pak, MD.

Guttate psoriasis. Courtesy of Hon Pak, MD.


 

Note characteristic lesions consisting of multipl...

Note characteristic lesions consisting of multiple, discrete, droplike papules with a salmon-pink hue. A fine scale, which is usually absent in early-stage lesions, may be appreciated on the more established ones. Courtesy of Hon Pak, MD.

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Note characteristic lesions consisting of multipl...

Note characteristic lesions consisting of multiple, discrete, droplike papules with a salmon-pink hue. A fine scale, which is usually absent in early-stage lesions, may be appreciated on the more established ones. Courtesy of Hon Pak, MD.


This variant of guttate psoriasis primarily occurs on the trunk and the proximal extremities, but it may have a generalized distribution. New guttate psoriasis lesions develop during the first month of disease, they remain stable during the second month, and the remission begins during the third month.1 The word guttate is derived from the Latin word gutta, meaning drop.
 
Guttate psoriasis is more common in individuals younger than 30 years, and a history of upper respiratory tract infection secondary to group A beta-hemolytic streptococci (eg, Streptococcus pyogenes) often precedes the eruption by 2-3 weeks.2 Streptococcal perianal dermatitis, a superficial bacterial infection of the anus and perianal skin in children, has also been linked with the appearance of guttate psoriasis.3,4 Although episodes may recur, especially those due to pharyngeal carriage of streptococci, isolated bouts have also been described. The sudden appearance of the papular lesions in response to streptococcal infection may be either the first manifestation of psoriasis in a previously unaffected individual or an acute exacerbation of long-standing plaque psoriasis. Uncommonly, guttate psoriasis may be chronic in nature and/or arise in the absence of preceding streptococcal infection.

Other eMedicine articles on psoriasis include Psoriasis, Plaque; Psoriasis, Nails; Psoriasis, Pustular; Psoriatic Arthritis; and Psoriasis (Ophthalmology).

Pathophysiology

The exact pathophysiologic mechanism in guttate psoriasis is undetermined. Guttate psoriasis is believed to result from an immune reaction triggered by a previous streptococcal infection in a genetically susceptible host.

Studies indicate the importance of chromosome 6 in determining the resultant psoriatic phenotype. HLA-Cw*0602–positive patients are more prone to develop the guttate form. Interactions of the HLA-C with killer immunoglobulin–like receptors (KIR) on natural killer cells or natural killer T cells can be deregulated by streptococcal infection. T lymphocytes and cytokines are believed to cause the characteristic inflammatory changes appreciated on histopathologic examination of lesional skin samples. An autoimmune phenomenon has also been postulated for guttate psoriasis because some streptococcal products and components have been found to cross-react with normal human epidermis.5,6 Electron microscopic studies of guttate psoriasis have shown that mast cell degranulation is an early and constant feature in the evolution of guttate psoriatic lesions.

Frequency

United States

The guttate form of psoriasis is relatively uncommon, occurring in less than 2% of the psoriatic population.

International

Surveys on the occurrence of the guttate form of psoriasis among patients with psoriasis range widely from 1.6-44%. A 2009 study has shown that the prevalence of psoriasis correlates with the distribution and mortality of streptococcal epidemics.7

Mortality/Morbidity

Guttate psoriasis is a nonfatal eruption that either can run a limited course over several weeks to a few months or can develop into the chronic plaque-type of psoriasis. Scarring is not a problem. Previously affected areas may show postinflammatory hypopigmentation or postinflammatory hyperpigmentation.

Race

Guttate psoriasis affects people of all races. 

Sex

In guttate psoriasis, both sexes are affected equally.

Age

The average age of psoriasis onset usually is the third decade of life.8 Guttate psoriasis is the second most common psoriasis variant in children.9

Clinical

History

  • The onset of the guttate psoriasis skin lesions often is acute, with multiple papules erupting on the trunk and the proximal extremities. The lesions are often accompanied by slight pruritus.
  • In most cases of guttate psoriasis, a history of an antecedent streptococcal infection, usually of the upper respiratory tract, such as pharyngitis or tonsillitis, 2-3 weeks prior to the eruption can be elicited.10,11
  • Perianal streptococcal infections, which often present with chronic pruritus of the anus in children, have also been associated with guttate psoriasis.3,4
  • Multiple other infectious agents have been implicated, although episodes of guttate psoriasis attributed to them are not as frequent as those attributed to streptococci. Associated organisms include the following: 
    • Bacteria -Staphylococcus aureus
    • Fungi -Malassezia, Candida
    • Viruses – Human papillomavirus (HPV), retroviruses, human endogenous retroviruses (HERVs)12
  • Drug therapy, including biologic agents, may sometimes precipitate a guttate-type flare. The most commonly implicated medications include lithium, beta-blockers, antimalarial drugs, and nonsteroidal anti-inflammatory drugs.12 Immunomodulatory drugs such as infliximab, etanercept, imatinib, and adalimumab have also been reported to cause guttate psoriasis.13,14,15
  • A positive family history of psoriasis may be present.16

Physical

  • Examination of the skin reveals characteristic lesions consisting of multiple, discrete, 1-10 mm in diameter, droplike papules with a salmon-pink hue. A fine scale, which is usually absent in early-stage lesions, may be appreciated on the more established ones, as shown in the image below.

  • Note characteristic lesions consisting of multipl...

    Note characteristic lesions consisting of multiple, discrete, droplike papules with a salmon-pink hue. A fine scale, which is usually absent in early-stage lesions, may be appreciated on the more established ones. Courtesy of Hon Pak, MD.

    [ CLOSE WINDOW ]
    Note characteristic lesions consisting of multipl...

    Note characteristic lesions consisting of multiple, discrete, droplike papules with a salmon-pink hue. A fine scale, which is usually absent in early-stage lesions, may be appreciated on the more established ones. Courtesy of Hon Pak, MD.

  • Beginning on the trunk and the proximal extremities, the lesions may sometimes spread to involve the face, the ears, and the scalp.
  • The palms and the soles are rarely affected in guttate psoriasis.
  • Nail changes in the form of pits, ridges, and the oil-drop sign, which are characteristic of chronic psoriasis, may be absent.
  • Additional findings may include pharyngeal or perianal erythema in cases associated with acute streptococcal infections. Ledoux et al emphasize a careful examination, including the perianal region, in children being examined for guttate psoriasis.4

Causes

  • Genetic predisposition
    • As in other types of psoriasis, genetic predisposition seems to play an important role in the development of an acute guttate psoriasis flare.17
    • Compared with control populations, a significant excess of HLA-BW17 has been found in patients with guttate psoriasis. Others have found an increase in HLA-B13 positivity. Moreover, the inability to produce normal amounts of antibody to streptolysin-O by HLA-B13–positive individuals might explain their high prevalence of guttate psoriasis.
    • Interestingly, an increased prevalence of HLA-Cw6*0602 has also been found, and these patients experience psoriasis at markedly higher rates than control subjects.18,19
    • Thus far, psoriasis is the only disease associated with HLA-C gene expression.5 HLA-B*57 and DRB1*07 have also been detected with increased frequency in psoriasis patients.20
    • Proteomic and immunohistochemistry studies have been able to demonstrate that guttate psoriasis and chronic plaque psoriasis are phenotypically distinguishable in their protein expression patterns.21,22
  • Streptococcal infection in guttate psoriasis
    • The association of guttate psoriasis with streptococcal infection has been recognized for more than 50 years. As many as 80% of patients with guttate psoriasis have clinical or laboratory evidence of streptococcal infection, usually in the form of tonsillopharyngitis.23
    • The ability of the streptococcal organism to trigger an eruption is not serotype specific. The serotypes present in patients with guttate psoriasis are similar to those seen in the general population. A number of cases of guttate psoriasis in children have also been triggered by streptococcal perianal cellulitis. Presumably, absorption of streptococci by-products produced by the streptococci occurs across the rectal mucosa, as with pharyngeal infections.
    • Unfortunately, although the association is definite, details regarding the exact mechanism by which streptococcal infection influences the actual formation of the psoriatic lesions are still largely theoretical.
    • Aside from group A streptococci, Lancefield groups C and G streptococci have also been related to guttate psoriasis.24,25 Although specific Lancefield groups have been associated with psoriasis, no association with any specific M serotype has been discovered.
    • Lotus et al demonstrated that guttate psoriasis patients expressing the HLA-Cw*0602 allele were twice as likely to have positive streptococcal throat cultures.6
  • Role of T lymphocytes in guttate psoriasis26
    • Histologic studies of early-stage psoriatic skin lesions reveal that the activation of T lymphocytes, endothelial cells, and macrophages precedes epidermal proliferation. The increased proliferation of the epidermal layer characteristic of psoriasis might be induced by activated T lymphocytes via the production of cytokines. Indeed, group A streptococcal antigen–specific T lymphocytes, which secrete high levels of gamma interferon, can be consistently isolated from guttate psoriatic skin lesions.
    • Consistent with the role of T lymphocytes is the concept of superantigenic stimulation by certain streptococcal components or products. Examples of superantigens produced by group A beta-hemolytic streptococci are streptococcal pyogenic exotoxins (SPE) types A, B, and C; a 22-kd pepsin fragment of M type-5 protein; S pyogenes– derived cytoplasmic membrane–associated protein (CAP); and secretion-type CAP (SCAP).27
    • In general, unlike a conventional peptide antigen, a superantigen stimulates T cells almost solely through the beta variable (Vß) portion of the T-cell receptor and induces an expansion of both CD4+ and CD8+ T cells. Therefore, an increased representation of Vß2+ T lymphocytes, such as that in both the epidermis and the dermis of guttate psoriatic lesions, compared with that of lymphocytes from the peripheral blood of the same patients and lymphocytes in normal skin strongly suggests that T-cell stimulation by a superantigen is probably involved.28
    • It appears that patients with guttate psoriasis respond to group A streptococcal antigen presentation in the same way as nonpsoriatic patients, but the magnitude of their response it much greater.2
  • Role of autoantibodies in guttate psoriasis24,29
    • Immunoblotting has demonstrated intense antistreptococcal antibody activity in the sera of patients with guttate psoriasis. Immunoglobulin G (IgG) antibodies against 3 different S pyogenes proteins, namely, a 60-, a 70-, and a 14-kd antigen, have been identified. Indirect immunofluorescence studies of these antibodies showed that they only react with autologous skin in patients with guttate psoriasis and not with normal skin or lesional skin from patients who do not have psoriasis.
    • Autoantibodies in psoriatic sera may recognize certain structures in the transformed keratinocytes of affected psoriatic skin. These autoantibodies cross-react with streptococcal antigens, and it has been demonstrated on immunofluorescent microscopy by using a monoclonal antibody (mAb 111-15504) to group A streptococci, which does not cross-react with antigens in normal human skin. These antigens were associated with class 1M protein and were mostly concentrated in the dermal papillae around the capillaries and inside the cells of the epidermal basal layer.
  • Drugs: Tumor necrosis factor blocker therapy has been associated with the development or worsening of guttate psoriasis.13,14,15,30

More on Psoriasis, Guttate

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

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Further Reading

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Keywords

psoriasis, guttate psoriasis, perianal streptococcal infection, Streptococcus pyogenes, S pyogenes, upper respiratory tract infection, URTI

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Contributor Information and Disclosures

Author

Cary Chisholm, MD, Resident Physician, Department of Pathology, Texas A&M Health Science Center College of Medicine
Cary Chisholm, MD is a member of the following medical societies: American Medical Association, College of American Pathologists, and Texas Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel D Bennett, MD, Assistant Professor, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine; Senior Staff, Department of Dermatology, Scott and White Memorial Hospital
Daniel D Bennett, MD is a member of the following medical societies: American Academy of Dermatology, American Contact Dermatitis Society, American Medical Association, Dermatology Foundation, National Psoriasis Foundation, Society for Investigative Dermatology, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Mark G Lebwohl, MD, Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Abbott Laboratories Honoraria Consulting; Actelion Honoraria Consulting; Amgen Honoraria Consulting; Astellas Honoraria Consulting; Centocor Honoraria Consulting; DermiPsor Honoraria Consulting; Galderma  Consulting; Genentech Honoraria Consulting; Helix BioMedix Honoraria Consulting; Medicis Honoraria Investigator

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Christen M Mowad, MD, Associate Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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