eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriasis, Guttate

Author: Charles R Taylor, MD, Assistant Professor of Dermatology, Harvard Medical School; Director of Phototherapy Unit, Department of Dermatology, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Aug 3, 2009

Introduction

Background

Guttate psoriasis refers to a distinctive, acute clinical presentation of an eruption characterized by small, droplike, 1-10 mm in diameter, salmon-pink papules, usually with a fine scale (see Media Files 1-3). The word guttate is derived from the Latin word gutta, meaning drop. This variant primarily occurs on the trunk and the proximal extremities, but it may have a generalized distribution.

More common in individuals younger than 30 years, a history of upper respiratory infection secondary to group A beta-hemolytic streptococci (eg, Streptococcus pyogenes) often precedes the eruption by 2-3 weeks. Although recurrent episodes may occur, especially those due to pharyngeal carriage of streptococci, isolated bouts are known to occur. The sudden appearance of the papular lesions may be either the first manifestation of psoriasis in a previously unaffected individual or an acute exacerbation of long-standing plaque psoriasis. On the other hand, guttate psoriasis may be chronic and unrelated to a streptococcal infection.

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

Pathophysiology

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

Recent 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 because some streptococcal products and components have been found to cross-react with normal human epidermis. Electron microscopic studies 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 eruption among patients with psoriasis range widely from 1.6-44%.

Mortality/Morbidity

Guttate psoriasis is a nonfatal eruption that either can run a limited course over several weeks to a few months or 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

Guttate psoriasis is more common in individuals younger than 30 years, and it is generally believed to be the type of psoriasis most likely to affect children and adolescents.

Clinical

History

• 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.
• Perianal streptococcal infections or viral infections, such as varicella, rubella, and roseola, have also been postulated as provocative factors, especially in children.
• A positive family history of psoriasis may be present.
• The onset of the guttate psoriasis skin lesions is often acute, with multiple papules erupting on the trunk and the proximal extremities. The lesions are often accompanied by slight pruritus.
• Drug therapy, including biologic agents, may sometimes precipitate a guttate-type flare.

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 (see Media File 3).

• 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.
• 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.¹ Ledoux et al emphasize a careful examination, including the perianal region, in children being examined for guttate psoriasis.²

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. 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 the high prevalence in guttate psoriasis. Interestingly, an increased prevalence of HLA-CW6 has also been found.³ Thus far, psoriasis is the only disease associated with HLA-C gene expression.⁴ Proteomic studies have been able to demonstrate that guttate psoriasis and chronic plaque psoriasis are phenotypically distinguishable in their protein expression patterns.⁵
• Streptococcal infection in guttate psoriasis⁶
  • 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. Aside from group A streptococci, groups C and G streptococci have also been related to guttate psoriasis.
  • 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.
• Role of T lymphocytes in guttate psoriasis⁷
  • Histologic studies of early-stage psoriatic skin lesions revealed 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).⁸
  • 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.
• Role of autoantibodies in guttate psoriasis⁹
  • 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.^10,11

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