Guttate Psoriasis
No Results
No Results
processing….
Guttate psoriasis is characterized by the acute onset of small, 1-10 mm diameter, droplike, erythematous-to-salmon-pink papules, usually with a fine scale, [1] as demonstrated in the images below.
See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.
This variant of psoriasis primarily occurs on the trunk and the proximal extremities, but it may have a generalized distribution. Lesions usually spread centripetally and are monomorphic. New guttate psoriasis lesions continue to develop during the first month of disease; they remain stable during the second month, and the remission begins during the third month. [2] The word guttate is derived from the Latin word gutta, meaning drop.
Guttate psoriasis is more common in individuals younger than 30 years. An upper respiratory tract infection from group A beta-hemolytic streptococci (eg, Streptococcus pyogenes) often precedes the eruption by 2-3 weeks. [3] 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. [4, 5]
Although episodes may recur, especially those due to pharyngeal carriage of streptococci, isolated bouts have commonly been described. Generally, the disease is self-limiting, but a certain percentage of cases progress to chronic plaque psoriasis.
The sudden appearance of the papular lesions in response to streptococcal infection could either be 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.
For more information, go to Psoriasis.
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. [6]
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 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 lesions. [7]
Psoriasis was originally classified as a Th1 disease, but Th17 cells have also been recognized to have an important role. Studies are also proposing a role for antimicrobial peptides and dendritic cells in the pathogenesis of psoriasis. Cathelicidin LL-37 is especially thought to lead to activation of dendritic cells, inducing production of interferons. Elevated levels of the cathelicidin LL-37 have been reported in patients with plaque and guttate psoriasis compared with healthy controls. [8, 9] Levels of inflammatory cytokines interleukin (IL)‒1RA, IL-2, IL-23, and interferon (IFN)‒gamma were also elevated in these patients. There was no significant difference in serum levels of inflammatory cytokines and LL-37 between the plaque type and guttate psoriasis group, but a positive correlation between disease activity and cytokine levels was noted. [8]
An autoimmune phenomenon has also been postulated to underlie guttate psoriasis because some streptococcal products and components have been found to cross-react with normal human epidermis. [10, 11] 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. Furthermore, Langerhans cell migration appears to be impaired during an acute episode of guttate psoriasis. [12]
The guttate form of psoriasis is relatively uncommon in the United States, occurring in less than 2% of the psoriatic population. International surveys on the guttate form of psoriasis among patients with psoriasis have found a wide range of prevalences, from 1.6-44%. A 2009 study has shown that the prevalence of psoriasis correlates with the distribution and mortality of streptococcal epidemics. [13]
Guttate psoriasis affects people of all races and affects males and females equally.
Guttate psoriasis is the second most common psoriasis variant in children. [14, 15]
The onset of the guttate psoriasis skin lesions often is acute, with multiple papules erupting on the trunk and the proximal extremities, in a centripetal fashion. 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 (eg, pharyngitis or tonsillitis), 2-3 weeks prior to the eruption can be elicited. [16, 17] Perianal streptococcal infections, which often present as chronic pruritus of the anus in children, have also been associated with guttate psoriasis. [4, 5]
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), varicella-zoster virus, [18] retroviruses, human endogenous retroviruses (HERVs) [19]
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. [19] Immunomodulatory drugs such as antiprogrammed cell death-1 (PD-1) inhibitors, infliximab, etanercept, imatinib, and adalimumab have also been reported to cause guttate psoriasis. [20, 21, 22, 23]
A positive family history of psoriasis may be present, and the outcome is generally good. [24, 25]
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.
The lesions of guttate psoriasis appear first on the trunk and the proximal extremities, progressing in a centripetal fashion. Lesions are commonly monomorphic and at the same stage of evolution. They 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. Ledoux et al emphasize a careful examination, including the perianal region, in children being examined for guttate psoriasis. [5]
The etiology of guttate psoriasis is not well understood. Genetic as well as environmental factors have been implicated in its pathogenesis.
As in other types of psoriasis, genetic predisposition seems to play an important role in the development of an acute guttate psoriasis flare. [26]
Compared with control populations, a significant excess of HLA-BW17 has been found in patients with guttate psoriasis. Other researchers 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. These patients experience psoriasis at markedly higher rates than control subjects. [27, 28]
Thus far, psoriasis is the only disease associated with HLA-C gene expression. [10] HLA-B*57 and DRB1*07 have also been detected with increased frequency in psoriasis patients. [29]
Proteomic and immunohistochemistry studies have demonstrated that guttate psoriasis and chronic plaque psoriasis are phenotypically distinguishable in their protein expression patterns. [30, 31]
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. [32]
The streptococcal serotypes in these patients are similar to those seen in the general population. Aside from group A streptococci, Lancefield groups C and G streptococci have also been related to guttate psoriasis. [33, 34] Although specific Lancefield groups have been associated with psoriasis, no association with any specific M serotype has been discovered.
A number of cases in children have also been triggered by streptococcal perianal cellulitis. Presumably, absorption of streptococcal by-products occurs across the mucosa, as with pharyngeal infections.
Unfortunately, although the association is definite, details regarding the exact mechanism by which streptococcal infection influences the formation of the psoriatic lesions are still largely theoretical.
Lotus et al demonstrated that guttate psoriasis patients expressing the HLA-Cw*0602 allele were twice as likely to have positive streptococcal throat cultures. [11]
Histologic studies of early-stage psoriatic skin lesions reveal that the activation of T lymphocytes, endothelial cells, and macrophages precedes epidermal proliferation. [35] 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). [36]
In general, unlike a conventional peptide antigen, a superantigen stimulates T cells almost solely through the beta variable (Vβ) portion of the T-cell receptor and induces an expansion of both CD4+ and CD8+ T cells. Therefore, an increased representation of Vβ2+ 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. [37]
It appears that patients with guttate psoriasis respond to group A streptococcal antigen presentation in the same way as nonpsoriatic patients. However, the magnitude of their response is much greater. [3]
The fungus Malassezia furfur has been associated with the appearance of psoriatic lesions, but a causative role has not been proven. A study by Aydogan et al showed that the prevalence of M furfur was similar in patients with psoriasis and those without. However, in psoriatic patients with M furfur, cytokines important in the regulation of helper T-lymphocytes (Th2 cells), such as IL-4, IL-10, and IL-13, were markedly downregulated as compared to normal controls and psoriatic patients without M furfur. Thus, cytokine dysregulation appears to be important in the development of psoriasis in this patient population. [38]
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 react only with autologous skin in patients with guttate psoriasis and not with normal skin or lesional skin from patients who do not have psoriasis. [33, 39]
Autoantibodies in psoriatic sera may recognize certain structures in the transformed keratinocytes of affected psoriatic skin. These autoantibodies cross-react with streptococcal antigens. Cross-reaction 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.
Epidermal Langerhans cell migration is inhibited in early-onset, plaque-type psoriasis. Altered Langerhans cell migration has recently also been demonstrated in patients with guttate psoriasis. A small study revealed decreased migration compared with healthy controls. In patients with resolved guttate psoriasis, the epidermal Langerhans cell migration was normal. [12]
Over the past years, concerns have been raised about vaccination as a possible trigger for new onset of psoriasis or exacerbation of existing disease. Several small studies have reported an association between influenza vaccination in the 2009-2010 flu season and psoriasis. Most cases presented as mixed/guttate psoriasis. [40] More studies are necessary for further evaluation, but a study by Sbidian et al suggested a very low incidence of associated cases and emphasized the relative safety and relevance of vaccinations. [41]
Tumor necrosis factor blocker therapy has been associated with the development or worsening of guttate psoriasis. [20, 21, 22, 42]
A careful history should be taken to exclude certain drugs, such as beta-blockers and lithium, which may cause an eruption similar to that of guttate psoriasis. Viral exanthema should also be considered.
Especially in patients with palmar and plantar lesions, serologic analysis should be performed to exclude secondary syphilis. Skin biopsy is probably the single most useful diagnostic test if the clinical diagnosis is not certain.
Histopathologic findings and severity do not correlate with the clinical severity or the Psoriasis Severity Index. [43]
The differential diagnosis of guttate psoriasis includes the following:
Levels of antibodies to streptolysin O, hyaluronidase, and deoxyribonuclease B may be elevated in more than half the patients with guttate psoriasis. Significant elevations of antistreptococcal M6 protein have been documented. Routine screening in asymptomatic patients is controversial. Patients with symptoms suggestive of a streptococcal infection should undergo appropriate laboratory testing.
A bacteriologic culture of the throat or the perianal area may be helpful to isolate the organism in selected cases. Throat culture continues to be the criterion standard to diagnose streptococcal pharyngitis.
Urine results are usually negative. Detection of blood and protein on urinalysis could suggest a rare case associated with a concomitant poststreptococcal acute glomerulonephritis. However, reported cases have failed to prove association of psoriasis and poststreptococcal renal disease. [44]
Because the clinical appearance is so characteristic, biopsy is seldom necessary to confirm the diagnosis of guttate psoriasis. Histopathologic changes may not be diagnostic when samples of early-stage papules are obtained at biopsy.
The epidermis shows hyperplasia and small foci of parakeratosis with an absence of the granular layer. Dermal changes consisting of capillary dilatation and edema may be more pronounced, and an infiltrate consisting of lymphocytes and macrophages is seen mostly in the upper dermis. A few polymorphonuclear leukocytes may be found at all levels. Early lesions exhibit more inflammation and less acanthosis, and very early lesions can show normal basket-weave orthokeratosis overlying parakeratotic changes.
In fully developed guttate lesions, vacuolated keratinocytes eventually disappear, leaving areas of agranulosis with overlying parakeratosis. Degenerated polymorphonuclear leukocytes on an otherwise orthokeratotic stratum corneum may be the earliest presentation of Munro microabscesses.
The term squirting papillae has been used to describe a phenomenon wherein neutrophils are discharged from the papillary capillaries, resulting in collections of neutrophils in association with parakeratotic mounds, as demonstrated in the image below. In some cases, marked exudation may lead to the formation of the highly diagnostic spongiform pustule of Kogoj, which is seen in psoriasiform variants. [15, 45] (See the images below regarding histologic findings.)
Histopathologic findings and severity do not correlate with the clinical severity or Psoriasis Severity Index. [43]
Usually, guttate psoriasis spontaneously resolves within a few weeks to months without treatment. In general, there is no firm consensus on specific treatment algorithms. [46]
As in other conditions, the choice of treatment should be tailored to the individual. Should guttate psoriasis result as a reaction to a new medication, removal of the offending medication may be warranted if other treatments do not ameliorate the symptoms.
Simple reassurance and emollients may be sufficient care. Topical steroids can be effective but their application can be cumbersome, especially when the eruption is extensive, as it is in most cases of guttate psoriasis.
A guideline summary from the American Academy of Dermatology, Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics, may be helpful. [47]
Topical corticosteroids are a critical addition to the successful treatment of many guttate psoriasis patients. The mechanisms believed to provide benefit include anti-inflammatory, antiproliferative, immunosuppressive, and vasoconstrictive effects.
Seven potency classes of corticosteroids exist, and the agent prescribed should be selected from a class appropriate to the location of disease. Lower-potency corticosteroids should be used for face and intertriginous areas, areas of thinned skin, and on infants. Higher-potency corticosteroids are generally acceptable in adults with lesions elsewhere on the body. Thick plaques may require therapy with the most potent corticosteroids. [48]
Because of the clear association with streptococcal infection seen in most cases of guttate psoriasis, laboratory testing in patients with a known history or symptoms suggestive of streptococcal infections and antibiotic therapy have been proposed. [49]
However, the efficacy of antibiotics in the management of psoriasis has been questioned and data are limited. [44] Dogan et al and Owen et al found no statistically significant improvement in streptococcal guttate psoriasis after treatment with penicillin or erythromycin or with no treatment. [50, 51] Nevertheless, some experts have used empiric antimicrobial therapy in streptococcal-related guttate psoriasis, with the following agents [52] :
Cephalexin (Keflex)
Amoxicillin
Penicillin VK
Erythromycin
Rifampin
Azithromycin, which is commonly prescribed for community-acquired pneumonia, is likewise an option.
The clearance of guttate lesions can be accelerated by judicious exposure to sunlight or by a short course of either broadband ultraviolet B (UV-B) or narrow-band UV-B phototherapy. [53, 54, 55] Koek et al reported that UV-B phototherapy administered to psoriasis patients in home-based setting was as effective as that administered as an outpatient treatment, with significantly lower patient burden. [56]
More resistant cases may benefit from oral psoralen plus exposure to ultraviolet A radiation (PUVA). The suit PUVA technique has been used in this setting. [53]
Aside from the usual mechanisms by which UV light is believed to exert its beneficial effects in psoriasis, a specific fibrosing response to PUVA via increased mast cell activation has been observed in guttate psoriasis and might underlie the mechanism of action behind UV-induced resolution of the lesions.
However, considering the developments in photomedicine over the last several years, particularly regarding the clinical efficacy of narrowband UV-B phototherapy, versus the risk of cutaneous malignancies with PUVA, treatment with narrowband UV-B is favored over treatment with PUVA.
Vitamin D analogues are also used for psoriasis. Randomized, placebo-controlled and double-blind studies have shown a marked improvement in disease as compared with response to other treatments. [48] Other therapies that have been reported in the literature include fish oil–derived n -3 fatty acid infusion, topical retinoids, and tar. [46, 48]
Should guttate psoriasis prove resistant to the above therapies, it may develop into a chronic plaque psoriasis, which may require systemic treatment with medications such as cyclosporine, acitretin, methotrexate, or a biologic agent.
Although unproven by large controlled clinical trials, tonsillectomy for patients with recurrent or chronic guttate psoriasis associated with poststreptococcal tonsillitis may be considered. [57, 58, 59]
Physicians should watch for possible hypersensitivity reactions to the above-mentioned antimicrobials, especially to penicillin. If hypersensitivity is suspected, the drug should be immediately discontinued. Patients who are hypersensitive to penicillin generally do well on erythromycin. Cephalosporins can also cover streptococci, but some cross-sensitivity with penicillins has been documented.
Areas of the skin that have been treated with high-potency topical steroids for long periods may show some atrophy, telangiectases, and hypopigmentation. Shifting to a preparation with a lower potency or to another treatment modality should be considered.
Patients on PUVA may experience a number of adverse effects, such as nausea and vomiting. These effects are sometimes remedied by taking psoralen pills after a meal. The psoralen-induced photosensitivity persists up to 24 hours after administration of the drug. Patients should be adequately informed about the need to wear protective lenses and to avoid sun exposure during this period.
Patients should be advised to minimize all forms of skin trauma, such as scratching or vigorous rubbing, which may lead to new psoriatic lesions on previously unaffected areas (Koebner phenomenon).
Patients should be advised to seek medical attention promptly for sore throat and other possible streptococcal infections. Early detection and treatment of such infections may prevent an acute flare of the skin disease.
For patient education information, see the Psoriasis Center, as well as Guttate Psoriasis, What Is Psoriasis?, Types of Psoriasis, Understanding Psoriasis Medications, and Nail Psoriasis.
Guttate psoriasis is a nonfatal eruption that either can run a limited course over several weeks to a few months, may recur, 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.
Data available on the prognosis of guttate psoriasis are sparse. Although guttate psoriasis often has a short-lived course, it may also represent the initial stage of chronic plaque-type psoriasis. Progression rates to chronic plaque psoriasis, reported in small studies, have ranged from one third to approximately two thirds (68%) of patients with gutatte psoriasis. [60, 61]
In a study of 15 patients, the probability of an individual developing chronic psoriasis within 10 years of a single episode of acute guttate psoriasis was suggested to be about 1 in 3, although further studies with larger numbers of patients are needed to more accurately determine the risk. [60]
Like other forms of psoriasis, guttate psoriasis tends to improve during the summer and worsen during the winter. Once an episode of acute guttate psoriasis has cleared, many patients will have limited or no evidence of psoriasis for prolonged periods.
Overview
What is the pathophysiology of guttate psoriasis?
What is the prevalence of guttate psoriasis in the US?
What are the demographic predilections in the prevalence of guttate psoriasis?
What are the signs and symptoms of guttate psoriasis?
Which organisms are associated with guttate psoriasis?
What are medical causes of guttate psoriasis?
Which physical findings are characteristic of guttate psoriasis?
What causes guttate psoriasis?
What is the role of genetics in the etiology of guttate psoriasis?
What is the role of streptococcal infection in the etiology of guttate psoriasis?
What is the role of T lymphocytes in the pathophysiology of guttate psoriasis?
What is the role of autoantibodies in the pathophysiology of guttate psoriasis?
What are implications of immunologic changes in the etiology of guttate psoriasis?
What is the role of vaccines in the etiology of guttate psoriasis?
What is the role of tumor necrosis factor blockers in the etiology of guttate psoriasis?
How is guttate psoriasis diagnosed?
What is included in the differential diagnoses of guttate psoriasis?
What is the role of serology in the evaluation of guttate psoriasis?
What is the role of culture in the diagnosis of guttate psoriasis?
What is the role of urinalysis in the evaluation of guttate psoriasis?
What are histologic features of guttate psoriasis?
What are the treatment options for guttate psoriasis?
What is the role of corticosteroids in the management of guttate psoriasis?
What is the role of lab testing in the management of guttate psoriasis?
What is the role of empiric antimicrobial therapy in the treatment of guttate psoriasis?
What is the role of phototherapy in the management of guttate psoriasis?
What is the role of vitamin D in the management of guttate psoriasis?
When are systemic medications indicated for the treatment of guttate psoriasis?
What is the role of surgery in the treatment of guttate psoriasis?
What are complications associated with guttate psoriasis?
What is included in patient education about guttate psoriasis?
What is the prognosis of guttate psoriasis?
Vence L, Schmitt A, Meadows CE, Gress T. Recognizing Guttate Psoriasis and Initiating Appropriate Treatment. W V Med J. 2015 Jul-Aug. 111 (4):26-8. [Medline].
Baker BS, Powles AV, Fry L. A possible role for vaccination in the treatment of psoriasis?. G Ital Dermatol Venereol. 2008. 143(2):105-117.
Nahary L, Tamarkin A, Kayam N, Sela S, Fry L, Baker B, et al. An investigation of antistreptococcal antibody responses in guttate psoriasis. Arch Dermatol Res. 2008 Sep. 300(8):441-9. [Medline].
Ulger Z, Gelenava T, Kosay Y, Darcan S. Acute guttate psoriasis associated with streptococcal perianal dermatitis. Clin Pediatr (Phila). 2007 Jan. 46(1):70-2. [Medline].
Ledoux M, Chazerain V, Saiag P, Mahe E. [Streptococcal perianal dermatitis and guttate psoriasis]. Ann Dermatol Venereol. 2009 Jan. 136(1):37-41. [Medline].
Shin MS, Kim SJ, Kim SH, Kwak YG, Park HJ. New Onset Guttate Psoriasis Following Pandemic H1N1 Influenza Vaccination. Ann Dermatol. 2013 Nov. 25(4):489-92. [Medline]. [Full Text].
Vanaki E, Ataei M, Sanati MH, Mansouri P, Mahmoudi M, Zarei F, et al. Expression patterns of Th1/Th2 transcription factors in patients with guttate psoriasis. Acta Microbiol Immunol Hung. 2013 Jun. 60(2):163-74. [Medline].
Hwang YJ, Jung HJ, Kim MJ, Roh NK, Jung JW, Lee YW, et al. Serum levels of LL-37 and inflammatory cytokines in plaque and guttate psoriasis. Mediators Inflamm. 2014. 2014:268257. [Medline].
Qian L, Chen W, Sun W, Li M, Zheng R, Qian Q, et al. Antimicrobial peptide LL-37 along with peptidoglycan drive monocyte polarization toward CD14(high)CD16(+) subset and may play a crucial role in the pathogenesis of psoriasis guttata. Am J Transl Res. 2015. 7 (6):1081-94. [Medline].
Holm SJ, Sakuraba K, Mallbris L, Wolk K, Stahle M, Sanchez FO. Distinct HLA-C/KIR genotype profile associates with guttate psoriasis. J Invest Dermatol. 2005 Oct. 125(4):721-30. [Medline].
Mallbris L, Wolk K, Sanchez F. HLA-Cw*0602 associates with a twofold higher prevalence of positive strepotococcal throat swab at the onset of psoriasis: a case control study. BMC Dermatol. 2009. 9:5.
Eaton LH, Chularojanamontri L, Ali FR, Theodorakopoulou E, Dearman RJ, Kimber I. Guttate psoriasis is associated with an intermediate phenotype of impaired Langerhans’ cell migration. Br J Dermatol. 2014 Mar 13. [Medline].
McFadden JP, Baker BS, Powles AV, Fry L. Psoriasis and streptococci: the natural selection of psoriasis revisited. Br J Dermatol. 2009 May. 160(5):929-37. [Medline].
Farber EM, Nall L. Epidemiology: Natural history and genetics. In: Roenigk HH, Maibach HI. Psoriasis. 1998. 3rd ed:
Krengel S, Schaumburg-Lever GM, Geilen CC, et al. Krengel S, Schaumburg-Lever GM, Geilen CC, et al. Psoriasis. 1998. 3rd:
Leung DY, Travers JB, Giorno R, Norris DA, Skinner R, Aelion J, et al. Evidence for a streptococcal superantigen-driven process in acute guttate psoriasis. J Clin Invest. 1995 Nov. 96(5):2106-12. [Medline]. [Full Text].
England RJ, Strachan DR, Knight LC. Streptococcal tonsillitis and its association with psoriasis: a review. Clin Otolaryngol Allied Sci. 1997 Dec. 22(6):532-5. [Medline].
Veraldi S, Lunardon L, Dassoni F. Guttate psoriasis triggered by chickenpox. G Ital Dermatol Venereol. 2009 Aug. 144(4):501-2. [Medline].
Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007 Nov-Dec. 25(6):606-15. [Medline].
Goiriz R, Dauden E, Perez-Gala S, Guhl G, Garcia-Diez A. Flare and change of psoriasis morphology during the course of treatment with tumour necrosis factor blockers. Clin Exp Dermatol. 2007 Mar. 32(2):176-9. [Medline].
Costa-Romero M, Coto-Segura P, Suarez-Saavedra S, et al. Guttate psoriasis induced by infliximab in a child with Crohn’s disease. Inflamm Bowel Dis. 2008. 14(10):1462-1463.
Cheng H, Geist DE, Piperdi M, Virk R, Piperdi B. Management of imatinib-related exacerbation of psoriasis in a patient with a gastrointestinal stromal tumour. Australas J Dermatol. 2009 Feb. 50(1):41-3. [Medline].
Yamamoto T. Anti-Programmed Cell Death-1-Induced Plaque and Guttate Psoriasis. Indian J Dermatol. 2018 Jan-Feb. 63 (1):88-89. [Medline].
Fan X, Yang S, Sun LD, Liang YH, Gao M, Zhang KY, et al. Comparison of clinical features of HLA-Cw*0602-positive and -negative psoriasis patients in a Han Chinese population. Acta Derm Venereol. 2007. 87(4):335-40. [Medline].
Pfingstler LF, Maroon M, Mowad C. Guttate psoriasis outcomes. Cutis. 2016 Feb. 97 (2):140-4. [Medline].
Zhang XJ, Zhang AP, Yang S, Gao M, Wei SC, He PP, et al. Association of HLA class I alleles with psoriasis vulgaris in southeastern Chinese Hans. J Dermatol Sci. 2003 Oct. 33(1):1-6. [Medline].
Fry L, Powles AV, Corcoran S, et al. HLA Cw*06 is not essential for streptococcal-induced psoriasis. Br J Dermatol. 2006. 154(5):850-853.
Gudjonsson JE, Karason A, Antonsdottir A, Runarsdottir EH, Hauksson VB, Upmanyu R, et al. Psoriasis patients who are homozygous for the HLA-Cw*0602 allele have a 2.5-fold increased risk of developing psoriasis compared with Cw6 heterozygotes. Br J Dermatol. 2003 Feb. 148(2):233-5. [Medline].
Atasoy M, Pirim I, Bayrak OF, Ozdemir S, Ikbal M, Erdem T, et al. Association of HLA class I and class II alleles with psoriasis vulgaris in Turkish population. Influence of type I and II psoriasis. Saudi Med J. 2006 Mar. 27(3):373-6. [Medline].
Carlen LM, Sanchez F, Bergman AC, Becker S, Hirschberg D, Franzen B, et al. Proteome analysis of skin distinguishes acute guttate from chronic plaque psoriasis. J Invest Dermatol. 2005 Jan. 124(1):63-9. [Medline].
Yazici AC, Karabulut AA, Ozen O, Eksioglu M, Ustun H. Expression of p53 in lesions and unaffected skin of patients with plaque-type and guttate psoriasis: a quantitative comparative study. J Dermatol. 2007 Jun. 34(6):367-74. [Medline].
Telfer NR, Chalmers RJ, Whale K, Colman G. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992 Jan. 128(1):39-42. [Medline].
Wilson AG, Clark I, Heard SR, Munro DD, Kirby JD. Immunoblotting of streptococcal antigens in guttate psoriasis. Br J Dermatol. 1993 Feb. 128(2):151-8. [Medline].
Gudjonsson JE, Thorarinsson AM, Sigurgeirsson B, Kristinsson KG, Valdimarsson H. Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study. Br J Dermatol. 2003 Sep. 149(3):530-4. [Medline].
Baker BS, Bokth S, Powles A, et al. Group A streptococcal antigen-specific T lymphocytes in guttate psoriatic lesions. Br J Dermatol. 1993. 128(5):493-499.
Villeda-Gabriel G, Santamaria-Cogollos LC, Perez-Lorenzo R, Reyes-Maldonado E, Saul A, Jurado-Santacruz F, et al. Recognition of Streptococcus pyogenes and skin autoantigens in guttate psoriasis. Arch Med Res. 1998 Summer. 29(2):143-8. [Medline].
Leung DY, Gately M, Trumble A, Ferguson-Darnell B, Schlievert PM, Picker LJ. Bacterial superantigens induce T cell expression of the skin-selective homing receptor, the cutaneous lymphocyte-associated antigen, via stimulation of interleukin 12 production. J Exp Med. 1995 Feb 1. 181(2):747-53. [Medline]. [Full Text].
Aydogan K, Tore O, Akcaglar S, Oral B, Ener B, Tunali S, et al. Effects of Malassezia yeasts on serum Th1 and Th2 cytokines in patients with guttate psoriasis. Int J Dermatol. 2012 Apr 18. [Medline].
Perez-Lorenzo R, Zambrano-Zaragoza JF, Saul A, Jimenez-Zamudio L, Reyes-Maldonado E, Garcia-Latorre E. Autoantibodies to autologous skin in guttate and plaque forms of psoriasis and cross-reaction of skin antigens with streptococcal antigens. Int J Dermatol. 1998 Jul. 37(7):524-31. [Medline].
Gunes AT, Fetil E, Akarsu S, Ozbagcivan O, Babayeva L. Possible Triggering Effect of Influenza Vaccination on Psoriasis. J Immunol Res. 2015. 2015:258430. [Medline].
Sbidian E, Eftekahri P, Viguier M, Laroche L, Chosidow O, Gosselin P, et al. National survey of psoriasis flares after 2009 monovalent H1N1/seasonal vaccines. Dermatology. 2014. 229 (2):130-5. [Medline].
Balato A, La Bella S, Gaudiello F, Balato N. Efalizumab-induced guttate psoriasis. Successful management and re-treatment. J Dermatolog Treat. 2008. 19(3):182-4. [Medline].
Kim BY, Choi JW, Kim BR, Youn SW. Histopathological findings are associated with the clinical types of psoriasis but not with the corresponding lesional psoriasis severity index. Ann Dermatol. 2015 Feb. 27 (1):26-31. [Medline].
Krishnamurthy K, Walker A, Gropper CA, Hoffman C. To treat or not to treat? Management of guttate psoriasis and pityriasis rosea in patients with evidence of group A Streptococcal infection. J Drugs Dermatol. 2010 Mar. 9(3):241-50. [Medline].
Mobini N, Toussaint S, Kamino H. Noninfectious erythematous, papular and squamous diseases. 10th ed. Lippincott-Raven Publishers; 2009. In: Lever’s Histopathology of the Skin:
Chalmers RJ, O’Sullivan T, Owen CM, Griffiths CE. A systematic review of treatments for guttate psoriasis. Br J Dermatol. 2001 Dec. 145(6):891-4. [Medline].
Menter A, Gottlieb A, Feldman SR, Van Voorhees AS, Leonardi CL, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008 May. 58(5):826-50. [Medline].
Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad Dermatol. 2009 Apr. 60(4):643-59. [Medline].
Rosenberg EW, Noah PW, Zanolli MD, Skinner RB Jr, Bond MJ, Crutcher N. Use of rifampin with penicillin and erythromycin in the treatment of psoriasis. Preliminary report. J Am Acad Dermatol. 1986 May. 14(5 Pt 1):761-4. [Medline].
Dogan B, Karabudak O, Harmanyeri Y. Antistreptococcal treatment of guttate psoriasis: a controlled study. Int J Dermatol. 2008 Sep. 47(9):950-2. [Medline].
Owen CM, Chalmers RJ, O’Sullivan T, Griffiths CE. A systematic review of antistreptococcal interventions for guttate and chronic plaque psoriasis. Br J Dermatol. 2001 Dec. 145(6):886-90. [Medline].
Baughman RD. Search for Streptococcus. Arch Dermatol. 1992 Jan. 128(1):103. [Medline].
Thappa DM, Laxmisha C. Suit PUVA as an effective and safe modality of treatment in guttate psoriasis. J Eur Acad Dermatol Venereol. 2006 Oct. 20(9):1146-7. [Medline].
Borroni G, Vignati G, Zaccone C, Gorani A, Brazzelli V, Rabbiosi G. Photofibrosis: a further histopathological change induced by PUVA therapy via the mast cell in guttate psoriasis. Preliminary report. Acta Derm Venereol Suppl (Stockh). 1994. 186:159-61. [Medline].
Fernández-Guarino M, Aboín-González S, Velázquez D, Barchino L, Cano N, Lázaro P. Phototherapy with Narrow-Band UVB in Adult Guttate Psoriasis: Results and Patient Assessment. Dermatology. 2016. 232 (5):626-632. [Medline].
Koek MB, Buskens E, van Weelden H, Steegmans PH, Bruijnzeel-Koomen CA, Sigurdsson V. Home versus outpatient ultraviolet B phototherapy for mild to severe psoriasis: pragmatic multicentre randomised controlled non-inferiority trial (PLUTO study). BMJ. 2009 May 7. 338:b1542. [Medline]. [Full Text].
Wilson JK, Al-Suwaidan SN, Krowchuk D, Feldman SR. Treatment of psoriasis in children: is there a role for antibiotic therapy and tonsillectomy?. Pediatr Dermatol. 2003 Jan-Feb. 20(1):11-5. [Medline].
Wu W, Debbaneh M, Moslehi H, Koo J, Liao W. Tonsillectomy as a treatment for psoriasis: a review. J Dermatolog Treat. 2014 Dec. 25(6):482-6. [Medline].
Cohn JE, Pfeiffer M, Vernose G. Complete resolution of guttate psoriasis after tonsillectomy. Ear Nose Throat J. 2018 Mar. 97 (3):62-63. [Medline].
Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis?. Arch Dermatol. 1996 Jun. 132(6):717-8. [Medline].
Williams RC, McKenzie AW, Roger JH, Joysey VC. HL-A antigens in patients with guttate psoriasis. Br J Dermatol. 1976 Aug. 95(2):163-7. [Medline].
Kirstin Altman, MD Assistant Professor of Dermatology, Texas A&M Health Science Center College of Medicine
Kirstin Altman, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Texas Dermatological Society
Disclosure: Nothing to disclose.
Daniel D Bennett, MD Associate Professor and Vice Chair for Clinical Affairs, Department of Dermatology, University of Wisconsin School of Medicine and Public Health
Daniel D Bennett, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Dermatology Foundation, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa
Disclosure: Nothing to disclose.
Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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: Received none from Amgen for consultant & investigator; Received none from Novartis for consultant & investigator; Received none from Pfizer for consultant & investigator; Received none from Celgene Corporation for consultant & investigator; Received none from Clinuvel for consultant & investigator; Received none from Eli Lilly & Co. for consultant & investigator; Received none from Janssen Ortho Biotech for consultant & investigator; Received none from LEO Pharmaceuticals for consultant & inves.
Elma D Baron, MD Assistant Professor of Dermatology, Case Western Reserve University, University Hospitals of Cleveland; Director of Skin Study Center, University Hospitals Research Institute; Acting Chief of Dermatology, Veterans Affairs Medical Center of Cleveland
Elma D Baron is a member of the following medical societies: American Academy of Dermatology, American Society for Photobiology, Photomedicine Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Cary Chisholm, MD Dermatopathology Fellow, Department of Dermatology, University of Texas Southwestern Medical Center
Cary Chisholm, MD is a member of the following medical societies: College of American Pathologists, Texas Medical Association, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
Charles R Taylor, MD Associate Professor of Dermatology, Harvard Medical School; Director of Phototherapy Unit, Department of Dermatology, Massachusetts General Hospital
Charles R Taylor, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Laser Medicine and Surgery, Massachusetts Medical Society, New England Dermatological Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Guttate Psoriasis
Research & References of Guttate Psoriasis |A&C Accounting And Tax Services
Source
0 Comments