Guttate psoriasis

INTRODUCTION — Psoriasis is a common skin disorder characterized by the development of inflammatory plaques on the skin. The spectrum of clinical manifestations of psoriasis is wide and includes chronic plaque, guttate, inverse, erythrodermic, pustular, and nail variants of the disease. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Patients with guttate psoriasis typically present with the acute onset of numerous small, inflammatory, scaly plaques on the trunk and extremities (picture 1A-B). Guttate psoriasis is most common among children and young adults, and a preceding history of streptococcal infection is often present.

The epidemiology, clinical manifestations, and treatment of guttate psoriasis will be reviewed here. Other manifestations of psoriasis are discussed separately. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis" and "Treatment of psoriasis in adults".)

EPIDEMIOLOGY — Psoriasis occurs in 0.6 to 4.8 percent of the general population [1], with chronic plaque psoriasis as the most common clinical presentation. Estimates of the proportion of patients with psoriasis who develop guttate disease vary widely; many studies cite a prevalence of less than 30 percent among patients with psoriasis [2-6].

Guttate psoriasis is most frequently diagnosed in children and young adults under the age of 30; however, older individuals may also be affected [7-9]. As an example, in a Spanish study that compared 1092 patients in whom psoriasis began between the ages of 0 and 30 years with 662 patients with disease onset later in life, patients in the younger-onset group were significantly more likely to have the guttate variant (15 versus 7 percent) [8].

A sex predilection for guttate psoriasis has not been established. Both males and females may develop this disease.

RISK FACTORS — Genetic and environmental factors likely contribute to the development of guttate psoriasis. The class I human leukocyte antigen HLA-Cw6 (in particular, the HLA Cw*0602 allele) and beta-hemolytic streptococci are the primary factors linked to the development of this disease.

Genetics — The HLA-Cw*0602 allele is strongly associated with psoriasis [10]. In a meta-analysis of 18 studies with approximately 3400 patients with psoriasis and 3300 healthy controls, participants who were positive for HLA-Cw*0602 were more than four times more likely to have psoriasis than participants who were negative for the allele (odds ratio 4.55, 95% CI 3.65-5.67) [11].

The association between psoriasis and the HLA-Cw*0602 allele appears to be particularly strong among patients with guttate psoriasis [5,12-16]. Examples of studies in support of an association include:

●In an Icelandic study that evaluated the correlation between HLA-Cw6 status and disease characteristics in patients with familial psoriasis, 31 of 33 patients (94 percent) whose symptoms began as an acute guttate eruption demonstrated HLA-Cw6 positivity [16]. An extension of this study that included patients without a family history of psoriasis (n = 1019) found the prevalence of guttate disease was significantly greater among HLA-Cw*0602 positive patients than among HLA-Cw*0602 negative patients (11 versus 3 percent) [14].

●In a Swedish case-control study, 56 of 77 patients with guttate psoriasis (73 percent) were positive for the HLA-Cw*0602 allele compared with 39 or 371 controls (11 percent) [12].

●In a United Kingdom study of 29 patients with guttate psoriasis and 604 controls, the HLA-Cw*0602 allele was detected in all patients with guttate psoriasis compared with only 20 percent of controls [15].

●A Chinese study found that HLA-Cw*0602 was strongly associated with guttate psoriasis; the guttate presentation accounted for 21 percent of psoriasis cases in HLA-Cw*0602 positive patients with psoriasis and 9 percent of psoriasis cases in HLA-Cw*0602 negative patients with psoriasis [5].

Streptococcal infection — Streptococcal infection often precedes the onset of guttate psoriasis [7,17-21]. A link between these entities is supported by studies that have documented a relationship between new-onset guttate psoriasis and acute streptococcal pharyngitis in 56 to 97 percent of patients [18]. In addition, perianal streptococcal infection has preceded guttate psoriasis in children [22,23]. The cutaneous manifestations of guttate psoriasis typically develop two to three weeks after an associated streptococcal infection [7].

New-onset guttate psoriasis may be more likely to be associated with streptococcal infections than guttate psoriasis that develops in patients with pre-existing chronic plaque psoriasis. In a prospective study, 19 of 33 patients (58 percent) with acute guttate psoriasis versus 7 of 27 patients (26 percent) with guttate exacerbations of chronic psoriasis had serologic evidence for recent streptococcal infection [19].

Other infections — Case reports have documented the development of guttate psoriasis following varicella [24,25] and Pityrosporum folliculitis [26,27]. A Koebner phenomenon, in which wound healing triggers hyperproliferative changes in the skin, may be a factor in these cases. Cases of guttate psoriasis following coronavirus disease 2019 (COVID-19) infection or vaccination have also been reported [28-31]. Guttate psoriasis has also developed in the site of a tattoo, a finding consistent with the theory of Koebnerization [32].

Drugs — Guttate psoriasis has been reported after treatment with tumor necrosis factor (TNF)-alpha inhibitors in case reports and case series [33-37]. The reason for this paradoxical observation is unclear but may involve disruption of the cytokine milieu, leading to unopposed interferon production [35].

PATHOGENESIS — The pathophysiology of guttate psoriasis is not well understood. Interplay between genetic and environmental factors leading to an aberrant immune response in the skin may contribute to disease development.

As noted above, strong associations between guttate psoriasis, streptococcal infection, and HLA-Cw*0602 positivity have been detected in patients with guttate psoriasis (see 'Risk factors' above). Examples of proposed mechanisms for the relationship between guttate psoriasis and streptococcal infection include [38]:

●Cross-reactivity between streptococcal M-proteins (the major pathogenic antigens on beta-hemolytic streptococci) presented to immune cells in the tonsils and structurally similar type I keratins in the epidermis (K16 and K17) trigger a T cell-mediated autoimmune response.

●Streptococcal superantigens in the tonsils may augment the expression of the skin-homing cutaneous lymphocyte antigen (CLA) on effector T cells, contributing to the migration of T cells into the skin; CD4+ cells migrate into the dermis, and CD8+ cells migrate into the epidermis. A study that found identical T cell receptor gene rearrangement in tonsils and psoriatic skin in patients with streptococcal-induced psoriasis supports direct migration of CLA+ cells in the tonsils to the skin [39].

●An innate immune-mediated inflammatory response occurs as a consequence of the binding of peptidoglycan or other streptococcal antigens to cell receptors.

The observed association between guttate psoriasis and HLA-Cw*0602 may be related to interactions between streptococci and this molecule [12]. In an in vitro study, homologous peptides from K17 and streptococcal M-protein that were predicted to bind to HLA-Cw6 were better able to stimulate interferon (IFN)-gamma production in T cells (mostly CD8+ T cells that also demonstrated CLA) from patients with psoriasis than T cells obtained from patients without psoriasis [40]. Moreover, the greatest responses were detected in T cells derived from HLA-Cw*0602 positive patients with psoriasis.

Another ex vivo study supports a role for interactions between streptococci and HLA-Cw*0602. Coculture of CLA+ T cells and autologous epidermal cells from patients with guttate psoriasis in the presence of Streptococcus pyogenes led to a higher Th17 response (higher production of interleukin [IL]-17A and IL-17F than IFN-gamma) with cells from carriers of HLA-Cw*0602 who had psoriasis flares associated with pharyngitis than with cells from HLA-Cw*0602 positive or negative patients who did not have flares associated with pharyngitis [41]. Th17 cells play an important role in the pathogenesis of psoriasis. (See "Pathophysiology of plaque psoriasis", section on 'T helper type 17 cells'.)

Clinical evidence of a relationship between HLA-Cw*0602 status, guttate psoriasis, and streptococcal infection was detected in a study of 439 patients with plaque psoriasis, 143 patients with guttate psoriasis, and 454 healthy controls. Patients with guttate psoriasis who were positive for HLA-Cw*0602 were more likely to have a positive streptococcal throat swab than patients who were HLA-Cw*0602 negative (odds ratio 3.5, 95% CI 1.5-8.7) [13]. A difference in throat swab positivity rates based upon HLA-Cw*0602 status was not detected among the healthy controls.

CLINICAL MANIFESTATIONS — Guttate psoriasis is characterized by the acute eruption of numerous small, erythematous papules and plaques. The term "guttate" is utilized to refer to the discrete, drop-like appearance of skin lesions. The eruption may present as a new-onset disorder in patients without a history of psoriasis or as a new presentation of psoriasis in patients with pre-existing chronic plaque-type disease [19].

Individual lesions usually measure between 2 and 15 mm in diameter and demonstrate fine, overlying scale (picture 1A-B). The trunk and proximal extremities are classically involved, although lesions may also occur in other sites, such as the scalp, hands, feet, and nails [7]. Pruritus and postinflammatory hyperpigmentation may occur.

DIAGNOSIS — Clinical examination is usually sufficient for the diagnosis of guttate psoriasis. A skin biopsy can be used to support the diagnosis in difficult cases.

Histopathology — The histopathologic findings of guttate psoriasis vary with the age of the lesion [42]. The findings in early lesions may be nondiagnostic, demonstrating mild acanthosis, papillary dermal edema, capillary dilatation, and a sparse lymphocyte-predominant dermal infiltrate.

Mature lesions more closely resemble the pathology findings in chronic plaque psoriasis. Such lesions have parakeratosis alternating with hyperkeratosis, epidermal acanthosis, rete ridge elongation, and collections of neutrophils in the epidermis that are also known as Munro microabscesses. Dermal findings include dilated, tortuous vessels and a superficial perivascular infiltrate containing lymphocytes, neutrophils, and macrophages.

Laboratory tests — No serologic tests provide a definitive diagnosis of guttate psoriasis. Routine assessment for evidence of a streptococcal infection in patients without infectious symptoms is controversial because a benefit of antibacterial therapy in guttate psoriasis is unproven [43]. In our opinion, laboratory testing is not necessary in patients without active signs or symptoms of streptococcal infection.

Patients who present with symptoms suggestive of streptococcal pharyngitis or other forms of streptococcal infection should be evaluated with appropriate laboratory studies to facilitate the identification and treatment of these conditions. Symptoms of streptococcal pharyngitis include sore throat, tonsillar exudate, tender cervical adenitis, and fever. (See "Evaluation of acute pharyngitis in adults" and "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis", section on 'Diagnosis'.)

Differential diagnosis — Multiple disorders may present with clinical features that resemble guttate psoriasis. In most cases, the clinical history and physical examination are sufficient for differentiating guttate psoriasis from other diseases. Occasionally, laboratory studies are needed to assist with diagnosis.

Examples of disorders in the differential diagnosis of guttate psoriasis include:

●Pityriasis rosea – Pityriasis rosea presents with the acute eruption of multiple oval inflammatory plaques (picture 2A-D). Like guttate psoriasis, the trunk and proximal extremities are prominent sites of involvement. The classic features of a "Christmas tree" pattern distribution and collarette of scale can be useful clues for the identification of pityriasis rosea. At least 50 percent also develop a large, oval plaque (also known as a herald plaque) prior to the development of the widespread eruption. (See "Pityriasis rosea".)

●Tinea corporis – Extensive tinea corporis may present with numerous annular plaques on the skin (picture 3A-B). Peripheral scale and central clearing are commonly seen. A potassium hydroxide (KOH) preparation is useful for diagnosis. (See "Dermatophyte (tinea) infections", section on 'Tinea corporis'.)

●Secondary syphilis – Secondary syphilis is characterized by the development of erythematous to brown macules, papules, or small plaques in a generalized distribution (picture 4A-C). Involvement of the palms and soles suggests the possibility of this diagnosis. Serologic findings and histopathologic examination are also useful for diagnosis. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Clinical manifestations'.)

●Pityriasis lichenoides chronica – Pityriasis lichenoides chronica is an uncommon skin disorder that presents with recurrent crops of erythematous to brown papules on the trunk and proximal extremities (picture 5A-B). Lesions often demonstrate an adherent (micaceous) scale. Pruritus may or may not be present. The disorder is most common in children and young adults. (See "Pityriasis lichenoides chronica".)

●Small plaque parapsoriasis – Small plaque parapsoriasis is a rare condition in which multiple small, oval patches with fine scale develop on the trunk and proximal extremities (picture 6A-B). The eruption may be asymptomatic or mildly pruritic. (See "Parapsoriasis (small plaque and large plaque parapsoriasis)", section on 'Small plaque parapsoriasis'.)

●Nummular dermatitis – Nummular dermatitis (also known as nummular eczema) may present with single or multiple oval, inflammatory plaques (picture 7A-C). Pruritus is typically prominent. Serous drainage may be present. (See "Overview of dermatitis (eczematous dermatoses)", section on 'Nummular eczema'.)

Although the cutaneous features of viral exanthems and maculopapular drug eruptions tend to differ from guttate psoriasis, the clinical scenarios in which guttate psoriasis develops (a new, widespread skin eruption in a patient with a recent history of upper respiratory symptoms or a history of streptococcal pharyngitis treated with antibiotics) may lead to consideration of these diagnoses (picture 8A-B). Recognition of the well-defined plaques with adherent scale that are characteristic of guttate psoriasis is useful for distinguishing this diagnosis.

CLINICAL COURSE — Guttate psoriasis may spontaneously remit, typically over the course of several weeks to several months, may intermittently recur, or may persist and progress into chronic plaque psoriasis [7,21,44,45]. Few data are available on the prognosis of guttate psoriasis, precluding reliable predictions about the disease course in individual patients. Examples include:

●The Stockholm Psoriasis Cohort study (n = 721) evaluated long-term outcomes in adolescents and adults with recent-onset psoriasis [46]. Of the 116 patients with guttate psoriasis who were re-examined after 10 years, 48 percent had minimal disease activity without treatment (as compared with 20 percent of 389 patients with plaque-onset psoriasis re-examined after 10 years).

●A retrospective study assessed 36 patients with childhood or adult-onset guttate psoriasis who lacked a preceding history of psoriasis [7]. Complete remission lasting for at least one year occurred in 22 patients (61 percent) with a mean time to disease clearance of 3.9±2.4 months, and the remaining 14 patients progressed to chronic plaque-type disease. Of note, three patients in the remission group had recurrence after one year. A wide variety of treatments for guttate psoriasis were utilized in the patients in this study.

●A retrospective study assessed 79 patients with guttate psoriasis and no prior history of psoriasis who were followed for a least one year (median follow-up period of five years). In the study, 20 patients (25 percent) progressed to plaque psoriasis [47]. The results of a molecular probe for streptococci appeared to correlate with risk for plaque psoriasis; however, additional data are necessary to confirm this finding. Among the 31 patients who had the molecular probe performed, none of the five patients who developed plaque psoriasis had a positive molecular probe for streptococci compared with 16 of 26 patients (62 percent) who did not develop plaque psoriasis. A similar correlation with antistreptolysin O titers was not detected.

Further study is necessary to determine whether a preceding history of guttate psoriasis is associated with greater severity of chronic plaque-type disease [21].

TREATMENT — The treatments used for guttate psoriasis overlap with those utilized for chronic plaque psoriasis. Although many treatments for chronic plaque psoriasis have been extensively studied, investigations focused specifically on treatment results in guttate psoriasis are limited [48-50]. (See "Treatment of psoriasis in adults".)

Given the possibility for spontaneous remission of guttate psoriasis within several weeks or several months, foregoing treatment is an option for patients who prefer to avoid therapy. However, since the time required for disease remittance is unpredictable and persistence of psoriasis is not uncommon, in our experience, many patients elect to proceed with treatment. (See 'Clinical course' above.)

First-line treatments for guttate psoriasis include phototherapy and topical agents. Although systemic antibiotic therapy has been advocated by some authors, the value of such treatment is unclear [43,51]. In addition, data on the efficacy of tonsillectomy, which aims to permanently remove a focus of streptococcal infection, are limited. Patients who progress to chronic plaque psoriasis can be managed according to the treatment approach for this variant. (See 'First-line therapies' below and 'Refractory disease' below.)

First-line therapies

Phototherapy — Ultraviolet (UV) phototherapy is considered a first-line therapy for guttate psoriasis. This designation is primarily due to its documented efficacy in other forms of psoriasis, its relative safety, and the ability to easily treat large body surface areas. The options for full-body phototherapy for psoriasis include narrowband ultraviolet B (UVB), broadband UVB, and psoralen plus ultraviolet A (PUVA) phototherapy.

The efficacy of phototherapy for plaque psoriasis is well documented, with narrowband UVB considered the preferred form of phototherapy [52,53]. Narrowband UVB has been more effective than broadband UVB in multiple small, prospective, split-body studies of patients with plaque-type psoriasis [52,54]. Although a randomized trial that compared narrowband UVB with a selective broadband UVB device in 100 patients with plaque-type psoriasis found a difference of efficacy in favor of narrowband UVB that was not statistically significant (56 versus 40 percent of patients achieved disease clearance), the study was underpowered to detect a difference [55]. PUVA was significantly more effective than narrowband UVB in a randomized trial (n = 93). However, the requirement for strict photoprotection following treatment makes PUVA a less favorable choice for therapy [56]. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy".)

Formal study of the efficacy of phototherapy in guttate psoriasis is limited since most psoriasis studies that have included patients with this variant have failed to stratify treatment results according to the type of psoriasis [48]. A prospective uncontrolled study in which 67 adults with guttate psoriasis were treated with narrowband UVB for guttate psoriasis supports benefit in this population; 52 (78 percent) achieved at least 90 percent improvement in the Psoriasis Area and Severity Index score, and 46 (88 percent) of those patients maintained this response during 18 months of follow-up without treatment [57]. Patients received an average of 20 treatments.

Potential adverse effects of phototherapy include burns, pruritus, and premature skin aging. Increased risks for squamous cell carcinoma and possibly melanoma are associated with long-term PUVA therapy. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy", section on 'Skin cancer'.)

Patients without access to phototherapy may experience improvement in guttate psoriasis with cautious outdoor sun exposure. The efficacy of this intervention has not been formally evaluated. Based upon clinical experience, 5 to 10 minutes of noontime sun exposure without sunscreen is typically sufficient. Sunburns should be avoided.

Topical corticosteroids and vitamin D analogs — Multiple randomized trials have supported the efficacy of topical corticosteroids and topical vitamin D analogs for chronic plaque psoriasis [58]. These agents have not been formally evaluated specifically in guttate disease [48].

A potential impediment to topical treatment of guttate psoriasis is the often widespread nature of the disease, which can make the application of topical agents impractical. Thus, phototherapy is usually preferred for the treatment of patients with numerous lesions. Topical agents may be used as an adjunct to phototherapy. (See 'Phototherapy' above.)

Cutaneous atrophy is a potential adverse effect of topical corticosteroid therapy. To minimize this risk, low-potency agents are typically used on atrophy-prone sites, such as the face and intertriginous areas (table 1). Medium- to high-potency agents may be applied to lesions on the trunk or extremities.

Topical corticosteroids are typically applied to active lesions once to twice daily for around two weeks. Longer courses may be utilized if necessary; however, monitoring for adverse effects is essential. (See "Treatment of psoriasis in adults", section on 'Corticosteroids' and "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Topical vitamin D analogs, such as calcitriol or calcipotriene, may be used alone or in conjunction with topical corticosteroid therapy. Cutaneous irritation is the most common adverse effect of these agents. (See "Treatment of psoriasis in adults", section on 'Topical vitamin D analogs'.)

Refractory disease — In a minority of patients, guttate psoriasis recurs multiple times per year or fails to improve with phototherapy or topical therapies. Although few data are available to support their use, tonsillectomy and systemic therapies used for chronic plaque psoriasis have been utilized in the management of these patients.

Tonsillectomy — Resolution of recurrent Streptococcus-associated guttate or chronic plaque psoriasis following tonsillectomy has been documented, including in a small randomized trial performed with patients with chronic plaque psoriasis and in case reports and uncontrolled studies [51,59,60]. In one uncontrolled study, five out of six patients with guttate psoriasis that flared with episodes of tonsillitis had complete clearance of the disease after tonsillectomy, and the remaining patient had a lesser degree of improvement [61]. Two of seven patients with chronic plaque psoriasis cleared.

Based upon the available data, it is conceivable that tonsillectomy may be effective for some patients with recurrent, tonsillitis-associated guttate psoriasis. However, data are insufficient to recommend the routine use of tonsillectomy, and further studies are necessary to evaluate the efficacy of this treatment [60]. (See "Tonsillectomy in adults: Techniques and perioperative issues" and "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications".)

Systemic psoriasis therapies — Based upon efficacy demonstrated in chronic plaque psoriasis, treatment with systemic immunomodulatory and immunosuppressive therapies utilized for chronic plaque psoriasis may be attempted in patients with persistent disease that fails to respond to first-line therapies. However, there is a lack of published evidence on the efficacy of these treatments, specifically in guttate psoriasis [48,49].

Other interventions

Systemic antibiotics — Due to the well-accepted association between streptococcal infection and guttate psoriasis, antibiotic therapy has been proposed as a treatment for this disease. Overall, data remain insufficient to support a routine recommendation for antibiotic therapy for skin disease in guttate psoriasis [51,62]. However, patients with active streptococcal infection (eg, streptococcal pharyngitis or perianal streptococcal infection) should be treated with antibiotic therapy to resolve these infections, as indicated. (See 'Streptococcal infection' above and "Treatment and prevention of streptococcal pharyngitis in adults and children".)

Evidence in support of antistreptococcal antibiotics is limited to a few uncontrolled studies that document improvement in guttate or plaque-type psoriasis after treatment with macrolides or treatment with rifampin given with or without other antistreptococcal agents [63-66]. The few randomized trials performed are of low quality and have not yielded favorable results [51]. In a randomized trial in 20 patients with psoriasis (19 with guttate psoriasis) that compared 14 days of treatment with penicillin V or erythromycin (both 250 mg four times daily) plus rifampin (300 mg twice daily) during the final five days of therapy with a 14-day treatment regimen consisting of penicillin or erythromycin monotherapy, neither treatment approach reduced disease severity [67].

A potential role for rifampin therapy resurfaced in a subsequent prospective uncontrolled study of 52 patients with guttate psoriasis. Monotherapy with rifampin (600 mg per day) for 60 days was associated with reductions of psoriasis severity scores regardless of the presence or absence of evidence of recent streptococcal infection. Based upon this finding, the authors postulated that immunomodulatory effects of rifampin may have contributed to the observed effect [66].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Psoriasis".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Guttate psoriasis is a variant of psoriasis that is characterized by the presence of small, erythematous papules and plaques on the skin. Guttate psoriasis is most frequently diagnosed in adolescents and young adults but may occur in other age groups. (See 'Epidemiology' above.)

●Risk factors – Genetic and environmental factors likely contribute to the development of guttate psoriasis. The HLA-Cw*0602 allele has been strongly linked to this disorder, and streptococcal infection often precedes its development. The latency period between streptococcal infection and the appearance of skin lesions is typically two to three weeks. (See 'Risk factors' above.)

●Pathogenesis – The relationship between streptococcal infection and guttate psoriasis is not fully understood. Cross-reactivity between streptococcal and epidermal antigens, stimulatory effects of streptococcal superantigens, and/or the induction of an innate immune response by streptococcal components may be involved. (See 'Pathogenesis' above.)

●Clinical manifestations – The skin lesions of guttate psoriasis are typically 2 to 15 mm in diameter with overlying, fine scale (picture 1A-B). The trunk and proximal extremities are the principle sites of involvement. (See 'Clinical manifestations' above.)

●Diagnosis – The diagnosis of guttate psoriasis can usually be made by clinical examination. In difficult cases, a skin biopsy may be used to support the diagnosis and rule out other conditions. (See 'Diagnosis' above.)

●Clinical course – Guttate psoriasis may spontaneously remit over the course of several weeks to months or may persist and progress to chronic plaque disease. The course of the disease is unpredictable. (See 'Clinical course' above.)

●Treatment:

•Initial treatment – For patients with widespread lesions of guttate psoriasis who desire treatment, we suggest treatment with narrowband ultraviolet B (UVB) phototherapy (Grade 2B). Topical corticosteroids, topical vitamin D analogs, and other forms of phototherapy are alternative treatments. (See 'First-line therapies' above.)

•Other therapies – Treatment with the systemic immunomodulatory and immunosuppressive agents utilized for plaque psoriasis may be attempted in patients with guttate psoriasis that fails to improve with phototherapy and topical therapies. The efficacy of such treatment in guttate psoriasis has not been well studied. (See 'Systemic psoriasis therapies' above.)

The use of tonsillectomy and systemic antibiotic therapy for the treatment of the skin manifestations of guttate psoriasis is controversial. Further study is necessary to explore the efficacy of these interventions. These interventions are not recommended for routine treatment of guttate psoriasis. Active streptococcal infection should be treated with antibiotics, as indicated. (See 'Tonsillectomy' above and 'Systemic antibiotics' above.)