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Gianotti-Crosti syndrome (papular acrodermatitis)

Gianotti-Crosti syndrome (papular acrodermatitis)
Literature review current through: Jan 2024.
This topic last updated: Oct 26, 2021.

INTRODUCTION — Gianotti-Crosti syndrome (GCS), also known as papular acrodermatitis, papular acrodermatitis of childhood, and infantile papular acrodermatitis, is a self-limited skin disorder that most often occurs in young children. Viral infections are common precipitating factors for GCS.

GCS typically manifests as a symmetric, papular eruption. Classic sites of involvement include the cheeks, buttocks, and extensor surfaces of the forearms and legs (picture 1A-F). GCS may be pruritic or asymptomatic, and papules typically resolve spontaneously within two months. Occasionally, GCS persists for longer periods.

The etiology, clinical manifestations, diagnosis, and management of GCS will be reviewed here. Other uncommon exanthems that primarily occur in children and in association with viral infections are reviewed separately. (See "Atypical exanthems in children".)

HISTORY AND TERMINOLOGY — Features consistent with GCS were first described by Gianotti and Crosti in the 1950s [1,2]. The disorder was initially considered limited to infants and children but has since been recognized in adolescents and adults [3-5].

The original description of GCS consisted of three cardinal manifestations [1,2,6-8]:

Nonrelapsing erythemato-papular dermatitis localized to the face and limbs, lasting approximately three weeks

Paracortical hyperplasia of lymph nodes

Acute hepatitis, usually anicteric, which could last for months and progress to chronic liver disease

However, it is now accepted that neither lymphadenopathy nor hepatitis is mandatory for the diagnosis of GCS, and the duration of the condition can vary. Some authors have utilized the term "Gianotti-Crosti disease" to refer to GCS that occurs specifically in association with hepatitis B virus infection [9].

EPIDEMIOLOGY — GCS occurs worldwide. The incidence and prevalence are unknown. Because many children with GCS are likely diagnosed with a "viral rash" or "nonspecific viral exanthem," GCS is probably underdiagnosed [10]. (See 'Differential diagnosis' below.)

GCS primarily affects children younger than five years of age. During childhood, there does not appear to be a sex predilection [11,12]. In contrast, case reports suggest that, among adults, females may be more likely to develop GCS than males [9].

Most reports of GCS describe isolated cases. However, outbreaks have been described in association with hepatitis B virus infection, Epstein-Barr virus infection, and idiopathic cases [13-18].

ETIOLOGY — The epidemiologic features (eg, young age of onset, equal sex distribution in children, and occurrences of outbreaks) support an infectious etiology for GCS [19]. Viral infections are considered the most common etiologic agents.

Viral infections — GCS usually occurs in association with a viral illness, most often Epstein-Barr virus (EBV) or hepatitis B virus (HBV) infection [20]. Case reports, case series, and retrospective studies support the association between EBV [11,21-30] and HBV infection [13-15,31-35]. Of note, HBV is an uncommon cause of GCS in locales where vaccination against HBV infection during infancy is routine, such as the United States [9]. (See "Clinical manifestations and treatment of Epstein-Barr virus infection" and "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents".)

GCS is less commonly reported in association with other viral pathogens. Examples include enteroviruses [36,37], cytomegalovirus [38-41], parvovirus [42,43], parainfluenza virus [44,45], hepatitis A virus [46,47], rotavirus [48,49], molluscum contagiosum [42,50], respiratory syncytial virus [37], HIV [51], and human herpesvirus 6 [52-54].

Other associations — Occasionally, GCS occurs in association with vaccination or bacterial infections. GCS has occurred following the administration of various antiviral vaccines, including vaccination against influenza [55-58], measles-mumps-rubella [59], hepatitis B [60,61], polio [62,63], hepatitis A [64], Japanese encephalitis [65], and varicella zoster virus infections [66]. One of the largest studies to evaluate the relationship between GCS and vaccination assessed 116 children diagnosed with GCS in close proximity to scheduled national days for receipt of the oral polio vaccine [63]. The study found that GCS was more often present one month after scheduled vaccination days (105 children, 90 percent) than one month prior to these days (11 children, 10 percent). Additional study is necessary to clarify the relationship between GCS and vaccines.

Associations between the development of GCS and bacterial infections have been documented in case reports, including Mycoplasma pneumoniae [67,68], beta-hemolytic streptococci [37], Bartonella henselae [69], and Borrelia burgdorferi [70].

PATHOGENESIS — The pathogenesis of GCS, including the reason for the acral distribution, is unknown. One hypothesis suggests that the clinical manifestations result from a delayed hypersensitivity reaction to viral infections [71].

The significance of immunoglobulin E (IgE)-mediated immunity in the pathogenesis of GCS and other viral exanthems is an area of investigation. GCS appears to be associated with atopy, which is characterized by the production of specific IgE following allergen exposure. A case-control study found that children with GCS were more likely to have had atopic dermatitis and to have a family history of atopy than control children who were being evaluated for recurrent infections (24 versus 7 percent for atopic dermatitis and 52 versus 31 percent for family history of atopy) [72]. In another case-control study with 37 children with GCS and matched controls, atopic dermatitis was more common among children with GCS than without GCS (76 versus 24 percent), and children with GCS were more likely to have at least one atopic disorder (84 versus 51 percent) [73]. (See "The relationship between IgE and allergic disease".)

CLINICAL FEATURES — The clinical manifestations of GCS typically consist of the cutaneous eruption and findings related to the associated infection.

Cutaneous manifestations — GCS classically presents as an acute, symmetric eruption of flat-topped, skin-colored or pink-brown papules or papulovesicles 1 to 10 mm in diameter that may coalesce into plaques (picture 1A-F) [9,74]. Although the face, buttocks, extensor aspects of forearms and legs, and feet are the predominant sites of involvement, involvement of the trunk does not exclude a diagnosis of GCS [75]. Truncal lesions are often more transient and fewer in number than acral lesions. Pruritus is usually mild to moderate but may be absent or severe.

The development of lesions at sites of skin trauma (ie, the Koebner phenomenon) may occur early in the course of GCS [11,76]. In addition, hemorrhagic lesions occasionally occur, particularly in areas subject to trauma [9,74,76,77]. It has been suggested that patients with petechial lesions are more likely to have hepatitis B virus infection [78]. However, the cutaneous findings of GCS are not a reliable indicator of the etiologic agent [31]. A vesiculobullous variant has also been reported in a child with Epstein-Barr virus (EBV) infection [79]. (See "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents".)

GCS does not cause mucosal lesions. However, mucosal or cutaneous features of certain associated viral infections may accompany the cutaneous manifestations of GCS. As an example, patients with enterovirus-associated GCS may have oral mucosal or palmoplantar skin lesions. (See "Hand, foot, and mouth disease and herpangina".)

Extracutaneous manifestations — Patients with GCS may experience symptoms of an upper respiratory or gastrointestinal illness during the week before the onset of the rash [9]. The initial illness may have resolved by the time the child presents with cutaneous manifestations. Patients may also present with concurrent malaise, low-grade fever, or diarrhea [9].

Lymphadenopathy occurs in 25 to 35 percent of patients, usually in the cervical, axillary, or inguinal regions [11,80]. The frequency of hepatic involvement is not known [9]. When hepatitis is present, it usually is anicteric (without clinically recognized jaundice) [8,81]. Splenomegaly may occur but is uncommon [9]. (See 'Diagnosis' below.)

Laboratory findings — There are no laboratory features characteristic of GCS. Patients may have modest lymphocytosis or lymphopenia [9]. Liver enzymes may be elevated in patients with EBV, cytomegalovirus, or hepatitis-associated disease.

COURSE — Most children with GCS have an excellent prognosis, although the course may be prolonged [9]. Spontaneous remission without active intervention is the rule.

During the initial two to three weeks, new papules and papulovesicles continue to occur, and the areas of involvement expand. The distribution is most classic in the middle phase of the disease.

GCS usually persists for 10 days to 6 months; however, durations ranging from 5 days to 12 months have been reported [80]. Most patients achieve resolution of papules and associated pruritus within two weeks to two months.

Near the end of the course, slow resolution of the skin lesions occurs. Recurrences are rare [82]. When present, lymphadenopathy and hepatomegaly (or hepatosplenomegaly) usually take longer to resolve than the cutaneous lesions [33,76].

COMPLICATIONS — Postinflammatory hypopigmentation or hyperpigmentation often follows resolution of the skin lesions in children with highly pigmented skin and can persist for up to six months, but eventually resolves [9,83]. Permanent scarring is uncommon.

Other potential complications are related to the underlying etiology. (See "Clinical manifestations and treatment of Epstein-Barr virus infection", section on 'Complications' and "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents".)

HISTOPATHOLOGY — The histopathologic findings of GCS are nonspecific. Typical findings include focal, epidermal spongiosis and parakeratosis with perivascular, lymphocytic infiltrates in the upper dermis [84].

DIAGNOSIS — GCS can usually be diagnosed based upon the history and physical examination. A skin biopsy is not usually necessary but may be useful in challenging cases. (See 'Differential diagnosis' below.)

The establishment of diagnostic criteria would help to facilitate the clinical diagnosis of GCS and future studies of the disease. It remains to be determined whether proposed, diagnostic criteria are the ideal criteria for the diagnosis of this disease [85]. More studies are necessary to assess the criteria-rated validity, test-test intraclinician reliability, and interclinician reliability [86].

History and physical examination — The history and physical examination should include an assessment of preceding or concurrent constitutional symptoms as well as the time course, distribution, and morphology of the eruption. A full skin examination should be performed.

A diagnosis of GCS is strongly suggested by the acute onset of a symmetrically distributed, papular or papulovesicular eruption in a young child that primarily involves the face, buttocks, and/or extensor surfaces of the extremities and does not have another identifiable cause (picture 1A-F). The presence of extracutaneous signs and symptoms (eg, malaise, fever, diarrhea, lymphadenopathy) is variable.

Skin biopsy — The histopathologic findings of GCS are nonspecific and cannot confirm the diagnosis. However, a skin biopsy may be necessary to exclude other diagnoses in atypical presentations (eg, atypical lesion morphology or distribution, or lack of spontaneous resolution within six months). A 4 mm punch biopsy is usually sufficient. (See 'Histopathology' above and 'Differential diagnosis' below and "Skin biopsy techniques".)

EVALUATION FOR UNDERLYING DISORDERS — The decision to proceed with laboratory tests to identify an etiologic agent for GCS should be made on an individual basis. Laboratory testing to identify an etiologic agent is not necessary for many patients. (See 'Etiology' above.)

However, testing of patients with GCS for specific viral infections is warranted in some scenarios, such as to identify patients who may benefit from close monitoring or treatment of a suspected underlying condition. GCS may be the only clinical manifestation of acute hepatitis B virus (HBV) infection in infants and young children; therefore, testing for HBV infection is particularly appropriate for patients with risk factors for HBV infection. Laboratory testing to screen for Epstein-Barr virus (EBV) infection is generally unnecessary in the absence of other indications for EBV testing, as supportive therapy is often sufficient. (See "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents", section on 'Epidemiology' and "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents", section on 'Screening'.)

Testing to identify an etiologic agent may also be of value in immunocompromised patients or in patients with close contact with immunocompromised individuals or pregnant women [87]. Moreover, investigative testing may also be warranted when extracutaneous clinical findings (eg, hepatomegaly) require further work-up. The clinical presentation directs the approach to evaluation.

DIFFERENTIAL DIAGNOSIS — The constellation of clinical features in GCS usually allows the diagnosis to be made relatively easily [9]. However, other conditions may warrant consideration, particularly in the setting of atypical presentations. Assessment of the course, associated symptoms, and lesion morphology and distribution is usually helpful for distinguishing GCS [76]:

Erythema infectiosum − Erythema infectiosum (EI; also known as "fifth disease") is a common childhood exanthem caused by parvovirus B19. Like GCS, EI begins with nonspecific prodromal illness and acral eruption. However, the rash of EI, which begins on the cheeks (picture 2) and spreads to the extremities (picture 3), often has a lacy, reticulated appearance. (See "Clinical manifestations and diagnosis of parvovirus B19 infection", section on 'Erythema infectiosum'.)

Erythema multiforme − Erythema multiforme (EM) typically affects adolescents and young adults, but may also occur in children [74]. EM is often caused by herpes simplex virus or Mycoplasma infection. Although target lesions are characteristic of EM (picture 4), the lesions may be papular early in the course. Mucosal lesions are present in some children with EM and may help to distinguish it from GCS. (See "Erythema multiforme: Pathogenesis, clinical features, and diagnosis".)

Hand, foot, and mouth disease − Hand, foot, and mouth disease (HFMD) is a common childhood illness that is usually caused by the group A coxsackieviruses. HFMD is characterized by fever; oral vesicles on the buccal mucosa and tongue; and peripherally distributed, small, tender, cutaneous macules, papules, or vesicles on the hands, feet, buttocks, and (less commonly) genitalia (picture 5A-C). The mucosal lesions and relatively short clinical course of HFMD distinguish it from GCS. (See "Hand, foot, and mouth disease and herpangina", section on 'Hand, foot, and mouth disease' and "Hand, foot, and mouth disease and herpangina".)

Scabies − Scabies is an infestation of the skin by the mite Sarcoptes scabiei that results in an intense pruritus and small, erythematous papules, pustules, or vesicles, often in a characteristic distribution (picture 6A-B). The degree of pruritus distinguishes scabies from GCS; pruritus associated with GCS is not usually severe. Characteristic scabies mite burrows may also be visible in patients with scabies. (See "Scabies: Epidemiology, clinical features, and diagnosis".)

Papular urticaria − Papular urticaria (also known as insect bite-induced hypersensitivity reaction) is defined by chronic or recurrent eruptions of papules, vesicles, target lesions, or wheals caused by hypersensitivity to insect bites (eg, fleas, mosquitoes, bedbugs, mites) in children. The lesions are symmetric, usually grouped in crops or clusters on exposed areas, and may take weeks to years to resolve. (See "Insect and other arthropod bites", section on 'Papular urticaria'.)

Less common conditions to consider in the differential diagnosis of GCS include lichen planus, drug eruptions, papular-purpuric gloves and socks syndrome (PPGSS), and immunoglobulin A (IGA) vasculitis (Henoch-Schönlein purpura (picture 7)). Petechial or purpuric lesions should prompt consideration of PPGSS and IgA vasculitis. (See "Atypical exanthems in children", section on 'Papular-purpuric gloves and socks syndrome' and "IgA vasculitis (Henoch-Schönlein purpura): Clinical manifestations and diagnosis".)

MANAGEMENT — GCS is a self-limited condition that can typically be managed with supportive therapy to minimize pruritus, when present. In addition, patients or caregivers of patients of GCS often benefit from a discussion of the diagnosis, expected course, and prognosis of GCS. (See 'Course' above.)

Pruritus — Interventions for GCS have not been evaluated in randomized trials. Clinical experience suggests that topical emollients provide adequate relief for most individuals. For patients with significant pruritus, lotions containing ingredients such as calamine, pramoxine, menthol, or camphor may help to alleviate pruritus. Low- or medium-potency topical corticosteroids have also been utilized. However, the ability of topical corticosteroids to alter the disease course has not been confirmed (table 1) [44]. The administration of a sedating antihistamine may be helpful when the pruritus interferes with sleep. (See "Pruritus: Therapies for generalized pruritus", section on 'Elimination of aggravating factors'.)

Return to daycare or school — Exclusion from daycare, school, or other activities is unnecessary for most children with GCS. The need for any infection precautions is based upon the risks of transmission of the underlying infectious disease. (See 'Etiology' above.)

Indications for referral — Referral to a pediatric dermatologist may be beneficial if the diagnosis is uncertain or the disease course is exceptionally prolonged (eg, longer than six months).

SUMMARY AND RECOMMENDATIONS

Gianotti-Crosti syndrome (GCS) is a self-limited cutaneous disorder that typically presents as a symmetric, papular eruption with an acral distribution. GCS primarily affects children younger than five years but can also occur in adolescents and adults. (See 'Epidemiology' above.)

GCS usually occurs in association with a viral illness, such as infection with Epstein-Barr virus, hepatitis B virus, or other viruses. GCS associated with antiviral vaccines or bacterial infections and idiopathic GCS have also been reported. (See 'Etiology' above.)

The diagnosis of GCS usually can be made based upon the patient history and physical findings. The characteristic presentation of GCS consists of symmetric, monomorphous, flat-topped, pink-brown or skin-colored papules or papulovesicles on the face, buttocks, feet, and extensor aspects of forearms and legs (picture 1A-F). Pruritus may be present. (See 'Clinical features' above.)

Noncutaneous findings in patients with GCS may include malaise, low-grade fever, and diarrhea. Lymphadenopathy is present in a subset of patients. Hepatitis, when present, is usually anicteric. (See 'Extracutaneous manifestations' above.)

GCS typically resolves spontaneously within two months. Supportive care for associated pruritus, such as emollients, topical antipruritic agents, and oral sedating antihistamines, is usually sufficient. Exclusion from daycare or school is not necessary for most children with GCS. (See 'Management' above.)

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