ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis

Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Sep 29, 2022.

INTRODUCTION — Psoriasis is a systemic, immune-mediated disease that is most often characterized by well-demarcated, erythematous plaques with adherent, micaceous scale. The onset of psoriasis can occur during childhood or adulthood.

Chronic plaque psoriasis is the most common clinical form of psoriasis in children; guttate, pustular, and erythrodermic psoriasis are additional presentations. Certain distributions of plaque psoriasis are more common in children than adults, including involvement of the face, scalp, and intertriginous skin. Psoriatic diaper rash (also known as "napkin psoriasis") can be the initial manifestation of psoriasis in infants and young children.

The epidemiology, clinical features, comorbidities, and diagnosis of psoriasis in children will be reviewed here. Detailed discussions of specific clinical variants of psoriasis, psoriatic arthritis in children, and the management of psoriasis in children are provided separately.

(See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)

(See "Guttate psoriasis".)

(See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis".)

(See "Pustular psoriasis: Management".)

(See "Erythrodermic psoriasis in adults".)

(See "Nail psoriasis".)

(See "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis".)

(See "Psoriatic juvenile idiopathic arthritis: Management and prognosis".)

(See "Psoriasis in children: Management of chronic plaque psoriasis".)

EPIDEMIOLOGY — Psoriasis is a common disorder that often begins in childhood. In a questionnaire survey of 5600 individuals with psoriasis (median age 44 years, range 1 to 92 years), approximately one-third reported onset of disease during the first two decades of life and 10 percent reported onset prior to the age of 10 years [1].

The prevalence of psoriasis varies geographically. Worldwide, prevalence estimates range from 0.51 to 11.3 percent of adults and 0 to 1.37 percent of children [2]. Psoriasis is more frequent in older children than young children. A review of data from 1.3 million individuals within a German statutory health insurance organization found an approximately linear increase in the proportion of patients with a diagnosis of psoriasis from 0.12 percent at age 1 year to 1.24 percent at age 18 years [3].

As in adults, the incidence of psoriasis in children has increased over time. A population-based study in Olmstead County, Minnesota, found that the annual incidence of pediatric psoriasis doubled between the periods of 1970 to 1974 and 1995 to 1999 (29.6 per 100,000 to 62.7 per 100,000, respectively) [4]. The rising prevalence of obesity, a risk factor for psoriasis, may contribute to this finding [4].

RISK FACTORS — A complex interplay of environmental and genetic factors contributes to risk for psoriasis. A family history of psoriasis is a common risk factor; in a multicenter study of 409 children with psoriasis, approximately 30 percent reported an immediate family member with psoriasis [5].

The most common predisposing genetic risk factor for early-onset psoriasis (onset under the age of 40 years) is the human leukocyte antigen (HLA) type Cw6 (PSOR1) [6]. Less common is a pathogenic mutation in CARD14 (caspase recruitment domain family 14; PSOR2), which is transmitted in an autosomal dominant fashion and may manifest as pityriasis rubra pilaris, erythrodermic psoriasis, pustular psoriasis, or plaque psoriasis [7,8].

Multiple environmental factors may trigger or exacerbate psoriasis [9]. Examples include skin trauma (Koebner phenomenon), infections (eg, streptococcal [most common], staphylococcal, and varicella zoster infections), Kawasaki disease, certain medications, and psychologic and physical stress [10-15].

Greater detail on the genetic and environmental risk factors for psoriasis is provided separately. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Risk factors'.)

PATHOGENESIS — Cutaneous inflammation in psoriasis is mediated by both the innate and adaptive immune systems. Activation of myeloid dendritic cells by tumor necrosis factor (TNF)-alpha, interferon-gamma, interleukin (IL) 6, and IL-1-beta stimulates the adaptive immune system via IL-23. The adaptive immune response is characterized by expression of primarily Th17 and TNF/IL-17 synergistic cytokines, in contrast to the Th2 response that predominates in atopic dermatitis. These proinflammatory cytokines stimulate further release of inflammatory mediators (including TNF) from keratinocytes, perpetuating the immune activation and resulting in the brightly erythematous, scaly plaques of psoriasis [16,17]. The pathophysiology of psoriasis is reviewed in greater detail separately. (See "Pathophysiology of plaque psoriasis".)

CLINICAL PRESENTATION — The classic erythematous and scaly plaques of psoriasis can occur in various forms and distributions. The major clinical variants of psoriasis include chronic plaque psoriasis, guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. In addition, certain distributions of psoriasis are more common in children than in adults, including face, scalp, intertriginous, and diaper area involvement (figure 1).

Chronic plaque psoriasis — Chronic plaque psoriasis is the most common presentation of psoriasis in both children and adults [18-20]. The classic cutaneous findings are round, brightly erythematous, well-demarcated plaques covered with silvery-white (mica-like or "micaceous") scale (picture 1A-D and figure 1). Children may also present with plaques with less distinct borders or thinner scale. In patients with highly pigmented skin (Fitzpatrick skin type V or VI (table 1)), erythema may not be prominent and plaques may appear violaceous or hyperpigmented rather than erythematous (picture 2A-B).

Plaque psoriasis may present with few plaques or in a more generalized distribution, but the distribution is often symmetric. As in adults, the elbows and knees are the most common sites for chronic plaque psoriasis. Other common areas of involvement include the scalp, lower back, and the anogenital region (figure 1). Formation of psoriasis plaques in sites of cutaneous trauma, termed the "Koebner phenomenon," is also characteristic. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Chronic plaque psoriasis'.)

Guttate psoriasis — Guttate psoriasis is a common initial presentation of psoriasis in children. In a multicenter study of 181 children with psoriasis, approximately 30 percent had a history of a guttate presentation [21].

Guttate psoriasis is characterized by the acute and generalized eruption of small, round, erythematous, and "drop-like" scaly papules (picture 3). As with chronic plaque psoriasis, plaques may appear violaceous or hyperpigmented in patients with darkly pigmented skin. Guttate psoriasis often occurs in association with group A streptococcal infection. (See "Guttate psoriasis".)

Pustular and erythrodermic psoriasis — Generalized pustular psoriasis and erythrodermic psoriasis are severe forms of psoriasis. These variants are rare in children.

Generalized pustular psoriasis is characterized by a generalized acute or subacute annular eruption of erythematous, thin plaques with numerous discrete pustules (picture 4). Children can present with pustules on preexisting psoriatic plaques or, more commonly, on previously normal skin. The pustules are usually sterile but can become secondarily infected. The pustules progress to crusts, and patients with acute disease ultimately progress to generalized erythroderma and exfoliation. Nail and mucous membrane involvement is not uncommon. Hospitalization is often required for acute generalized pustular psoriasis due to associated abnormalities in temperature regulation and cardiovascular stability. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis".)

Pustular psoriasis may also present with involvement limited to the palms and soles (pustulosis palmaris et plantaris) or intertriginous distribution that begins in infancy [22]. (See "Palmoplantar pustulosis: Epidemiology, clinical features, and diagnosis".)

Pustular psoriasis may be an indicator of rare genetic syndromes. Pustular psoriasis in infancy, especially when there is associated sterile osteomyelitis or periostitis, should raise suspicion for abnormalities of interleukin (IL) 1 (deficiency of IL-1 receptor antagonist [DIRA]) or IL-36 (deficiency of IL-36 receptor antagonist [DITRA]), rare autosomal recessive disorders that present with pustular psoriasis [23-27]. Pustular psoriasis is also a less common manifestation of a CARD14 mutation [7,8]. (See "Autoinflammatory diseases mediated by miscellaneous mechanisms".)

The presentation of erythrodermic psoriasis overlaps with pustular psoriasis. Erythrodermic psoriasis is characterized by widespread cutaneous erythema and associated scale and exfoliation. (See "Erythroderma in children", section on 'Psoriasis' and "Erythrodermic psoriasis in adults".)

Paradoxical psoriasis — The term "paradoxical psoriasis" describes the drug-induced development of psoriatic skin lesions in patients treated with biologic tumor necrosis factor (TNF)-alpha inhibitors. In a systematic review that included 210 pediatric patients with paradoxical psoriasis, plaque psoriasis and alopecia due to psoriatic inflammation on the scalp were the most common manifestations, and the scalp and ears were the most common sites of involvement [28].

Special sites — Facial, scalp, intertriginous, and diaper area involvement are particularly common distributions of psoriasis in children (figure 1):

Facial involvement – Facial psoriasis is more common in children than in adults and is the sole manifestation of psoriasis in 4 to 5 percent of children [11,20,29,30]. In children, facial psoriasis often presents as erythematous, scaly patches or plaques on the eyebrows, nasolabial folds, perioral skin, or other facial areas (picture 5C) [30].

Scalp involvement – Scalp psoriasis is common in children with psoriasis, occurring in up to 79 percent [21]. Scalp psoriasis is more common in girls than boys, which may be secondary to the Koebner phenomenon (lesion development in sites of skin trauma) induced by frequent combing, brushing, or vigorous shampooing [21].

Well-demarcated, erythematous, scaly plaques are typical, although the plaques may also have a salmon-colored, greasy appearance similar to seborrheic dermatitis (picture 5A-B). While seborrheic dermatitis tends to remain within the hairline, psoriasis plaques often extend beyond the hairline to the upper forehead, pre- and postauricular skin, and nuchal areas (picture 6).

Inverse psoriasis – Inverse psoriasis occurs more frequently in the pediatric population than in adults. Shiny, erythematous, thin plaques occur in a flexural distribution (eg, axillae, inguinal skin, gluteal cleft), sparing the extensor surfaces (picture 5D) [31]. Scale is minimal or absent.

Diaper area involvement – Psoriatic diaper rash (also known as "napkin psoriasis") may be the initial manifestation of psoriasis in young children, with or without psoriasis present elsewhere on the body [20]. Children typically have brightly erythematous and well-demarcated plaques on skin covered by the diaper (picture 7A-C). Scale is often masked by the increased moisture in the diaper area. Psoriatic diaper rash often resolves with toilet training, suggesting that the Koebner phenomenon contributes to development. Children may continue to have anogenital psoriasis past infancy.

Nail psoriasis – Nail involvement affects 25 to 50 percent of children with psoriasis and is more common in boys than girls [21]. Pitting is the most common manifestation but discoloration, onycholysis, and subungual hyperkeratosis also occur (picture 8A-B). (See "Nail psoriasis" and "Overview of nail disorders".)

COMORBIDITIES — Pediatric psoriasis is associated with increased risk for various comorbidities, including obesity and other cardiovascular risk factors, arthritis, psychiatric disorders, and other diseases [9].

Obesity and cardiovascular risk — Obesity is the most common comorbidity of pediatric psoriasis. In an international, cross-sectional study of 409 children with psoriasis, children with psoriasis were significantly more likely to be obese (body mass index [BMI] ≥95th percentile) than controls (odds ratio [OR] 4.29, 95% CI 1.96-9.39) [5]. Both children with severe psoriasis and children with milder psoriasis exhibited elevated risk for obesity (OR 4.92, 95% CI 2.20-10.99 and OR 3.60, 95% CI 1.56-8.30).

Children with psoriasis also appear to have increased risk for other components of the metabolic syndrome. Population-based studies have found increased rates of hyperlipidemia, hypertension, and diabetes in children with psoriasis [3,32].

However, although psoriasis is independently associated with an increased risk of metabolic syndrome, this risk appears to be largely driven by obesity. In a retrospective cohort study using administrative claim data from a large database of privately insured patients over a 10-year period, nearly 30,000 children with psoriasis were compared with a similar-size cohort of age- and sex-matched children without psoriasis [33]. Nonobese children with psoriasis had an approximately 40 to 75 percent increased risk of elevated lipid levels, hypertension, diabetes, and metabolic syndrome compared with nonobese children without psoriasis. In contrast, these risks were 6 to 20 times higher in children with psoriasis who were also obese and were similar to those estimated in obese children without psoriasis.

Psoriatic arthritis — Psoriatic arthritis is estimated to occur in less than 6 percent of children with psoriasis [5]. Psoriatic arthritis may precede or follow the onset of cutaneous manifestations of psoriasis. Younger children tend to have dactylitis and small joint involvement, while older children more often have enthesitis and axial joint disease [34,35]. Psoriatic arthritis in children is reviewed in detail separately. (See "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis".)

Psychosocial effects — Psoriasis has a negative effect on the quality of life of both affected children and their families [36,37]. In a study of 208 children (ages 4 to 17 years) with moderate to severe plaque psoriasis, health-related quality of life was similar to children with arthritis and asthma and worse than children with diabetes [38]. Children with psoriasis also have an increased risk of anxiety and depression [39,40].

Other — Less common disorders that may occur with increased frequency in children with psoriasis include Crohn disease (but not ulcerative colitis), rheumatoid arthritis, and uveitis [3,41,42].

A general review of comorbidities of psoriasis is provided separately. (See "Comorbid disease in psoriasis".)

DIAGNOSIS — The diagnosis of psoriasis in children usually can be made based upon the clinical features. A skin biopsy is not necessary for the diagnosis of most patients.

Clinical assessment — Performance of a full skin examination is helpful for diagnosis and assessing the extent of disease. The classic clinical findings of plaque psoriasis are well-demarcated, erythematous plaques (figure 1). Of note, erythema may be less obvious in patients with highly pigmented skin (Fitzpatrick skin type V or VI) (picture 2A-B). Plaques may appear violaceous or hyperpigmented rather than erythematous in these patients.

Certain features strongly suggest specific clinical forms of psoriasis:

Chronic plaque psoriasis – Presents with erythematous plaques with micaceous scale and sharply demarcated borders, often involving sites such as the elbows, knees, scalp, or lower back (picture 1A-B, 1D and figure 1). Children may also exhibit plaques with thinner scale or less distinct borders. Removal of scale from plaques often results in pinpoint areas of bleeding (Auspitz sign). Facial, intertriginous, and diaper-area involvement are also common in children; however, scale may be minimal or absent in these areas.

Guttate psoriasis – Presents with numerous, small, "drop-like," erythematous papules and plaques, particularly when involving the trunk and proximal extremities (picture 3). Plaques are erythematous.

Generalized pustular psoriasis and erythrodermic psoriasis – Acute generalized pustular psoriasis presents with widespread erythema, pustules, and scale. Erythrodermic psoriasis presents with widespread erythema and scale. Patients with these disorders often appear systemically ill.

Inverse psoriasis – Presents with well-demarcated, shiny, erythematous, thin plaques within skin folds and/or on anogenital skin (picture 5D). Scale is minimal or absent.

Diaper area (napkin) psoriasis – Presents with shiny, erythematous patches involving skin covered by diaper; there is minimal or absent scale (picture 8A-B). Psoriasis involving other sites also may be present.

Additional features that support a diagnosis of psoriasis, but are not required for diagnosis, include:

Family history of psoriasis

Concomitant nail dystrophy consistent with nail psoriasis (see "Nail psoriasis")

Onset associated with known disease trigger (eg, streptococcal infection) (see 'Risk factors' above)

History of the Koebner phenomenon (development of skin disease in sites of skin trauma)

Joint or axial symptoms or signs suggestive of psoriatic arthritis (see "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical manifestations')

Skin biopsy — Skin biopsies are almost never performed in children with psoriasis. When the diagnosis is in question, however, a confirmatory biopsy can be performed; this is most often necessary with pustular psoriasis. The histologic findings of psoriasis include epidermal thickening, retention of nuclei in the stratum corneum (parakeratosis), and a mononuclear infiltrate with collections of neutrophils in the stratum corneum and/or subcorneal layer.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of psoriasis includes atopic dermatitis as well as other papulosquamous disorders that can occur in children (figure 1). Most often, the history and physical examination are sufficient to distinguish psoriasis from these conditions, but a skin biopsy can be helpful in ambiguous presentations.

Disorders commonly in the differential diagnosis of guttate and plaque psoriasis include:

Atopic dermatitis – Atopic dermatitis is common in children (figure 1). In infants, atopic dermatitis often manifests as erythematous, scaly patches on the face, extensor surfaces, and/or scalp (picture 9A-B). The diaper area is usually spared (picture 9B). Older children usually have erythematous patches or lichenified plaques in flexural areas (eg, antecubital and popliteal fossae, volar wrists, ankles, or neck (picture 10)). Occasionally, children present with an overlap of atopic dermatitis and psoriasis, consisting of lesions with intermediate morphology or the presence of lesions characteristic of each condition, which can complicate a clinical diagnosis [20]. The plaques of psoriasis tend to be more well-defined and less pruritic than those of atopic dermatitis. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

Pityriasis rosea – Pityriasis rosea is a benign, self-limited disorder that may be confused with guttate psoriasis. Pityriasis rosea often begins with a single lesion ("herald patch") followed by a secondary eruption. The herald patch tends to be a well-demarcated, scaly patch on the trunk, upper arm, neck, or thigh with a slightly elevated outer border. The secondary eruption consists of smaller, often pruritic papules with a collarette of scale (picture 11A-B). The papules most often occur in a characteristic "Christmas tree" distribution on the trunk, usually sparing the face and distal extremities. Spontaneous resolution usually occurs within a few months. The histopathologic features of pityriasis rosea are not diagnostic, but the characteristic distribution and natural history helps to distinguish this condition from guttate psoriasis. (See "Pityriasis rosea".)

Pityriasis lichenoides chronica – Pityriasis lichenoides chronica (PLC) is rare inflammatory skin condition, which is part of the spectrum of pityriasis lichenoides. PLC can develop de novo or progress from pityriasis lichenoides et varioliformis acuta (PLEVA). Clinically, PLC consists of multiple and diffuse, scaly, erythematous to brown papules and plaques that remit (with residual dyspigmentation) and relapse over months to years (picture 12). Unlike psoriasis, PLC tends not to improve with topical corticosteroids but may resolve with systemic antibiotic therapy. Histopathologic evaluation of biopsy specimens can further distinguish PLC from psoriasis if clinical assessment is insufficient. (See "Pityriasis lichenoides chronica".)

Pityriasis rubra pilaris Pityriasis rubra pilaris (PRP) is a skin condition typically characterized by follicular papules coalescing into hyperkeratotic plaques and accompanied by salmon-colored palmoplantar keratoderma (picture 13). The clinical course varies from resolution within 6 to 12 months to a more protracted course, with remissions and exacerbations similar to psoriasis. When unable to distinguish psoriasis and PRP morphologically, pathology can be helpful. Biopsy of follicular-based PRP lesions reveals follicular keratosis, alternating epidermal parakeratosis and orthokeratosis, and dermal mononuclear cell infiltrates. Some patients may at times show features of PRP and at other times psoriasis; it is possible that these patients harbor a heterozygous mutation in CARD14, which may variably manifest as PRP, psoriasis, or erythrodermic psoriasis with pustules [7,8]. (See "Pityriasis rubra pilaris: Pathogenesis, clinical manifestations, and diagnosis".)

The differential diagnosis of localized and generalized pustular psoriasis includes other pustular disorders that can occur in children, such as infectious pustulosis, eosinophilic pustular folliculitis in infants, and infantile acropustulosis. A culture can distinguish infectious pustulosis from the sterile pustules of pustular psoriasis. Eosinophilic pustular folliculitis in infancy typically begins within the first few weeks of life and is characterized by recurrent crops of pustules on the scalp and face. Less frequently, other body areas are involved. Acropustulosis of infancy usually begins within the first several months of life and presents with recurrent crops of pruritic vesicles and pustules, with a predilection for acral skin (picture 14). A skin biopsy can help to distinguish eosinophilic folliculitis and infantile acropustulosis from pustular psoriasis when needed. (See "Vesicular, pustular, and bullous lesions in the newborn and infant".)

ADDITIONAL EVALUATION — Psoriatic arthritis is a common comorbidity of psoriasis. Children should be assessed for signs or symptoms of psoriatic arthritis at the time of diagnosis of psoriasis and periodically thereafter. Helpful screening questions include inquiring about joint redness and swelling, limp, and joint pain and stiffness after inactivity. Suggestive clinical findings include oligoarthritis, spinal or sacroiliac arthritis, enthesitis, dactylitis, and uveitis. The diagnosis of psoriatic arthritis in children is reviewed separately. (See "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnosis'.)

Given the association of psoriasis with increased risk for other diseases (eg, obesity, hypertension, hyperlipidemia, diabetes), clinicians treating children for psoriasis should be cognizant of recognizing children who may benefit from screening for comorbidities [43]. (See 'Comorbidities' above.)

Psoriasis can have negative psychosocial effects. Asking children about their feelings about their psoriasis may help to identify children who may benefit from emotional support or other interventions. National support groups, such as the National Psoriasis Foundation, offer education and support. (See 'Psychosocial effects' above.)

In sum, we agree with the pediatric psoriasis comorbidity screening guidelines outlined in the joint American Academy of Dermatology-National Psoriasis Foundation (AAD-NPF) guidelines of care for the management and treatment of psoriasis in pediatric patients [9]. Some of the recommendations for screening for specific disorders, including insulin resistance, dyslipidemia, hypertension, nonalcoholic fatty liver disease, and mental health, overlap with recommendations for children without psoriasis, and screening can be performed as part of routine health assessment visits in the primary care setting.

The AAD-NPF screening guidelines for children with psoriasis include:

Obesity – Routinely assess for obesity status. Routinely assess obese patients for comorbidities of obesity. (See "Clinical evaluation of the child or adolescent with obesity".)

Cardiovascular disease – Screen for cardiovascular risk factors when history and physical examination findings show a potential risk. Patients who have cardiovascular risk factors (eg, obesity, dyslipidemia, diabetes, hypertension, or metabolic syndrome) should be referred to appropriate specialists for additional evaluation and management. (See "Pediatric prevention of adult cardiovascular disease: Promoting a healthy lifestyle and identifying at-risk children", section on 'Identifying children at risk for cardiovascular disease'.)

Insulin resistance – Screen or refer for screening for insulin resistance and diabetes mellitus every three years in obese children (or overweight children with other risk factors for insulin resistance) beginning at age 10 or the onset of puberty, whichever is first. (See "Epidemiology, presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents", section on 'Screening'.)

Dyslipidemia – Screen or refer for screening for dyslipidemia (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride levels) between the ages of 9 and 11 years and between the ages of 17 and 21 years. Patients with increased risk for dyslipidemia may be screened more often based upon the clinician's discretion. Refer patients with dyslipidemia to their primary care clinician or an endocrinologist for additional evaluation and management. (See "Dyslipidemia in children and adolescents: Definition, screening, and diagnosis".)

Hypertension – Screen for hypertension annually beginning at three years of age. (See "Definition and diagnosis of hypertension in children and adolescents".)

Nonalcoholic fatty liver disease – Obtain or refer for obtainment of alanine aminotransferase measurement starting at nine years of age for obese children and overweight children. Screening should be repeated every two to three years. (See "Metabolic dysfunction-associated steatotic liver disease in children and adolescents", section on 'Screening'.)

Psoriatic arthritis – Screen for arthritis through a thorough history and physical examination as part of standard ongoing management of children with psoriasis. Patients who show signs and symptoms of inflammatory arthritis should be referred to a rheumatologist with pediatric expertise, if available, for additional evaluation and management. (See "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnosis'.)

Mental health – Routinely screen or refer for screening for depression and anxiety in all children with psoriasis. Screen yearly for substance abuse beginning at 11 years of age. Refer patients with mental health or substance abuse concerns to an appropriate health care professional for assessment and management. (See "Screening tests in children and adolescents", section on 'Depression and suicide risk screening' and "Screening tests in children and adolescents", section on 'Nicotine, alcohol, and substance use'.)

Inflammatory bowel disease – For patients with signs and symptoms of inflammatory bowel disease, consider consultation with a gastroenterologist with pediatric expertise, if available, for further evaluation and management. (See "Clinical presentation and diagnosis of inflammatory bowel disease in children".)

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".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Psoriasis (The Basics)" and "Patient education: Psoriatic arthritis in children (The Basics)")

Beyond the Basics topics (see "Patient education: Psoriasis (Beyond the Basics)" and "Patient education: Psoriatic arthritis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Epidemiology – Psoriasis is a common immune-mediated disease that may begin during childhood or adulthood. Approximately one-third of adults with psoriasis have a history of disease onset during the first two decades of life. (See 'Epidemiology' above.)

Risk factors – A complex interplay of environmental and genetic factors contributes to risk for psoriasis. The human leukocyte antigen type Cw6 (PSOR1) is the most common predisposing genetic risk factor for early-onset psoriasis (psoriasis before age 40 years). (See 'Risk factors' above.)

Clinical presentation:

Variants – The major clinical forms of psoriasis are similar in children and adults. Chronic plaque psoriasis is the most common form of psoriasis in children. Guttate, pustular, and erythrodermic psoriasis are less frequent. (See 'Clinical presentation' above.)

Chronic plaque psoriasis is characterized by the presence of well-demarcated, erythematous plaques with silvery-white, mica-like scale (picture 1A-D and figure 1). In children with highly pigmented skin (Fitzpatrick skin type V or VI), erythema may be less prominent and plaques may appear violaceous or hyperpigmented (picture 2A-B). (See 'Chronic plaque psoriasis' above.)

Sites of involvement – Children with psoriasis are more likely to present with psoriasis involving the face, scalp, or intertriginous skin than adults (picture 5A-D). Involvement of the diaper area (also known as "napkin psoriasis") can be the initial manifestation of psoriasis in infants and young children (picture 7A-C). (See 'Special sites' above.)

Comorbidities – Children with psoriasis have increased risk for a variety of other diseases. Examples include psoriatic arthritis, obesity, hypertension, diabetes, hyperlipidemia, depression, and anxiety. (See 'Comorbidities' above.)

Diagnosis – The diagnosis of psoriasis in children usually can be made based upon the clinical features (figure 1). Skin biopsies are reserved for patients in whom the diagnosis remains uncertain after the clinical evaluation. (See 'Diagnosis' above.)

  1. Farber EM, Nall ML. The natural history of psoriasis in 5,600 patients. Dermatologica 1974; 148:1.
  2. Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol 2017; 31:205.
  3. Augustin M, Glaeske G, Radtke MA, et al. Epidemiology and comorbidity of psoriasis in children. Br J Dermatol 2010; 162:633.
  4. Tollefson MM, Crowson CS, McEvoy MT, Maradit Kremers H. Incidence of psoriasis in children: a population-based study. J Am Acad Dermatol 2010; 62:979.
  5. Paller AS, Mercy K, Kwasny MJ, et al. Association of pediatric psoriasis severity with excess and central adiposity: an international cross-sectional study. JAMA Dermatol 2013; 149:166.
  6. Nair RP, Duffin KC, Helms C, et al. Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nat Genet 2009; 41:199.
  7. Jordan CT, Cao L, Roberson ED, et al. PSORS2 is due to mutations in CARD14. Am J Hum Genet 2012; 90:784.
  8. Eytan O, Qiaoli L, Nousbeck J, et al. Increased epidermal expression and absence of mutations in CARD14 in a series of patients with sporadic pityriasis rubra pilaris. Br J Dermatol 2014; 170:1196.
  9. Menter A, Cordoro KM, Davis DMR, et al. Joint American Academy of Dermatology-National Psoriasis Foundation guidelines of care for the management and treatment of psoriasis in pediatric patients. J Am Acad Dermatol 2020; 82:161.
  10. Shah KN. Diagnosis and treatment of pediatric psoriasis: current and future. Am J Clin Dermatol 2013; 14:195.
  11. Nyfors A, Lemholt K. Psoriasis in children. A short review and a survey of 245 cases. Br J Dermatol 1975; 92:437.
  12. Pouessel G, Ythier H, Carpentier O, et al. Childhood pustular psoriasis associated with Panton-Valentine leukocidin-producing Staphylococcus aureus. Pediatr Dermatol 2007; 24:401.
  13. Ito T, Furukawa F. Psoriasis guttate acuta triggered by varicella zoster virus infection. Eur J Dermatol 2000; 10:226.
  14. Ergin S, Karaduman A, Demirkaya E, et al. Plaque psoriasis induced after Kawasaki disease. Turk J Pediatr 2009; 51:375.
  15. Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009; 361:496.
  16. Guttman-Yassky E, Nograles KE, Krueger JG. Contrasting pathogenesis of atopic dermatitis and psoriasis--part II: immune cell subsets and therapeutic concepts. J Allergy Clin Immunol 2011; 127:1420.
  17. Cai YH, Lu ZY, Shi RF, et al. Enhanced proliferation and activation of peripheral blood mononuclear cells in patients with psoriasis vulgaris mediated by streptococcal antigen with bacterial DNA. J Invest Dermatol 2009; 129:2653.
  18. Fan X, Xiao FL, Yang S, et al. Childhood psoriasis: a study of 277 patients from China. J Eur Acad Dermatol Venereol 2007; 21:762.
  19. Mallbris L, Larsson P, Bergqvist S, et al. Psoriasis phenotype at disease onset: clinical characterization of 400 adult cases. J Invest Dermatol 2005; 124:499.
  20. Morris A, Rogers M, Fischer G, Williams K. Childhood psoriasis: a clinical review of 1262 cases. Pediatr Dermatol 2001; 18:188.
  21. Mercy K, Kwasny M, Cordoro KM, et al. Clinical manifestations of pediatric psoriasis: results of a multicenter study in the United States. Pediatr Dermatol 2013; 30:424.
  22. Bellet JS, Chamlin SL, Yan AC, Paller AS. Intertriginous pustular psoriasis. J Am Acad Dermatol 2009; 60:679.
  23. Minkis K, Aksentijevich I, Goldbach-Mansky R, et al. Interleukin 1 receptor antagonist deficiency presenting as infantile pustulosis mimicking infantile pustular psoriasis. Arch Dermatol 2012; 148:747.
  24. Marrakchi S, Guigue P, Renshaw BR, et al. Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis. N Engl J Med 2011; 365:620.
  25. Posso-De Los Rios CJ, Pope E. New insights into pustular dermatoses in pediatric patients. J Am Acad Dermatol 2014; 70:767.
  26. Sugiura K, Takemoto A, Yamaguchi M, et al. The majority of generalized pustular psoriasis without psoriasis vulgaris is caused by deficiency of interleukin-36 receptor antagonist. J Invest Dermatol 2013; 133:2514.
  27. Farooq M, Nakai H, Fujimoto A, et al. Mutation analysis of the IL36RN gene in 14 Japanese patients with generalized pustular psoriasis. Hum Mutat 2013; 34:176.
  28. Cyrenne BM, Parpia AS, Sibbald C. Paradoxical psoriasis in pediatric patients: A systematic review. Pediatr Dermatol 2021; 38:1086.
  29. Nanda A, Kaur S, Kaur I, Kumar B. Childhood psoriasis: an epidemiologic survey of 112 patients. Pediatr Dermatol 1990; 7:19.
  30. Farber EM. Facial psoriasis. Cutis 1992; 50:25.
  31. Benoit S, Hamm H. Childhood psoriasis. Clin Dermatol 2007; 25:555.
  32. Koebnick C, Black MH, Smith N, et al. The association of psoriasis and elevated blood lipids in overweight and obese children. J Pediatr 2011; 159:577.
  33. Tollefson MM, Van Houten HK, Asante D, et al. Association of Psoriasis With Comorbidity Development in Children With Psoriasis. JAMA Dermatol 2018; 154:286.
  34. Zisman D, Gladman DD, Stoll ML, et al. The Juvenile Psoriatic Arthritis Cohort in the CARRA Registry: Clinical Characteristics, Classification, and Outcomes. J Rheumatol 2017; 44:342.
  35. Stoll ML, Zurakowski D, Nigrovic LE, et al. Patients with juvenile psoriatic arthritis comprise two distinct populations. Arthritis Rheum 2006; 54:3564.
  36. Tollefson MM, Finnie DM, Schoch JJ, Eton DT. Impact of childhood psoriasis on parents of affected children. J Am Acad Dermatol 2017; 76:286.
  37. Randa H, Lomholt JJ, Skov L, Zachariae R. Health-related quality of life in adolescents with psoriasis: an interview-based study. Br J Dermatol 2018; 178:1404.
  38. Varni JW, Globe DR, Gandra SR, et al. Health-related quality of life of pediatric patients with moderate to severe plaque psoriasis: comparisons to four common chronic diseases. Eur J Pediatr 2012; 171:485.
  39. Kimball AB, Wu EQ, Guérin A, et al. Risks of developing psychiatric disorders in pediatric patients with psoriasis. J Am Acad Dermatol 2012; 67:651.
  40. Bilgic A, Bilgic Ö, Akış HK, et al. Psychiatric symptoms and health-related quality of life in children and adolescents with psoriasis. Pediatr Dermatol 2010; 27:614.
  41. Niccoli L, Nannini C, Cassarà E, et al. Frequency of iridocyclitis in patients with early psoriatic arthritis: a prospective, follow up study. Int J Rheum Dis 2012; 15:414.
  42. Rosenbaum JT. Uveitis in spondyloarthritis including psoriatic arthritis, ankylosing spondylitis, and inflammatory bowel disease. Clin Rheumatol 2015; 34:999.
  43. Osier E, Wang AS, Tollefson MM, et al. Pediatric Psoriasis Comorbidity Screening Guidelines. JAMA Dermatol 2017; 153:698.
Topic 110152 Version 7.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟