Are There Any Skin Conditions That Mimic Eczema
J Clin Med. 2015 May; four(5): 884–917.
Diagnosis of Atopic Dermatitis: Mimics, Overlaps, and Complications
Elaine C. Siegfried
1Saint Louis University, Fundamental Glennon Children's Infirmary, 1465 South Grand Avenue, St. Louis, MO 63104, United states
Adelaide A. Hebert
2University of Texas-Houston Medical School, 6655 Travis, Suite 980, Houston, TX 77030, USA; E-Mail: ude.cmt.htu@trebeH.A.edialedA
Sebastien Barbarot, Academic Editor and Kim Thomas, Bookish Editor
Received 2015 Jan 31; Accustomed 2015 Apr 21.
Abstract
Atopic dermatitis (Advertizement) is i of the well-nigh common skin diseases affecting infants and children. A smaller subset of adults has persistent or new-onset AD. Advertisement is characterized past pruritus, erythema, induration, and scale, just these features are also typical of several other conditions that can mimic, coexist with, or complicate AD. These include inflammatory skin conditions, infections, infestations, malignancies, genetic disorders, immunodeficiency disorders, nutritional disorders, graft-versus-host affliction, and drug eruptions. Familiarity of the spectrum of these diseases and their distinguishing features is critical for correct and timely diagnosis and optimal handling.
Keywords: atopic dermatitis, differential diagnosis, eczema, adult, boyish, child, eczema herpeticum, eczema coxsackium, immunodeficiency, seborrheic dermatitis, psoriasis
1. AD Diagnosis
Atopic dermatitis (AD) is the most common chronic pare affliction in children, typically presenting in patients less than two years of age. Prevalence is highest among blackness children [i] with age-related gender variation. A slight predominance has been documented in male pre-schoolhouse-aged children and in adult females [2].
The diagnosis is based on age-specific clinical criteria that include pruritus and chronic or relapsing spongiotic dermatitis involving the face, trunk, and/or extensor extremities in infants, flexural surfaces like the wrists/ankles and antecubital/popliteal fossae in children, or the easily in adults (Table 1). The "diaper area"/groin and axillae are typically spared. Generalized xerosis is a ubiquitous feature, often with fibroid ichthyosiform scale and palmoplantar hyperlinearity. Skin lesions are typically diffuse and very pruritic. Advertizement is characterized by interval flares, frequently without obvious triggers. Acutely flaring AD features erythema, edema, and scale, often with multiple and widespread excoriations (Figure 1). Papular follicular changes are more prominent in darker peel types. In more severe cases, fine vesicles/papules are obvious, with serous drainage and crusting. Lichenification and dyspigmentation are chronic changes, and are more prominent in darker skin types. Frequent comorbidities include sleep impairment, psychiatric and mood disorders, asthma, allergic rhinitis, and allergic conjunctivitis. Eosinophilic gastroenteritis and celiac disease are as well frequent comorbidities of Advert; however, there is currently no evidence to support implementing nutrient elimination diets (including gluten-complimentary diets) in the absence of suggestive signs or symptoms.
Table 1
American Academy of Dermatology (AAD) Diagnostic Criteria for Atopic Dermatitis. Advertising indicates atopic dermatitis; IgE, immunoglobulin E.
Atopic dermatitis: clinical features.
Associated laboratory abnormalities include high levels of immunoglobin E (IgE) and circulating eosinophils, but pathognomonic biomarkers take not yet been identified, then diagnosis is based on personal/family history of atopy and physical examination to exclude other weather condition. A number of mimics, overlaps, and complications of Advertisement be and these differ past historic period group (Table 2 and Table 3). Department ii, Section iii, Section 4, Section 5, Section six, Department 7, Department 8 and Department ix discuss how these conditions may be dislocated with, coexist with, and/or complicate AD. Blood and skin testing for food and ecology allergic triggers should simply be considered for patients with suggestive signs temporally related to exposure (i.eastward., urticaria, gastrointestinal or respiratory symptoms, anaphylaxis), or those with AD that is unresponsive to optimized treatment.
Table 2
Diagnosis of atopic dermatitis: common mimics, overlaps, and complications and relative prevalence by age grouping.
| Diagnosis | Relative Prevalence | |||
|---|---|---|---|---|
| Infants | Children | Adolescents/Adults | ||
| Inflammatory Skin Conditions (Run across Section ii) | seborrheic dermatitis | common | uncommon | common |
| psoriasis | less common | less common | common | |
| nummular dermatitis | less common | common | less common | |
| contact dermatitis a | common | common | mutual | |
| dermatographism a | less mutual | common | common | |
| pityriasis alba a | mutual | common | uncommon | |
| overlap (see Section 2.seven) | common | common | common | |
| Infections (See Department 3) | impetigo a | common | common | less common |
| secondary syphilis | rare | rare | rare | |
| molluscum dermatitis a | common | common | less common | |
| eczema herpeticum a | uncommon | uncommon | rare | |
| eczema vaccinatum a | rare | rare | rare | |
| eczema coxsackium a | emerging | emerging | rare | |
| viral exanthem | mutual | common | less mutual | |
| tinea (as AD mimic) | uncommon | uncommon | uncommon | |
| candidiasis | common | less mutual | less mutual | |
| Infestations (See Section 4) | scabies (prevalence varies by region) | may exist common | may exist common | may exist common |
| Genetic Disorders (See Department 6) | keratosis pilaris | less common | common | not mutual |
| ichthyosis vulgaris a | mutual | common | common | |
| Immunodeficiency Disorders (Come across Department 7) | HIV/AIDS-related pare changes (prevalence varies past region) | less common | less common | may exist common |
| Other (See Section 9) | drug eruptions | less common | common | common |
Table three
Differential diagnosis of atopic dermatitis: Rare disorders by age group. Ig indicates immunoglobulin.
| Infants | Children | Adolescents/Adults | |
|---|---|---|---|
| Malignancies (Run across Section 5) | ● Letterer-Siwe Disease | ● Letterer-Siwe Illness | ● Letterer-Siwe Affliction |
| ● cutaneous T-prison cell lymphoma | ● cutaneous T-jail cell lymphoma | ● cutaneous T-jail cell lymphoma | |
| Genetic Disorders (See Section 6) | ● 10-linked recessive ichthyosis (males only) | ● 10-linked recessive ichthyosis (males only) | ● X-linked recessive ichthyosis (males only) |
| ● lamellar ichthyosis | ● lamellar ichthyosis | ||
| ● nonbullous ichthyosiform erythroderma | ● nonbullous ichthyosiform erythroderma | ● nonbullous ichthyosiform erythroderma | |
| Immunodeficiency Disorders (See Department 7) | ● Netherton syndrome | ● IgA deficiency ● IgM deficienc | ● IgA deficiency |
| ● STAT3 deficiency | |||
| ● DOCK8 deficiency | |||
| ● Wiskott-Aldrich syndrome (males simply) | |||
| ● Leiner Phenotype | |||
| ○ astringent combined immunodeficiency | |||
| ○ Omenn syndrome | ● IgM deficiency | ||
| ● hypohidrotic ectodermal dysplasia/NEMO | |||
| ● autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) | |||
| Nutritional Disorders (See Section 8) | ● cystic fibrosis | ● | ● dermatitis herpetiformis |
| ● phenylketonuria | |||
| ● zinc deficiency | |||
| ● biotin deficiency | |||
| Other (See Section 9) | ● maternal-fetal graft-versus-host illness | ● graft-versus-host disease | ● graft-versus-host disease |
Accurate diagnosis is critical to optimal patient intendance. Standard arroyo to handling begins with education regarding the chronic relapsing nature of Advertisement, which is be best controlled by bland skin care and adequate amounts of topical corticosteroids (TCS) for flares [4,5], In addition, topical calcineurin inhibitors (TCIs) or mild-to-moderate TCS can be used for proactive maintenance treatment in moderate-to-severe chronic disease.
2. Inflammatory Skin Conditions
2.1. Seborrheic Dermatitis
Seborrheic dermatitis (SD) is a mutual inflammatory peel status about prominent on sebum-rich skin of the scalp and face up. Onset is related to hormone-driven sebum production during early infancy, which wanes forth with prevalence in childhood and increases once again in adolescence and machismo.
Both AD and SD are common in infants, and tin can occur together [6] frequently leading to defoliation. SD is distinguished by a lack of excoriations and slumber harm. In infants, SD typically involves the confront, scalp, and posterior auricular, nuchal, axillary, and/or inguinal folds. SD in adolescents and adults characteristically involves the scalp besides every bit alar and mesiolabial folds. SD lesions almost oft appear every bit salmon-pink patches with thick or greasy, white, fair, or yellow scales (Figure ii). Lesions are many times hypopigmented, peculiarly in patients with darker skin types, and may be misinterpreted every bit vitiligo.
SD affects male and female patients equally. Unlike AD, SD in infants normally resolves before two years of age. SD may be more than prevalent in adults with neurologic or psychiatric illness. Associated alopecia is rare, so tinea capitis (encounter Section iii.3.i) should be considered in children with both hair loss and scalp lesions. The differential diagnosis of thick, tenacious scalp scale with or without associated alopecia includes psoriasis (see Section 2.2). Acute worsening with associated tenderness is characteristic of superimposed streptococcal intertrigo (see Section 3.1).
The crusade of SD is not completely understood, merely it is often associated with Malassezia species (previously Pityrosporum), because this organism heavily colonizes sebum-rich skin [7]. For this reason, topical anti-yeast treatment is oft effectively used for long-term command [eight], while TCS and TCIs may exist used to chop-chop minimize redness and scaling [9].
two.2. Psoriasis
Psoriasis can bear upon patients of whatever age with no credible gender bias. The acme age of onset appears to be adolescence/early on adulthood [10,11], although psoriasis may be nether-recognized in infants and children. Psoriasis vulgaris, or plaque psoriasis, is the most mutual form of psoriasis and is characterized by sharply circumscribed, persistent erythematous, indurated plaques with silvery-white, adherent scale and a predilection for extensor surfaces of the elbows or knees, or for the thumb in infants who suck their thumb ("thumb sign") via the Köebner phenomenon (localization to areas of micro-trauma; Figure iii). Notwithstanding, other presentations are not uncommon and include acute widespread guttate, flexural ("inverse"), annular, palmoplantar, pustular, and scalp (pityriasis amiantacea, ofttimes accompanied by alopecia) psoriasis as well as psoriasis-eczema overlap (come across Section 2.7) [12].
In infants and children, psoriasis may be misdiagnosed as Advertizing because scaling is often less prominent and the distribution of lesions more ofttimes includes the face up. Unlike AD, psoriasis is frequently encountered in the diaper area. Nail interest (fine pits) is a subtle feature that can assistance differentiate psoriasis or coexisting psoriasis from AD in infants and children. Family history is often used as supporting bear witness for diagnosis; however, only nearly one-third of patients take a family history of psoriasis, which suggests that it may be underdiagnosed.
Although Streptococcal pharyngitis or pharyngeal colonization is a well-recognized psoriasis trigger, impetigo, or other peel infections are rare [11].
TCS are ofttimes used every bit start-line treatment [12], but long-term TCS monotherapy can be associated with suboptimal response and rebound. In these cases, addition of a topical steroid-sparing medication (due east.chiliad., vitamin D analog [thirteen], salicylic acrid [14] or TCI [xv]) may improve efficacy and increment the chances of remission.
2.iii. Nummular Dermatitis
Nummular dermatitis (ND) is characterized past round or oval (i.e., nummular), well-demarcated lesions that are sometimes itchy. Lesions are ordinarily asymmetrically distributed on the limbs, rarely on the face, just the rash may affect any expanse. Different AD, ND is unusual before age v [16].
The cause of ND is unknown, merely because many cases are associated with localized microtrauma (e.grand., insect bite, scratching), some consider this status to be a form of psoriasis. Other suspected factors include Staphylococcus aureus colonization, contact allergens or irritants, xerosis, or stasis dermatitis.
two.iv. Contact Dermatitis
Contact dermatitis (CD) is the most mutual form of dermatitis and like all dermatitis, acute CD is characterized by cutaneous erythema and edema. CD tin exist acute, chronic, persistent, or relapsing and it has been classically categorized every bit either irritant or allergic, simply both types can coexist. In infants and children, allergic CD often occurs in the same distribution equally irritant CD and may be underappreciated.
Allergic CD is a delayed-type hypersensitivity reaction, with onset subsequently several hours to days after allergen exposure. The distribution is classically geographic and oftentimes asymmetric. Irritant CD is a more rapid response to concrete bulwark microtrauma, typically occurring within minutes, and is often less itchy, less geographic, and more than symmetric (except in instances when allergen exposure is bilateral such as footwear or gloves) than allergic CD. Recognition of isolated CD relies on temporal pattern, too every bit suggestive distribution (Figure 4).
CD usually complicates other skin disease, including Advertizement. Impaired peel barrier part has been a suspected risk factor simply results of studies have been conflicting and take a chance may exist allergen-specific [17,xviii,nineteen,20]. Recognition of CD in the setting of coexisting skin affliction requires a loftier index of suspicion based on personal/family history, presence of xerosis, and, if necessary, results of "patch testing" (although the sensitivity of patch testing is less than 70%). Diagnostic skill is also important for recognition of a less common manifestation of allergic CD called autoeczematization or "id" reaction, characterized by advent of widespread, symmetrically distributed ectopic lesions [21,22].
Older adults take both greater lifetime risk of repeated allergen exposure and reduced skin barrier repair mechanisms, and and so may be specially prone to allergic CD [23]. Nonetheless, CD can bear upon patients of whatever age including infants and children, contrary to what had been previously believed [21,24]. In pediatric patients, irritant CD is about common on the face up, dorsal attribute of the hands, and "diaper area", often triggered by frequent cycles of skin wetting and drying besides as exposure to endogenous (e.k., drool, lip-licking, urine, and feces) or exogenous (e.g., cleansing products, highly alkaline or acidic foods) irritants. In adults, irritant and allergic CD about often presents as "hand dermatitis" triggered by frequent paw washing in healthcare and food industry workers. Common topical allergens include emulsifiers, preservatives, and fragrances used in topical products (e.g., diaper wipes, hand sanitizers, emollient lotions, and creams). Recognition of these triggers may be especially difficult when the allergen is an ingredient contained in products that accept been used as a treatment for dermatitis. In some cases, sensitization with ane allergen contained in a circuitous topical product volition enable cosensitization to another ingredient in the same product. Nickel is some other common sensitizer. Nickel allergic CD is classically localized to the infraumbilical surface area (from jean snaps) or ear lobules. Ear piecing in infancy is an important risk factor for nickel allergy.
The most effective manner to alleviate CD is with strict avoidance of likely triggers. When triggers cannot be identified/avoided or there is residual dermatitis after triggers take been removed, TCS [25,26] or TCIs [27,28,29] may reduce inflammation; however, chronic apply of TCS should be avoided, especially on the face and diaper area. Long term and frequent (greater than in one case daily) application of TCS (peculiarly higher potency preparations) is contraindicated, due to an increased risk of skin barrier compromise and systemic exposure.
2.5. Dermatographism
Dermatographism is an immunologic response to pressure level applied the peel, characterized past local wheal-and-flare erythema followed by edema and crawling (Figure v). Alternately known as dermographism, dermatographic urticaria, or mechanical urticaria, signs and itch classically begin within five min of stimulation and persist for 15–30 min. Delayed-type dermatographism is much less common, presenting as an urticarial response 3–half-dozen h afterwards stimulation, and lasting for 24–48 h, not ever preceded past an immediate wheal-and-flare. "White dermatographism" is a modest diagnostic benchmark for Advertising and presents every bit pallor rather than erythema, with subsequent erythematous halo (Figure 6).
White dermatographism (typically observed in atopic dermatitis).
Patients of whatsoever historic period can exist affected by dermatographism just it is most often diagnosed in young adults. Onset is generally gradual and resolution is often within v years [30]. Dermatographism can affect whatsoever region of the trunk including the palms and soles, simply not ordinarily the scalp or genitals. Tight clothing is a common trigger. Diagnosis is clinical and confirmed by the appearance of a wheal in response to mechanical stimulation. Although dermatographism is usually idiopathic, in some cases it is associated with drug reactions, scabies, stress/anxiety, or an underlying systemic disease (e.g., hyperthyroidism, type two diabetes mellitus). Trigger avoidance is the nigh effective mode to control dermatographism.
2.6. Pityriasis Alba
Pityriasis alba (PA) is a common, idiopathic, generally asymptomatic condition, often noted as an incidental finding on peel test. PA is associated with Advert, equally a minor diagnostic criterion. PA is well-nigh often found in school-historic period children with no gender bias [31].
PA appears every bit subtle, poorly circumscribed, hypopigmented patches with fine papular follicular accentuation, most frequently on the proximal upper extremities, although the face up and body are sometimes involved (Effigy vii). Patches become more prominent with increased summer sunday exposure, as surrounding skin tans. In winter, hypopigmentation is less prominent, and the patches feature powdery, white scale. Some reports take suggested that PA is more common in patients with darker skin, simply the condition is equiprevalent in all skin types, just more apparent on darker skin tones [31]. Astringent cases of PA are clinically indistinguishable from hypopigmented mycosis fungoides (see Section 5.ii).
Emollients tin minimize scaling but will not impact hypopigmentation, which may persist for months to years despite control of xerosis and inflammation. A few reports take documented efficacy of TCIs [32,33].
two.7. Overlap
"Overlap" is a term used to describe i or more circumstantial inflammatory skin diseases. The most well described combination may be psoriasis-eczema overlap (PsE), too known as eczematous psoriasis and PsEma. Patients with PsE typically present with a combination of flexural eczema and psoriatic lesions that lack thick plaques and are more likely to experience itch than patients with isolated psoriasis (Figure viii) [12,34,35]. In 1 study, PsE responded well to psoriasis handling strategies including TCS [34].
Psoriasis-eczema overlap.
3. Infections
3.1. Bacterial Infections
iii.1.one. Impetigo
Impetigo is a superficial, cutaneous bacterial infection that virtually often occurs at sites of minor skin trauma (e.1000., traumatic injury, irritation, dermatitis, insect bites). Impetigo is most often acquired by Due south. aureus or Streptococcus pyogenes and is characterized by erythema, edema, and tenderness, often with honey-xanthous crusting (Figure 9). Less common variants include bullous impetigo and Streptococcal intertrigo, which are classically superimposed on SD (come across Department ii.1). Pharyngeal or perianal Streptococcus carriage is a risk gene for Streptococcal impetigo. Impetigo is most common in young children, merely can occur at any historic period, with a college incidence in males [36].
Both Staphylococcal and Streptococcal impetigo are easily treated with peel cleansing and topical antibiotics. Dilute bleach baths may also exist helpful and will not contribute to the hazard of microbial resistance. Oral antibiotics are indicated for widespread disease, or accompanying fever. Patients with recurrent impetigo may do good from peel surface, nares, pharyngeal, or perianal cultures for mucosal carriage detection, bacterial identification, and antimicrobial resistance conclusion.
Patients with Ad are heavily colonized with S. aureus, on both dermatitic and normal-appearing skin, so skin cultures cannot differentiate colonization from true infection. True impetiginization in AD is most oftentimes characterized by acute onset with peel tenderness and crops of pustules. Despite frequent use of antibiotics among patients with Advertising, a high incidence of methicillin-resistant S. aureus (MRSA) has not been found in this population [37,38,39]. Mupirocin resistance is emerging [twoscore]. Command of impetiginized Ad may be initially managed with dilute bleach baths.
iii.i.2. Secondary Syphilis
Widespread availability of antibiotics has fabricated secondary syphilis (SS) a rare condition in all but immunocompromised patients; however, this condition, historically known as "the bully mimicker", is hands cured and should not be disregarded. In contrast to the local reaction observed in primary syphilis (oft a unmarried chancre), SS classically presents every bit a widespread eruption several weeks to months afterwards advent of the primary chancre (Figure ten) [41]. Near syphilitic disease in children is congenital and thus secondary due to the hematogenous spread from mother to fetus in utero (Figure 11).
Secondary syphilis can manifest in a number of ways but most frequently as a diffuse macular eruption that evolves into maculopapular or pustular lesions on the trunk and proximal extremities; however, any peel surface can be involved including the palms and soles [42]. Scaling, mucosal ulceration, patchy hair loss, and condyloma latum (greyish-white moist raised patches institute on moist skin surfaces) may also be nowadays. SS is non associated with pruritus. Cutaneous symptoms are often accompanied by fever, lymphadenopathy, angst, weight loss, and headache.
3.2. Viral Infections
3.ii.ane. Molluscum Dermatitis
In virtually patients, molluscum contagiosum (MC) causes a relatively benign infection characterized by scattered clusters of small, umbilicated, flesh-colored, pinkish, or "pearly" white papules. For some patients, diffuse or discoid dermatitis develops surrounding some of these MC papules (molluscum dermatitis; Md) frequently masking the papules birthday (Effigy 12). Patients (with or without Advertizing) that develop Physician take a prolonged and/or more severe grade [43,44] mayhap due scratching and autoinoculation to other skins sites; all the same, in some patients the credible "spread" of MC lesions may be due to autoeczematization [45]. Secondary infection is uncommon and characterized by acute onset of tenderness and drainage.
Children are primarily affected with no apparent gender bias. Approximately one-quarter of patients with MC develop Medico [44,46] while one-half of patients with AD do so [44]. There is some speculation that patients with AD may also be more susceptible to MC, merely data are non conclusive [44,46,47,48].
Uncomplicated MC does not usually require treatment; however, for Physician, short-course TCS may help control the dermatitis and forestall spread [44]. Data are alien as to the event of TCS on recurrence rate [44,46].
3.2.2. Eczema Herpeticum
Eczema herpeticum (EH), is an acute-onset, potentially life-threatening viral infection caused by herpes simplex virus occurring almost exclusively in patients with a history of chronic peel disease, peculiarly Advertizement. Patients nowadays with widespread tender "punched out" erosions with a predilection for the face and areas of chronic dermatitis (Effigy 13). Regional lymphadenopathy is often present.
EH may be easily mistaken for impetigo (see Section 3.iii.1.), especially for recurrent EH in patients with severe Advertisement ("EH incognito"). Positive skin surface bacterial civilisation for with Staphylococcal or Streptococcal bacteria is common, and does not exclude EH. Diagnosis tin can be confirmed by pare scraping for Tzanck smear, viral civilization, PCR, or immunofluorescence, only sensitivity is low for all these techniques, so a loftier index of suspicion is important. Empiric antiviral treatment is oft indicated; all the same, acyclovir resistance is emerging [49]. Continued monitoring subsequently clearance is recommended because EH recurs in about half of patients [50].
EH can touch patients of any age, but it is most common in infants and children. Approximately 10%–20% of patients with AD develop EH and those that do typically take more astringent/earlier onset Advertisement, college prevalence of atopic comorbidities, and are more than likely to have a history of South. aureus or MC infection [50,51]. Previous TCS use has been cited every bit a possible risk factor for EH [52]. Thus far, data are not sufficient to determine the effect of TCIs on EH risk [52,53,54].
iii.2.iii. Eczema Vaccinatum
Kaposi'south varicelliform eruption was used historically to refer to eczema vaccinatum (EV) or EH, conditions with similar clinical features and risk factors. EV is a rare, potentially life-threatening eruption that develops in predisposed individuals either after immunization for smallpox with live, attenuated vaccinia virus or physical contact with a recently vaccinated private [48]. Although universal smallpox vaccination successfully eradicated the disease in the 1970s, contempo bioterrorism concerns accept prompted a reinstitution of smallpox vaccination for military personnel leading to a few recent reports of EV.
Adventure factors include a history of atopy (even in the absence of circumstantial dermatitis), or other principal skin illness featuring barrier dysfunction (e.yard., dermatitis herpetiformis (DH; come across Section 8.four) or primary immunodeficiency disorders (run into Department seven.3)). EV presents equally a quickly progressing generalized, vesiculopustular, smallpox-similar eruption appearing kickoff and more densely in areas of cutaneous compromise.
iii.2.iv. Eczema Coxsackium
Initially reported in 2013, a new variant of Kaposi's varicelliform eruption (eczema coxsackium (EC)), attributable to coxsackievirus A6 (CSVA6), is being increasingly recognized. EC is related to the well-described hand, pes, and rima oris affliction (HFMD), which is most oft caused by CSVA16. Over half of CSVA6-related HFMD manifests every bit EC [55].
In contrast to the oral erosions and gray-white, oval vesicles on the easily, feet, and buttocks typically associated with HFMD, EC manifests as EH-like lesions with a predilection for hemorrhagic vesicles within dermatitic skin (Figure 14). While the cutaneous findings of EC are the well-nigh dramatic presenting sign, children with AD typically take associated fever and ramble symptoms as well as subsequent onychomadesis.
A bulk of patients with EC have a history skin illness, most often AD, and patients with a history of AD are significantly more probable to manifest EC [55]. A diagnosis of EC is most reliably confirmed past serum PCR for coxsackievirus. Treatment is supportive, with antipyretics and bland skin care.
three.2.5. Viral Exanthem
Viral exanthems (VE) are a heterogeneous group of skin findings associated with a wide variety of systemic viral infections. The most common VE is acute onset of generalized morbilliform eruption, featuring widespread, fine, pink macules and/or papules that may be confused with Advertising (Figure 15). Other VEs include more pathognomonic features: unilateral laterothoracic exanthem (asymmetric periflexural exanthem of childhood), purpuric socks and gloves syndrome, infantile popular acrodermatitis (Gianotti-Crosti syndrome), and 5th disease [56]. VEs are generally self-limited and handling is supportive.
three.three. Fungal Infections
3.three.1. Tinea
Tinea, or "band worm", is a dermatophyte infection of the skin that characteristically appears every bit well demarcated, annular, red, scaly, usually pruritic patches with fundamental clearing and advancing border (Figure 16 and Figure 17). Infections may exist astute with sudden onset and rapid spread or chronic with a slow extension of mild rash.
Infants and children well-nigh often present with tinea capitis [57]. Tinea capitis tin vary in presentation from pruritus and scales with patches of alopecia, broken hairs, and crusting on the scalp to tender boggy plaques and pustules (kerion) (Figure 18). In many cases, cervical or suboccipital lymphadenopathy is besides present. Prevalence is greatest among African Americans and amongst children ages 3–9 [58]. Children presenting with tinea corporis or faciei often harbor occult tinea capitis. Definitive tinea capitis treatment requires systemic antifungal for 4–6 weeks.
Data do not back up an increase susceptibility to tinea amidst patients with Advertizement; withal, the broken pare, erosions, and excoriations associated with Advertising are subject field to tinea fungal infections. Tinea misdiagnosed as AD may amend but not clear after application of TCS, a status known every bit "tinea incognito".
three.3.ii. Candidiasis
Although irritant CD is the most common cause of diaper rash, Candida is a frequent cofactor (Figure 19). Widespread cutaneous Candida infection is uncommon, occurring most oftentimes in infants. In adolescents and adults, cutaneous Candidiasis well-nigh oftentimes localizes to skin folds, peculiarly in individuals with predisposing factors such as obesity, diabetes, and immunosuppression. Infantile candidiasis has been categorized into two subsets: built and neonatal. Built candidiasis presents at birth with generalized erythroderma and "burn-like" desquamation that may obscure the diagnosis. At chance infants are premature, low both weight, and born to mothers heavily colonized with Candida, frequently treated with antenatal antibiotics. Congenital candidiasis is associated with significant morbidity and mortality. Neonatal Candidiasis presents in the first 1–2 weeks of life with patchy redness and scaling in an otherwise healthy, by and large total-term infant with proximal boom dystrophy and paronychia as a subtle associated finding.
Candida culture-positive diaper dermatitis.
4. Infestations
4.i. Scabies
Scabies is an allergic reaction to the eggs and feces of the female Sarcoptes scabei. The reaction is characterized by minor, red papulovesicles or dermatitic lesions. In infants, the most commonly affected areas are palms, soles, face, and scalp. In adults, finger webs, wrists, areolar area, and genitals are most often affected (Figure twenty). Patients frequently report an insidious onset of pruritus that is especially intense at night, although non all patients will experience itch.
Scabies is most often diagnosed in young children and young adults [59], but it is not limited to these age groups or to a detail socioeconomic group. The presence of gradual onset of itch, lack of xerosis, and other family members being itchy with similar time of onset helps to confirm diagnosis. Visualization of the mite's linear burrows (tiny grey irregular tracks) or positive scrapings for mites, eggs, or scybala is definitive (Figure 21).
Scabies infestation with visible couch.
Patients with Advertizing are more than prone to and have more severe reactions to the scabies mite. Treatment with TCS may meliorate appearance ("scabies incognito"), simply prolong the infestation.
5. Malignancies
5.1. Letterer-Siwe Disease
Letterer-Siwe Disease (LSD) is a malignant form of Langerhans cell histiocytosis (LCH) and is the type of LCH most likely to exist mistaken for AD. LCH classically presents in infants with crusted, scaly, SD-like dermatitis or ulcerations on the scalp (most often), periauricular, perineal, and/or axillary regions. Reddish-dark-brown purpuric pustules (petechiae) may too exist present.
5.2. Cutaneous T-Cell Lymphoma
Cutaneous T-cell lymphoma (CTCL) onset before the age of 50 is rare, but an increasing incidence in the pediatric population has been reported over the past 10 years [60]. The early stages of CTCL present as slowly-progressing scaly patches/plaques (mycosis fungoides) or quickly-progressing generalized erythema (Sézary syndrome) on the trunk. Tumors and pruritus are generally nowadays at later stages. In children, CTCL nearly oftentimes presents with wide-spread poorly confining hypopigmented macules (hypopigmented mycosis fungoides), indistinguishable from severe PA (see Section 2.6). Lesions may respond favorably to TCS, delaying diagnosis. There is bear witness that severe Advertizement may be a take a chance gene for CTCL [61,62]. Lack of atopy, adult onset, and symptoms accompanied past weight loss or malaise are key to differential diagnosis.
6. Genetic Disorders
six.1. Keratosis Pilaris
Keratosis pilaris (KP) is a beneficial, generally asymptomatic disorder of follicular hyperkeratinization causing small, rough papules associated with varying degrees of erythema and sometimes-balmy pruritus (Effigy 22). This characteristic stippled or "gooseflesh" appearance is usually observed with dry scaly skin on the cheeks or extensor surfaces of the upper arms, upper legs, and buttocks. KP is often associated with Advertizement or ichthyosis vulgaris (IV; see Department 6.2).
TCIs (tacrolimus specifically) take been constructive in reducing erythema [63]. Emollients containing urea, salicylic acid, lactic acid, or glycolic acid may temporarily improve the advent of the papules (but worsen the erythema).
half dozen.2. Ichthyoses
Ichthyoses are a group of congenital diseases characterized past universal scaling, amid which IV is the near mutual [64].
half dozen.2.i. Ichthyosis Vulgaris
IV is characterized by xerosis and fine, or sometimes coarse, light grey, centrally adherent scale that normally appears ii–half-dozen months afterward birth, increases though puberty, and decreases with age thereafter. Changes are accentuated on the legs where scales may take on a mosaic appearance (Figure 23). The palms and soles of patients with IV are characteristically, but non always, hyperlinear.
Ichthyosis vulgaris (left) and associated palmar hyperlinearity (correct).
Approximately half of patients with IV develop Ad [64] and the xerosis observed with Advertizing may be difficult to differentiate from IV. IV is associated with earlier onset and severity of AD as well as atopy [65]. IV is also associated with KP (encounter Section 6.1). Different Advertisement, few patients experience pruritus or pare inflammation.
Four tin be distinguished from near other forms of ichthyosis by sparing of antecubital and popliteal fossae.
6.ii.2. Other Ichthyoses
Infantile presentation of other ichthyoses is virtually identical, then distinguishing between them is nearly incommunicable until after the first twelvemonth of life, when distinctive features brainstorm to manifest. X-linked recessive ichthyosis (XLRI), a recessive ichthyosis plant overwhelmingly in males, is characterized by erythema and generalized scaling at or within weeks of birth. The large, translucent, peeling scales present early give way to adherent, light chocolate-brown or grey, rhomboid scales as the patient ages. Scaling is almost prominent on the extensor surfaces, neck, face, trunk, and buttocks. Palms and soles are not afflicted.
Babies with autosomal recessive congenital ichthyosis (ARCI) are generally born with or develop soon after birth a thickened collodion-like canvas that encases the entire body (i.eastward., "collodion baby"). Subsequently approximately one month, this "sail" is replaced by varying degrees of generalized scaling in a majority of patients. In lamellar ichthyosis, a course of ARCI, scaling is large, dark chocolate-brown, plate-like scaling (without erythema) that is most prominent on flexural surfaces, the forehead, and lower limbs. The nonbullous ichthyosiform erythroderma course of ARCI is characterized by fine, white scales with generalized erythroderma (but on the legs scaling may be darker, larger, and plate-like). Pruritus is a common feature of ARCI.
vii. Immunodeficiency Disorders
7.ane. Netherton Syndrome
Netherton syndrome (NS) is a rare condition that by and large presents shortly after birth with severe erythema and scaling typically on the scalp, confront, and eyebrows. In some cases, patients develop a pruritic eczematous rash that is unresponsive to treatment. At 1–2 years of age, the erythroderma may be replaced by an annular and polycyclic blueprint of lesions (ichthyosis linearis circumflexa), especially in girls.
Severe skin inflammation and related infections may exist life threatening. Dehydration and failure thrive are also typically present. The presence of "bamboo pilus" (trichorrhexis invaginata; brusque, brittle, lusterless hair) is diagnostic.
TCS are not recommended for NS due to a loftier risk of systemic exposure. Systemic exposure is also high for topical tacrolimus (a TCI) [66]. Systemic exposure for topical pimecrolimus (another TCI) was detectible, merely lower than expected and pimecrolimus treatment has been effective and well tolerated in NS [67].
7.ii. HIV/AIDS-Related Skin Changes
Every bit of 2011, 57 different cutaneous peel disorders take been linked to HIV/AIDS and about every patient with HIV/AIDS will experience some cutaneous changes, many of which mimic AD [68]. These HIV/AIDS-related cutaneous changes are more often than non secondary to immunosuppression (i.e., opportunistic infections or increased susceptibility to malignancy); however, a significant number of inflammatory dermatoses are directly related to HIV infection. The mechanisms by which HIV infection furnishings these changes has non been completely elucidated merely there is evidence to suggest that they may exist related to changes in sweat/oil production, depletion of Langerhans cells, decreased CD4+ T prison cell function, and/or shifts in cytokine profile.
SD (run across Section ii.i), psoriasis (see Section two.2), eosinophilic folliculitis (erythematous urticarial vesiculopapular or pustular rash affecting the face, cervix, and upper chest/back), primary HIV viremia (morbilliform eruption affecting the body and limbs), pruritic papular eruption of HIV (diffuse red rash affecting the trunk and face), xerosis, and AD have each been linked directly to HIV infection. AD is observed in ~30%–50% of HIV/AIDS patients, particularly AIDS patients [68]. Patients with HIV/AIDS too often report drug eruptions (DE; run into Section 9.2) perchance related to HIV-related changes in immune part and/or metabolic dysfunction.
Handling is ofttimes disappointing, as HIV-related cutaneous changes are particularly resistant to treatment and/or prone to recurrence. Highly active antiretroviral therapy has significantly reduced the incidence of opportunistic infections and Kaposi's sarcoma, but it has had trivial event on the incidence of inflammatory dermatoses. TCS have limited efficacy [68].
7.iii. Other Immunodeficiency Disorders
STAT3 deficiency and DOCK 8 deficiency are rare phenotypes of main immunodeficiency that feature elevated serum IgE, eosinophilia, susceptibility to cutaneous and sinopulmonary infections, predisposition for malignancy (predominantly lymphoma), and eczematous dermatitis [69,70,71]. The cutaneous symptoms associated with STAT3 deficiency usually begin as a pustular rash on the face or scalp at or just after birth, much before than Advertizing. The rash may resolve or persist and evolve into eczematous dermatoses. On the other hand, patients with DOCK8 deficiency tend to develop eczematous dermatoses a few months after birth, much like AD. These cutaneous symptoms are often the first symptom of immunodeficiency. Treatment is mainly palliative and may be difficult every bit TCS or TCIs may exacerbate cutaneous infections.
Wiskott-Aldrich syndrome (WAS) is an rare 10-linked recessive disorder characterized by elevated IgE, lymphopenia, susceptibility to infections, predisposition for malignancy (primarily hematopoietic), eczematous dermatitis, and/or haemorrhage due to thrombocytopenia and platelet dysfunction [69]. The first clinical sign of WAS is oft bleeding-related, withal eczematous dermatitis generally develops inside the showtime few months of life [69] and is indistinguishable from Advertizing including in its anatomical distribution. Much similar Advert, WAS-related dermatitis is pruritic and ofttimes improves with age. Patients are also prone to atopy. TCS have been effective in treating cutaneous symptoms [69].
Immunoglobulin (Ig) A deficiency (IgAD) and IgM deficiency are associated with eczematous dermatitis which is often mistaken for Advertising.
Leiner phenotype is a broad spectrum of immunodeficiency disorders (including astringent combined immunodeficiency syndrome [SCID]) in infants characterized clinically by exfoliative dermatitis, chronic diarrhea, failure to thrive, and recurrent bacterial and Candida infections. These infants manifest noncongenital or caused erythroderma within the offset few weeks of life. Patients with SCID generally present in early on infancy with recurrent mucocutaneous infections, erythroderma, and morbilliform or SD-like eruptions. Individuals may also present with cutaneous manifestations of graft-versus-host affliction (GVHD; come across Section 9.1) such as exfoliative dermatitis, a lichenoid rash, or sclerodermoid skin changes [72]. Without handling, SCID is lethal. Cyclosporine can be used to treat dermatitis. There are nine described SCID subtypes, each caused by a different genetic mutation. Amongst these, patients with Omenn syndrome (OS) nowadays with erythroderma, eosinophilia, failure to thrive, chronic diarrhea, lymphadenopathy, and hepatosplenomegaly. Symptoms usually manifest before the age of six months. Presence of lymphadenopathy and hepatosplenomegaly distinguish Os from other forms of SCID and may lead to information technology being confused with graft-versus-host disease (GVHD; run across Section 9.one).
Hypohidrotic ectodermal dysplasia (HED) is an X-linked trait caused by hypomorphic mutation in the IKBKG (or EDA) gene, encoding nuclear cistron κB essential modulator (NEMO). HED presents in males as persistent and extensive SD- or Advertisement-like skin eruptions, intertrigo, and facial ectodermal dysplasia including absent or sparse hair growth, delayed tooth eruption, baldness, dry wrinkled skin, and signs of immunodeficiency such as sepsis, pneumonia, otitis media, sinusitis, lymphadenitis, bronchiectasis, pare and soft tissue infections, and/or infections of the bones and gastrointestinal tract. Heterozygous females show milder symptoms, if whatsoever.
Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome is an extremely rare autosomal recessive genetic disorder. Patients with APECED initially present with recurrent mucosal and cutaneous Candidiasis typically before the age of 5 with no other opportunistic infections [69]. Subsequently, hyperparathyroidism and autoimmune adrenal insufficiency develop. Individuals may too have blazon 1A diabetes, hypogonadism, pernicious anemia, malabsorption, baldness, and vitiligo.
In rare cases, patients with iatrogenic immune deficiency develop paradoxic inflammatory skin disease (PISD) with features of chronic eczema or psoriasis [73]. The most well described PISD is psoriasis triggered by anti-TNF therapy (infliximab, etanercept, adalimumab). Less well appreciated is an Advertising-like chronic skin affliction observed in immunocompromised children treated with long-term systemic calcineurin inhibitors (cyclosporine, tacrolimus). Recognition of PISD requires a high index of suspicion and handling is challenging.
8. Nutritional Disorders
Cutaneous symptoms of nutritional disorders can be the consequence of poor nutrient intake/anorexia (Kwashiorkor (Figure 24), zinc deficiency (ZD)), malabsorption (dermatitis herpetiformis (EH), nutritional deficiency dermatitis of cystic fibrosis (CFNDD)), or impaired end-organ response (phenylketonuria (PKU), biotinidase deficiency (BD)).
8.1. Cystic Fibrosis
In infants, the initial symptoms of CF may exist CFNDD. This potentially life threatening nutritional deficiency presents as erythematous annular papules that are distributed periorally, periocularly, or in the "diaper area". The eruption so spreads to the flexural surfaces of the extremities and takes on a "peeling paint" scaly appearance. In addition, patients demonstrate sparse brittle hair, periorbital and extremity edema, and failure to thrive. CFNDD mostly presents during the first weeks to months of infancy and precedes pulmonary and gastrointestinal symptoms by a few months. Though this is an extremely rare presentation, these manifestations are associated with false-negative sweat test results [74], making diagnosis hard.
CFNDD is related to malabsorption of nutrients either every bit a direct upshot of membrane dysfunction or indirectly via reduced digestive enzyme availability and pancreatic dysfunction due to aberrant ion transport [75]. With nutritional intervention, CFNDD should subside.
Although data are express, CF does appear to be associated with atopy (but non AD) and increased risk of cutaneous drug reactions [75].
viii.ii. Phenylketonuria
Later the get-go few months of nascency, patients with PKU may present with astringent acute dermatitis on near of the body. Individuals may likewise exist photosensitive, hypopigmented relative to siblings and parents, and nowadays with a "musty odor" in sweat and urine due to a buildup of phenylalanine metabolic byproducts [76]. The severities of other symptoms depend on age and generally include intellectual disability, microcephaly, seizures, and movement disorders.
8.three. Zinc Deficiency and Biotin Deficiency
Most cases of ZD occur in premature infants who are all the same breast feeding at three months of age when zinc levels in mother's milk drop every bit the infant's zinc requirements increment. Typical presentation includes a "horseshoe" pattern of facial dermatitis or crusty erosions on the cheeks and chin. "Diaper area" interest typically features sharply demarcated plaques with peripheral calibration that, unlike Candidiasis, classically spares the folds. In older children, lesions localize to the extensor surfaces of the elbows and knees. Paronychia, baldness, diarrhea, and recurrent skin infections are also common. Children with ZD tend to be irritable although there is no xerosis or pruritus. Until solid food is introduced, zinc supplementation improves clinical signs.
BD, or multiple carboxylase deficiency, is a rare autosomal recessive trait based on reduced activity of any or all three associated biotin-dependent carboxylases. BD presents with alopecia and maculopapular erythemic rash around the eyes, nose, oral cavity, ears, and genitals. The eruption is often accompanied by airsickness, apnea, hypotonia, seizures, lethargy, recurrent infections, metabolic acidosis, organic aciduria, hyperammonemia, and difficulty feeding. Symptoms by and large present inside the outset twelvemonth of life. Family history of BD is an important risk factor. Biotin supplementation improves symptoms.
8.4. Food Allergy
Cutaneous reactions are the most mutual presentation of nutrient allergy/intolerance in children and tin manifest as Advert, allergic or irritant CD (run across Section 2.four), or DH.
Dermatitis Herpetiformis
Although gastrointestinal symptoms may not be present, DH is directly related to gluten-sensitive enteropathy (GSE); however, the severity of DH does non announced to be related to the severity of abdominal inflammation [77]. DH most oft presents every bit symmetrical circular groupings of polymorphic erythremic papulovesicles on extensor surfaces of the limbs, back, or buttocks; withal, due to intense pruritus (which sometimes precedes lesion development), excoriations, and crusting may exist evident instead. The face and scalp are sometimes affected and urticaria may be nowadays. Lichenification and hypopigmentation may develop due to chronic lesions and scratching.
Prevalence of DH is greater in Caucasians [78]. Prepubertal children by and large manifest GSE as celiac disease characterized past gastrointestinal symptoms, while in early to middle adulthood, DH is more common. Diagnosis requires a high index of suspicion and is confirmed by observation of granular IgA deposits forth the dermal-epidermal border via directly immunofluorescence. Oral corticosteroids have piffling effect, but potent-to-very strong TCS may help alleviate pruritus [78].
9. Other Differential Diagnoses
9.1. Graft-versus-Host Disease
The nigh common clinical manifestation of acute GVHD (occurring within 100 days of transplant) is a pruritic or tender maculopapular rash commonly involving the palms, soles, cervix, ears, and/or shoulders, which may progress to involve the whole body [79,80]. Findings are often subtle just astringent cases may progress to erythroderma, bullae, or desquamation and, rarely, epidermal necrolysis. Mucositis and hepatic and/or gastrointestinal signs and symptoms back up the diagnosis. Like symptoms of acute GVHD may develop in infants with SCID (see Department 7.3) due to engraftment by transplacentally acquired maternal T cells (maternal-fetal GVHD) [81].
nine.2. Drug Eruptions
Drug eruptions (DE), are the virtually common rashes managed past physicians [57]. Most oft, DE manifest as erythema, urticaria, erythema multiforme (EH-similar reaction), or fixed drug eruption. Erythematous lesions may be maculopapular or morbilliform, and generally begin on the trunk and are symmetrically distributed (Figure 25). Urticaria may be an immediate- or delayed-type reaction, and presents with small papules to big annular plaques that are often pruritic. Fixed drug eruptions are solitary or multiple eruptions that occur in the aforementioned location with each drug exposure and may include central blisters, which are rarely pruritic.
DEs can mimic a broad range of dermatoses. Most are diagnosed from medical history and clinical examination, but skin biopsy may exist helpful. DE should be considered in any patient presenting with cutaneous symptoms without prior history of pare illness, including Advertizement.
Treatment is supportive and primarily includes cessation of the drug, if possible. Dermatitis can exist treated with TCS.
x. Distinguishing Features
Differentiating AD from other potential diagnoses can be difficult. Not simply are in that location a number of "imitators" with similar clinical features, but there are several diagnoses that can coexist with and/or complicate Ad.
At that place is no definite laboratory test for AD. Patch testing (to diagnose CD), bacterial culture (to diagnose impetigo), microscopy (to diagnose tinea, scabies), or biopsy and other laboratory parameters such as cell catamenia cytometry (to diagnose CTCL) may be helpful, but in most cases, diagnosis is based on clinical signs merely. In our clinical experience, several key features distinguish AD from other diagnoses (Tabular array 4).
Tabular array 4
Distinguishing clinical features of most prominent differential diagnoses. [blank] indicates rare/unusual; ✓, sometimes; ✓ +, often/usually; ✓ ++, ever/nearly ever/most oftentimes; Δ, variable; –, not applicative; AD, atopic dermatitis; ARCI, autosomal recessive congenital ichthyosis; CS, corticosteroids; CTCL, cutaneous T-jail cell lymphoma; TCS, topical corticosteroids; XLRI, X-linked recessive ichthyosis; a Concurrent disease may be observed (i.eastward., "overlap").
| History | Signs/Symptoms | Distribution | Other Distinguishing/Diagnostic Features | ||||
|---|---|---|---|---|---|---|---|
| Infantile Onset | Associated with AD | Pruritus/Excoriations | Xerosis | Well Circumscribed Lesions | |||
| Atopic Dermatitis | ✓++ | – | ✓++ | ✓++ | infants: face, body, extensor extremities | chronic with intermittent flares | |
| children: flexors | |||||||
| adults: hands | |||||||
| all ages: spares "diaper expanse"/groin, axilla | |||||||
| Seborrheic Dermatitis a | ✓++ | ✓ | scalp, face, skin folds | coarse, greasy, yellow scale | |||
| Psoriasis a | ✓ | ✓ | ✓++ | extensors, scalp, "diaper area"; "Köebnerizes" | thick, silvery-white scaling | ||
| Nummular Dermatitis a | ✓ | ✓ | ✓+ | ✓++ | extremities | very TCS-responsive | |
| Irritant Contact Dermatitis | ✓ | ✓+ | ✓+ | ✓+ | ✓+ | geographic, often asymmetric | history of irritant exposure |
| Allergic Contact Dermatitis a | ✓ | ✓++ | ✓ | ✓+ | often bilaterally symmetric | history of allergen exposure | |
| Dermatographism | ✓+ | ✓++ | ✓+ | "Köebnerizes" | clinical response to mechanical stimulation | ||
| Pityriasis Alba | ✓+ | ✓+ | ✓+ | face, trunk, extremities | poorly circumscribed, hypopigmented lesions; nonpruritic | ||
| Impetigo | ✓+ | ✓ | ✓+ | face, trunk, extremities | honey-colored crust, tenderness | ||
| Secondary Syphilis | ✓+ | ✓+ | trunk, extremities | mucous membrane and palmoplantar involvement | |||
| Molluscum Dermatitis | ✓+ | ✓+ | ✓+ | ✓+ | face, body, extremities | frequently localized; umbilicated papules (oft subtle) | |
| Eczema Herpeticum/Vaccinatum | ✓+ | ✓+ | ✓+ | ✓+ | face, AD-afflicted areas | "punched out" lesions | |
| Eczema Coxsackium | ✓+ | ✓+ | ✓+ | ✓+ | Advertizing-affected areas | astute onset, fever, subsequent onychomadesis | |
| Viral Exanthem | ✓++ | ✓ | ✓ | face, torso extremities | acute onset, associated constitutional symptoms | ||
| Tinea | ✓ | ✓ | ✓++ | scalp, face, trunk, extremities | trailing border scale, lymphadenopathy, pilus loss | ||
| Candidiasis | ✓++ | ✓ | ✓ | ✓ | skin folds, genitalia | paronychia and/or thrush | |
| Scabies | ✓+ | ✓++ | ✓ | infants: palms, soles, face, scalp adults: finger webs, wrists, periareolar, genitals | visible burrows, palmoplantar pustules | ||
| Letterer-Siwe Disease | ✓++ | ✓ | peel fold and scalp accentuation | telangiectatic, hepatosplenomegaly | |||
| Early on-Stage CTCL | ✓ | trunk, extremities | symptoms accompanied by weight loss or malaise | ||||
| Keratosis Pilaris | ✓ | ✓+ | ✓ | ✓+ | cheeks, extensor extremities | follicular keratotic papules, underlying macular erythema | |
| Ichthyosis Vulgaris | ✓+ | ✓+ | ✓ | ✓++ | spares popliteal and antecubital fossae | plate-like scale, palmoplantar hyperlinearity, not-responsive to CS | |
| XLRI (males just) | ✓++ | ✓ | ✓++ | extensor surfaces, neck, face, trunk, buttocks | grey adherent scale | ||
| ARCI | ✓++ | ✓ | ✓++ | face, torso, extremities | "collodion baby" | ||
| Immunodeficiency Disorders | ✓++ | ✓ | Δ | Δ | variable | laboratory confirmation | |
| Nutritional Disorders | ✓ | ✓ | Δ | ✓ | variable | laboratory confirmation | |
| Astute Graft-versus-Host Disease | ✓ | ✓++ | face, trunk, extremities | oral mucous membrane/palmar involvement | |||
| Drug Eruptions | ✓ | ✓ | ✓ | face up, trunk, extremities | clinico-pathological correlations | ||
eleven. Conclusions
Although many differential diagnoses have been discussed, few are as mutual as Advertizing. Historic period of onset, presence of xerosis and/or pruritus, distribution and appearance of lesions, and accompanying symptoms are key to successful diagnosis. Clinicians should keep in mind that inflammatory skin diseases tin can coexist ("overlap") and may be complicated by or predispose patients to infections and infestations. Keratosis pilaris and ichthyosis vulgaris may be nowadays as a small-scale characteristic of Ad, or may exist present exterior the context of AD. Dermatitis is associated with serious immunodeficiency disorders, ichthyoses, malignancies, nutritional disorders, and other conditions (graft-versus-host disease, drug eruptions), and should not be overlooked.
Acknowledgments
All manuscript content was developed contained of funding source. Jennifer Jaworski, a total-time employee of Prescott Medical Communications Group (Chicago, IL, The states) assisted with training of the manuscript at the direction of the authors with financial support from Valeant Pharmaceuticals N America LLC.
Author Contributions
Elaine C. Siegfried and Adelaide A. Hebert both contributed to the concept of this paper, critically reviewed each draft, and approved the final version as submitted.
Conflicts of Interest
Elaine C. Siegfried has received consulting fees, and/or served on Advisory Boards for Valeant Pharmaceuticals North America LLC and Astellas Pharma US. She has also participated in contract inquiry with Astellas and Novartis Pharmaceuticals Corporation.
Adelaide A. Hebert has received consulting fees, been a member of Speakers' Bureaus, and/or served on Advisory Boards for Valeant Pharmaceuticals North America LLC and Astellas Pharma United states of america. She has too served equally a fellow member of Information Rubber Monitoring Boards for Valeant and Novartis. In add-on, she has participated in contract enquiry with Astellas and Novartis Pharmaceuticals Corporation for which all enquiry funds were paid to the Academy of Texas Medical School at Houston.
References
i. Shaw T.E., Currie G.P., Koudelka C.W., Simpson Due east.L. Eczema prevalence in the Us: Information from the 2003 National Survey of Children'due south Health. J. Investig. Dermatol. 2011;131:67–73. doi: 10.1038/jid.2010.251. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
2. Chen Westward., Mempel Yard., Schober Westward., Behrendt H., Ring J. Gender divergence, sexual practice hormones, and immediate type hypersensitivity reactions. Allergy. 2008;63:1418–1427. doi: 10.1111/j.1398-9995.2008.01880.x. [PubMed] [CrossRef] [Google Scholar]
3. Eichenfield Fifty.F., Hanifin J.Grand., Luger T.A., Stevens Southward.R., Pride H.B. Consensus conference on pediatric atopic dermatitis. J. Am. Acad. Dermatol. 2003;49:1088–1095. doi: ten.1016/S0190-9622(03)02539-8. [PubMed] [CrossRef] [Google Scholar]
4. Eichenfield L.F., Tom W.50., Berger T.G., Krol A., Paller A.S., Schwarzenberger Grand., Bergman J.N., Chamlin S.L., Cohen D.E., Cooper Thou.D., et al. Guidelines of intendance for the management of atopic dermatitis: Section 2. Management and treatment of atopic dermatitis with topical therapies. J. Am. Acad. Dermatol. 2014;71:116–132. doi: x.1016/j.jaad.2014.03.023. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
5. Sidbury R., Tom Westward.L., Bergman J.N., Cooper K.D., Silverman R.A., Berger T.G., Chamlin S.L., Cohen D.E., Cordoro K.M., Davis D.G., et al. Guidelines of treat the management of atopic dermatitis: Section four. Prevention of disease flares and utilise of adjunctive therapies and approaches. J. Am. Acad. Dermatol. 2014;71:1218–1233. doi: 10.1016/j.jaad.2014.08.038. [PMC costless commodity] [PubMed] [CrossRef] [Google Scholar]
half dozen. Alexopoulos A., Kakourou T., Orfanou I., Xaidara A., Chrousos Grand. Retrospective analysis of the relationship between infantile seborrheic dermatitis and atopic dermatitis. Pediatr. Dermatol. 2014;31:125–130. doi: 10.1111/pde.12216. [PubMed] [CrossRef] [Google Scholar]
7. Sampaio A.L., Mameri A.C., Vargas T.J., Ramos-e-Silva M., Nunes A.P., Carneiro S.C. Seborrheic dermatitis. An. Bras. Dermatol. 2011;86:1061–1071. doi: 10.1590/S0365-05962011000600002. [PubMed] [CrossRef] [Google Scholar]
8. Apasrawirote W., Udompataikul Chiliad., Rattanamongkolgul S. Topical antifungal agents for seborrheic dermatitis: Systematic review and meta-analysis. J. Med. Assoc. Thail. 2011;94:756–760. [PubMed] [Google Scholar]
9. Kastarinen H., Oksanen T., Okokon Eastward.O., Kiviniemi V.V., Airola Yard., Jyrkka J., Oravilahti T., Rannanheimo P.K., Verbeek J.H. Topical anti-inflammatory agents for seborrhoeic dermatitis of the face or scalp. Cochrane Database Syst. Rev. 2014;v doi: 10.1002/14651858.CD009446.pub2. [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]
10. Augustin Thou., Reich Yard., Glaeske M., Schaefer I., Radtke Thou. Co-morbidity and age-related prevalence of psoriasis: Assay of health insurance data in Germany. Acta Derm. Venereol. 2010;90:147–151. doi: 10.2340/00015555-0770. [PubMed] [CrossRef] [Google Scholar]
11. Guttman-Yassky East., Nograles K.E., Krueger J.Grand. Contrasting pathogenesis of atopic dermatitis and psoriasis—Part I: Clinical and pathologic concepts. J. Allergy Clin. Immunol. 2011;127:1110–1118. doi: x.1016/j.jaci.2011.01.053. [PubMed] [CrossRef] [Google Scholar]
12. Wilsmann-Theis D., Hagemann T., Jordan J., Bieber T., Novak N. Facing psoriasis and atopic dermatitis: Are at that place more similarities or more differences? Eur. J. Dermatol. 2008;eighteen:172–180. [PubMed] [Google Scholar]
13. Scott Fifty.J., Dunn C.J., Goa Thou.L. Calcipotriol ointment. A review of its use in the management of psoriasis. Am. J. Clin. Dermatol. 2001;two:95–120. doi: 10.2165/00128071-200102020-00008. [PubMed] [CrossRef] [Google Scholar]
14. Hendriks A.M., Keijsers R.R., de Jong Eastward.M., Seyger M.M., van de Kerkhof P.C. Combinations of classical time-honoured topicals in plaque psoriasis: A systematic review. J. Eur. Acad. Dermatol. Venereol. 2013;27:399–410. doi: 10.1111/j.1468-3083.2012.04640.x. [PubMed] [CrossRef] [Google Scholar]
fifteen. Wang C., Lin A. Efficacy of topical calcineurin inhibitors in psoriasis. J. Cutan. Med. Surg. 2014;eighteen:8–14. [PubMed] [Google Scholar]
xvi. Krol A., Krafchik B. The differential diagnosis of atopic dermatitis in childhood. Dermatol. Ther. 2006;nineteen:73–82. doi: 10.1111/j.1529-8019.2006.00058.ten. [PubMed] [CrossRef] [Google Scholar]
17. Fonacier L.S., Aquino M.R. The role of contact allergy in atopic dermatitis. Immunol. Allergy Clin. Northward. Am. 2010;xxx:337–350. doi: 10.1016/j.iac.2010.06.001. [PubMed] [CrossRef] [Google Scholar]
18. Spiewak R. Contact dermatitis in atopic individuals. Curr. Opin. Allergy Clin. Immunol. 2012;12:491–497. doi: 10.1097/ACI.0b013e328357b05a. [PubMed] [CrossRef] [Google Scholar]
nineteen. De Waard-van der Spek F.B., Andersen M.Due east., Darsow U., Mortz C.G., Orton D., Worm One thousand., Muraro A., Schmid-Grendelmeier P., Grimalt R., Spiewak R., et al. Allergic contact dermatitis in children: Which factors are relevant? (review of the literature) Pediatr. Allergy Immunol. 2013;24:321–329. doi: ten.1111/pai.12043. [PubMed] [CrossRef] [Google Scholar]
20. Aquino 1000., Fonacier Fifty. The office of contact dermatitis in patients with atopic dermatitis. J. Allergy Clin. Immunol. Pract. 2014;2:382–387. doi: 10.1016/j.jaip.2014.05.004. [PubMed] [CrossRef] [Google Scholar]
21. Bruckner A.50., Weston Westward.L. Allergic contact dermatitis in children: A applied approach to direction. Pare Ther. Lett. 2002;seven:3–5. [PubMed] [Google Scholar]
22. Pigatto P., Martelli A., Marsili C., Fiocchi A. Contact dermatitis in children. Ital. J. Pediatr. 2010;36:2. doi: 10.1186/1824-7288-36-2. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
23. Seyfarth F., Schliemann S., Antonov D., Elsner P. Dry peel, bulwark function, and irritant contact dermatitis in the elderly. Clin. Dermatol. 2011;29:31–36. doi: 10.1016/j.clindermatol.2010.07.004. [PubMed] [CrossRef] [Google Scholar]
24. Simonsen A.B., Deleuran M., Johansen J.D., Sommerlund M. Contact allergy and allergic contact dermatitis in children—A review of current information. Contact Dermatitis. 2011;65:254–265. doi: 10.1111/j.1600-0536.2011.01963.x. [PubMed] [CrossRef] [Google Scholar]
25. Ramsing D.W., Agner T. Efficacy of topical corticosteroids on irritant skin reactions. Contact Dermatitis. 1995;32:293–297. doi: ten.1111/j.1600-0536.1995.tb00784.x. [PubMed] [CrossRef] [Google Scholar]
26. Levin C., Maibach H.I. An overview of the efficacy of topical corticosteroids in experimental human nickel contact dermatitis. Contact Dermatitis. 2000;43:317–321. doi: ten.1034/j.1600-0536.2000.043006317.x. [PubMed] [CrossRef] [Google Scholar]
27. Anderson B.Due east., Marks J.G., Jr., Mauger D.T. Efficacy of tacrolimus ointment in the prevention and treatment of contact dermatitis. Dermatitis. 2004;xv:158–159. doi: x.2310/6620.2004.03007. [PubMed] [CrossRef] [Google Scholar]
28. Day I., Lin A.Due north. Use of pimecrolimus cream in disorders other than atopic dermatitis. J. Cutan. Med. Surg. 2008;12:17–26. [PubMed] [Google Scholar]
29. Fonacier Fifty.Due south., Aquino M.R., Mucci T. Current strategies in treating severe contact dermatitis in pediatric patients. Curr. Allergy Asthma Rep. 2012;12:599–606. doi: x.1007/s11882-012-0305-0. [PubMed] [CrossRef] [Google Scholar]
30. Mecoli C.A., Morgan A.J., Schwartz R.A. Symptomatic dermatographism: Current concepts in clinical do with an emphasis on the pediatric population. Cutis. 2011;87:221–225. [PubMed] [Google Scholar]
31. Lin R.L., Janniger C.Grand. Pityriasis alba. Cutis. 2005;76:21–24. [PubMed] [Google Scholar]
32. Fujita Due west.H., McCormick C.50., Parneix-Spake A. An exploratory study to evaluate the efficacy of pimecrolimus cream 1% for the handling of pityriasis alba. Int. J. Dermatol. 2007;46:700–705. doi: 10.1111/j.1365-4632.2007.03145.x. [PubMed] [CrossRef] [Google Scholar]
33. Rigopoulos D., Gregoriou S., Charissi C., Kontochristopoulos G., Kalogeromitros D., Georgala S. Tacrolimus ointment 0.1% in pityriasis alba: An open up-characterization, randomized, placebo-controlled study. Br. J. Dermatol. 2006;155:152–155. doi: 10.1111/j.1365-2133.2006.07181.ten. [PubMed] [CrossRef] [Google Scholar]
34. Kapila S., Hong E., Fischer G. A comparative study of childhood psoriasis and atopic dermatitis and greater understanding of the overlapping condition, psoriasis-dermatitis. Australas. J. Dermatol. 2012;53:98–105. doi: 10.1111/j.1440-0960.2012.00878.10. [PubMed] [CrossRef] [Google Scholar]
35. Abramovits W., Cockerell C., Stevenson 50.C., Goldstein A.Thousand., Ehrig T., Menter A. PsEma—A hitherto unnamed dermatologic entity with clinical features of both psoriasis and eczema. Skinmed. 2005;four:275–281. doi: ten.1111/j.1540-9740.2005.03983.10. [PubMed] [CrossRef] [Google Scholar]
36. Kiriakis K.P., Tadros A., Dimou A., Karamanou Thou., Banaka F., Alexoudi I. Case detection rates of impetigo by gender and age. Infez. Med. 2012;20:105–107. [PubMed] [Google Scholar]
37. Ortega-Loayza A.M., Diamantis Due south.A., Gilligan P., Morrell D.Southward. Label of Staphylococcus aureus cutaneous infections in a pediatric dermatology tertiary health care outpatient facility. J. Am. Acad. Dermatol. 2010;62:804–811. doi: 10.1016/j.jaad.2009.07.030. [PubMed] [CrossRef] [Google Scholar]
38. Matiz C., Tom W.L., Eichenfield L.F., Pong A., Friedlander Due south.F. Children with atopic dermatitis appear less probable to be infected with customs acquired methicillin-resistant Staphylococcus aureus: The San Diego experience. Pediatr. Dermatol. 2011;28:6–xi. doi: 10.1111/j.1525-1470.2010.01293.10. [PubMed] [CrossRef] [Google Scholar]
39. Bell Thousand.C., Stovall S.H., Scurlock A.M., Perry T.T., Jones S.G., Harik Northward.S. Addressing antimicrobial resistance to treat children with atopic dermatitis in a third pediatric allergy clinic. Clin. Pediatr. (Phila) 2012;51:1025–1029. doi: ten.1177/0009922812441669. [PubMed] [CrossRef] [Google Scholar]
40. Hetem D.J., Bonten M.J. Clinical relevance of mupirocin resistance in Staphylococcus aureus. J. Hosp. Infect. 2013;85:249–256. doi: ten.1016/j.jhin.2013.09.006. [PubMed] [CrossRef] [Google Scholar]
41. Brown D.Fifty., Frank J.E. Diagnosis and management of syphilis. Am. Fam. Physician. 2003;68:283–290. [PubMed] [Google Scholar]
42. Baughn R.E., Musher D.M. Secondary syphilitic lesions. Clin. Microbiol. Rev. 2005;18:205–216. doi: 10.1128/CMR.18.one.205-216.2005. [PMC complimentary commodity] [PubMed] [CrossRef] [Google Scholar]
43. Dohil Yard.A., Lin P., Lee J., Lucky A.West., Paller A.S., Eichenfield L.F. The epidemiology of molluscum contagiosum in children. J. Am. Acad. Dermatol. 2006;54:47–54. doi: 10.1016/j.jaad.2005.08.035. [PubMed] [CrossRef] [Google Scholar]
44. Berger E.One thousand., Orlow S.J., Patel R.R., Schaffer J.V. Experience with molluscum contagiosum and associated inflammatory reactions in a pediatric dermatology practice: The crash-land that rashes. Curvation. Dermatol. 2012;148:1257–1264. doi: x.1001/archdermatol.2012.2414. [PubMed] [CrossRef] [Google Scholar]
45. Netchiporouk Eastward., Cohen B.A. Recognizing and managing eczematous id reactions to molluscum contagiosum virus in children. Pediatrics. 2012;129:e1072–e1075. doi: 10.1542/peds.2011-1054. [PubMed] [CrossRef] [Google Scholar]
46. Osio A., Deslandes Due east., Saada V., Morel P., Guibal F. Clinical characteristics of molluscum contagiosum in children in a private dermatology practice in the greater Paris area, France: A prospective study in 661 patients. Dermatology. 2011;222:314–320. doi: 10.1159/000327888. [PubMed] [CrossRef] [Google Scholar]
47. Hayashida S., Furusho N., Uchi H., Miyazaki S., Eiraku One thousand., Gondo C., Tsuji G., Hachisuka J., Fukagawa S., Kido M., et al. Are lifetime prevalence of impetigo, molluscum and herpes infection really increased in children having atopic dermatitis? J. Dermatol. Sci. 2010;lx:173–178. doi: 10.1016/j.jdermsci.2010.09.003. [PubMed] [CrossRef] [Google Scholar]
48. Olsen J.R., Gallacher J., Piguet V., Francis N.A. Epidemiology of molluscum contagiosum in children: A systematic review. Fam. Pract. 2014;31:130–136. doi: x.1093/fampra/cmt075. [PubMed] [CrossRef] [Google Scholar]
49. Frisch S., Siegfried E.C. The clinical spectrum and therapeutic claiming of eczema herpeticum. Pediatr. Dermatol. 2011;28:46–52. doi: 10.1111/j.1525-1470.2010.01356.ten. [PubMed] [CrossRef] [Google Scholar]
50. Brook Fifty.A., Boguniewicz Grand., Hata T., Schneider Fifty.C., Hanifin J., Gallo R., Paller A.S., Lieff Southward., Reese J., Zaccaro D., et al. Phenotype of atopic dermatitis subjects with a history of eczema herpeticum. J. Allergy Clin. Immunol. 2009;124:260–269. doi: 10.1016/j.jaci.2009.05.020. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
51. Peng W.M., Jenneck C., Bussmann C., Bogdanow M., Hart J., Leung D.Y., Bieber T., Eis-Hubinger A.Grand., Novak N. Run a risk factors of atopic dermatitis patients for eczema herpeticum. J. Investig. Dermatol. 2007;127:1261–1263. doi: 10.1038/sj.jid.5700657. [PubMed] [CrossRef] [Google Scholar]
52. Aronson P.L., Shah S.S., Mohamad Z., Yan A.C. Topical corticosteroids and hospital length of stay in children with eczema herpeticum. Pediatr. Dermatol. 2013;30:215–221. doi: 10.1111/j.1525-1470.2012.01859.10. [PubMed] [CrossRef] [Google Scholar]
53. Lubbe J., Pournaras C.C., Saurat J.H. Eczema herpeticum during treatment of atopic dermatitis with 0.1% tacrolimus ointment. Dermatology. 2000;201:249–251. doi: 10.1159/000018497. [PubMed] [CrossRef] [Google Scholar]
54. Osawa K., Etoh T., Ariyoshi Northward., Ishii I., Ohtani Thousand., Kariya Due south., Uchino M., Kitada M. Relationship between Kaposi's varicelliform eruption in Japanese patients with atopic dermatitis treated with tacrolimus ointment and genetic polymorphisms in the IL-18 gene promoter region. J. Dermatol. 2007;34:531–536. doi: 10.1111/j.1346-8138.2007.00326.x. [PubMed] [CrossRef] [Google Scholar]
55. Mathes E.F., Oza 5., Frieden I.J., Cordoro K.M., Yagi South., Howard R., Kristal L., Ginocchio C.C., Schaffer J., Maguiness South., et al. "Eczema coxsackium" and unusual cutaneous findings in an enterovirus outbreak. Pediatrics. 2013;132:e149–e157. doi: ten.1542/peds.2012-3175. [PMC gratis commodity] [PubMed] [CrossRef] [Google Scholar]
56. Biesbroeck L., Sidbury R. Viral exanthems: An update. Dermatol. Ther. 2013;26:433–438. doi: 10.1111/dth.12107. [PubMed] [CrossRef] [Google Scholar]
57. Sanfilippo A.M., Barrio V., Kulp-Shorten C., Callen J.P. Mutual pediatric and adolescent peel weather condition. J. Pediatr. Adolesc. Gynecol. 2003;16:269–283. doi: 10.1016/S1083-3188(03)00147-5. [PubMed] [CrossRef] [Google Scholar]
58. Ely J.W., Rosenfeld Due south., Seabury Rock G. Diagnosis and management of tinea infections. Am. Fam. Dr.. 2014;ninety:702–710. [PubMed] [Google Scholar]
59. Orrico J.A., Krause-Parello C.A. Facts, fiction, and figures of the Sarcoptes scabiei infection. J. Sch. Nurs. 2010;26:260–266. doi: x.1177/1059840510375413. [PubMed] [CrossRef] [Google Scholar]
sixty. Pope Eastward., Weitzman S., Ngan B., Walsh S., Morel One thousand., Williams J., Stein South., Garzon K., Knobler E., Lieber C., et al. Mycosis fungoides in the pediatric population: Report from an international Childhood Registry of Cutaneous Lymphoma. J. Cutan. Med. Surg. 2010;fourteen:i–vi. doi: x.2310/7750.2009.08091. [PubMed] [CrossRef] [Google Scholar]
61. Carr West.Westward. Topical calcineurin inhibitors for atopic dermatitis: Review and handling recommendations. Paediatr. Drugs. 2013;15:303–310. doi: 10.1007/s40272-013-0013-9. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
62. Tennis P., Gelfand J.M., Rothman Yard.J. Evaluation of cancer hazard related to atopic dermatitis and use of topical calcineurin inhibitors. Br. J. Dermatol. 2011;165:465–473. doi: 10.1111/j.1365-2133.2011.10363.10. [PubMed] [CrossRef] [Google Scholar]
63. Breithaupt A.D., Alio A., Friedlander S.F. A comparative trial comparison the efficacy of tacrolimus 0.ane% ointment with Aquaphor ointment for the treatment of keratosis pilaris. Pediatr. Dermatol. 2011;28:459–460. doi: 10.1111/j.1525-1470.2011.01497.x. [PubMed] [CrossRef] [Google Scholar]
64. Traupe H., Fischer J., Oji V. Nonsyndromic types of ichthyoses—An update. J. Dtsch. Dermatol. Ges. 2014;12:109–121. [PubMed] [Google Scholar]
65. Bremmer South.F., Hanifin J.G., Simpson Eastward.L. Clinical detection of ichthyosis vulgaris in an atopic dermatitis clinic: Implications for allergic respiratory disease and prognosis. J. Am. Acad. Dermatol. 2008;59:72–78. doi: x.1016/j.jaad.2008.03.029. [PubMed] [CrossRef] [Google Scholar]
66. Allen A., Siegfried E., Silverman R., Williams Chiliad.L., Elias P.M., Szabo S.K., Korman N.J. Significant assimilation of topical tacrolimus in 3 patients with Netherton syndrome. Curvation. Dermatol. 2001;137:747–750. [PubMed] [Google Scholar]
67. Yan A.C., Honig P.J., Ming M.E., Weber J., Shah 1000.N. The safe and efficacy of pimecrolimus, i%, cream for the treatment of Netherton syndrome: Results from an exploratory study. Arch. Dermatol. 2010;146:57–62. doi: 10.1001/archdermatol.2009.326. [PubMed] [CrossRef] [Google Scholar]
68. Cedeno-Laurent F., Gomez-Flores M., Mendez North., Ancer-Rodriguez J., Bryant J.L., Gaspari A.A., Trujillo J.R. New insights into HIV-1-main pare disorders. J. Int. AIDS Soc. 2011;14:v. doi: x.1186/1758-2652-14-5. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
69. Paller A.S. Genetic immunodeficiency disorders. Clin. Dermatol. 2005;23:68–77. doi: 10.1016/j.clindermatol.2004.09.011. [PubMed] [CrossRef] [Google Scholar]
seventy. Freeman A.F., Holland S.K. Clinical manifestations of hyper IgE syndromes. Dis. Markers. 2010;29:123–130. doi: 10.1155/2010/580197. [PMC costless article] [PubMed] [CrossRef] [Google Scholar]
71. Minegishi Y., Saito M. Cutaneous manifestations of Hyper IgE syndrome. Allergol. Int. 2012;61:191–196. doi: 10.2332/allergolint.12-RAI-0423. [PubMed] [CrossRef] [Google Scholar]
72. Sillevis Smitt J.H., Kuijpers T.W. Cutaneous manifestations of primary immunodeficiency. Curr. Opin. Pediatr. 2013;25:492–497. doi: 10.1097/MOP.0b013e3283623b9f. [PubMed] [CrossRef] [Google Scholar]
73. Fiorino G., Danese South., Pariente B., Allez M. Paradoxical allowed-mediated inflammation in inflammatory bowel disease patients receiving anti-TNF-alpha agents. Autoimmun. Rev. 2014;xiii:15–19. doi: x.1016/j.autrev.2013.06.005. [PubMed] [CrossRef] [Google Scholar]
74. Hebert A.A. Laboratory evaluation of the kid with recalcitrant eczema. Dermatol. Clin. 1994;12:109–121. [PubMed] [Google Scholar]
75. Bernstein M.L., McCusker M.Thou., Grant-Kels J.1000. Cutaneous manifestations of cystic fibrosis. Pediatr. Dermatol. 2008;25:150–157. doi: x.1111/j.1525-1470.2008.00620.x. [PubMed] [CrossRef] [Google Scholar]
76. Mitchell J.J. Phenylalanine hydroxylase deficiency. In: Pagon R.A., Adam Thousand.P., Ardinger H.H., Bird T.D., Dolan C.R., Fong C.T., Smith R.J.H., Stephens Chiliad., editors. GeneReviews® [Cyberspace] University of Washington, Seattle; Seattle, WA, USA: 1993–2015. [(acccessed on 16 Jan 2015)]. Available online: http://world wide web.ncbi.nlm.nih.gov/books/NBK1504 [Google Scholar]
77. Zone J.J. Skin manifestations of celiac disease. Gastroenterology. 2005;128:S87–S91. doi: 10.1053/j.gastro.2005.02.026. [PubMed] [CrossRef] [Google Scholar]
78. Caproni Thousand., Antiga Due east., Melani L., Fabbri P. Guidelines for the diagnosis and treatment of dermatitis herpetiformis. J. Eur. Acad. Dermatol. Venereol. 2009;23:633–638. doi: 10.1111/j.1468-3083.2009.03188.x. [PubMed] [CrossRef] [Google Scholar]
79. Goker H., Haznedaroglu I.C., Chao N.J. Acute graft-vs.-host disease: Pathobiology and direction. Exp. Hematol. 2001;29:259–277. doi: x.1016/S0301-472X(00)00677-9. [PubMed] [CrossRef] [Google Scholar]
80. Jacobsohn D.A., Vogelsang G.B. Astute graft versus host disease. Orphanet J. Rare Dis. 2007;2:35. doi: ten.1186/1750-1172-2-35. [PMC costless commodity] [PubMed] [CrossRef] [Google Scholar]
81. Muller Southward.Grand., Ege M., Pottharst A., Schulz A.S., Schwarz G., Friedrich W. Transplacentally acquired maternal T lymphocytes in severe combined immunodeficiency: A study of 121 patients. Blood. 2001;98:1847–1851. doi: 10.1182/blood.V98.6.1847. [PubMed] [CrossRef] [Google Scholar]
Articles from Journal of Clinical Medicine are provided here courtesy of Multidisciplinary Digital Publishing Found (MDPI)
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470205/
Posted by: chambersfelf1972.blogspot.com
0 Response to "Are There Any Skin Conditions That Mimic Eczema"
Post a Comment