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Year : 2016  |  Volume : 17  |  Issue : 3  |  Page : 167-172

Annular erythema in pediatric population

1 Department of Dermatology, College of Medicine and Sagore Dutta Hospital, Kamarhati, India
2 Department of Dermatology, Burdwan Medical College and Hospital, Burdwan, India
3 Department of Dermatology, All Institute of Medical Sciences, Bhubaneswar, Odisha, India

Date of Web Publication5-Jul-2016

Correspondence Address:
Joly Seth
Street No: 88; Qrs No: 15/D, Chittaranjan, Burdwan - 713 331, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2319-7250.185502

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The term Annular Erythema encompases a great number of entity which commonly present as annular lesions. Differention of one from another is sometimes difficult. Consideration of different aspects such as age, sex, onset, duration etc of these so called less discussed entities as well as clinic-pathological correlation is required to solve the puzzle. We brought about a concise yet lucid review of annular erythema compraising salient features of each entity. We also went through extensive literature search to highlight latest updates and scientific information of the same.

Keywords: Annular erythema, diagnostic challenge, rare

How to cite this article:
Saha A, Seth J, Pradhan S. Annular erythema in pediatric population. Indian J Paediatr Dermatol 2016;17:167-72

How to cite this URL:
Saha A, Seth J, Pradhan S. Annular erythema in pediatric population. Indian J Paediatr Dermatol [serial online] 2016 [cited 2021 Sep 28];17:167-72. Available from: https://www.ijpd.in/text.asp?2016/17/3/167/185502

  Introduction Top

Annular erythema is a descriptive term that includes a group of cutaneous disorders typified by annular, arcuate, circinate, polycyclic, or serpiginous configuration which may spread peripherally or remain fixed. In the literature, this entity has been described and classified under the rubric terms such as figurate, gyrate, or reactive erythemas. The conditions classically described under this salutation are erythema annulare centrifugum (EAC), erythema marginatum, erythema chronicum migrans, erythema gyratum repens (EGR), aanular erythema of infancy, neonatal lupus erythematosus (NLE), erythema atrophicans transiens neonatal, etc. Some of the conditions represent a hypersensitivity reaction pattern to underlying associated disease or cutaneous manifestation of a well-defined disease; whereas in others, the etiopathogenesis is still a crux. Marked clinic-histopathological overlap among the individual entity makes exact diagnosis a challenging one. Tenuous differences in morphological pattern, age of onset, duration and course of the disease enable us to differentiate one member of this group from the others. While erythema migrans is most commonly encountered entity in childhood, EGR is yet to be described in pediatric population.

  Erythema Annulare Centrifugum Top

EAC is considered under persistent forms of annular erythemas. Lesions are migratory in nature and commonly affect adults. However, reports state that infant and children can also be affected. Pathogenesis is still an enigma. This entity is conceptualized to be a cutaneous hypersensitivity reaction to an underlying antigen. Several infections (tuberculosis, candidiasis, dermatophytosis, Epstein–Barr virus, and ascariasis) are implicated as etiological factors in its causation. Recently, herpes zoster infection is also found to be associated with EAC.[1] Other etiological factors are drugs (amitriptyline, hydroxychloroquine, cimetidine), food (blue cheese), and systemic diseases (sarcoidosis, liver diseases, hypereosinophilic syndrome and Graves'disease). Sometimes, EAC might be aparaneoplastic expression of underlying malignancy. Common malignancies associated are Hodgkin lymphoma, leukemia, and multiple myeloma. Recently, EAC is reported to be associated with breast carcinoma.[2] Only few literatures showed association between EAC and pregnancy, and they linked it with elevated level of estrogen and/or progesterone.[3],[4] In most of the instances, however, no definite cause can be elicited. The exact incidence is very difficult to determine because most of the literatures are case reports or small series study.

Classically, the lesions start as erythematous papules which migrate (2–3 mm/day) and enlarge peripherally to acquire polycyclic configuration with central clearing. Site of predilection are trunk and proximal extremities. There are two variants; superficial and deep. Superficial variant is pruritic with trailing of scales and rarely vesicles at the border. The deep one is characterized by indurated border with lack of scales and pruritus. Individual lesion persists for weeks and heals with residual hyper pigmentation. However, new lesions continue to appear for months and years together.

In this regard, two other forms of persistent annular erythema are worth mentioning. Though erythema gyratumperstans fall within the spectrum of EAC can be distinguished from the latter with early age of onset, more persistent course (more than 15 years), associated slight to severe pruritus, and constant vesiculation at the margin. Familial annular erythema is distinguished by autosomal dominant inheritance, onset at early infancy and more consistent presence of scaling, vesiculation, and pruritus. Geographic tongue may be an associated feature.

Histologically superficial variant is typified by lymphohistocytic infiltration around superficial vascular plexus with epidermal changes; spongiosis, parakeratosis. In deep variant, in addition to superficial vascular plexus, the same type of infiltration mentioned above also surrounds deep plexus forming coat-sleeve. Epidermal changes are characteristically absent here. A report by Nayak et al. described deep variant of EAC with vasculitis like changes.[5]

Any abnormal laboratory test indicates toward underlying disorder. Treatment with topical steroid, topical calciprotriol,[6] or tacrolimus [7] and oral antihistaminic may be beneficial for that episode only. Treatment of underlying disease can only break the persistent nature of the disease, if any.

Recent study by Ziemer et al. challenged the age old conventional concept regarding EAC.[8] They claimed that EAC should not be considered as a separate clinicopathological entity. Clinicopathological evaluation of ninety patients presenting with EAC-like lesions revealed lupus erythematosus (32%), spongiotic dermatitis (28%), and pseudolymphoma (18%), respectively. According to them, EAC can be considered as clinical variants of above mentioned diseases.

  Erythema Gyratum Repens Top

Clinical description of this entity is hidden within its name. The term “gyratum” literally means winding round a central point and “repens” means crawl or creep. It is characterized by rapidly migrating (1 cm/day) erythematous concentric bands (resembling wood grains) with trailing scales at the margin commonly affecting trunk and extremities with sparing offace, palms, and soles. Lesions are usually associated with significant pruritus. Middle aged and elderly adults are exclusive victims. To the best of our knowledge, this entity has not been reported in pediatric age group. Serdar et al. reported EGR-like persistent nonpruritic figurate erythema confined to the hands in a 16-year-old girl.[9]

Etiology is unknown. It is described as most specific paraneoplastic syndrome which precedes, follows, or occurs concomitantly with an underlying malignancy in more than 80% cases. Like EAC, it is supposed to be a hypersensitivity reaction to underlying tumor antigens. Most common associated neoplasm is of the lung followed by esophagus, breast, and genitourinary tract.[10],[11] Other association may be pulmonary tuberculosis,[11] ichthyosis, palmoplantar keratosis, pityriasis rubrapilaris, psoriasis, and CREST syndrome. Piqué et al. described an interesting EGR like presentation of leukocytoclastic vasculitis in a systemic lupus erythematosus patient.[12] Recently, Mohanan et al. reported a case of lepromatous leprosy presenting with EGR-like configuration.[13] This entity has been reported to occur in healthy individuals without any associated malignancy.[14],[15] Histopathology is nonspecific. Any abnormal laboratory test reflects further evaluation for underlying malignancy.

Identification and treatment of underlying malignancy result in resolution of cutaneous lesions. EGR-like eruption in healthy individuals respond well to topical steroid only.[16] Though almost never reported in pediatric age group; proper knowledge about age of onset, clinical features, and associations increases diagnostic skill of the physician to pick up any unusual presentation of annular erythemas.

  Annular Erythema of Infancy Top

It is a rare benign disorder of early infancy with asymptomatic, erythematous, urticarial papule which slowly enlarges to form arcuate or polycyclic lesions with cord like firm, raised palpable border. Vesiculation and scaling are characteristically absent at the border. Individual lesions resolve completely within few days without any residual skin changes, but new lesions continue to appear in cyclic fashion until complete resolution within 1 year. The term “persistent annular erythema of infancy” is attributed where lesions persist longer than 1 year.[17] Histopathology is marked by the presence of eosinophils in addition to lymphohistocytic infiltration around superficial and deep vascular plexus. Neutrophilic figurate erythema refers to the presence of neutrophils and leukocytoclasia in the infiltrate.[18],[19] This entity is supposed to be a hypersensitivity reaction to an unidentified antigen. According to some authors, it can be subdivided into two types; with known etiology and with signature pattern without any etiology.[20] No therapy is warranted for this self-limiting condition.

The importance of knowing this benign entity lies in the fact that it should be differentiated from its close differentials to assess the merit of individual case in terms of therapy and prognosis. This transient form of annular erythema can be differentiated from EAC by early age of onset, lack of scaling and vesiculation, shorter duration of individual lesion, healing without any residual stigmata, presence of eosinophils in perivascular infiltrate, and complete resolution within 1 year (transient). NLE is a must to be ruled out entity with poor prognosis. Age of onset may not give sufficient clue because here lesions may appear at birth or few weeks of age. Presence of scaly annular plaque with preferential distribution in scalp, periorbital, and malar region; stigmata of residual atrophy, hypopigmentation and telangiectasia and aggravation or induction by sun exposure are points toward NLE. Prompt screening for relevant antibodies and echocardiography should be instituted in these cases to avoid unfortunate outcomes. Erythema gyratum atrophicans transient neonatal, a close mimicker of NLE, should also be evaluated properly with serology.

  Erythema Gyratum Atrophicans Transient Neonatalae Top

This self-resolving entity was first reported by Gianotti and Ermacora.[21] Erythematous arcuate patches develop within few days of life with concentration around head and neck region. Within few weeks, transformation of the lesions into annular plaque with erythematous raised border and central atrophy do occur. Complete resolution occurs within 1 year without any residual stigmata. Histopathology demonstrates epidermal atrophy, basal cell degeneration, and mononuclear cell infiltrate in the dermis. Immunofluorescence study shows granular deposits of immunoglobulin G (IgG) and C3 along dermoepidermal junction and around capillaries. Some authors described it to be a variant of NLE.[22],[23]

  Earythema Marginatum Top

This evanescent migratory annular erythema is considered as one of the major manifestations in revised Jone's criteria for rheumatic fever.[24] Approximately, 10–20% of children with acute rheumatic fever presented with erythema marginatum.[25]

Classical lesions are asymptomatic annular erythematous plaque with central clearing with predilection for trunk and extremities. Scales or any epidermal changes are typically absent. The signature signs of the entity are evanescent nature (few hours to days) and rapid migration (up to 10 mm in 12 h). Recurrent outbreak may continue for several weeks.

Skin biopsy shows perivascular neutrophilic infiltration in upper dermis.

No specific treatment is required because of its asymptomatic and evanescent nature. Treatment with penicillin and anti-inflammatory medications should be targeted to eradicate streptococcal infection and to control over carditis and arthritis, respectively. Prognosis depends on the severity of cardiac involvement. The appearance of this annular erythema is associated with active episodes of carditis and arthritis.[26],[27]

Ergin et al. reported one case of Type 1 hereditary angioneurotic edema (HANO) with recurrent arthritis and erythema marginatum-like rash but with normal immunoglobulin and negative rheumatologic serology.[28] The patient was initially misdiagnosed as acute rheumatic fever and did not respond to benzathine penicillin.

Another study conducted in Farkas et al. described erythema marginatum as a prodromal sign of HANO which can predict an impending acute edematous attack.[29] Erythema marginatum is found to be a presenting feature even in acquired angioneurotic edema, where bradykinin is supposed to be the key mediator.[30] All lesions of erythema marginatum disappeared following subcutaneous injection of icatibant (bradykinin B2 receptor antagonist). These observations definitely questioned the reliability of erythema marginatum as a major criterion of rheumatic fever.

  Erythema Migrans Top

It is the most characteristic skin manifestation of Lyme borreliosis. Lag phase between tick bite and appearance of rash ranges from 5 to 14 days. This prolonged lag phase may be attributed to slow replication capability of spirochaete in comparison with bacteria. Children are more frequently affected by Lyme disease with erythema migrans being the presenting complaint in more than 90% of cases.[31],[32],[33] Initial localized redness within few hours of tick bite may be a manifestation of immediate hypersensitivity reaction which fades away within several days. Common sites of involvement are skin folds (groins, sub mammary region, axillae), back and scalp as they favors undisturbed attachment of ticks. Head and neck regions are more frequently involved in children. This asymptomatic annular erythematous rash spreads slowly from the tick attachment site. The advancing edge may have stronger color and gives false impression of outer ring. Homogeneous in early stage, some lesion develop central clearing and described as bull's eye. Central clearing is absent in more than 50% of cases.[34] This self-limiting entity fades away within weeks to months by its own, though appropriate antibiotic therapy hastens the fading process within days.

Several species of Borrelia have been implicated as causative organisms with their distinctive features. Borrelia burgdorferi sensu stricto infection is characterized by faster evolution, lack of central clearing, sometimes with multiple erythema migrans,[35] and systemic involvement such as arthritis and neurological complications. In contrary, Borrelia afzelii infection develops slowly but ends up with large lesion with central clearing with little systemic involvement. Erythema migrans lesions by Borrelia garinii develop faster with high propensity to systemic involvement. Recently, Borrelia spielmanii has been implicated as a causative agent of Lyme's disease.[36],[37],[38]

According to some authors, development of central clearing is solely dependent upon the duration of lesion rather on species of the infective organism.[39] Presence of multiple erythema migrans and subclinical hepatitis should alert the physician about the possible development of early disseminated borreliosis.[40]

Distinctive feature of classical lesion allows clinical diagnosis even in absence of laboratory confirmation. Therefore, in endemic area, any clinically suspected case of Lyme disease should promptly be treated with appropriate antibiotics as sensitivity of serological tests is very low during initial 2 week.[41],[42] Patients in early Lyme disease may present with atypical rash such as uniform red or red-blue color with central vesiculation and lack of central clearing.[43],[44] This observation demands proper awareness and vigilant attitude of the clinician to consider erythema migrans as differential of an atypical rash, especially in an endemic area. The term “mini-erythema” denotes rash <5 cm in size with positive culture/polymerase chain reaction result showing B. burgdorferi sensu lato.[45] Practically, this entity poses a considerable diagnostic dilemma for the clinician. Identification and fast institution of curative antibiotics are very crucial because mini erythema migrans serves as an important but unusual feature of early Lyme borreliosis.

  Neonatal Lupus Erythematosus Top

This entity is caused by maternally transmitted auto antibodies through placenta, hence can be designated as passively acquired autoimmune disease. Precise mechanisms of these antibodies are not conclusive till date.[46],[47],[48] The expression of the disease is limited to a small proportion of infants. Only 5% of mother with anti-Ro and anti-La antibodies give birth to an affected child and surprisingly, mothers of an affected baby are absolutely alright in spite of having these culprit antibodies in their blood. It is also seen that NLE does not occur in every pregnancy and fraternal twins are discordant for the same. These observations speak in favor of role of the host factors such as TNF-alfa polymorphism [49] and maternal and/or sibling microchimerism.[50] As far as environmental factor is concerned, presence of cutaneous lesions at birth challenges role of ultraviolet ray as precipitating factor. Epidemiological data is very limited due to rarity of the entity and its transient nature of the rash.

The clinical manifestations of NLE in decreasing order of frequency are dermatologic, cardiac, and hepatic abnormalities.[51],[52],[53]

Cutaneous lesions used to appear within the first few weeks of life; however, they can also be present at birth.[54],[55] The lesions in the form of annular erythematous or polycystic plaques with or without fine scales appear predominately on the scalp, neck, or face (typically periorbital in distribution), but similar lesions can also appear on trunk and extremities.[51],[54] The lesions with increased density in the periorbital area giving an “eye-mask” or “owl-eye'' appearance is a very common characteristic of NLE.[51],[55] At times urticarial, desquamative, ulcerative, or crusted lesions may be found.[56],[57] Bullous lesions with particular predilection for palms and soles are found in some cases.[53] In a study apart from erythema tours patches, subacute cutaneous lupus erythematosus lesions, petechiae, persistent cutis marmorata, and discoidal lesions were found in NLE.[51]

There have been reports of atypical skin manifestations in neonatal lupus in the form of multiple morphea, papulo-erythematosus rash, congenital cutaneous lupus with atrophic lesions, and papulo-nodular lesions on the palmar and plantar surfaces.[58],[59],[60]

The lesions usually last for weeks or months and then resolve spontaneously with disappearance of maternal antibodies in the neonatal circulation.[54] The lesions usually subside with dyspigmentation, scarring, or atrophy. Dyspigmentation is frequent but usually resolves spontaneously whereas scarring and atrophy persist.[51],[55] Telangiectasia is often prominent and is the sole cutaneous manifestation reported in some patients.

Skin biopsy is useful in patients with NLE when the diagnosis is in doubt which shows interface dermatitis, keratinocyte damage, moderate hyperkeratosis, follicular plugging, and vacuolar degeneration in the basal cell layer. Epidermal atrophy may be found.[54] In case of bullous NLE intense inflammatory infiltrate is found. Immunofluorescence study reveals granular deposition of IgG at the dermoepidermal junction and sometimes IgM and C3 deposition are also evident.

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