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REVIEW ARTICLE
Year : 2012  |  Volume : 13  |  Issue : 1  |  Page : 21-26

Lupus erythematosus: A pediatric perspective


Department of Dermatology, Venereology and Leprosy, Shri BM Patil Medical College, Hospital and Research Center, BLDE University, Bijapur, Karnataka, India

Date of Web Publication23-Oct-2012

Correspondence Address:
Arun C Inamadar
Department of Dermatology, Venerology and Leprosy, Shri BM Patil Medical College, Hospital and Research Center, BLDE University, Bijapur- 586 103, Karnataka
India
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Source of Support: None, Conflict of Interest: None


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  Abstract 

Lupus erythematosus (LE) is an autoimmune multisystem disorder with varied clinical manifestations. There are many similarities and differences between pediatric and adult disease in regard to epidemiological, clinical and therapeutic aspects. In general, the disease in children has a more aggressive course and need for prolonged treatment is frequent, which implies a greater incidence of therapy-related adverse effects. This review addresses various aspects of pediatric LE and how they differ from or are similar to adult disease.

Keywords: Childhood LE, neonatal LE, Autoimmune multisystem disorder


How to cite this article:
Adya KA, Inamadar AC, Palit A. Lupus erythematosus: A pediatric perspective. Indian J Paediatr Dermatol 2012;13:21-6

How to cite this URL:
Adya KA, Inamadar AC, Palit A. Lupus erythematosus: A pediatric perspective. Indian J Paediatr Dermatol [serial online] 2012 [cited 2020 Sep 19];13:21-6. Available from: http://www.ijpd.in/text.asp?2012/13/1/21/102805


  Introduction Top


Systemic lupus erythematosus (SLE) is an autoimmune multisystem disease characterized by production of autoantibodies and deposition of complement-fixing immune complexes in various tissues, resulting in their damage. In patients with SLE, a multitude of antibodies are produced that include many "organ-specific" ones that target their respective tissues producing a wide range of clinical manifestations, which are characterized by remissions and exacerbations. There are several similarities as well as differences between pediatric and adult-onset lupus erythematosus (LE) in regard to etiology, clinical manifestations, complications and prognosis. LE in the pediatric age group represents both a special challenge and a special opportunity. Early onset allows observation of the natural history of the disease and investigation of potential etiologies, free from confounding factors that are frequently present in older patients. [1]


  Epidemiology Top


The true incidence and prevalence of pediatric LE are still unknown. [2] Although better numbers have been provided by countries where every child with a specific diagnosis is reported to a central registry, these countries have lacked the ethnic diversity that is found in larger countries, making their data inapplicable. Because of such difficulties in assessing the incidence of SLE, the prevalence can only be estimated. [3] The influences of sex and racial origin on the occurrence and manifestations of SLE are widely recognized. [4],[5],[6],[7] In childhood, the influence of race is striking. The age and sex-adjusted prevalence of SLE in African American, Asian and Hispanic children were more than three-fold that of white children at one large center. [4] The same study found a 60% increase in the frequency of post-pubertal SLE compared with pre-pubertal SLE in male children. The corresponding figures for females were a 246% increase in white female children, 434% in African American females, 406% in Asian females and 181 in Hispanic females.


  Etiopathogenesis Top


The exact cause of SLE is unknown. LE can best be described as a disorder in which the interplay between host factors (genetic factors, hormonal factors, etc.) and environmental factors (ultraviolet [UV] radiation, viruses, drugs, etc.) leads to loss of self-tolerance and induction of autoimmunity, which is followed by activation of the immune system with subsequent immunological injury to the end organs. [8]


  Genetic Factors Top


Considerable evidence support the role of genetic factors in the pathogenesis of LE. [9] The condition has been reported in identical twins, [10],[11] with a concordance rate of 65%. [11] The onset of SLE in identical twins occurred within 2 years, compared with an interval of 9 years between siblings and 20 years between parents and offspring. [12]


  Autoantibodies Top


Non-organ-specific humoral autoantibodies are the hallmark of SLE. A host of autoantibodies are found in LE, among which some are more disease specific (anti-double-stranded DNA and anti-Sm antibodies) and some are much more commonly found (antinuclear and anti-Ro antibodies). Disease could be produced by the development of such antibodies against tissue antigens to which tolerance has been lost by failure of homeostatic immunological mechanisms. [13],[14] Anti-Ro or closely related antibodies are associated with neonatal lupus erythematosus (NLE) and possibly in other childhood SLE. Antiphospholipid autoantibodies are also frequently found in children with SLE and in their family members. [15],[16],[17]


  Immunologic Abnormalities Top


Childhood SLE is more frequently associated with immunological abnormalities. Complement deficiency [18] (especially C2 or C4 deficiency) and IgA deficiency [19] are the frequent findings in childhood SLE.


  Environmental Factors Top


Current evidence suggests that environmental factors like UV radiation, viruses (especially Epstein-Barr virus), [1] drugs, etc. may produce altered immunological response in a genetically predisposed individual and lead to development of the disease.


  Clinical Features Top


Dermatologic Manifestations

All the cutaneous lesions of LE are induced or exacerbated by UV radiation, but definite photosensitivity is seen in about 16% of childhood SLE. [20] The typical butterfly rash is seen only in 30-50% of childhood SLE. [21] This rash is frequently associated with vasculitic involvement of hard palate, which serves as a useful confirmatory sign.

Discoid lupus erythematosus is uncommon in childhood. There appears to be no female preponderance, there is less photosensitivity and the frequency of progression to systemic disease is higher. The other clinical features are similar to those in adults. [22]

Other dermatologic manifestations of LE in childhood include recurrent urticaria, bullous lesions and vasculitic lesions like nodules or ulceration, with the latter being associated with active disease. Bullous lesions may resemble bullous pemphigoid and are found more commonly in boys. [23]

Systemic Manifestations

Unexplained fever, malaise and weight loss are the most common systemic features of SLE in childhood and adolescents. These symptoms, especially in the context of an otherwise unexplained anemia and/or thrombocytopenia, should prompt a thorough investigation for LE in this age group. Other systemic manifestations are described in [Table 1]. A higher frequency of aggressive renal disease, and thus a higher requirement for steroids and immunosuppressive drugs, has been reported among children with lupus compared with their adult counterparts. [3]
Table 1: Systemic manifestations in childhood LE

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  Laboratory Evaluation Top


No laboratory findings are unique to SLE in childhood. Hypogammaglobulinemia, pancytopenia, a positive antinuclear antibody (ANA) test, organ-specific and non-organ-specific autoantibodies and other abnormalities are found in a similar manner as in adults. Positive ANA tests may also be found in children with juvenile rheumatoid arthritis and in normal healthy children. The titers of the ANA are generally higher in those with SLE. [3] Antibodies to ribosomal P protein, previously implicated in SLE-associated psychosis and depression, have been shown to be more prevalent in childhood compared with adult-onset SLE. A recent cluster autoantibody analysis study conducted in Toronto reported an increased prevalence of anti-U1RNP and anti-Sm antibodies within non-Caucasian populations. The same study identified three clusters of autoantibodies (anti-dsDNA, anti-dsDNA+antichromatin+antiribosomal P+anti-U1 RNP+anti-Sm+anti-Ro+anti-La and anti-dsDNA+anti-RNP+anti-Sm) associating with different clinical courses (mild disease with no major organ involvement, high frequency of nephritis/serositis/hemolytic anemia and NP disease/nephritis, respectively). [30]


  Treatment Top


Pediatric SLE has a more aggressive course, with increased incidence of renal and central nervous system disease. Hence, the use of higher doses of corticosteroids for longer duration is more frequent in this age group than in adults. [Table 2] outlines the various drugs used in the management of LE in childhood. [3] Milder manifestations are managed by non-steroidal anti-inflammatory drugs and antimalarials. In the presence of severe disease manifestations, corticosteroids and immunosupressives (especially for nephritis) are used. Other modalities include monoclonal antibodies, autologous stem cell transplantation [31] and intravenous immunoglobulin. As regards monoclonal antibodies, rituximab is currently being used in immune thrombocytopenia and rheumatoid arthritis in children, and its therapeutic role in SLE is being investigated.
Table 2: Drugs used in the management of childhood LE

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  Neonatal Lupus Erythematosus Top


NLE is a disorder thought to be caused by the transplacental passage of maternal antibodies. It is characterized by transient skin lesions resembling subacute cutaneous LE and/or congenital heart block (CHB), occurring in the babies of mothers with clinical or subclinical autoimmune connective tissue disease and associated with the transplacental passage of maternal autoantibodies to the ribonucleoproteins (RNPs), Ro-SSA, La-SSB or U1-RNP. [32] A considerable proportion of mothers of affected infants are asymptomatic (40%). [33]


  Etiopathogenesis Top


Among the above-mentioned transplacentally transferred maternal autoantibodies, the Ro-SSA is associated with 95% of NLE. [33],[34] In cases where only anti-U 1 RNP antibodies are found, only cutaneous disease has been reported. [33] Two main Ro/SS-A proteins exist (52 and 60 kDa), and studies suggest the former being frequently found in CHB, [35],[36] whereas the latter is more frequently associated with cutaneous disease. [37] The presence of Ro and La antigens has been demonstrated in fetal skin and cardiac-conducting tissue. [38],[39] The antibodies bind to the antigens at these sites after which a sequence of apoptosis, opsonization and fibrosis follows. [40]


  Clinical Features Top


About 90% of neonates have skin lesions, and both skin and cardiac lesions are seen in 10%. [41],[42] In about two-thirds of NLE with skin lesions, the lesions are present at birth, [43],[44] and, in the remainder, they may appear later as the 5 th month. [41] But, generally, the lesions appear within the first 2 months of life and resolve within 4-6 months with disappearance of maternal antibodies.

Cutaneous

An erythematous, scaly eruption on the face and periorbital skin (raccoon sign) is the most common cutaneous finding in NLE, with the scalp, trunk, extremities, neck and intertriginous involvement occurring in decreasing order of frequency. [45] The eruption may be aggravated by UV exposure, and there are reports of the rash being triggered by phototherapy for neonatal jaundice. [46],[47] The rash may sometimes be present at birth, when it becomes difficult to implicate UV exposure as the etiology. [48] Other manifestations include a vitiligo-like eruption, [49] morphea-like lesions [50] and papules on the feet. [51] Occasionally, NLE presents as extensive reticulate erythema with atrophy, closely resembling cutis marmorata telangiectatica congenita. [52],[53] In most cases, the lesions resolve within a year. Occasionally, atrophy, telangiectasia and scarring may remain as residua.

Cardiac

The incidence of CHB in the offspring of anti-Ro-positive women is 1-2%, and the risk of recurrence of complete atrioventricular (AV) block is almost 10-times higher in the following pregnancies. Substantial morbidity (65% require lifelong pacing) and mortality (20%) are associated with CHB. [54] Associated features may also include pericardial effusions, pleural effusions, ascites, intrauterine growth retardation and hydrops fetalis. [55] Dilated cardiomyopathy occurs in up to 20%, and has a significant mortality in the first year of life. [56]

Other Systemic Manifestations

A smaller proportion of infants have combinations of hepatomegaly, splenomegaly, lymphadenopathy, autoimmune hemolytic anaemia, thrombocytopenia and pneumonitis, which are generally mild in degree and fairly transient.


  Treatment Top


Cutaneous lesions are transient and generally resolve without any residua. However, photoprotection is necessary. Up to 50% of patients with heart blocks may require pacing in the newborn period, and others may require pacemaker insertion at a later date. [55]


  Prevention Top


Serial echocardiograms to detect early fetal abnormalities, such as premature atrial contractions or moderate pericardial effusion, which might precede complete heart block and obstetric sonograms perfor-med biweekly starting from the 16 th week of gestational age in the presence of anti-Ro/SSA antibodies, seems to be the best current recommendation. [57] Effective management of these early fetal cardiac abnormalities may prevent the development of complete AV block. Intravenous immunoglobulin had been used to prevent the development of CHB in eight high-risk mothers (anti-Ro/SSA positive and previous pregnancy with CHB), and, in one case, CHB recurred (12.5%). [58]

Learning Points

  • Pediatric LE represents both a special challenge and a special opportunity. There are several similarities and differences between pediatric and adult-onset LE in regard to etiology, clinical manifestations, complications and prognosis
  • True incidence and prevalence of pediatric LE are still unknown. In childhood LE, the influence of race is striking
  • Childhood LE is more frequently associated with immunological abnormalities like complement and immunoglobulin A deficiency
  • Definite photosensitivity is seen only in 16% of childhood LE, and the typical malar rash is seen in 30-50%. Discoid LE is rare in childhood
  • Fever, malaise and musculoskeletal pains are the most common manifestations of childhood LE. Renal involvement is seen in 2/3 rds of the cases
  • Neonatal LE is a rare condition seen in neonates born to mothers with antibodies against Ro/SSA, La/SSB or U 1 RNP. It is characterized by transient photosensitive rash, and, in about 10%, heart blocks
  • In general, pediatric LE has a more aggressive course. The use of higher doses of corticosteroids for a longer duration is more frequent in this age group than in adults
  • Systematic use of cyclophosphamide and other safer alternatives like MMF, azathioprine, etc., has significantly improved the prognosis of children with LE
  • Newer management options like stem cell therapy, monoclonal antibodies, etc., may promise a brighter tomorrow to these patients with regard to the survival and quality of life


 
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  In this article
Abstract
Introduction
Epidemiology
Etiopathogenesis
Genetic Factors
Autoantibodies
Immunologic Abno...
Environmental Fa...
Clinical Features
Laboratory Evalu...
Treatment
Neonatal Lupus E...
Etiopathogenesis
Clinical Features
Treatment
Prevention
References
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