Systemic lupus erythematosus and related disorders of childhood.
Systemic lupus erythematosus (SLE) remains a challenging autoimmune disease in term of its etiology, pathogenesis, and management. Much progress has been made in the past year in searching for the SLE susceptibility genes, particularly by several genome-wide screening groups. Cumulative evidence about the association of infections and hormones with SLE has been gathered. Researchers believe that childhood SLE involves more severe organ involvement than adult SLE. Central nervous system complicated lupus continues to be problematic because functional imaging can be abnormal in otherwise asymptomatic lupus individuals. Whether these abnormalities result from subclinical central nervous system involvement or from false positives remains to be determined. With the wide use of corticosteroids as a cornerstone therapy for major organ involvement in childhood SLE, potential complications, especially those involving the growing bone or osteoporosis, are a cause of concern. Evidence suggests that regular exercise, as well as calcium and vitamin D supplementation, may help alleviate bone complications. Researchers have also updated information about pediatric antiphospholipid antibody syndrome. Follow-up studies on neonatal lupus and its pathogenesis have progressed, leading to a better understanding of its natural history and, in turn, to proper counseling of mothers of infants with neonatal lupus and of women with positive anti-Ro or anti-La antibodies. Drug-induced lupus in children is not uncommon. Minocycline and zafirlukast have been increasingly used, and were reported to induce lupus in children.
Arkachaisri
T
T
Division of Pediatric Rheumatology, The Hospital for Special Surgery, New York, New York 10021, USA.
Lehman
T J
TJ
D002493:Central Nervous System Diseases / Q000209:etiology*; D002648:Child; D020022:Genetic Predisposition to Disease; D006801:Humans; D008171:Lung Diseases / Q000209:etiology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000235:genetics; D010024:Osteoporosis / Q000209:etiology*