Lupus Immunological diseases // Drug Repurposing

Lupus Immunological diseases

Neonatal autoimmune diseases are distinctly rare. Most neonatal autoimmune diseases result from the transplacental transfer of maternal antibodies directed against fetal or neonatal antigens in various tissues. These results are consistent with a crude estimate based upon the 0.5 percent prevalence of anti-SSA/Ro antibodies in asymptomatic pregnant women and the rate of congenital heart block (1 in 15, 000 to 1 in 22, 000 live births)

Neonatal lupus erythematosus (NLE) is an autoimmune disease affecting the fetus as a result of transplacental transfer of anti-Ro autoantibodies. Neonatal lupus erythematosus (NLE) is an autoimmune disease characterized primarily by transient skin lesions and/or permanent congenital heart block. Other clinical findings include self-limited cytopenias, hematologic and hepatic abnormalities and liver disease. The syndrome results from the passive transfer of maternal anti-SSA, anti-SSB, or anti-U1RNP autoantibodies to the fetus across the placenta. The cutaneous manifestations are generally analogous to those of subacute cutaneous lupus erythematosus (SCLE) and consist of small, erythematous macules that progress to annular plaques with delicate scaling. The skin lesions usually resolve within the first 6 months of life as maternal autoantibodies are cleared from the infant’s circulation

Creating-hashtag-on-twitterTypically, it presents in the first few months of life with an annular form of subacute cutaneous lupus erythematosus. The most common clinical manifestations are cardiac, dermatologic, and hepatic. Some infants may also have hematologic abnormalities. The majority of infants with NLE exhibit isolated congenital heart block, cutaneous lesions analogous to those of adult subacute cutaneous lupus erythematosus, or both.

Neonatal lupus (NL) is a passively transferred autoimmune disease. It occurs in about 1 to 2 percent of babies born to mothers with autoimmune disease, primarily systemic lupus erythematosus (SLE) and Sjogren’s syndrome, and antibodies to SSA/Ro and/or SSB/La. However, many cases occur in children of mothers who have the same autoantibodies, but who do not have symptoms of lupus or other autoimmune disease at the time of the baby’s birth. About half of these mothers go on to develop autoimmune disease (more commonly Sjogren syndrome than SLE). The most serious complication of NL is complete heart block (about 10 percent have an associated cardiomyopathy at the initial diagnosis or develop it later).

While autoantibodies have been detected in patients with neonatal autoimmune disease, the pathogenic role of autoantibodies has not been well defined. Other mechanisms may play a role in the development of neonatal autoimmunity, including fetal/maternal microchimerism and aberrant apoptosis of fetal cells.

The pathophysiologic basis for the development of neonatal autoimmunity is not entirely clear, but differences in the neonatal immune system compared with the adult immune system, as well as unique characteristics of target antigens in the newborn period may be important factors.

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