Despite many studies on the subject, the causal relationships between viruses and presentation/exacerbation of autoimmune diseases are still elusive. The possibility of false positive IgM antibody tests for human cytomegalovirus (CMV) in patients with systemic lupus erythematosus (SLE) has been pointed out. Here we report a case of a patient who developed lupus nephritis, with biochemical and clinical markers of CMV infection with intestinal involvement. At first, the antibodies to CMV were regarded as spurious aspecific signs of autoimmune disease. The patient had had serious flare-ups of the disease, hemolytic-uremic syndrome with thrombotic microangiopathy superimposed on SLE nephritis, and life-threatening infections for three years until CMV infection was confirmed by the persistence of anti-CMV IgM-antibodies coupled with positive results of tests for viral replication. After therapy with ganciclovir, his clinical and biochemical condition improved and remained stable for three years, with only very low maintenance steroid coupled with hydroxychloroquine. IgM anti-CMV were no longer detectable in spite of the persistence of other autoantibodies such as anti-DNA and ANA. Keeping in mind that CMV-IgM has been reported in only 5% of patients with SLE nephritis, the history of our patient indicates that CMV infection must be carefully excluded before IgM antibodies against CMV can be simply classified as an aspecific sign of cross-reacting autoantibodies formed in SLE patients.
IgM antibodies against cytomegalovirus in SLE nephritis: viral infection or aspecific autoantibody?
MAZZUCCO, Gianna;
2002-01-01
Abstract
Despite many studies on the subject, the causal relationships between viruses and presentation/exacerbation of autoimmune diseases are still elusive. The possibility of false positive IgM antibody tests for human cytomegalovirus (CMV) in patients with systemic lupus erythematosus (SLE) has been pointed out. Here we report a case of a patient who developed lupus nephritis, with biochemical and clinical markers of CMV infection with intestinal involvement. At first, the antibodies to CMV were regarded as spurious aspecific signs of autoimmune disease. The patient had had serious flare-ups of the disease, hemolytic-uremic syndrome with thrombotic microangiopathy superimposed on SLE nephritis, and life-threatening infections for three years until CMV infection was confirmed by the persistence of anti-CMV IgM-antibodies coupled with positive results of tests for viral replication. After therapy with ganciclovir, his clinical and biochemical condition improved and remained stable for three years, with only very low maintenance steroid coupled with hydroxychloroquine. IgM anti-CMV were no longer detectable in spite of the persistence of other autoantibodies such as anti-DNA and ANA. Keeping in mind that CMV-IgM has been reported in only 5% of patients with SLE nephritis, the history of our patient indicates that CMV infection must be carefully excluded before IgM antibodies against CMV can be simply classified as an aspecific sign of cross-reacting autoantibodies formed in SLE patients.
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