Autoantibodies May Precede Sjogren's Symptoms by Years

November 05, 2013

By Megan Brooks

NEW YORK (Reuters Health) Nov 05 - Patients who develop Sjogren's syndrome may have autoantibodies characteristic of the disease in their blood years before any symptoms present, Swedish researchers say.

In a research letter in JAMA this week, they say "Autoantibody profiling may identify individuals at risk many years before disease onset. However, the significance of these presymptomatic autoantibodies for determining prognosis and treatment remains to be determined."

The presence of various autoantibodies is a hallmark of primary Sjogren's syndrome and may be involved in the development of the autoimmune disease, although data on the presence of presymptomatic autoantibodies are limited, note Dr. Gunnel Henriksson and colleagues from Lund University in Malmo, Sweden.

To investigate, they studied serum samples obtained from 44 patients with primary Sjogren's an average of seven years before symptom onset, and 44 matched controls.

In 29 Sjogren's cases (66%), autoantibodies -- primarily antinuclear antibodies (ANA), followed by rheumatoid factor (RF), anti-Ro60/SSA, anti-Ro52/SSA, and anti-La/SSB -- were detected before symptom onset.

"All 29 cases had autoantibodies in their earliest available serum sample, as early as 18 years before symptom onset," the authors note. There was no statistically significant difference in the time between a positive test result and symptom onset for the different autoantibodies assessed.

The likelihood for developing Sjogren's syndrome was high for both anti-Ro60/SSA (odds ratio, 15.0) and anti-La/SSB (OR, 10.0) antibodies.

"This study mirrors earlier studies demonstrating similar findings in systemic lupus and rheumatoid arthritis, where the characteristic autoantibodies of these diseases have also been shown to precede clinical disease onset by many years," Dr. Alan Baer, who heads the Jerome L. Greene Sjogren's Syndrome Center at Johns Hopkins University School of Medicine in Baltimore, Maryland, told Reuters Health by email.

Dr. Baer, who wasn't involved in the study, said the findings are important for two reasons.

First, they provide "evidence that the autoimmune abnormalities of Sjogren's syndrome are present years before symptom onset and are likely the cause of the salivary and lacrimal gland dysfunction," he said. He noted that, in some mouse models of Sjogren's syndrome, dysfunction of the salivary glands precedes development of the autoantibodies, "raising the possibility in these models that an intrinsic (ie. non-autoimmune) glandular defect may occur first and then trigger an autoimmune reaction."

Dr. Baer said the findings also raise the possibility that multiple events are required to trigger the development of autoimmune diseases, including Sjogren's syndrome.

"Thus, the observation that patients destined to develop Sjogren's syndrome have abnormalities of their immune system for up to 18 years before symptom onset suggests that the disease may either be very slow in its development or that additional stochastic events (e.g. viral infections, drug or chemical exposures) must occur to trigger the disease in a host already demonstrating an abnormal immune system," Dr. Baer explained.

He cautioned that "the presence of autoantibodies typical of lupus or Sjogren's (e.g. anti-SSA and anti-SSB) in an asymptomatic individual does not necessarily mean that the individual will develop one of these diseases."


JAMA 2013;310:1854-1855.


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