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WASHINGTON –
“We observed a consistent association between infections and the subsequent development of primary Sjögren’s syndrome,” said Johannes Mofors of the department of medicine at the Karolinska University Hospital, Stockholm, in his presentation. “Infections of certain anatomical sites have different associations to Sjögren’s.”
With risk measurements primarily reliant on detecting the presence of MHC genes, this knowledge could be helpful in identifying at-risk patients and give physicians the chance to act before the syndrome emerges, according to Mr. Mofors.
Investigators conducted a retrospective, multicenter, controlled cohort study of 9,993 Swedish individuals from the country’s national patient registry to observe the association between infections and Sjögren’s.
Patients were an average age of 55 years, with either an SSA or SSB infection, with an average observational period of 16 years before diagnosis.
Of the patients with Sjögren’s disease, 21% reported one or more infections prior to diagnosis, compared with 12% among the control group.
When assessing patients by their type of infection, Mr. Mofors and his colleagues found the likelihood of developing Sjögren’s varied depending on which infection was present.
“We looked at respiratory infections, with the SSA/Ro-, SSB/Ro-positive patients having a stronger association than the corresponding rate of SSA-, SSB-negative patients,” explained Mr. Mofors. “Interestingly, as we looked at patients with skin infections, we observed an association with the SSA-, SSB-positive patients having a stronger association than the negative patients.”
Investigators also tested gastrointestinal infections, but found no clear association to Sjögren’s.
Presence of more than one infection also appeared to increased disposition of patients to Sjögren’s syndrome, although it depended on the type of infection, Mr. Mofors said at the meeting, which was sponsored by Johns Hopkins University and the National Institutes of Health.
Patients with multiple respiratory infections showed a stronger association to Sjögren’s, patients with SSA- or SSB-positive infection displaying even stronger prevalence, and patients with skin infections showed a dose-response pattern.
Patients with SSA or SSB pattern showed no significant association.
It is possible, said Mr. Mofors, that patients became more susceptible to infection as their Sjögren’s manifested, so investigators extended the omission period of their study from 3 to 7 years.
“As the omission period was extended, in the aggregated group of cases we saw a less prominent association; however, for the respiratory infections the change in relationship was insignificant,” said Mr. Mofors.
For SSA- and SSB-negative patients, the association between infections and predisposition to Sögren’s was not significant when the omission period was extended.
Mr. Mofors reported no relevant financial disclosures.
WASHINGTON –
“We observed a consistent association between infections and the subsequent development of primary Sjögren’s syndrome,” said Johannes Mofors of the department of medicine at the Karolinska University Hospital, Stockholm, in his presentation. “Infections of certain anatomical sites have different associations to Sjögren’s.”
With risk measurements primarily reliant on detecting the presence of MHC genes, this knowledge could be helpful in identifying at-risk patients and give physicians the chance to act before the syndrome emerges, according to Mr. Mofors.
Investigators conducted a retrospective, multicenter, controlled cohort study of 9,993 Swedish individuals from the country’s national patient registry to observe the association between infections and Sjögren’s.
Patients were an average age of 55 years, with either an SSA or SSB infection, with an average observational period of 16 years before diagnosis.
Of the patients with Sjögren’s disease, 21% reported one or more infections prior to diagnosis, compared with 12% among the control group.
When assessing patients by their type of infection, Mr. Mofors and his colleagues found the likelihood of developing Sjögren’s varied depending on which infection was present.
“We looked at respiratory infections, with the SSA/Ro-, SSB/Ro-positive patients having a stronger association than the corresponding rate of SSA-, SSB-negative patients,” explained Mr. Mofors. “Interestingly, as we looked at patients with skin infections, we observed an association with the SSA-, SSB-positive patients having a stronger association than the negative patients.”
Investigators also tested gastrointestinal infections, but found no clear association to Sjögren’s.
Presence of more than one infection also appeared to increased disposition of patients to Sjögren’s syndrome, although it depended on the type of infection, Mr. Mofors said at the meeting, which was sponsored by Johns Hopkins University and the National Institutes of Health.
Patients with multiple respiratory infections showed a stronger association to Sjögren’s, patients with SSA- or SSB-positive infection displaying even stronger prevalence, and patients with skin infections showed a dose-response pattern.
Patients with SSA or SSB pattern showed no significant association.
It is possible, said Mr. Mofors, that patients became more susceptible to infection as their Sjögren’s manifested, so investigators extended the omission period of their study from 3 to 7 years.
“As the omission period was extended, in the aggregated group of cases we saw a less prominent association; however, for the respiratory infections the change in relationship was insignificant,” said Mr. Mofors.
For SSA- and SSB-negative patients, the association between infections and predisposition to Sögren’s was not significant when the omission period was extended.
Mr. Mofors reported no relevant financial disclosures.
WASHINGTON –
“We observed a consistent association between infections and the subsequent development of primary Sjögren’s syndrome,” said Johannes Mofors of the department of medicine at the Karolinska University Hospital, Stockholm, in his presentation. “Infections of certain anatomical sites have different associations to Sjögren’s.”
With risk measurements primarily reliant on detecting the presence of MHC genes, this knowledge could be helpful in identifying at-risk patients and give physicians the chance to act before the syndrome emerges, according to Mr. Mofors.
Investigators conducted a retrospective, multicenter, controlled cohort study of 9,993 Swedish individuals from the country’s national patient registry to observe the association between infections and Sjögren’s.
Patients were an average age of 55 years, with either an SSA or SSB infection, with an average observational period of 16 years before diagnosis.
Of the patients with Sjögren’s disease, 21% reported one or more infections prior to diagnosis, compared with 12% among the control group.
When assessing patients by their type of infection, Mr. Mofors and his colleagues found the likelihood of developing Sjögren’s varied depending on which infection was present.
“We looked at respiratory infections, with the SSA/Ro-, SSB/Ro-positive patients having a stronger association than the corresponding rate of SSA-, SSB-negative patients,” explained Mr. Mofors. “Interestingly, as we looked at patients with skin infections, we observed an association with the SSA-, SSB-positive patients having a stronger association than the negative patients.”
Investigators also tested gastrointestinal infections, but found no clear association to Sjögren’s.
Presence of more than one infection also appeared to increased disposition of patients to Sjögren’s syndrome, although it depended on the type of infection, Mr. Mofors said at the meeting, which was sponsored by Johns Hopkins University and the National Institutes of Health.
Patients with multiple respiratory infections showed a stronger association to Sjögren’s, patients with SSA- or SSB-positive infection displaying even stronger prevalence, and patients with skin infections showed a dose-response pattern.
Patients with SSA or SSB pattern showed no significant association.
It is possible, said Mr. Mofors, that patients became more susceptible to infection as their Sjögren’s manifested, so investigators extended the omission period of their study from 3 to 7 years.
“As the omission period was extended, in the aggregated group of cases we saw a less prominent association; however, for the respiratory infections the change in relationship was insignificant,” said Mr. Mofors.
For SSA- and SSB-negative patients, the association between infections and predisposition to Sögren’s was not significant when the omission period was extended.
Mr. Mofors reported no relevant financial disclosures.
REPORTING FROM ISSS
Key clinical point: Infections can be used to identify predisposition to Sjögren’s syndrome.
Major finding: Of the observed Sjögren’s syndrome patients, 21% had an infection prior to diagnosis, compared with 12% in the control group.
Study details: A controlled, multicenter, retrospective cohort study of 9,993 patients collected from the Swedish national patient database.
Disclosures: The investigators reported no relevant financial disclosures.