WEDNESDAY, March 20, 2024 (HealthDay News) — People with autoimmune disorders such as lupus, type 1 diabetes and rheumatoid arthritis tend to have fewer children, and women with this class of illnesses often have higher risks for complications of pregnancy, new research shows.
Researchers in Finland compared pregnancy and childbirth outcomes for the roughly 8% of Finnish adults who have some form of autoimmune disorder to people without such illnesses. They published their findings March 20 in Rheumatology.
Women with certain illnesses — Addison’s disease, lupus, juvenile arthritis, vitamin B12 anemia and rheumatoid arthritis — did tend to experience childlessness more often, and had fewer children on average, said a team led by Anne Kerola. She’s a resident in rheumatology at the Helsinki University Central Hospital.
Men with immune-related conditions also had a higher rate of childlessness, the study found, especially men with myasthenia gravis, Addison’s disease and vitamin B12 deficiency anemia.
When it came to complications of pregnancy, the research showed that risks for pre-eclampsia, low birth weight, preterm delivery, non-elective C-sections and the need for intensive care of newborns was raised for women with various autoimmune disorders.
Specifically, women with lupus, type 1 diabetes and Addison’s disease had more than double the odds for these complications, the Finnish data showed.
Speaking in a journal news release, lead author Kerola stressed that despite these elevated risks, “many of the complications are still fairly rare.”
She said doctor-patient discussions are key to helping ease these issues.
“Family planning should actively be discussed between patients, both men and women, with rheumatic diseases and their healthcare providers,” Kerola said. “Pregnancies in women with rheumatic diseases are carefully followed up to tailor medications appropriately, which helps reduce risks.”
More information
Find out more about autoimmune illnesses at the National Institute of Environmental Sciences.
SOURCE: Oxford University Press, news release, March 20, 2024
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