Bronchiectasis (BR) occurs in about 3% of patients with rheumatoid arthriti
s (RA). Defective antibody production is a rare but well-recognised cause o
f both BR and inflammatory arthritis. We examined the hypothesis that subtl
e specific antibody defects might play a role in the pathogenesis of BR ass
ociated with RA. Identification of defects in antibody production is import
ant because substantial benefits may be gained from immunoglobulin replacem
ent. Specific antibody production was assessed in 20 patients with RA and B
R, 20 with BR alone. 20 with RA alone and 20 healthy controls (all groups m
atched for age and sex). All had normal total IgG, IgA and IgM and IgG subc
lass levels. Specific antibody production was assessed by assay of antibodi
es to representative polysaccharide and protein antigens. Subjects with sub
protective titres were challenged with the appropriate vaccine. Defective a
ntibody production was defined as a subprotective level despite immunisatio
n. Three out of 20 patients with RA and BR had a defective IgG(2) response
to the polysaccharide antigen, but normal responses to the protein antigen.
All of the subjects in the BR alone or healthy control group had normal an
tibody production. Two out of 20 patients with RA alone had defective produ
ction of antibodies against both protein and polysaccharide antigens; both
were receiving gold therapy, a recognised cause of functional antibody defe
cts. It was concluded that some patients with RA and BR have functional ant
ibody defects and may benefit from antibody replacement. An unexpectedly hi
gh proportion of patients with RA alone also have functional antibody defec
ts, possibly secondary to gold therapy.