title: The effect of non-steroidal anti-inflammatory drugs on faecal flora and bacterial antibody levels in rheumatoid arthritis.
abstract: The faecal flora and bacterial antibody levels of 22 patients with active rheumatoid arthritis (RA) were compared with those of 26 patients with osteoarthritis (OA) undergoing comparable treatment with non-steroidal anti-inflammatory drugs (NSAIDs), and a further 22 patients with OA who were not receiving NSAIDs. Faecal counts of Clostridium perfringens were significantly higher in the RA patient group and in those OA patients receiving NSAIDs, compared with those OA patients not taking NSAIDs (P = 0.032, P = 0.0004 respectively). Total aerobic and anaerobic counts were, however, identical in all three groups. Levels of serum IgA antibody to the alpha toxin of Cl. perfringens were higher in the RA group and in the OA group taking NSAIDs than in OA patients not taking NSAIDs (P = 0.011, P = 0.055). Serum IgG antibody to alpha toxin was higher in the RA group than in OA patients both on and off NSAIDs (P = 0.019, P = 0.0072) and also a group of normal controls (P = 0.032). These results suggest that the increased faecal counts of Cl. perfringens together with the associated increased antibody levels seen in this and previous studies are more likely to result from NSAID therapy used to treat the disease than from a disease specific change in bowel flora.
authors.affiliation: Clinical Pharmacology Unit, Royal Bath Hospital, Harrogate.
authors.forename: S M
authors.initials: SM
authors.lastname: Dearlove
authors.forename: K
authors.initials: K
authors.lastname: Barr
authors.forename: V
authors.initials: V
authors.lastname: Neumann
authors.forename: A
authors.initials: A
authors.lastname: Isdale
authors.forename: H A
authors.initials: HA
authors.lastname: Bird
authors.forename: H C
authors.initials: HC
authors.lastname: Gooi
authors.forename: V
authors.initials: V
authors.lastname: Wright
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000032:analysis*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology*; D001427:Bacterial Toxins / Q000276:immunology; D002135:Calcium-Binding Proteins; D003016:Clostridium perfringens / Q000187:drug effects* / Q000254:growth & development / Q000276:immunology; D015169:Colony Count, Microbial; D005243:Feces / Q000382:microbiology*; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology; D010738:Type C Phospholipases
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000907:Antibodies, Bacterial; D001427:Bacterial Toxins; D002135:Calcium-Binding Proteins; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D010738:Type C Phospholipases; C040649:alpha toxin, Clostridium perfringens