Search tips
Search criteria 


Logo of annrheumdAnnals of the Rheumatic DiseasesVisit this articleSubmit a manuscriptReceive email alertsContact usBMJ
Ann Rheum Dis. 1999 September; 58(9): 585–587.
PMCID: PMC1752943

Old drug, new tricks: haloperidol inhibits secretion of proinflammatory cytokines


OBJECTIVES—It was noted that treatment of a patient with acute mania by haloperidol was associated with marked improvement in activity of rheumatoid arthritis. The objective of this study was to examine the effects of haloperidol on inflammatory cytokine release in vitro, as a potential mechanism to explain the in vivo anti-inflammatory effects of haloperidol.
METHODS—The effect of haloperidol on the production of inflammatory cytokines interleukin 1β (IL1β) and tumour necrosis factor α (TNFα) was measured in bacterial lipopolysaccharide stimulated whole blood cultures and on the promonocyte cell line THP-1, using commercial and in house enzyme linked immunosorbent assays to measure cytokine concentrations.
RESULTS—Haloperidol inhibited lipopolysaccharide stimulated production of both IL1β and TNFα in vitro in a dose dependent manner and over a prolonged time period. Marked inhibition was seen over a range of concentrations of haloperidol from 0.5 µg/ml to 50 µg/ml, including those predicted to occur in the patient's blood.
CONCLUSIONS—Haloperidol treatment seemed to alleviate inflammation in rheumatoid arthritis. In vitro experiments would suggest that the mechanism is by direct inhibition of proinflammatory cytokine release. This phenomenon requires further investigation and may potentially lead to the development of novel treatment.

Figure 1
Inhibition of release of inflammatory cytokines (A) IL1β and (B) TNFα by haloperidol at concentrations from 50 µg/ml down to 0.5µg/ml, compared with medium control: LPS stimulated whole blood.     ...
Figure 2
Production of IL1β by the human promonocytic cell line THP-1 was determined in the presence of varying concentrations of haloperidol, and as control, diazepam.

Articles from Annals of the Rheumatic Diseases are provided here courtesy of BMJ Publishing Group