Recently, it has been shown that some well-known pathogenic mediators in
rheumatoid arthritis (RA), such as interleukin-1β (IL-1β) and
tumor necrosis factor (TNF), could play a pathogenic role in
insulin resistance and (IR) and
type 2 diabetes (T2D).In this 6-month longitudinal study, we aimed at investigating if the inhibition of
IL-1 or TNF is associated with an improvement of IR in RA patients with comorbid T2D and the possible effects on selected serum
adipokines. RA patients with comorbid T2D were recruited among those undergoing treatment with
anakinra (ANA) or with
TNF inhibitor (TNFi). The 1998-updated version of the Homeostasis Model Assessment (HOMA2) was used to calculate surrogate indexes of IR (HOMA2-IR) and steady-state beta cell function (%B) from fasting values of
glucose and
C-peptide.
Glucagon,
adiponectin,
adipsin,
leptin, and
resistin were also measured. All these parameters were collected at baseline, after 3 and 6 months of treatment.ANA-treated patients showed a significant improvement in HOMA2-%β, HOMA2-IR, and
glucagon. In TNFi-treated patients, no significant difference was observed analyzing these metabolic parameters.
Adipsin and
resistin decreased after 6 months in ANA-treated patients whereas, no difference was recognized analyzing
adiponectin and
leptin. In TNFi-treated patients,
leptin and
resistin significantly increased, whereas no difference was found analyzing
adiponectin and
adipsin, during the follow-up.Our data may suggest a beneficial effect of
IL-1 inhibition on measures of metabolic derangement in RA-associated T2D. If further confirmed by larger studies,
IL-1 targeting
therapies may represent a tailored approach in these patients.