Multiple lines of evidence have increasingly suggested a pathogenic connection between rheumatoid arthritis (RA) and the mechanisms of type 2 diabetes (T2D) in a vicious circle perpetuated by glucose derangement and inflammatory mediators. These findings have been further reinforced by clinical studies showing that the inhibition of interleukin (IL)-1 and IL-6 may allow the treatment of RA and concomitant T2D at the same time. Interestingly, IL-1 inhibition induced a more evident reduction of glycated haemoglobin (HbA1c) in patients with concomitant RA and T2D than in previous studies on IL-1 inhibition in patients with this metabolic disease alone. Thus, the inflammatory pathogenic mechanisms of T2D could be exaggerated in the context of a rheumatic disease, possibly explaining these findings. In fact, IL-1 inhibition could not only palliate glycaemia, but also decrease the progressive decline in insulin secretion associated with T2D, interfering with apoptosis of beta-cells, improving their function, and ameliorating the peripheral insulin resistance. Moreover, the maintenance of clinical remission of rheumatic disease could further improve the glucose derangement and reduce the occurrence of T2D in RA. On these bases, the presence of T2D may allow the physicians to perform a better profile of patients with RA according to the principles of precision medicine, tailoring the medical treatment to the individual characteristics. In this context, the benefits of targeting the inflammatory process, mainly by IL-1 inhibition, may be suggested in patients with RA and concomitant T2D.

Rheumatoid Arthritis Treatment Options and Type 2 Diabetes: Unravelling the Association

Di Muzio, Claudia;Cipriani, Paola;Ruscitti, Piero
2022-01-01

Abstract

Multiple lines of evidence have increasingly suggested a pathogenic connection between rheumatoid arthritis (RA) and the mechanisms of type 2 diabetes (T2D) in a vicious circle perpetuated by glucose derangement and inflammatory mediators. These findings have been further reinforced by clinical studies showing that the inhibition of interleukin (IL)-1 and IL-6 may allow the treatment of RA and concomitant T2D at the same time. Interestingly, IL-1 inhibition induced a more evident reduction of glycated haemoglobin (HbA1c) in patients with concomitant RA and T2D than in previous studies on IL-1 inhibition in patients with this metabolic disease alone. Thus, the inflammatory pathogenic mechanisms of T2D could be exaggerated in the context of a rheumatic disease, possibly explaining these findings. In fact, IL-1 inhibition could not only palliate glycaemia, but also decrease the progressive decline in insulin secretion associated with T2D, interfering with apoptosis of beta-cells, improving their function, and ameliorating the peripheral insulin resistance. Moreover, the maintenance of clinical remission of rheumatic disease could further improve the glucose derangement and reduce the occurrence of T2D in RA. On these bases, the presence of T2D may allow the physicians to perform a better profile of patients with RA according to the principles of precision medicine, tailoring the medical treatment to the individual characteristics. In this context, the benefits of targeting the inflammatory process, mainly by IL-1 inhibition, may be suggested in patients with RA and concomitant T2D.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/197753
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