Tesi etd-10012021-093932 |
Link copiato negli appunti
Tipo di tesi
Tesi di laurea magistrale LM6
Autore
MORICONI, FRANCESCA ROMANA
URN
etd-10012021-093932
Titolo
The JAK-STAT pathway, an emerging target for cardiovascular risk in rheumatoid arthritis and myeloproliferative neoplasms: an assessment of current literature and a Pisan case study
Dipartimento
RICERCA TRASLAZIONALE E DELLE NUOVE TECNOLOGIE IN MEDICINA E CHIRURGIA
Corso di studi
MEDICINA E CHIRURGIA
Relatori
relatore Prof. De Caterina, Raffaele
correlatore Prof.ssa Baldini, Chiara
correlatore Prof.ssa Galimberti, Sara
correlatore Prof.ssa Baldini, Chiara
correlatore Prof.ssa Galimberti, Sara
Parole chiave
- Atherosclerosis
- Baricitinib
- Cardiovascular disease
- Inflammation
- JAK-STAT pathway
- Myeloproliferative neoplasm
- Rheumatoid arthritis
- Ruxolitinib
- Tofacitinib
- Upadacitinib
Data inizio appello
26/10/2021
Consultabilità
Non consultabile
Data di rilascio
26/10/2091
Riassunto
Inflammation contributes to many cardiovascular (CV) diseases, and anti-inflammatory treatments can reduce CV events. The Jak-STAT pathway is an emerging target in inflammatory disorders, such as rheumatoid arthritis (RA) and myeloproliferative neoplasms (MPNs). Our objectives are to study the prevalence of CV risk factors in RA and MPNs; to verify the correlation between disease activity and CV risk factors; to compare CV risk factors before and after Jak inhibitor treatment with evidence from the literature. We followed 74 patients, 42 with RA and 32 with MPN, from baseline to interruption of the Jak inhibitor treatment. Patients enrolled were involved in a regular routine follow-up at the hospital Units of Rheumatology and Hematology at the Santa Chiara Pisa University Hospital. We have found that:as disease severity increased, CV risk profile also worsened. Jak inhibitors were effective in controlling disease activity both in RA and MPN patients, with a reduction in inflammation indices (more obvious in the RA group). The RA group showed an increase in total cholesterol; CV risk score, in general, remained stable. Specifically: tofacitinib users featured a reduction, while baricitinib users showed an increase in CV risk score. None of RA patients enrolled experienced new CV events. These results are in line with the existing literature. The group with MPN has decreased total cholesterol levels, at variance from previous literature, but they have an overall increase in CV risk score. MPN patients experienced 8 CV events during the follow-up period. Since these results are in agreement with the literature describing CV risk in patients with MPN, we conclude that these events are linked to the disease natural history. Our study and a review of the previous literature have highlighted a link between CV risk, disease severity, and Jak inhibitors. At this time, we cannot yet clearly conclude on the existence of a definite – favorable or unfavorable – relationship between events and Jak inhibitor therapies. A longer study on a larger sample should provide clarification on this important issue.
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Tesi non consultabile. |