1. What data in particular will be shared?
   Response - All of the individual participant data collected during the trial, after de-identification.
   


2. What additional supporting information will be shared?
   Response -  Study Protocol
   Response -  Statistical Analysis Plan
   Response - Informed Consent Form
   Response - Clinical Study Report
   Response -  Analytic Code
   
   
3. Who will be able to view these files?
   Response - Anyone
   


4. For what types of analyses will this data be available?
   Response - Any purpose.
   


5. By what mechanism will data be made available?
   Response - Proposals should be directed to [jugalborajhss@gmail.com].
   


6. For how long will this data be available start date provided 01-04-2026 and end date provided 30-04-2030?
   Response - Immediately following publication. No end date.
   


7. Any URL or additional information regarding plan/policy for sharing IPD? 
   Additional Information - NIL

Rheumatoid arthritis is a common autoimmune disease characterised by inflammatory arthritis.Rheumatoid arthritis is primarily considered a disease of the joints but abnormal immune responses are evident and can cause a variety of extra articular manifestations such as vasculitis, nodules and accelerated atherosclerosis. It has been observed that rheumatoid arthritis patients have greater rate of cardiovascular mortality and morbidity. Dyslipidemia is highly prevalent in RA and appears to be present very early in the RA disease process. Apart from the usual risk factors , chronic inflammatory state and dyslipidemia have been proposed as the reasons for accelerated premature atherosclerosis in RA leading to an increased risk for cardiovascular disease. Most studies have shown that the lipid profile of patients with active or untreated RA is primarily characterised by a decrease in the  serum levels of HDL cholesterol. The significant reduction in HDL increases the total cholesterol by HDL ratio which represents the atherogenic index and this could explain the increased coronary artery disease risk in these patients. Reduction in HDL also correlated with the disease activity suggesting a potential role for inflammation in the atherogenic risk observed in RA.