mcgj.brouwers@mumc.nl
26 november 2020 bij 17:46- Antwoorden
interesting study. Would you advocate to use your score in large epidemiological studies (when imaging is absent) or clinical practice?
S.C. Boone (Leiden)
26 november 2020 bij 18:16- Antwoorden
Thank you for your question and the interesting reference! The question is complex. I’ve briefly looked through the reference and I agree that NAFLD or gene variants that lead to it might play a role in the development of CVD. However, this leaves somewhat unanswered if simple steatosis (without steatohepatitis) elevates CVD risk to such an extent that screening for steatosis is worthwhile. The elevated risk could for example mostly be concentrated in individuals who are further down the spectrum of NAFLD (i.e. with inflammatory features/steatohepatitis).
Even then, if simple steatosis also increases your risk it would still be important to investigate in more detail how large this increase is and if it would be worthwhile to intervene on the steatosis. I think this is relevant not only for the patient but also from a healthcare organization/cost perspective. Steatosis prevalence in Western societies is quite high from recent estimates (30% or even more) so you would be looking at a large potential group of patients if you are thinking about treating these individuals.
Back to my own model/presentation and your question. I am not sure if I would advocate for its use, because the errors around the predicted values are quite substantial and it’s unclear if such a predicted value could lead to any treatment benefit at this time.
mcgj.brouwers@mumc.nl
26 november 2020 bij 17:48- Antwoorden
Of note: it can be debated whether simple steatosis is as benign as you suggest, see PMID: 31713012
3 Reacties
interesting study. Would you advocate to use your score in large epidemiological studies (when imaging is absent) or clinical practice?
Thank you for your question and the interesting reference! The question is complex. I’ve briefly looked through the reference and I agree that NAFLD or gene variants that lead to it might play a role in the development of CVD. However, this leaves somewhat unanswered if simple steatosis (without steatohepatitis) elevates CVD risk to such an extent that screening for steatosis is worthwhile. The elevated risk could for example mostly be concentrated in individuals who are further down the spectrum of NAFLD (i.e. with inflammatory features/steatohepatitis).
Even then, if simple steatosis also increases your risk it would still be important to investigate in more detail how large this increase is and if it would be worthwhile to intervene on the steatosis. I think this is relevant not only for the patient but also from a healthcare organization/cost perspective. Steatosis prevalence in Western societies is quite high from recent estimates (30% or even more) so you would be looking at a large potential group of patients if you are thinking about treating these individuals.
Back to my own model/presentation and your question. I am not sure if I would advocate for its use, because the errors around the predicted values are quite substantial and it’s unclear if such a predicted value could lead to any treatment benefit at this time.
Of note: it can be debated whether simple steatosis is as benign as you suggest, see PMID: 31713012