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MASH – the race to organ death
July 4, 2022
Which organ decompensates first?
The race to organ death is not a show you want to be a part of. The main cause of death in patients with metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) is liver and cardiovascular complications, while disease activity remains a major feature of liver fibrosis progression.
Metabolic associated steatohepatitis (MASH, formerly NASH) is a consequence of metabolic problems including obesity and is often characterized by multiple organ failure, with hepatic cirrhosis driving organ decompensation. But what is the true event and death rate of MASH patients? What do they suffer from and why do they die? And how do we know which organ decompensates first?
The answer is simple.
It is essential to measure the functions of different organs and their activity/progression rates, including the liver, heart, and kidney.
Can we thus assume that for MASH patients, the smallest problem is the liver-related event? Yes and no. The liver is important, but we need to consider the patient as a normal human – with not just a liver, but a heart, kidney, and other organs. These patients are also in the highest risk group for osteoarthritis (OA) and inflammatory bowel diseases (IBD), albeit that is not the focus of this blog article.
We can conclude that it is central to measure several organ functions and their activity/progression rates – which has been the exact focus for Nordic in the recent period. Our technologies, biomarkers, and drug development projects are perfectly aligned for this.
For example, PRO-C3 (also available on the high-precision Roche Cobas platform), a biomarker of type III collagen formation, is an excellent marker of MASH progression of fibrogenic activity in the liver. PRO-C3 is FDA approved and utilizes Nordic Bioscience’s protein fingerprint technology.
In relation to the organ death race, Nordic Bioscience received a Letter of Support (LoS) from the FDA for the first serological biomarker for enrichment in clinical studies and trials in heart failure (HFpEF).
Our protein fingerprint biomarkers can be measured in serum and they specifically target the neo-epitopes that are released during protein formation of degradation and signaling the extent of fibrogenesis or fibrolysis.
