Liver scarring
Hepatic architectural distortion↓
Also searched as Hepatic architectural distortion.
You want to never arrive. This pathway exists on the map so the earlier ones are understood as the place where the work actually pays.
In depth
Scarring so extensive the liver's architecture is replaced. Ten languages agreed on one thing: everything before this stage can come back, and this stage cannot. Published estimates of how many heavy drinkers reach it range from about 10% to 30%.
What drives it
Tissue scarring increases it.
10.3389/fphar.2014.00167 — Nbk482419 — the reversibility boundary, and it is the most important line on this MAP. German-language source (fettleber.org): 'Eine leberzirrhose (fibrose-stadium F4) gilt ... als NICHT MEHR VOLLSTÄNDIG REVERSIBEL. ALLE STADIEN DAVOR (F0-F3) KÖNNEN SICH ... ZURÜCKBILDEN.' Arabic-language source gives the rate: 20-30% of heavy drinkers reach cirrhosis. Korean kasl gives the pace: heavy drinking carries roughly 2% per year to cirrhosis. The evidence covers nothing on this blend has been shown to reverse established cirrhosis in a person, and pivens showed vitamin e did not even improve fibrosis ('improvement in fibrosis was not observed'). NO copy may imply otherwise. doi 10.3389/fphar.2014.00167
Liver inflammation increases it.
Verbatim (pmc8960636, Osipova et al.): 'The progression spectrum of NAFLD starts from non-alcoholic fatty liver (nafl), non-alcoholic steatohepatitis (NASH), anD to cirrhosis which is one kind of the end-stage liver disease. And NASH had been the second leading indication for liver transplantation for adults in the united states in 2015.' scope: the Mexican guideline warns the stages are not a queue — 'Esteatosis y hepatitis representan grados variables de lesión, PERO NO son REQUISITOS para EL DESARROLLO DE CIRROSIS.'.
What it drives
It increases Liver-tissue risk.
The terminal edge. PMC11675116, a prospective study of 299 cirrhotic patients with liver and spleen elastography by a single blinded operator: 'LSM has shown high accuracy for diagnosing liver cirrhosis, as well as for predicting decompensation and HCC development'; median LSM 25.7 kPa, median spleen stiffness 44.6 kPa. And the direction is reversible in at least one setting: 'liver stiffness regression after sustained virological response by direct-acting antivirals reduces the risk of outcomes' (Piedade et al., Sci Rep 2021;11:11681), and after resection 'achieving LSM <=8 kPa suggested a reduced risk of late recurrence (HR 0.519; 95% CI 0.307-0.877; p = 0.014)'. Stiffness falling tracks risk falling. Both regression findings ARE in viral hepatitis treated with ANTIVIRALS OR surgery, not in metabolic OR alcoholic fatty liver, and not with any supplement. The Russian-language source also records that HCC risk persists after abstinence once cirrhosis exists. PMC11675116
It increases Portal pressure.
Verbatim (s1665268123002831, on Baveno vii): 'the development of portal hypertension is the most critical milestone in the natural history of advanced chronic lIVER disease. Portal hypertension is defined as an increase in portal pressure gradient between the portal vein and the inferior vena cava above 5 mmHg. Cirrhosis is by far the most common cause of portal hypertension.' And pmc10311004: 'Cirrhosis transcends various progressive stages from compensation to decompensation driven by the severity of portal hypertension.'.
It reduces Blood protein status.
Loss of functional hepatocyte mass in cirrhosis reduces albumin synthesis and lowers serum albumin. doi 10.22416/1382-4376-2022-32-4-7-16
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.