increasing alcoholic liver disease

2 recent articles confirmed (yet again) the adverse effects of drinking alcohol: the 1^st (below) found  an increasing prevalence of alcoholic fatty liver disease (see alcohol fatty liver dz inc JAMA2019 in dropbox, or Wong T. JAMA 2019; 321 (17): 1724), and the 2^nd showed that even small amounts of alcohol are associated with cancer, will send out next.

Details:

-- data from the National Health and Nutrition Examination Survey (NHANES), from 2001-2016, a nationally representative survey of non-institutionalized US population, which includes both interviews and health examinations

-- alcoholic fatty liver disease (AFLD) was defined based on alcohol use (> 28 g/d for women and> 42 g/d for men), in conjunction with elevated AST or ALT levels but no elevation of total bilirubin, evidence of hepatitis B or C infections, or of metabolic syndrome

-- alcoholic fibrosis was assessed using the validated instruments of the AST/platelet ratio, and the Fibrosis-4 score

Results:

-- 34,423 respondents: about 4.5% were identified with AFLD (61% men, 63% non-Hispanic white, mean age 40), and this prevalence remained constant comparing the 2001-2002 to the 2015-2016 data

-- AFLD with stage II or greater fibrosis increased almost three-fold from 0.6% (0.5%-0.8%) to 1.5% (1.3%-1.8%), p<0.001

    -- for men it increased from 0.7% to 1.8%, for women from 0.5% to 1.3%

    -- there was at least a doubling of prevalence for all age groups (20-44, 45-64, and >65), and for the race/ethnicities of white, black/African-American, and Hispanic

-- AFLD with stage III or greater fibrosis doubled from 0.1% (0.02%-0.1%) to 0.2% (0.2%-0.4%), p=0.045

    -- for men it increased from 0.1% to 0.4%, women from 0.05% to 0.1%

    -- there was at least a doubling for all of the age groups assessed

    -- there was at least a doubling for all of the race/ethnicity groups

Commentary:

-- although the overall prevalence of AFLD among US adults was basically stable, the prevalence of AFLD with stage II or greater fibrosis as well as the prevalence of stage III or greater fibrosis increased significantly

-- the big concern here is that fibrosis is the strongest predictor of progression to cirrhosis as well as liver cancer and death

    -- alcoholic liver disease had become the leading indication for US liver transplants in 2016

    -- a 2018 US population-based study found that increasing cirrhosis death rates were largely driven by alcoholic cirrhosis

-- it is not clear from the study why the degree of fibrosis was increasing, in light of the same prevalence of alcoholic fatty liver disease.

    -- Is it increased amounts of alcohol consumed over time? One study suggested that though alcohol consumption in the US is lower than most high-income countries, it is the only country where per capita alcohol consumption has been increasing, from 6.7 L in 2000 to 7.0 L in 2014 (see https://ourworldindata.org/alcohol-consumption ). Of course, this is just an average, and the group with AFLD may well be drinking significantly more alcohol more recently. Other data suggest that in 2015, there were 17.3 million heavy alcohol users, 12.5% of the 138.3 million current alcohol users (see https://www.samhsa.gov/data/sites/default/files/NSDUH-FFR1-2015/NSDUH-FFR1-2015/NSDUH-FFR1-2015.pdf ). One encouraging trend is that alcohol consumption has been decreasing among teens over time (see http://gmodestmedblogs.blogspot.com/2018/11/teen-drug-use-in-us-2016-survey.html )

    -- is it exposure to other hepatotoxins? Environmental? Occupational? Medications? Infections? Or some combo of these? Would be useful to know.

So, a pretty concerning trend. Whatever the reason for the increases in alcoholic fatty liver disease, there are several concerns:

-- once a drinker has evidence of elevated liver enzymes, they are at increased risk of progressing to  fibrosis and the above cascade of cirrhosis, etc (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846480/ )

-- with multiple hits on the liver (alcohol plus any other liver toxins), the effect on the liver tends to be multiplied

-- so, it is important that we clinicians screen for alcohol use, check for the effects on liver enzymes, and really engage patients in decreasing their alcohol consumption to zero if elevated. of course, no alcohol use is best for the population (eg, see next blog, as well as http://gmodestmedblogs.blogspot.com/2015/02/moderate-alcohol-and-cardioprotection.html , which rebuffs the prevalent belief that moderate alcohol confers cardioprotection )

geoff​

If you would like to be on the regular email list for upcoming blogs, please contact me at gmodest@uphams.org

to get access to all of the blogs:

1. go to http://gmodestmedblogs.blogspot.com/ to see them in reverse chronological order

2. click on 3 parallel lines top left, if you want to see blogs by category, then click on "labels" and choose a category​

3. or you can just click on the magnifying glass on top right, then  type in a name in the search box and get all the blogs with that name in them

please feel free to circulate this to others. also, if you send me their emails, i can add them to the list