prohibition and cirrhosis

a comment was made in today's pharmacology lecture-

"US alcohol prohibition reduced rates of liver cirrhosis, and therefore was good for public health in this particular instance."

i think because none of use had ever looked into this question combined with the fact that it seemed so intuitive, we all took it as fact. however i was interested in seeing whether any data exist to support this claim.

national board of economic research published a paper, Alcohol Prohibition and Cirrhosis, by Dills and Miron, in 2003. The paper examined death rates in the context of state and federal prohibitions. All the cirrhosis death rates declined during the prohibition period by 10-20%, they caution concluding this solely to prohibition for the following reasons:

-there have been substantial fluctuations in cirrhosis death rates comparable to the ones seen during prohibition, outside of periods of prohibition

-cirrhosis did not increase to pre-prohibition levels upon repeal

-cirrhosis levels had declined by the time prohibition began, allow little time for this effect

you decide!

random pharmacology notes

clinical pharmacology notes

takes 3 half lives of elimination to achieve steady state, so drugs w/long half lives o elimination (amiodarone - 40 days) can fool one into changing them before they've reached steady state. don't make any changes to meds unless they have been in patient for greater than 3 half lives.

aminoglycosides and fluoroquinolones are concentration dependent for bacterial infections

penicillins are time dependent

thus don't underdose fluoroquinolones, don't short course penicillins

quinidine is the most potent inhibitor of CYP2D6 in man

clinical clue: nail through the tennis shoe- think s. aureus or p. aeruginosa because these bacteria grow great in sneakers.

fluoroquinolone with Ca2+ (as in milk or iron fortified OJ) going to form Ca fluoroquinolone precipitates in the gut and less antibiotic will be available. this is bad because fluoroquinolones are concentration dependent anti-bacterial agents

interesting findings surrounding acetaminophen and EtOH. Chronic EtOH induces CYP2E1 for which acetaminophen is a substrate. the acetaminophen is metabolized to a hepatotoxic byproduct associated w/liver failure, thus the total recommended daily dosage for acetaminophen for someone who has at least 2 drinks a day is 2gms! interestingly, in binge drinking college kids - EtOH acutely inhibits CYP2E1, thus they are not bound by the same restriction of 2gm/day of acetaminophen-