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BTW I used to work as a registered nurse and my girlfriend (who agrees with this) holds a MSc in pain management.
BTW I used to work as a registered nurse and my girlfriend (who agrees with this) holds a MSc in pain management.
Funny, spouse had acute liver failure and I remember the ER doc saying this to me face to face. He did not look to be the "joking" kind of doc, nor does I think he was bull#ting me for the pleasure...
It does exacerbate liver damage and increases the chance of death in very severe cases of acute liver failure.
originally posted by: PeterMcFly
a reply to: PaddyInf
I hope that you understand that you base your argumentation on an appeal to authority:
A systematic review of methodologically sound short-term studies suggested that the use of therapeutic dosing of acetaminophen in patients with chronic alcoholism has not been associated with liver injury, but no studies of longer-term therapy have been performed.15 Thus, less than 4 g/d of acetaminophen appears safe for short-term dosing in patients with mild to moderate alcohol intake, but most hepatologists (written communication, expert opinion: see end of article for list of sources) advocate for lower dosing at 2 g or less per day, given the small margin for error in a nonstudy population. Data do not exist for long-term acetaminophen use in patients with active alcohol use. Multiple hepatologists agree that 2 g or less per day of acetaminophen would be recommended for these patients (written communication, expert opinion).
The half-life of acetaminophen is prolonged in patients with chronic liver disease. However, a study by Benson showed that repeated maximal dosing did not lead to accumulation in patients with chronic stable liver disease (CSLD).18 In that study, 20 patients with CSLD were given 4 grams per day of acetaminophen for 13 days without signs of toxicity. When compared to normal patients, Forrest et al demonstrated similar levels of cysteine and mercapturic acid conjugates, suggesting intact detoxification of NAPQI.19
Recent reviews have concluded that paracetamol is a safe
and effective first line agent in almost all patients
regardless of liver disease aetiology. Although the need for
dose reduction in the healthy population seems largely
unnecessary, it may be warranted in certain severe or decompensated
hepatic disease states, particularly if patients
are malnourished, are not eating or have a dry weight less
than 50 kg.
Actually, you generally see people with end-stage hepatic disease being given acetaminophen for fever and headache, and being told to avoid NSAIDS like the plague
originally posted by: PeterMcFly
a reply to: Bedlam
We are talking here about ACUTE liver failure and NOT chronic liver problems. Your key to enlightenment might be on reading the difference.
Hepatic failure/problem mean loss of coag. Tylenol is one of the few if not the only practical one that is not an antiplatelet.
Paracetamol metabolism is altered during acute viral hepatitis.
It has been suggested that the 24 hour intake of paracetamol in patients
with acute liver disease should be restricted to around 2g/day4.
We are talking here about ACUTE liver failure and NOT chronic liver problems. Your key to enlightenment might be on reading the difference.