If a normal daily dose of aspirin builds up in the body over time and causes symptoms, it is called a chronic overdose. This may happen if your kidneys do not work correctly or when you are dehydrated.
Aspirin can cause several forms of liver injury: in high doses, aspirin can cause moderate to marked serum aminotransferase elevations occasionally with jaundice or signs of liver dysfunction, and in lower doses in susceptible children with a febrile illness aspirin can lead to Reye syndrome.
(Salicylism)
Salicylate poisoning can cause vomiting, tinnitus, confusion, hyperthermia, respiratory alkalosis, metabolic acidosis, and multiple organ failure. Diagnosis is clinical, supplemented by measurement of the anion gap, arterial blood gases, and serum salicylate levels.
When taken as directed, regular use of aspirin does not seem to increase the risk of kidney disease in people who have normal kidney function. However, taking doses that are too large (usually more than six or eight tablets a day) may temporarily and possibly permanently reduce kidney function.
Aspirin produces hepatotoxic reactions as a cumulative phenomenon, requiring days or weeks to develop. Patients with active rheumatic or collagen disease, as well as children, are especially susceptible. Blood levels of salicylate higher than 25 mg/dL are particularly likely to lead to hepatic injury.
As mentioned above, aspirin is rapidly biotransformed into the active metabolite, salicylate. Therefore, aspirin has a very short half-life. Salicylate, in turn, is mainly metabolized by the liver.
Ibuprofen has the highest liver safety profile among NSAIDs and showed no severe liver injury in larger studies. Along with paracetamol and aspirin, it is considered one of the most common over the counter NSAIDs sold in the world.
Acetaminophen. Taking acetaminophen in excess is the leading cause of drug-induced liver injury.
Daily aspirin use was associated with less severe histologic features of nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH), and with lower risk for progression to advanced fibrosis with time, according to a study recently published in Clinical Gastroenterology and Hepatology.
Acetaminophen (paracetamol), when taken in reduced doses (maximum 2–3 grams per day), is generally considered to be the safest pain relief option for your liver.
The most effective fatty liver treatment involves a change in lifestyle. Weight loss is helpful. “But the weight loss has to be pretty significant,” says Loomba. You have to lose about 7% of your body weight to resolve NASH.
The maximum dose within a 24-hour period must never be exceeded. Paracetamol overdose is one of the leading causes of acute liver failure. Adults can usually take one or two 500mg tablets every 4-6 hours, but shouldn't take more than 4g (eight 500mg tablets) in the space of 24 hours.
Paracetamol can cause acute liver damage especially in people with excessive alcohol intake, people with advanced liver disease (such as cirrhosis), or people with kidney disease. Aspirin relieves mild to moderate pain and treats fever.
NSAIDs and aspirin should be avoided in patients with advanced CLD or cirrhosis. Low-dose acetaminophen should be used instead of NSAIDs.
HEPATOTOXICITY RISK FACTORS
While acute liver injury can occur when used at or below the recommended daily maximum dose (4000 mg)[4], paracetamol toxicity is often the result of ingestion of paracetamol over this maximum dose.
Acetaminophen remains the drug of choice for occasional use in patients with kidney disease because of bleeding complications that may occur when these patients use aspirin.
Should you take a daily aspirin? Don't start taking a daily aspirin without talking to your health care provider. Taking an occasional aspirin or two is usually safe for most adults to use for headaches, body aches or fever. But daily use of aspirin can have serious side effects, including gastrointestinal bleeding.
Important. Do not take more than 12 tablets in 24 hours. Wait at least 4 hours between doses.
Salicylate poisoning causes respiratory alkalosis and, by an independent mechanism, metabolic acidosis. Consider salicylate toxicity in patients with nonspecific findings (eg, alteration in mental status, metabolic acidosis, noncardiogenic pulmonary edema, fever), even when a history of ingestion is lacking.
The second phase of aspirin toxicity results in an anion gap metabolic acidosis. This occurs because salicylate interrupts aerobic respiration by uncoupling oxidative phosphorylation and interfering with the krebs cycle. This results in the anaerobic production of lactate.