Because I know how common it is for people to develop dental problems, after you are diagnosed with liver disease or cirrhosis, I thought it was worth making this post, to tell you about what happened to my husband recently when he started taking 3 prescriptions given to him by his dentist. What I have concluded is that antibiotics (particularly when mixed with pain killers) can be VERY dangerous for someone with any degree of liver disease and they can make a person very sick!!! And DO NOT expect your dentist, or pharmacist, to ask you if you have any degree of fibrosis... they will not!
My husband had two teeth pulled recently (and unfortunately those weren't the first, since he was diagnosed with cirrhosis). Once your liver becomes cirrhotic, your body is unable to process calcium properly, and you will be subjected to extreme bone loss, and your teeth will probably start to fall out! It will be especially bad if you are taking proton pump inhibitors.
My husband has had implants put in. The amount of money he's spent on getting JUST A FEW teeth fixed is equivalent to what it would have cost to buy a professional grade PEMF machine, a detox water machine, and a few years' worth of supplements! I recently talked to a woman who told me her boyfriend (who got cirrhosis the same way Jake did) spent $65,000.00 on having all his teeth replaced!
So please, people... do whatever you can to prevent cirrhosis, before it even starts. The amount of money you would spend, fixing the problems, is FAR more than you would spend to prevent it (AND YOU WILL ENJOY YOUR LIFE WAY MORE).
For anyone who has cirrhosis via alcohol (like my husband did), please, quit drinking alcohol ASAP. Get help to deal with the emotions and/or whatever you are suppressing that is making you want to drink. Get into either a rehab facility or start listening to motivational autiotapes and books to turn your life around. Join a fitness program like 24 hour fitness, or Phoenix Multisport if you have one in your area.
OK sorry I am getting off track but you know certain things I just cannot stress enough!
Anyway, when I got home, I looked up all those medications his dentist gave my husband, and sure enough... although liver failure is not necessarily common when you take these medications, they do list it on the websites for a reason.
Please have a look at this video if you get a chance.
(UPDATE... oy... I don't know if Big Pharma threatened the people who posted this video or if it was a copyright infringement, but it's removed. I am leaving the old version here in case you want to try to look up the title and see if you can find it).
You would think that the pharmacist at Costco would have been able to look at his history of medications and say, "Hmmm... it looks like you were diagnosed with cirrhosis at some point, and could still have some form of liver disease.... are you sure you want to be taking this?" Sorry...even though pharmacists typically make about $82,000.00 per year, they are just not required to go that far. I was actually the person who picked up all these medications for my husband, and the pharmacist read all the instructions to me (it took about 2 minutes for her to go over everything)... but she never mentioned anything about possible damage to the liver.
I suppose I can understand this, since they see soooo many sick people who have so many health problems, if they made everyone stand in line to listen to a long speech about every one of the potential side effects of every medication...that line at the pharmacy would be soo long, people would be more annoyed than they already are. I already get impatient when I have 2 or 3 people in front of me and have to wait more than 5 minutes in the pharmacy line!
UPDATE 11/15/16: I have been meaning to tell you guys... about a month ago, a man told me that his pharmacist - who was his long time pharmacist and friend, actually told him, I could lose my job over this, but I have to tell you... I don't think you should take this antibiotic the doctor prescribed for you... because you have cirrhosis, it could kill you. I... kid... you... not. There seems to be soooo much that doctors and dentists and pharmacists do NOT tell the majority of us! When I heard that, I wanted to shout, I KNEW IT!!! Like when a woman from the Czech republic told me her husband developed encephalopathy from drinking MILK (not even meat). There is just sooooo much that we will NOT learn from our doctors and the people who are supposed to be authorities on this subject. We're left to figure it all out on our own!
I feel kind of stupid for just now realizing, oh yeah, duh... Acetaminophen is the same thing as Tylenol, which I've heard is bad for the liver, but somehow when you see commercials you whole life, showing all these healthy, happy people (aka ACTORS) who are taking it and they seem just fine... it has a way of making you forget how serious the side effects can be, if a person has a damaged liver.
UPDATE: I have to add, a few days later he showed me he was even developing some swelling in his legs and a few weeks later, he started getting some fluid in his abdomen!!!! This is serious, people. Please believe me when I say, those prescrition drugs - especially when they are all mixed together - can be DANGEROUS.... luckily his swelling seems to be going down, but it really had me scared for a while! He started using a different setting on the water machine and I am so grateful for that machine because it actually seemed to work and he said he felt a lot better! I cannot advise anyone else to use that setting, I am just saying this is what he did.
I am not really worried about my husband because we are very lucky to have a water machine and a PEMF machine at home, and we have learned through trial and error what supplements are the most helpful. So I am confident that whatever problems he is having with his liver, can be reversed fairly soon.
Amoxicillin is considered a third generation or aminopenicillin and is one of the most commonly prescribed antibiotics. Amoxicillin and other aminopenicillins have been linked with idiosyncratic liver injury, but only rarely and in isolated case reports.
Amoxicillin (a mox' i sil' in) is an orally available aminopenicillin that has been available in the United States since 1980, for which currently more than 50 million prescriptions are filled yearly. Amoxicillin is used to treat mild to moderate infections caused by susceptible agents, such as (but not limited to) Escherichia coli, Hemophilis influenzae, Listeria monocytogenesis, Neisseria gonorrhoeae, Proteus mirabilis, Salmonella, Shigella, Staphylococcus aureus (non-penicillinase producing), Staphyloccocus epidermidis, and Streptococcus pneumoniae. Amoxicillin is available in multiple generic formulations as tablets or capsules of 250, 500 and 875 mg and is usually given in doses of 250 to 850 mg every 8 hours for 7 to 14 days. Pediatric formulations in liquid suspension and chewable tablets are also available.
Rare instances of idiosyncratic liver injury have been reported in persons receiving the aminopenicillins including amoxicillin. Cases are characterized by a short latency period of a few days to as long as two weeks. The onset of liver injury can occur after the antibiotic is stopped. The serum enzyme pattern associated with aminopenicillin liver injury has included a hepatocellular pattern with marked elevations in ALT and AST, and minimal elevations in alkaline phosphatase and rapid recovery after withdrawal. In addition, cholestatic forms of hepatic injury with marked alkaline phosphatase elevations (as also seen with penicillin-induced liver injury) have also been described, some of which have been associated with prolonged cholestasis (Case 1). The onset of hepatic injury may be accompanied by signs or symptoms of hypersensitivity such as eosinophilia, rash and arthralgias, and in some cases is accompanied by toxic epidermal necrolysis or Stevens Johnson syndrome.
Likelihood score: B (highly likely but rare cause of clinically apparent liver injury).
Much more common than liver injury from amoxicillin alone is the typically cholestatic hepatitis that occurs after treatment with the combination of amoxicillin and clavulanate. Indeed, this combination is currently the most common cause of idiosyncratic acute liver injury in the United States, Europe and Australia. The injury, however, is usually attributed to the clavulanate rather than amoxicillin. The clinical features are similar but perhaps not completely the same. In cases of liver injury seeming due to amoxicillin, an extra effort should be made to make sure that it was not amoxicillin/clavulanate [Augmentin] that was taken.
Mechanism of Injury
The cause of the liver injury associated with amoxicillin use is probably hypersensitivity or allergy. Recurrence with reexposure is highly likely, but intentional rechallenge has not been described.
Outcome and Management
In the few cases that have been described, the majority of patients have recovered, although recovery has been slow in some cholestatic instances (2 to 6 months). Rare instances of acute liver failure and several cases of vanishing bile duct syndrome have been reported with aminopenicillin induced liver injury. Corticosteroids have often been used to treat the allergic manifestations of penicillin related immunoallergic hepatitis; while corticosteroid therapy may improve fever and rash promptly, their efficacy in ameliorating the accompanying liver disease has not been shown. Instances of recurrence of liver injury with unintentional reexposure to aminopenicillins and recurrence with exposure to cephalosporins have been reported. Patients with aminopenicillin induced hepatitis should avoid reexposure to other penicillins and should take cephalosporins with caution.
References to the hepatotoxicity and safety of amoxicillin are given in the Overview section on the aminopenicillins.
Drug Class: Antiinfective Agents, Aminopenicillins
Other Drugs in the Subclass, Aminopenicillins: Amoxicillin
/Clavulanate, Ampicillin, Ampi cillin-Sulbactam, Bacampicillin, Pivampicillin
Case 1. Cholestatic hepatitis due to amoxicillin therapy.
from Bolzan H, Spatola J, Castelletto R, Curciarello J. Cholestasis
intrahepatica inducida por amoxicilina sola. Gastroenterol Hepatol 2000;
A 24 year old woman developed anorexia and weakness followed by dark urine and itching 5 days into a 10 day course of amoxicillin for pharyngitis and fever. Within days of finishing the 10 day course, a friend told her that she looked jaundiced. Ten days after stopping the antibiotic, she sought medical care for continuing jaundice and pruritus. Serum ALT, AST and alkaline phosphatase were only modestly elevated, but total serum bilirubin was 10.5 mg/dL with a direct fraction of 8.0 mg/dL. There was no eosinophilia, rash or fever. Tests for viral hepatitis and autoantibodies were negative. An ultrasound of the liver was normal. Her jaundice deepened, and she underwent endoscopic retrograde pancreato-cholangography (ERCP) which was also normal. A liver biopsy showed intrahepatic cholestasis, mild portal inflammation, but little hepatocellular injury, compatible with a resolving cholestatic hepatitis secondary to a medication. She had taken no other medications, herbals or over-the-counter products and had no previous history of liver disease or alcohol abuse.
|Medication:||Amoxicillin (1500 mg daily for 10 days)|
|Severity:||3+ (jaundice and hospitalization)|
Metronidazole is a nitroimidazole derivative bactericidal agent widely used in the treatment of many anaerobic and certain protozoan and parasitic infections. Metronidazole has been linked to rare instances of acute, clinically apparent liver injury.
Metronidazole (met" roe nid' a zole) is a nitroimidazole antibiotic that is activated by reduction of its nitro group by susceptible organisms. The activated form of metronidazole is a highly reactive radical anion which targets and damages large protein molecules and DNA. Mammalian cells do not ordinarily activate metronidazole, which accounts for its lack of toxicity in humans. Metronidazole was approved for use in the United States in 1963 and currently several million prescriptions are filled yearly. Metronidazole is indicated for treatment and prophylaxis of infections with susceptible anaerobic bacteria and protozoa. The recommended dosage is 500 to 750 mg taken orally three times daily for 5 to 10 days. Metronidazole is available alone in tablets of 250, 375, 500 and 750 mg as well as in combination with other medications, in multiple generic formulations and under several brand names including Flagyl, Metryl, Noritate, Pylera and Helida. Other formulations include injectable solutions, extended release tablets, suppositories, and topical creams. The most common side effects include metallic taste, nausea, vomiting, abdominal discomfort and diarrhea.
Despite the wide use of metronidazole, only rare cases of hepatotoxicity have been reported, and metronidazole is not listed among causes of drug induced liver injury and acute liver failure in large case series. High doses of metronidazole given parenterally or in an overdose can cause elevations in serum aminotransferase levels, but these are usually self-limited and minimally symptomatic (Case 1). Acute, clinically apparent liver injury from metronidazole is rare. Ornidazole, another synthetic nitroimidazole that was available in Europe, was implicated in several cases of drug induced liver injury, with a latency of a few days or weeks and a hepatocellular pattern of injury. Metronidazole has been associated with a similar acute hepatitis-like syndrome with a short incubation period, but much more rarely. Fever, rash and eosinophilia are uncommon as are autoimmune features. A fatal recurrence of acute liver injury after reexposure to metronidazole has been published (Case 2). Strikingly, multiple instances of metronidazole hepatoxicity have been reported in the rare genetic disease, Cockayne syndrome in which there is an absence or deficiency in an important DNA repair enyzme responsible for nucleotide excision repair. The cases were marked by a short latency (1 to 7 days) to onset of jaundice, a hepatocellular pattern of enzyme elevations and severe course with a high mortality rate.
Mechanism of Injury
The cause of acute liver injury due to metronidazole is probably immunoallergic, given the short latency period and recurrence with rechallenge. However, the frequency of severe hepatotoxicity in children with Cockayne syndrome suggests a direct toxic effect, probably involving breaks in double stranded DNA.
Outcome and Management
The liver injury from metronidazole is rare, but can result in liver failure and death. In typical cases, recovery is expected in 1 to 3 months. Rechallenge results in prompt recurrence and should be avoided.
Drug Class: Antiinfective Agents; Gastrointestinal Agents
Other Drugs in the Subclass, Nitroimidazoles: Tinidazole
Before taking this medicine
- liver disease;
- a stomach or intestinal disease such as Crohn's disease;
- a blood cell disorder such as anemia (lack of red blood cells) or leukopenia (lack of white blood cells);
- epilepsy or other seizure disorder; or
- nerve disorders.
Case 1. Elevations in serum aminotransferase levels during intravenous metronidazole therapy.
[Modified from: Appleby DH, Vogtland HD. Suspected metronidazole hepatotoxicity. Clin Pharm 1983; 2: 373-4. PubMed Citation]
58 year old man underwent prostate biopsy and cystoscopy and 32 hours
later developed fever and was admitted for treatment of suspected
urosepsis. After a combination of cephalosporin and tobramycin failed
to affect his course, intravenous metronidazole (500 mg every 6 hours)
was added. He had rapid clinical improvement, but then complained of
abdominal pain, nausea, headache, and a metallic taste. Metronidazole
was stopped after 5 days, and he was switched on oral cefaclor. At the
same time, serum ALT and alkaline phosphatase levels were found to be
elevated. Physical exam showed slight hepatomegaly without jaundice.
Hepatitis B serology was negative. Over the following week, the patient
recovered symptomatically and was discharged home. All laboratory
tests were normal 4 weeks after stopping metronidazole.
|Medication:||Metronidazole, 500 mg iv every 6 hours for 5 days|
|Severity:||1+ (ALT elevations without jaundice)|
|Recovery:||24 days after stopping|
|Other medications:||Cefaclor, tobramycin|
|Time After Starting||Time After Stopping||ALT (U/L)||Alk P (U/L)||Bilirubin (mg/dL)||Other|
|Pre||Pre||65||Prostate biopsy, cystoscopy|
|Fever 104 oF: cefapirin, tobramycin|
|0||Start iv metronidazole||Continued fever|
|5 days||0||Stop metronidazole||Started cefaclor|
|6 days||1 day||720||200||0.4||GGT 459|
|7 days||2 days||238||0.5|
|9 days||4 days||464||191||0.9|
|10 days||5 days||319|
|2 weeks||9 days||167||71||Discharged|
|4 weeks||24 days||42||80||0.3|
The serum enzyme elevations were compatible with mild metronidazole hepatotoxicity, given the short latency period and rapid recovery after stopping. The rapid onset and rapid recovery after high doses of intravenous metronidazole suggest direct hepatic injury. However, idiosyncratic cases are also marked by short latency period and rechallenge, even with oral metronidazole should be avoided.
Case 2. Acute hepatocellular injury due to metronidazole with fatal recurrence on reexposure.
from: Björnsson E, Nordlinder H, Olsson R. Metronidazol as a probable
cause of severe liver injury. Hepatogastroenterology 2002; 49: 252-4. PubMed Citation]
24 year old woman was treated with metronidazole for Clostridium
difficile infection after a course of penicillin for a tooth abscess.
Her diarrhea improved, but a few days later she developed nausea and
vomiting followed by jaundice. Her past medical history included asthma
and frequent upper respiratory infections. Laboratory tests showed
total bilirubin of 7.9 mg/dL with marked elevations in serum
aminotransferase levels, but modest increase in alkaline phosphatase
(Table). Tests for hepatitis A, B ad C and for autoantibodies were
negative. An ultrasound showed no evidence of biliary obstruction.
Metronidazole was discontinued and she began to improve, but her
recovery was slow and symptoms persisted for at least two months and
laboratory tests did not return to normal for at least nine months. Two
years later, she was treated for bacterial vaginitis with metronidazole
and tetracycline and one week later developed nausea, vomiting and
jaundice. Serum bilirubin was 12.2 mg/dL, ALT and AST were more than
100 fold elevated, and prothrombin index was <9%. She was
transferred to a liver transplant center where she developed progressive
hepatic coma. Tests for hepatitis A, B and C were again negative. She
underwent liver transplantation, but died in the perioperative period.
Explant showed massive hepatic necrosis and cholestasis.
|Medication:||Metronidazole (dose and duration not given)|
|Severity:||3+ initially (jaundice and hospitalization)|
5+ on reexposure (liver transplantation, death)
|Recovery:||10 months after initial exposure|
|Other medications:||Oral tetracycline|
|Time After Starting||Time After Stopping||ALT* (U/L)||Alk P* (U/L)||Bilirubin *(mg/dL)||Other|
|0||Metronidazole given for C difficile|
|15 days||5 days||3000||500||20.1|
|1 mo||1 mo||104||450||10.5|
|2.5 mos||2.5 mos||102||492||1.0|
|9 mos||9 mos||84||<300||1.0|
|26 mos||Metronidazole given for bacterial vaginitis|
|~7 days||0||11104||810||12.2||Protime index < 9%|
|~10 days||~3 days||20.5||Liver transplant, post-operative death|
*Values estimated from Figure 1. Bilirubin results converted from mol to mg/dL (17.1) and enzyme results converted from kat to U/L (0.01667).
Severe acute hepatocellular injury from a short course of metronidazole with slow recovery, followed by tragic rapid and fatal recurrence on reexposure.
REPRESENTATIVE TRADE NAMESMetronidazole – Generic, Flagyl®
DRUG CLASSAntiinfective Agents