Now, if this was the first person I'd ever talked to, who told me this, I might think nothing of it. But I've had so many people tell me they couldn't figure out how they got their cirrhosis.... and they just happened to be taking Metformin...
Things that make you go, HMMMM!
Today was that day I finally got around to looking into this a little further.
She did say that she had a lot of dental work done. And I told her that my husband experienced liver problems after getting dental work done, because a liver with fibrosis (even if it's not CIRRhosis) can react poorly to the anesthesia you get in a dental chair. She said yes, she'd had dental work done. So I am guessing that is a contributing factor.
Then, my next call was with a woman who just got a water machine this weekend. She called to tell me that her Dad looked more clear headed than she's seen him in a long time, and her Mom (who is also on Metformin) agreed. Her Mom has had a lot of health issues also.
OK so here is my OPINION on the whole Metformin thing.
In my OPINION, metformin may cause more liver toxicity, than people realize, especially when it's taken for extended periods of time. And it's taken by someone with Diabetes, who is already struggling with health issues. People with type 2 diabetes would usually, greatly benefit from a change in their diet, and may already have a certain amount of liver issues that have steadily been building, for several years (the liver can take a LOT of damage, until all of a sudden, it's like.... glaring loud warning signals like a fire alarm going off).
So, it doesn't really surprise me that people on Metformin will gradually start having a LOT of different health issues. When you rely on taking lots of medications, to fix your health issues, without changing your diet... it's just like a guaranteed recipe for disaster.
I'd read once, that ALL prescription medications are toxic to the liver, to some degree, and I believe it. The problem is that doctors make it sound like it's NORMAL for a person to be on medications, for the rest of their lives. And I truly believe that if doctors made NO MONEY whatsoever, from prescriptions... it would be an entirely different story. Kickbacks for prescription medications should be ILLEGAL.
Below is some info I pasted from this page.... decide for yourself.
Maybe the instance is low, but... somehow, these people and their relatives manage to keep finding my blog!
https://www.livestrong.com/article/245459-metformin-effects-on-the-liver/
Mild Liver Dysfunction
According to LiverTox, a publication of the U.S. National Library of Science drug database, Metformin may occasionally cause mild liver toxicity, characterized
by minor elevations in liver enzymes. It occurs in less than 1 percent
of the patients taking Metformin and usually appears within the first
one to eight weeks of treatment, according to LiverTox. Liver problems
usually resolve quickly once you stop taking the Metformin, according to
LiverTox.
Knowing the Signs
Your
liver is a critical organ that is responsible for detoxifying your
blood. While Metformin influences the liver in some positive ways that
result in decreased glucose output, it's
capable, under rare circumstances, of negatively affecting liver
function. Seek immediate medical attention if you notice signs of liver
toxicity, which include weakness, fatigue or jaundice.
is some info I pasted from this page:
https://livertox.nlm.nih.gov/Metformin.htm
OVERVIEW
Metformin
Metformin
Introduction
Metformin is a first line agent for the treatment of type 2 diabetes that can be used alone or in combination with sulfonylureas, thiazolidinediones or other hypoglycemic agents. Metformin has not been linked to serum enzyme elevations during therapy and is an exceeding rare cause of idiosyncratic clinically apparent acute liver injury.
Background
Metformin (met for' min) is a biguanine and acts as an insulin sensitizing agent, probably through activation of adenosine monophosphate dependent (AMP) kinase in liver and muscle tissue. Metformin is often associated with weight loss making it a preferred, first line agent for management of overweight patients with type 2 diabetes. Initial concerns about the possibility that metformin (like the related biguanine phenformin) could induce lactic acidosis have been largely resolved, although the agent is contraindicated in patients with renal dysfunction because of this reason and should be used with caution in patients with significant liver disease. Metformin was approved for use in the United States in 1995 and is currently one of the most commonly used drugs for the therapy of diabetes, with more than 30 million prescriptions filled in the United States yearly. Metformin is available in many generic forms in tablets of 500, 850 or 1000 mg, the recommended regimen being to start with 500 or 850 mg once daily and increase based upon tolerance to 1000 to 2550 mg daily taken in two divided doses. Commercial formulations include Glucophage, Glumetza, Fortamet and Riomet. Metformin is also available in extended release formulations and in combinations with sulfonylureas such as glipizide (Metaglip) or glyburide (Glucovance), DDP-4 inhibitors such as alogliptin (Kazano), linagliptin (Jentadueto), saxagliptin (Kombiglyze) and sitagliptin (Janumet), as well as thiazolidinediones such as pioglitazone (Actoplus) and rosiglitazone (Avandamet). Metformin is generally well tolerated but side effects can include diarrhea, gastrointestinal upset, abdominal pain, nausea, weakness, headache, dizziness and rash.
Hepatotoxicity
Minor enzyme elevations have been reported to occur during metformin therapy in less than 1% of patients. Indeed, metformin may actually lower elevated aminotransferase levels in patients with fatty liver disease. Clinically apparent liver injury from metformin is very rare, fewer than a dozen cases having been described in the literature despite widespread use of this agent for several decades. The liver injury usually appears after 1 to 8 weeks, typically with symptoms of weakness and fatigue followed by jaundice. Various combinations of hepatocellular and cholestatic injury have been described, and many have been mixed. Allergic manifestations are not typical but rash, fever and eosinophilia have been described. Autoantibody formation is also not typical. Because this agent is usually given in combination with other hypoglycemic agents, many of which also cause liver injury, it can be difficult to establish whether the injury is due to metformin or another agent. The timing of injury is perhaps most characteristic, the injury arising soon after the agent is started and not during long term therapy. Recovery is usually rapid after metformin is stopped.
Mechanism of Injury
The mechanism of liver injury due to metformin is unknown. Metformin may actually be beneficial for some forms of liver disease, such as nonalcoholic steatohepatitis and need not be avoided in patients with mild, preexisting serum enzyme abnormalities. Acute liver injury from metformin may have a metabolic basis, arising after weeks to months of therapy. Rechallenge can lead to recurrence, but also requires weeks to months of therapy before injury reappears.
Outcome and Management
The liver injury from metformin usually resolves rapidly once the agent is stopped. Chronic injury has not been described. No convincing cases of fulminant hepatic failure from metformin have been reported. In cases in which multiple hypoglycemic agents were being used when the liver injury appears, rechallenge with the agent least likely associated with the injury is appropriate. There is no cross reactivity in hepatotoxicity with other antidiabetic medications.
Drug Class: Antidiabetic Agents
Top of page
CASE REPORTS
Metformin
Metformin
Case 1. Acute hepatitis due to metformin.
[Modified from: Deutsch M, Kountouras D, Dourakis SP. Metformin hepatotoxicity. Ann Intern Med 2004; 140: 408-9. PubMed Citation]
A 67 year old woman with diabetes was started on metformin (500 mg twice daily) and developed fatigue, weakness and jaundice five weeks later. She had no history of liver disease or risk factors for viral hepatitis and did not drink alcohol. She had coronary artery disease and medications taken chronically included aspirin, isosorbide mononitrate, diltiazem and acarbose. On admission, 6 weeks after starting metformin, she had a total bilirubin of 4.8 mg/dL (Table). Tests for hepatitis A, B and C were negative. She had antinuclear antibodies (1:320). An abdominal ultrasound and CT scan were normal. Liver biopsy showed acute inflammation. Metformin and acarbose were withdrawn and gliclazide started. The jaundice slowly resolved over the next three months, but metformin was subsequently restarted, and jaundice reappeared 3 months later. Metformin was again withdrawn and her liver injury improved slowly.
Key Points
| Medication: | Metformin (500 mg twice daily) |
| Pattern: | Hepatocellular (R=26) |
| Severity: | 3+ (hospitalization for jaundice) |
| Latency: | 5 weeks |
| Recovery: | Complete within 2 months |
| Other medications: | Acarbose, diltiazem, aspirin, isosorbide mononitrate |
Laboratory Values
| Time After Starting | Time After Stopping | ALT* (U/L) | Alk P (U/L) | Bilirubin* (mg/dL) | Other |
|---|---|---|---|---|---|
| 6 weeks | 0 | 905 | 121 | 4.8 | ANA: 1:320 |
| 7 weeks | 1 week | 960 | 4.5 | Liver biopsy | |
| 8 weeks | 2 weeks | 1160 | 3.0 | ||
| 9 weeks | 3 weeks | 1080 | 3.0 | ||
| 3 months | 6 weeks | 280 | 4.0 | ||
| 4 months | 10 weeks | 120 | |||
| 12 weeks | 40 | 1.0 | |||
| Metformin restarted approximately 4 months later | |||||
| 12 weeks | 0 | 880 | 3.0 | ||
| 13 weeks | 1 week | 1240 | 2.5 | ANA still present | |
| 14 weeks | 2 | 1120 | 2.2 | ||
| 15 weeks | 3 | 920 | 2.1 | ||
| 4 months | 4 | 800 | 2.5 | ||
| 5 months | 9 | 480 | 1.0 | ||
| 6 months | 13 | 40 | 1.0 | ||
| Normal Values | <40 | <130 | <1.2 | ||
* Values of ALT and bilirubin were estimated from the figure and converted from times upper limit of normal to absolute values based upon normal values provided.
Comment
This patient developed an acute hepatitis-like illness with mild jaundice after 5 weeks of therapy with metformin which was somewhat slow to resolve. Upon rechallenge, there was a recurrence of the liver injury, but only after metformin had been given for several months. Nevertheless, the pattern and subsequent course of the liver injury was similar to the original episode making it likely that metformin was the cause of the injury. While most causes of liver injury were excluded (hepatitis A, B and C, cholecystitis), the presence of a strongly positive ANA raises the possibility that the patient had autoimmune hepatitis with an acute, fluctuating onset and course. The liver biopsy apparently did not suggest autoimmune hepatitis, but this possibility can be excluded only by further follow up. In assessing hepatotoxicity from commonly used medications such as metformin, the possibility of an unusual presentation of a common liver disease must always be considered.
Case 2. Acute hepatitis-like injury due to metformin.
[Modified from: Kutoh E. Possible metformin-induced hepatotoxicity. Am J Geriatr Pharmacother 2005; 3: 270-3. PubMed Citation]
A 73 year old Japanese woman with poorly controlled diabetes, despite therapy with a sulfonylurea and pioglitazone, was started on metformin (500 mg twice daily) and developed fatigue, weakness and jaundice 3 weeks later. She was known to have had normal liver tests before starting metformin. On admission, laboratory testing showed a total bilirubin of 6.5 mg/dL and a hepatocellular pattern of serum enzyme elevations (Table). All oral antidiabetic agents were stopped and she was managed on insulin. Tests for hepatitis B and C infection were negative as were autoantibodies. Ultrasound, CT and ERCP were unremarkable. Her serum enzymes improved rapidly once metformin was stopped and were normal 7 weeks later.
Key Points
| Medication: | Metformin (500 mg twice daily) |
| Pattern: | Hepatocellular (R=21) |
| Severity: | 3+ (hospitalization for jaundice) |
| Latency: | 3 weeks |
| Recovery: | Complete within 2 months |
| Other medications: | Nateglinide and pioglitazone for 6 months |
Laboratory Values
| Time After Starting | Time After Stopping | ALT (U/L) | Alk P (U/L) | Bilirubin (mg/dL) | Other |
|---|---|---|---|---|---|
| Pre | 16 | 337 | 0.7 | ||
| 3 weeks | 0 | 772 | 635 | 6.5 | Admission |
| 4 weeks | 1 weeks | 353 | 480 | 3.2 | |
| 6 weeks | 3 weeks | 101 | 2.6 | Symptoms resolved | |
| 8 weeks | 5 weeks | 65 | 1.7 | ||
| 10 weeks | 7 weeks | 13 | 0.6 | ||
| Normal Values | <36 | <359 | <1.2 | ||
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