Pitavastatin

[keengkong]

I just went through prior auth with my insurance (very good platinum ins) who denied them using pita and stated I would need to show intolerance to EVERY single other statin before they would authorize it. Sooooo I went to Costplus sans insurance for 26 bucks shipped to my house.

It looks like it was a good thing that it was delayed due to insurance. My endocrinologist wants me to avoid taking the pitavastatin until my liver enzyme numbers return to normal. He wants to confirm that my only liver problem is from the statin before I add the pitavastatin. Even though I believe pitavastatin is unlikely to cause the same type of liver injury, it does appear reasonable, in my non-expert opinion, to confirm that the Lipitor was the sole cause of the liver injury before adding another statin back.

 

[Wizbang]

It looks like it was a good thing that it was delayed due to insurance. My endocrinologist wants me to avoid taking the pitavastatin until my liver enzyme numbers return to normal. He wants to confirm that my only liver problem is from the statin before I add the pitavastatin. Even though I believe pitavastatin is unlikely to cause the same type of liver injury, it does appear reasonable, in my non-expert opinion, to confirm that the Lipitor was the sole cause of the liver injury before adding another statin back.

Pitavastatin works through a different liver pathway than all the others, I believe it doesn't utilize CYP450 like all the others, cant remember what it does utilize off the top of my head but elevated liver values from pita are rare. But better to be safe than sorry.

 

[Ghoul]

Pitavastatin, uniquely among statins, isn't primarily metabolized by liver enzymes oxidizing the drug, so it doesn't raise ALT / AST by any significant amount.

Instead 90% of Pita is eliminated via glucuronidation. This is the liver’s way of “wrapping up” a fat-soluble drug molecule in a water-friendly coating (the glucuronic acid tag), and it gets pooped out.

The other 10% is metabolized via CYP2C9, which very few drugs get metabolized by. This is why Pita has the lowest risk of drug interactions.

 

[Wizbang]

Yeah! What he said!

 

[keengkong]

Pitavastatin, uniquely among statins, isn't primarily metabolized by liver enzymes oxidizing the drug, so it doesn't raise ALT / AST by any significant amount.

Instead 90% of Pita is eliminated via glucuronidation. This is the liver’s way of “wrapping up” a fat-soluble drug molecule in a water-friendly coating (the glucuronic acid tag), and it gets pooped out.

The other 10% is metabolized via CYP2C9, which very few drugs get metabolized by. This is why Pita has the lowest risk of drug interactions.

Ghoul, I was prepared to disagree with you and instead follow my endocrinologist's advice (going against the advice of the prescribing cardiologist) but then I looked things up at Livertox.

Livertox is a great resource. It's an excellent use of our tax dollars.

Lipitor (atorvastatin), Crestor (rosuvastatin) and simvastatin all receivr an "A," defined as "well known but rare cause of clinically apparent liver injury." In contrast, there are no confirmed cases of pitavastatin causing liver injuries although it has been associated with transitory increases in liver enzyme levels.

"Less information is available on the potential hepatotoxicity of pitavastatin in comparison to other more widely used statins. In large clinical trials, pitavastatin therapy was associated with mild, asymptomatic and usually transient serum aminotransferase elevations in approximately 1% of patients, but levels above 3 times the upper limit of normal (ULN) were infrequent and no cases of clinically apparent hepatitis were reported from the preregistration clinical trials. Since marketing of pitavastatin, however, the sponsor has received reports of jaundice, hepatitis and hepatic failure including fatal cases. However, the clinical features and typical course of the liver injury associated with pitavastatin have not been defined in the published literature. On the other hand, the other statins have all been implicated in cases of clinically apparent acute liver injury that typically arise after 1 to 6 months of therapy with either a cholestatic or hepatocellular pattern of serum enzyme elevations. Rash, fever and eosinophilia are uncommon, but some cases have been marked by autoimmune features including autoantibodies, chronic hepatitis on liver biopsy and a clinical response to corticosteroid therapy. This pattern has yet to be shown to apply to pitavastatin." Livertox (pitavastatin).

I'm not sure what I'll do. The pharmacy benefit manager did approve the prior authorization for pitavastatin; I'll pick up the pitavastatin later today.

 

[Ghoul]

Ghoul, I was prepared to disagree with you and instead follow my endocrinologist's advice (going against the advice of the prescribing cardiologist) but then I looked things up at Livertox.

Livertox is a great resource. It's an excellent use of our tax dollars.

Lipitor (atorvastatin), Crestor (rosuvastatin) and simvastatin all receivr an "A," defined as "well known but rare cause of clinically apparent liver injury." In contrast, there are no confirmed cases of pitavastatin causing liver injuries although it has been associated with transitory increases in liver enzyme levels.

"Less information is available on the potential hepatotoxicity of pitavastatin in comparison to other more widely used statins. In large clinical trials, pitavastatin therapy was associated with mild, asymptomatic and usually transient serum aminotransferase elevations in approximately 1% of patients, but levels above 3 times the upper limit of normal (ULN) were infrequent and no cases of clinically apparent hepatitis were reported from the preregistration clinical trials. Since marketing of pitavastatin, however, the sponsor has received reports of jaundice, hepatitis and hepatic failure including fatal cases. However, the clinical features and typical course of the liver injury associated with pitavastatin have not been defined in the published literature. On the other hand, the other statins have all been implicated in cases of clinically apparent acute liver injury that typically arise after 1 to 6 months of therapy with either a cholestatic or hepatocellular pattern of serum enzyme elevations. Rash, fever and eosinophilia are uncommon, but some cases have been marked by autoimmune features including autoantibodies, chronic hepatitis on liver biopsy and a clinical response to corticosteroid therapy. This pattern has yet to be shown to apply to pitavastatin." Livertox (pitavastatin).

I'm not sure what I'll do. The pharmacy benefit manager did approve the prior authorization for pitavastatin; I'll pick up the pitavastatin later today.

I should probobly point out that in cases of actual liver failure, not NAFLD aka fatty liver but seriously reduced liver function, Pitavastatin isn't the best choice, since it relies on the liver's glucuronidation to be cleared out, if liver function is fucked Pita can build up to a toxic level, and those folks need to use a statin (pravastatin I think?) that gets cleared mostly by kidneys. This warning applies to most other statins too of course since they also rely on the liver.

The good thing about Pita being eliminated via glucuronidation is that it's very gentle on the liver, a process that's not harmful to liver cells at all, unlike CYP enzyme metabolism.

 

[keengkong]

Ghoul, I was prepared to disagree with you and instead follow my endocrinologist's advice (going against the advice of the prescribing cardiologist) but then I looked things up at Livertox.

Livertox is a great resource. It's an excellent use of our tax dollars.

Lipitor (atorvastatin), Crestor (rosuvastatin) and simvastatin all receivr an "A," defined as "well known but rare cause of clinically apparent liver injury." In contrast, there are no confirmed cases of pitavastatin causing liver injuries although it has been associated with transitory increases in liver enzyme levels.

"Less information is available on the potential hepatotoxicity of pitavastatin in comparison to other more widely used statins. In large clinical trials, pitavastatin therapy was associated with mild, asymptomatic and usually transient serum aminotransferase elevations in approximately 1% of patients, but levels above 3 times the upper limit of normal (ULN) were infrequent and no cases of clinically apparent hepatitis were reported from the preregistration clinical trials. Since marketing of pitavastatin, however, the sponsor has received reports of jaundice, hepatitis and hepatic failure including fatal cases. However, the clinical features and typical course of the liver injury associated with pitavastatin have not been defined in the published literature. On the other hand, the other statins have all been implicated in cases of clinically apparent acute liver injury that typically arise after 1 to 6 months of therapy with either a cholestatic or hepatocellular pattern of serum enzyme elevations. Rash, fever and eosinophilia are uncommon, but some cases have been marked by autoimmune features including autoantibodies, chronic hepatitis on liver biopsy and a clinical response to corticosteroid therapy. This pattern has yet to be shown to apply to pitavastatin." Livertox (pitavastatin).

I'm not sure what I'll do. The pharmacy benefit manager did approve the prior authorization for pitavastatin; I'll pick up the pitavastatin later today.

I do want to thank you, Ghoul, for your efforts here. Although I'm confident that you're not being paid by those who produce pitavastatin, you are great salesman for it. I'm confident that your efforts are merely motivated by the desire to keep people alive. Also, I do plan on following your general advice about taking something else (bempoic acid and/or ezetimibe) if necessary (as I suspect it will be) to keep my LDL under 70. Yesterday the NP from the cardiologist's office said something about there being plaque build-up in my coronary arteries. I don't recall hearing that before. I looked through my online medical records and couldn't find any record of that or any diagnosis matching that. I'll bring that up the next time I'm at the cardiologist. I'm hoping that I'll get to see the doctor (for whom I'm scheduled to see) because in this particular case I believe the doctor knows far more than the NP.

 

[thestruggle]

I’m

Does PCT 24X7 ship to Europe?

Asked them. They don't.

 

[Ghoul]

I do want to thank you, Ghoul, for your efforts here. Although I'm confident that you're not being paid by those who produce pitavastatin, you are great salesman for it. I'm confident that your efforts are merely motivated by the desire to keep people alive. Also, I do plan on following your general advice about taking something else (bempoic acid and/or ezetimibe) if necessary (as I suspect it will be) to keep my LDL under 70. Yesterday the NP from the cardiologist's office said something about there being plaque build-up in my coronary arteries. I don't recall hearing that before. I looked through my online medical records and couldn't find any record of that or any diagnosis matching that. I'll bring that up the next time I'm at the cardiologist. I'm hoping that I'll get to see the doctor (for whom I'm scheduled to see) because in this particular case I believe the doctor knows far more than the NP.

Thanks man.

I can’t count the number of times over the years I hear “You’re XX is a little high” and that was always the end of it.

Hard to get motivated about BP or Lipids if the medic mentioning it doesn’t take action.

Too much blind trust led to too much, unnecessary accumulated damage.

Little did I realize how few doctors were following the lax, always outdated guidelines they were supposed to use back then, never mind keeping up with and treating based on current evidence based best practices.

In hindsight, and now that I’m immersed in the medical science, with some foresight too, it’s so damned EASY to prevent the major causes of disability and death.

Few cardiologists would argue with the premise it’s best to stop plaque buildup as soon as possible. We’re blessed to have all the tools necessary to do so without causing other harms as a tradeoff, the unfortunate reality decades ago with semi-toxic meds. There’s no justifiable reason, from a health perspective, to let plaque accumulation go on, to delay addressing it, other than cost. Cost to the payer (insurance, government), cost to the provider (in time and effort), and ultimately, the cost is shifted to the patient, in the form of needless suffering and premature death.

 

[Catteni]

View attachment 349827

Running Prava, thanks for the visual.