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179856 tn?1333547362

High Cholesterol After Treatment

Well my cholesterol was always one of the only perfect things I had...and now that is gone.  I have to go on a low fat diet and increase exercise! AS you know, Lipitor is not indicated for people with liver disease...so I'm going to have to do it I guess.  Low fat? After doing treatment and becoming so used to ice cream and things like that it's going to be torture!

I was wondering if anybody else had their cholesterol go up after treatment?  If it was an after tx complication or just that I'm getting not so young anymore and would have happened anyway?

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568322 tn?1370165440
PART 2....

In animal studies, statins have been found to cause severe liver injury. Inhibition of mevalonic acid synthesis leading to centrizonal hepatocellular necrosis is thought to be the mechanism responsible for statin hepatotoxicity and can be prevented by mevalonate supplements in animal studies. However, in human studies, statins can also cause mild elevation in liver enzymes without clinically significant liver damage (Hepatology 2005;41:690–695). Pfeffer et al, in the prospective pravastatin pooling project, observed that 0.5% of the patients who received 40 mg of pravastatin had ALT levels >5 times ULN and 0.2% had ALT levels >9 times ULN (Circulation 2002;105:2341–2346). Interestingly, during several statin trials, investigators observed similar incidence of increased liver enzymes in patients receiving placebo. This observation has been demonstrated by De Denus et al in a meta-analysis reviewing 13 placebo-controlled trials with total of 49,275 subjects. Statin therapy was not associated with a significant increase in liver enzymes compared with placebo (OR, 1.26; 95% CI, 0.99–1.62; Pharmacotherapy 2004;24:584–591). Despite frequent concerns for statin hepatotoxicity, acute liver failure leading to death or liver transplantation seems to be extremely rare. Of 51,741 patients who underwent liver transplantation in the United States between 1990 and 2002, there were 3 patients who had acute liver failure presumably caused by statins (Liver Transpl 2004;10:1018–1023) and many experts argue that these few cases of acute liver failure may be unrelated to statins and reflect the expected incidence of acute liver failure of unknown cause.

Several investigators have demonstrated the safety of using statins in the treatment of hypercholesterolemia in patients with chronic liver disease. Chalasani et al retrospectively compared the incidence of statin hepatotoxicity over a 6-month period in 342 hyperlipidemic patients with elevated baseline liver enzymes who received statins with 1,437 hyperlipidemic patients with normal aminotransferase levels who received statins (statin controls) and 2,245 patients with elevated liver enzymes who did not receive statins (liver disease controls). Compared with statin controls, patients with elevated baseline liver enzymes had higher incidence of mild-to-moderate elevations (4.7% vs 1.9%; P = .002) but not severe elevations (0.6% vs 0.2%; P = .2). The authors found that patients with elevated baseline liver enzymes who received statins did not have higher incidence of mild-to-moderate elevations (4.7% vs 6.4%; P = .2) or severe elevations (0.6% vs 0.4%; P = .6) than the liver disease controls who did not receive statins (Gastroenterology 2004;128:1287–1292). Khorashadi et al studied the safety of using statins in treatment of hypercholesterolemia in patients with HCV. In this study, biochemical evidence of statin hepatotoxicity over a 12-month period was assessed in 166 subjects with HCV who received statins compared with 332 HCV subjects who did not receive statins and 332 subjects without HCV who did receive statins. The authors found no association between HCV positivity and biochemical evidence of statin hepatotoxicity, and concluded that statin therapy is safe in HCV patients with hyperlipidemia (Clin Gastroenterol Hepatol 2006;4:902–907).

More recently, Segarra-Newnham et al retrospectively reviewed 146 patients with HCV and hypercholesterolemia who were treated with statins between January 1995 and September 2003. Lipid profiles and aminotransferase levels at baseline and at 3 and 6 months after starting the statin were collected with a mean follow-up of 22 months. A significant decrease in LDL-C levels from their baseline values was seen with no significant increase in serum ALT levels. Only 1 patient discontinued statin owing to an ALT value elevated >3 times the ULN (Pharmacotherapy 2007;27:845–851). Ritzel et al, in a small pilot study, demonstrated the safety of using statins in patients with primary biliary cirrhosis (J Hepatol 2002;36:454–458).

The study by Lewis et al is the first prospective, randomized, double-blind, placebo-controlled trial of using statins in patients with chronic liver disease. This well-designed study provides the strongest evidence that statin use in patients with chronic liver diseases is safe and effective. In fact, the observation of improvement in liver enzymes in patients who received statins warrants future studies looking at the therapeutic role of statins and possible improvement in liver histology. Strengths of the study include the use of strict criteria for the safety endpoint (doubling of ALT either from normal or baseline value as a sign of liver injury); therefore, even mild liver injury was likely to be detected biochemically. Because statin hepatotoxicity is thought to be dose related, the investigators also used a high therapeutic dose of pravastatin (80 mg/d). The study cohort was large and the follow-up period of 36 weeks was reasonably long enough to detect most episodes of statin-induced liver injury.

Ultimately, there are some questions that remain unanswered. Patients with decompensated or severe liver diseases were excluded from the trial, so the results of this study cannot be applied to this group of patients; however, the role of therapy for dyslipidemia in this group of patients is unclear. The other point worth mentioning is that the majority of the subjects had NAFLD and the role of statins in treatment of NAFLD continues to evolve. Overall, this trial provides strong evidence that the use of statin agents among patients with chronic liver disease is safe, effective in managing dyslipidemia, and may even be beneficial in improving liver chemistries. The challenging question which faces many physicians is not can we use these drugs safely, but rather do we still need to monitor patients on statins for possible hepatotoxicity and if so, how often?

http://www.gastrojournal.org/article/S0016-5085(08)01189-X/fulltext
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568322 tn?1370165440
"AS you know, Lipitor is not indicated for people with liver disease."

That's not true.


July 2008

Statins Are Safe for the Treatment of Hypercholesterolemia in Patients With Chronic Liver Disease.

Lewis JH, Mortensen ME, Zweig S, et al. (Georgetown University Medical Center, Washington, DC, USA).

The benefits of statins in the primary and secondary prevention of cardiovascular disease have been well-demonstrated in clinical trials, showing that statins decrease the mortality from coronary artery disease and decrease the incidence of myocardial infarction, stroke, and peripheral vascular disease (Circulation 2002;106:1024–1028). These medications are safe and >10 million prescriptions were given to patients in the United States in 2003. Although clinically significant liver injury is extremely rare from statins, mild increases in liver enzymes can occur in 1%–3% of patients. Because of the concern of possible hepatotoxicity, statins are labeled as contraindicated in patients with liver disease. Given the prevalence of liver diseases in the population, such as nonalcoholic fatty liver disease (NAFLD), hepatitis C (HCV), and others, many patients have not benefitted from the cardiovascular protective effects of statins. In clinical practice, gastroenterologists and hepatologists are often consulted to evaluate patients who develop liver enzymes abnormalities while receiving statins and also are frequently asked about the safety of prescribing statins in patients with hypercholesterolemia and chronic liver disease. Several retrospective studies have looked at the safety of statins in patients with established liver disease and suggest that statins are safe in patients with compensated liver disease.

In this setting, Lewis et al prospectively assessed the efficacy and safety of using pravastatin in patients with hypercholesterolemia and chronic liver disease (Hepatology 2007;46:1453–1463). Between March 5, 2003, and July 23, 2004, 630 subjects underwent initial screening. During the screening period, the subjects were not permitted to take any lipid-lowering treatments and entered a 4-week, single-blind, placebo lead-in period, during which time they were to have adhered to the National Cholesterol Education Program Step 1 diet. At the end of the placebo lead-in period, 326 subjects with persistent hypercholesterolemia (mean low-density lipoprotein cholesterol [LDL-C] ≥100 mg/dL and triglycerides [TG] 5 times the ULN, decompensated liver disease (cirrhosis with a Child–Pugh score >5), treated with antiviral therapy for hepatitis B or C, prior lipid-lowering medications for ≥8 weeks, or with other significant comorbid conditions (eg, cancer, significant cardiovascular, uncontrolled diabetes mellitus) were excluded.

All pre-enrollment liver enzymes levels were similar for both treatment groups. The mean historical ALT and AST values were statistically significantly lower in the pravastatin group than in the placebo group (P = .0073), but were not considered clinically significant. All baseline lipid values were similar for both treatment groups. The mean HDL-C was modestly (but statistically significantly) higher at the baseline in the pravastatin group than in the placebo group (P = .0392). At week 12, the treatment group had statistically significant reduction in the mean LDL-C, TC, and TG values compared with the placebo group. The difference in HDL-C between groups was statistically significant, favoring pravastatin, only at weeks 4 and 8 (P = .005 and P = .003, respectively).

After 36 weeks of treatment, the cumulative proportion of patients who reached the primary safety endpoint was lower in the pravastatin group than in the placebo group (8% vs 13%; 95% confidence interval [CI], −11.6 to 1.6; P = .1379). In fact, the mean ALT values declined from baseline in the pravastatin group, whereas the mean ALT and AST were increased from baseline in the placebo group. None of the subjects in either treatment group had an elevation of total bilirubin >2 times the ULN. Outcomes were similar in all subgroups regardless of etiology of liver disease. The overall incidence of adverse events was similar in the pravastatin group (26.4%) and in the placebo recipients (25.2%), with the most common adverse event being a headache in both treatment groups. No clinically apparent hepatotoxicity was seen in either group. No subject experienced acute exacerbation of underlying liver disease during the trial. One death was reported (in a placebo recipient) owing to myocardial infarction that was considered unrelated to the study drug by the investigators. The authors concluded that statin therapy should not be denied to patients on the basis of liver disease. Moreover, they join others in suggesting that the current labeling for pravastatin and other statins that contraindicates their use in liver disease should be reviewed and amended.
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Avatar universal
OATMEAL, stop smoking, use the stairs!  less fat, your not old honey, your body is just changing, oh agrees on the fudgecycles!

I think a lot of people have to deal with this at a certain age, husband is now, he isn't HCV, but  cooking for us is strange sometimes, he is no fat, I am fat, like jack sprat and his wife.

Deb
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412832 tn?1219075345
Ask your doctor about Zetia... It's not hamful to the liver like a statin drug.  

I also recommend another good book by Dr. Agatston called "South Beach Heart Progam."  I just read it and am going to have several blood tests done to measure other indicators of heart disease.  Shocking for me to read that having normal cholesterol levels doesn't mean your heart is healthy...

Trust me after "surviving" tx, I want to make sure I'm as healthy as can be!

pK
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Avatar universal
Jim has mentioned it before but check out the South Beach Diet by Arthur Agatston, M.D.
CS
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362971 tn?1201987034
  Hi
I can give you my experience. I have had hep-c for about 30 years. I don't know what my cholesterol was back then but I started paying attention to it about 15 years ago when it was 150. I assume that as my liver desease progressed it  got lower. The last 8 years it has hovered between 90 and 110.
  
   Guess what. In June which was 3 months after the end of treatment my cholesterol was 177. The highest that I know of. This tells me that my Liver is healing and making more of it. I just hope it doesn't keep going up. I will have to wait and see.  
  
A compromised Liver sometimes doesn't make enough of it. If we do end up on Lipitor, we probably would of anyway if we didn't have hep-c.

Bobby
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96938 tn?1189799858
Here is the question to which I referred:

http://www.medhelp.org/posts/show/534318
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487070 tn?1313665952
Just out of curiosity, if one has say, stage 4 does is neccesasarily recover back to an uninflammed Liver? Can't it only go back to a stage 2 having at least some improvement. I can understand a stage 1 or 2 going fully back. Won't a bx after tx actually tell? Do many people have a bx any time after tx.
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96938 tn?1189799858
You're paying for the fudgicles now.  But really, do you even have liver disease?  As the famous Dr. says (see a question from me to him in July'ish) your liver should recover. So, with a recovered liver and the absence of hcv - you might not have liver disease and therefore might be 'eligible' for those thing that you weren't when you 'had' that stuff. Nothing wrong with diet, exercise and twigs and pebbles on your dinner plate, I suppose.
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Avatar universal
Oh, and one other thing as I was told recently by a poster with impeccable credentials, back off the sugar.

jasper
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Avatar universal
The last part I’m not going to touch but seeings how your thyroid is gone it may have something to do with it besides at your age a little exercise will not hurt.
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