I have never seen any data that Incivek causes elevated "Uric Acid " ,however there are numerous articles and studies done that the other two medications (Peg/Riba) can cause these levels to rise.(see link below)
The normal reference range for serum UA is 3.5 -7.2 mg/dl so at 12 yours is quite elevated.
I know there are medications to control this so possibly a discussion with your doctor about it.
Best to you..
CONCLUSION: Peg-IFNalpha2b plus ribavirin combination therapy induced an elevation of uric acid concentration, although the elevated levels were still within normal limit in many cases. It may be that ribavirin plays a leading role in its elevation and other factors may also be involved.
I remember having uric acid tested on a few of my labs during the Incviek stage.
Here is the gist of it:
Uric Acid: During the Incivek combination treatment period, 73% of subjects had elevated uric acid levels compared to 29% for those treated with peginterferon alfa and ribavirin alone. Shifts to greater than or equal to 12.1 mg per dL from baseline in uric acid levels were also more frequent among subjects treated with Incivek (7%) compared to peginterferon alfa and ribavirin (1%). Less than 1% of subjects had clinical events of gout/gouty arthritis; none were serious and none resulted in treatment discontinuation.
Uric Acid: During the INCIVEK combination treatment period, 73% of subjects had elevated uric acid levels compared to 29% for those treated with peginterferon alfa and ribavirin alone. Shifts to greater than or equal to 12.1 mg/dL from baseline in uric acid levels were also more frequent among subjects treated with INCIVEK (7%) compared to peginterferon alfa and ribavirin (1%). Less than 1% of subjects had clinical events of gout/gouty arthritis; none were serious and none resulted in treatment discontinuation.
This is straight from the prescribing information from Incevik. I seem to recall at the FDA hearings that there was a pretty heated discussion about this and potential risk -- but I have not found it yet in the FDA briefing document.
My spouse is doing triple therapy with Victrelis. His uric acid level was around 12 pretreatment, but was overlooked. He had never had any symptoms of gout ever before. Around week 9 or so he started with gout symptoms and few days later went into uric acid crisis (also called tumor lysis syndrome) and went into acute renal failure. His level was then 17, I believe. The doctors told us that he should have been pretreated before starting therapy. Apparently chemo doctors screen for this routinely before starting chemo, which is essentially what some of these drugs are. What a horrible experience, I hope everyone gets screened and pretreated if needed. We have continued on and hope to complete treatment.
My elevated uric acid during treatment was caused by the rapid turnover of red blood cells. Some articles on uric acid refer to hemolytic anemia as a cause. Incivek can make hemolytic anemia worse (it certainly did for me!).
I did not get a gout attack until near the end of treatment. After a lot of discomfort and pain, and right after treatment ended, that attack was resolved with an extremely heavy duty anti-inflammatory (indocin).
A week later I got gout in both feet and I couldn't walk for a week -- the carpet burns on my butt from dragging
myself to the bathroom are finally gone! This episode was treated with allopurinol and colcrys.
Six weeks post treatment my uric acid is back in.the normal range, but my left foot is still recovering. Cheers, GB
Thanks Sentinel13. I hope I can get mine to lower by just quitting eating sugary stuff. I asked my nurse if there was anything that she knew of I could take to help lower it down and she said nothing that she knew of.
You may want to talk to your doctor about "insulin resistance"
High uric acid is associated with having insulin resistance and hyperinsulinemia.
Best of luck..
"In the present study, URIC ACID had an independent, significant association with metabolic syndrome in different logistic analyses, SHOWING A CONSISTENT RELATION TO INSULIN RESISTANCE. Uric acid actually correlated significantly with the fasting and two-hour insulin levels (r = 0.34). These findings are in agreement with the previous studies, in which uric acid has been connected with insulin resistance as measured with the euglycemic clamp technique or the insulin suppression test (Modan et al. 1987, Facchini et al. 1991, Vuorinen-Markkola & Yki-Järvinen 1994). This relationship persisted when the differences in age, sex, overall obesity and abdominal obesity were taken into account. Facchini et al. found (1991) that URINARY URIC ACID CLEARANCE DECREASES IN PROPORTION TO INCREASES IN INSULIN RESISTANCE in normal volunteers, leading to an increase in the serum uric acid concentration. The mechanism explaining the observed association is unclear. On the one hand, there are mechanisms implying DECREASED RENAL EXCRETION OF URIC ACID IN THE PRESENCE OF HYPERINSULINEMIA, including increased levels of ketoacids and increased sodium reabsorption with the elevation of uric acid (Modan et al. 1987). On the other hand, there are mechanisms associated with increased production of uric acid. Uric acid is a purine base that may originate from turnover and degradation of various phosphate nucleosides, such as ATP, or dinucleotides. Increased ATP turnover has, in turn, been shown to explain hyperuricemia induced by ethanol, acetate and fructose." (Vuorinen-Markkola & Yki-Järvinen 1994).
J Med Virol. 2008 Apr;)
"Is serum uric acid a predictive factor of response to IFN-treatment in patients with chronic hepatitis C infection?"
Several factors, including metabolic profile, are predictive of response to standard antiviral therapy in patients with chronic hepatitis C. In a retrospective study, it was investigated whether uric acid, involved in metabolic syndrome, could be included. A total of 153 patients (56.2% males; mean age 45.7 +/- 11.3 years) treated with pegylated-interferon and ribavirin were included. Eighty-five were infected with hepatitis C virus (HCV) genotype 1 or 4 and 68 with genotype 2 or 3. Viral load was >1,000,000 IU/ml in 101, or =5.8 mg/dl (OR = 0.46; 95% CI: 0.30-0.62), viral load (OR = 0.29; 95% CI: 0.09-0.92) and HCV genotype (OR = 0.23; 95% CI: 0.09-0.60) were identified as the most important factors independently influencing clinical outcome. The prognostic role of serum uric acid was confirmed on the sub-sample reporting Ishak fibrosis score (OR = 0.49; 95% CI: 0.28-0.85). SERUM URIC ACID
LEVEL > or =5.8 mg/dl IS PREDICTIVE OF POOR RESPONSE TO HCV TREATMENT. Prospective studies are needed to clarify the issue.
I was mistaken on the Uric Acid. My base was 8.5 and at week 4 labs it was up to 10.6. I think according to what I have read less than 6.0 mg/dL is normal and hyperuricemia is at a level above 6.8 mg/dL.
The problem is not with the amount of uric acid produced by the body, but the fact that the kidneys cannot excrete it well. It can damage the kidneys (so keep an eye on the BUN, creatinine and blood pressure) and accumulate in joints triggering inflammation and a strong immune response. High blood levels of uric acid are also associated with high blood pressure are a strong predictor of death from cardiovascular disease
According to studies, vitamin C lowers uric acid (some studies used 500mg daily). Obviously, don't take anything without first checking with your doctor.
I just checked my historical uric acid lab results. My pre-treatment uric acid was 7.0. After a few weeks on treatment, it spiked to 9.7 then slowly declined until treatment was over where it ended at 7.9.
My gout started materializing at about treatment week 20 (out of 24). It began with discomfort in the joint below my big toe and then escalated from there.
Recommend being vigilant for signs of gout and, if the treatment is not contraindicated with your HCV treatment, treat it aggressively -- I feel it is easier to get a handle on the gout if it is treated early.
There are many articles on gout, Here is my favorite:
My research indicates that not everyone with high uric acid gets gout.
I don't understand why your nurse told you she didn't know of anything to lower your uric acid level. There are meds that are specifically designed to lower uric acid levels (e.g., Allopurinol, which is what I am taking). Now, I can't say whether these meds are okay while you are undergoing HCV treatment, but they do exist.
Some articles I've read indicate that cherries (or cherry juice) and celery seed extract help gout. I can't say one way or the other, but that is what some people say.
Since high uric acid does not guarantee you will get gout, I personally would not take meds at this point in an attempt to lower my uric acid level, but I would be very aware of gout signs and symptoms and expeditiously talk to your doctor about treating them if the symptoms arise.
As I previously indicated, I believe my high uric acid was caused by hemolytic anemia (you can Google "gout uric acid hemolytic anemia"). As some previous responders indicated, there are other causes of high uric acid.
What is causing the high uric acid may not be as important as expeditiously treating the gout if it occurs.
One thing I learned when I had gout is DO NOT TAKE A LONG HOT BATH WITH YOUR FOOT IN THE WATER. OUCH!
My uric acid was never checked but I noticed that my urine smells strong although I drink a lot and urine looks very diluted. Told Md he checked for infection but that was negative.Iam assigned tonew MD after week 12.Thanks God.1more week to go.Good luck
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