I just finished my Hepc treatment after six months and I feel great, except for one thing; I have gout. This started 2 weeks after the treatment. I've been to the doctor for this , the pain has subsided but I'm still limping. I've stopped taking the prescriptions and trying the natural stuff. It seems to be working but ever so slow. Excersize seems to help also. I suggest to keep moving and do not let it get the best of you. After six months of Pegasys, and six weeks of procrit, God will help me conquer this. Next week I will have a serious talk about this. I'm glad to see that I'm not the only one who is having the problem (well I'm not glad) and I thank you gus for the information. We must all detox the cure for HepC out of our systems. I believe that Gout is a side effect. Hang in there guys, study, research with love and let's keep each other informed.
Numerous and various sides to Tx. My biggest mistake was letting all my doctors convince me it was all in my head. Since finding this forum I now have a pro-active open minded Hepatologist. I am off all anti-depressants and pain medications and feel like I'm slowly waking from a nightmare of doubt and un-certainty that was probably being caused by the drugs.
Exercise is not recommended with Gout.
There are articles which link uric acid levels (high uric acid is associated with Gout) with HCV and interferon but I don't think that gout is a side effect of HCV or treatment. If that were the case I think I would have seen a lot more posts on the subject - I can't remember one). I treated 3 times and my last ended in June 2004. I never had gout until May 2009. Too often we attribute every malady we have to HCV or treatment but it's more often that not wrong.
and what do you attribute your gout to now? Genetics? Age? Curious. After Tx I awoke with Olcrannon Bursas on both elbows. One resolved and the other had to be removed surgically. Orthopedist said it could have been triggered by Interferon. New Hepatologist a fellow for UT MD Anderson Hosp said that as of now 3% of Post Tx patients go on to never clear Sxs. And that many genetic flaws can be triggered by Tx during and after Tx and may never resolve. He also said that number is likely to increase.
I don't know what to attribute my recent Gout episode to. I had blood work from 4 weeks earlier and my uric acid level was well within normal limits. I'm sure you've read the same stuff I have about food triggering an episode. Two days before the Gout really started I had eaten sausage which I very rarely eat. That is the only thing I can think of. I treated with Prednisone because my transplant team ruled out the other common treatments. It resolved within 1.5 days but I continued the drug for 5 days. The other strange thing is that I got it in my second toe and the vast majority of reported cases indicate that Gout affects the big toe.
Olecranon Bursae is associated with Gout and, though I don't know much about it, I haven't read that is autoimmune related which is often cited as a side effect of HCV treatment. I wouldn't argue the 3% long term side effects but I have no independent knowledge that would corroborate that number. I have never heard that treatment is associated with Gout but I don't know for certain that it isn't or couldn't be. In my case I seriously doubt that treatment was the cause or a contributing factor because it has been 4 years and I haven't had any autoimmune issues or any side effects that I believe are interferon/ribavirin based.
I do sympathize with your elbow problems and the Gout too. I was shocked at the pain I experienced from Gout. It was debilitating until I started the Prednisone.
I hope you recover quickly and don't have another episode of either disease.
Investigation of hyperuricemia during pegylated-interferon-alpha2b plus ribavirin combination therapy in patients with chronic hepatitis C.
Yamashita N, Enjoji M, Kotoh K, Kato M, Ueda A, Horikawa Y, Tajiri H, Higuchi N, Kinukawa N, Nakamuta M, Takayanagi R. Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
OBJECTIVE: Hyperuricemia has been reported as being an adverse effect of pegylated-interferon-alpha2b (Peg-IFNalpha2b) and ribavirin combination therapy for chronic hepatitis C and hyperuricemic changes occur in some patients during the therapy. However, detailed investigation of the elevation of uric acid has not been carried out previously. The incidence and mechanism of hyperuricemia were investigated in this study. METHODS: The data of 50 patients with chronic hepatitis C who had been treated with Peg-IFNalpha2b and ribavirin combination therapy or pegylated-interferon-alpha2a monotherapy for more than 24 weeks were analyzed. The effects of these treatments were evaluated clinically by the serum uric acid level and its urinary excretion rates. RESULTS: In patients with pegylated-interferon-alpha2a monotherapy, no significant elevation was shown either in serum uric acid concentrations or excretion rates. On the other hand, serum uric acid concentrations were significantly elevated during the combination therapy, reaching > or =7.0 mg/L in men and > or =6.5 mg/L in women in 15% of patients. The urinary uric acid excretion rate was also elevated significantly. 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.
You say: "Gout is a side effect of treatment. " I don't see that conclusion in the abstract.
It says: "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.'
Gout isn't mentioned and I don't see where the elevation is significant or permanent. It may be both and the hyperuricimea that results may be associated with Gout but, if so, I don't see evidence of it here. Note that the uric acid "elevated levels were still within normal limit in many cases."
It's relevant but I don't think it's conclusive about anything.. The study cohort was quite small and the findings seem somewhat vague.
thank you Cowriter that backs up what my Hepatologist said and my Psychologist. Mike, Thank you also. The Tx is a miracle with teeth. Some of us get bitten-some don't. What are the alternatives? They'te working on them and learning from us. In the future they'll come up with a vaccine. I only have one complaint really-the original Hepatologist and my other doctors convincing me the Tx is harmless and all sides would clear soon after treatment-they didn't and I spent a fortune on ADs and unnecessary testing. It costs all of us in the rear when doctors don't just say yes, there can be everlasting sides in 3 % of patients. Then at least we know It Isnt In Our Heads!
I believe gout is listed on the medication insert as a side effect.
Incidence of Adverse Events
Individual serious adverse reactions occurred at a frequency less than or equal to 1% and included suicide attempt, suicidal ideation, severe depression; psychosis, aggressive reaction, relapse of drug addiction/overdose; nerve palsy (facial, oculomotor); cardiomyopathy, myocardial infarction, angina, pericardial effusion, retinal ischemia, retinal artery or vein thrombosis, blindness, decreased visual acuity, optic neuritis, transient ischemic attack, supraventricular arrhythmias, loss of consciousness; neutropenia, infection (sepsis, pneumonia, abscess, cellulitis); emphysema, bronchiolitis obliterans, pleural effusion, gastroenteritis, pancreatitis, GOUT, hyperglycemia, hyperthyroidism and hypothyroidism, autoimmune thrombocytopenia with or without purpura, rheumatoid arthritis, interstitial nephritis, lupus-like syndrome, sarcoidosis, aggravated psoriasis, urticaria, injection site necrosis, vasculitis and phototoxicity."
Here's a study that says that gout is frequent on liver transplant recipients.....
J Clin Rheumatol. 2008 Oct
Musculoskeletal manifestations in liver transplantation recipients.
Diep JT, Kerr LD, Barton C, Emre S. Department of Medicine, Division of Rheumatology, Mount Sinai Medical Center, New York, New York, USA.
BACKGROUND: The prevalence and type of musculoskeletal problems among liver transplant recipients have not been well characterized in the current literature. OBJECTIVE: We conducted a retrospective analysis of both outpatients and inpatients (total 234) who underwent liver transplantation or had rheumatologic consultation during 2002-2004, to document the cause for their rheumatologic symptoms. We hypothesized that infection, crystal diseases, and corticosteroid complications would be more common in this cohort of immunosuppressed patients as compared with de novo connective tissue disease. RESULTS: Among the outpatients, we found that arthralgia presumably secondary to tacrolimus/sirolimus; osteoarthritis, peripheral neuropathy, and myalgia were the most common diagnoses. The only autoimmune disease documented was Hepatitis C Virus-associated cryoglobulinemic vasculitis. Hyperuricemia was also prevalent in this patient population. Infection and GOUT were seen frequently among the inpatients. CONCLUSIONS: It is important for physicians to be cognizant of the variety and prevalence of musculoskeletal disorders in the liver transplantation patient population.
Is your doctor giving you medication for it? Because a uric acid level > 5.8 is predictive of poor response to Hepatitis C treatment.
Is serum uric acid a predictive factor of response to IFN-treatment in patients with chronic hepatitis C infection?
Pellicano R, Puglisi G, Ciancio A, Balzola F, Saracco G, Ciccone G, Baldi I, Abate ML, Smedile A, Rizzetto M. Department of Gastro-Hepatology, San Giovanni Battista (Molinette) Hospital, Torino, Italy.
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 =1,000,000 IU/ml in 35 and unknown in 17 patients. Ishak fibrosis score was 4 in 15 and unknown in 57 patients. Mean serum uric acid was 5.05 +/- 1.3 mg/dl. Sustained virological response (negative serum HCV-RNA 6 months after treatment cessation) was achieved in 102 patients (67%). In the final logistic model, serum uric acid level > 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.
Cherries are supposed to lower uric acid and inflammation.
Consumption of cherries lowers plasma urate in healthy women.
Jacob RA, Spinozzi GM, Simon VA, Kelley DS, Prior RL, Hess-Pierce B, Kader AA.
U.S. Department of Agriculture/ARS Western Human Nutrition Research Center, University of California at Davis, Davis, CA
To assess the physiologic effects of cherry consumption, we measured plasma urate, antioxidant and inflammatory markers in 10 healthy women who consumed Bing sweet cherries. The women, age 22-40 y, consumed two servings (280 g) of cherries after an overnight fast. Blood and urine samples were taken before the cherry dose, and at 1.5, 3 and 5 h postdose. Plasma urate decreased 5 h postdose, mean +/- SEM = 183 +/- 15 micro mol/L compared with predose baseline of 214 +/- 13 micro mol/L (P < 0.05). Urinary urate increased postdose, with peak excretion of 350 +/- 33 micro mol/mmol creatinine 3 h postdose compared with 202 +/- 13 at baseline (P < 0.01). Plasma C-reactive protein (CRP) and nitric oxide (NO) concentrations had decreased marginally 3 h postdose (P < 0.1), whereas plasma albumin and tumor necrosis factor-alpha were unchanged. The vitamin C content of the cherries was solely as dehydroascorbic acid, but postdose increases in plasma ascorbic acid indicated that dehydroascorbic acid in fruits is bioavailable as vitamin C. The decrease in plasma urate after cherry consumption supports the reputed anti-gout efficacy of cherries. The trend toward decreased inflammatory indices (CRP and NO) adds to the in vitro evidence that compounds in cherries may inhibit inflammatory pathways.
Consumption of Bing sweet cherries lowers circulating concentrations of inflammation markers in healthy men and women.
Kelley DS, Rasooly R, Jacob RA, Kader AA, Mackey BE. U.S. Department of Agriculture/ARS, Western Regional Research Center, Department of Nutrition, University of California, Davis, CA 95616, USA.
The purpose of this study was to determine the effects of consuming sweet cherries on plasma lipids and markers of inflammation in healthy humans. Healthy men and women (n = 18) supplemented their diets with Bing sweet cherries (280 g/d) for 28 d. After a 12-h fast, blood samples were taken before the start of cherry consumption (study d 0 and 7), 14 and 28 d after the start of cherry supplementation (study d 21 and 35), and 28 d after the discontinuation (study d 64) of cherry consumption. After cherries were consumed for 28 d, circulating concentrations of C-reactive protein (CRP), regulated upon activation, normal T-cell expressed, and secreted (RANTES), and NO decreased by 25 (P < 0.05), 21 (P < 0.05), and 18% (P = 0.07) respectively. After the discontinuation of cherry consumption for 28 d (d 64), concentrations of RANTES continued to decrease (P = 0.001), whereas those of CRP and NO did not differ from either d 7 (pre-cherries) or d 35 (post-cherries). Plasma concentrations of IL-6 and its soluble receptor, intercellular adhesion molecule-1, and tissue inhibitor of metalloproteinases-2 did not change during the study. Cherry consumption did not affect the plasma concentrations of total-, HDL-, LDL-, and VLDL- cholesterol, triglycerides, subfractions of HDL, LDL, VLDL, and their particle sizes and numbers. It also did not affect fasting blood glucose or insulin concentrations or a number of other chemical and hematological variables. Results of the present study suggest a selective modulatory effect of sweet cherries on CRP, NO, and RANTES. Such anti-inflammatory effects may be beneficial for the management and prevention of inflammatory diseases.
I eat a lot of Bing Cherries so that's a plus.
The negatives are I had HCV, I treated for 3.5 years and another 6 months of mini-treatment and I am a liver transplant recipient.
I guess I will be eating the cherries for the rest of my life.
It's fortunate for me that I love Bing Cherries.
Thanks for the information Co.
a couple things come to mind and your mention of sausage trigger my memories.
You are aware that your SOC for HCV can trigger many diseases at any time.
The next question becomes why does SOC trigger such things?
Well because it whacks out and messes with normal immune responses.
That's why tx is known for causing RA in quite a few people..because it turns the body on itself, and instead of just scavenging for abberant cells or virusess sometimes the cells lose sight of what to attack and begin to attack heatlth tissue. With RA that is joint cartilage primarily.
Gout can mean your acids are off true, and kidneys are stressed. But it can also be just a reaction to drugs, or even to a food.
So you mentioned sausage and I thought allergic reaction or cytokine storm.
Because I already have autoimmune stuff I know a little here. Pork protein or ANY protein can at ANY time become a trigger for systemic reactions, especially when the body has been through a chemo therapy or has and liver or kidney damage.
If the body does not like a protein, it turns on a histamine reaction which draws fluid filled with fighter cells to the area. If the histamine reaction does not shut off (which can happen anytime the body is run down or worn from anything, an autoaccident, and rough day, let alone chemo...then the reaction can beome a chain reaction..where the cells turn on the histamine and forget to turn it off...(RNA/DNA damage contribute to this and both HCV and SOC tx cause this.)
anyway a quick reaction would cause swelling of throat and breathing can be cut off..
a slower reaction can cause tissues (which received the offending protein) swell, in which case it tends to be limbs rather than strict anaphylaxis that sets in.
If your kidney function tests were normal then my guess...I am NOT a doctor...
would be allergic reaction or possibly a cytokine event.
People don't all know this, but if you are immune compromised (as all chemo patients are by the chemo itself) you should introduce new or exotic foods very sparingly.
As a liver patient you should avoid shellfish entirely as it's proteins and bacterium are highly toxic.
Transplant patient are at even higher risk do to all the drugs and the new tissue within ones body.
Did you get an fever when this started?
Wikipedia is pretty good on cytokine storms, read that, and read up on allergic reactions.
When prednisone or a similar compound settles down such an event the next question should be, well the steroid settled down the inflammation, but what set if off...
that way you can avoid another repeat perhaps.
cherries might help, unless one had a fruit nut allergy, in which case the proteins in cherries or almonds, apples or pears, hazelnuts and more make this not a good fix.
In case this person might have what I theorized as the trigger he may want to read up
on Fruit and Nut allergy. It is almost as common as hayfever, and can begin at ANY time of life, and they can be life threatening. Sometimes that apple a day can make the doctor a lot of cashola!!!
My only side effect from treatment is a recurrent joint pain in the knees, hips, wrists and hands (worse at rest and when I first move after resting or sleeping). It is not RA. I doubt that it's gout, but maybe next time I'm having a flare up I'll test for it just to rule it out.
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