Keith’s GoutPal Story 2020 Forums Please Help My Gout! Gout Related Allopurinol is safer at higher doses?

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    Stumbled upon this article online…not sure of its validity though.

    Gout Drug Should Be Used High-Dose

    March 4, 2002 – Regular high-dose allopurinol may improve survival in heart failure patients. Dr. Allan Struthers identified 1760 CHF patients. He compared heart-related events in patients taking allopurinol (in several different ways) to heart-related events in patients not taking the gout drug.
         Mortality was similar between groups except that patients taking long-term, low-dose allopurinol had worse mortality than the other groups. Patients taking long-term, high-dose allopurinol had the same mortality risk as the no-allopurinol group. This suggests that CHFers with gout should take at least 300mg allopurinol per day even if a lower dose keeps the gout under control.
      Jon's note – Be wary of studies that examine old data as opposed to trials that test a theory in real patients with specific endpoints.


    An excellent find – the full study is online as “Effect of allopurinol on mortality and hospitalisations in chronic heart failure: a retrospective cohort study”.

    As Jon(*) notes it is right to be wary of statistical analysis, but it is a clear pointer that allopurinol saves lives. That should not be interpreted to mean that all gout sufferers are at risk, or all gout sufferers will be saved. However, those gout sufferers also at risk of cardiovascular problems should certainly be alert to the dangers. Perhaps their inflated uric acid is due to underlying inflammatory problems that also increase cardiovascular risks.

    One thing that does rankle me about the study is the complete lack of any uric acid data. I can understand this not being available for all cases, but anyone who is taking allopurinol should be having uric acid tests.

    The authors note:

    It also raises the hypothesis that patients with CHF who have gout ought to receive ≥ 300 mg allopurinol/day even if a lower dose keeps the gout under clinical control.

    To me, the conclusion is that there is no reason to believe that gout was properly under control in this group. It points for the need for more studies to correlate uric acid levels with mortality and morbidity.

    A typical gout patient who is under-dosed on allopurinol is unlikely to question the fact. More importantly, how many doctors are going to recognise the continuing risk if the lab test comes back “normal?”

    (*)I've traced Jon to, a site for Congestive Heart Failure sufferers. I haven't studied his site in depth, but his story has some echoes to my own – couldn't find a decent website about his condition, so he created one.


    Just taking this a step further, the allopurinol study is cited in Canadian Cardiovascular Society Consensus Conference recommendations on heart failure update 2007: Prevention, management during intercurrent illness or acute decompensation, and use of biomarkers

    Those recommendations include:

    Patients with heart failure are at increased risk of gout due to low cardiac output, reduced renal function, chronic loop diuretic use and possibly increased total body water fluctuation. The standard therapy treatment for gouty arthritis, NSAIDs or cyclooxygenase 2 inhibitors, have known adverse renal effects and are associated with increased hospitalizations (and possibly death) in patients with heart failure (88,129–132). They should, therefore, be avoided when other adequate treatments are available. Oral colchicine is an effective therapy and is generally safe to use in heart failure patients. Alternatively, a short-term oral steroid for one to two weeks or an intra-articular steroid (when feasible, such as with a certain single joint involvement) may be used for a lower level of fluid retention and other side effects (133). Allopurinol may be started approximately two weeks after the acute episode is completed. Small studies have hypothesized that allopurinol may be beneficial in chronic heart failure, possibly due to its antioxidant properties, although this is has not been proven (84,129–131,134).

    The numbers in brackets are references to further studies that may be of interest to anyone researching links between gout and heart disease. I wonder why they recommend the 2 week delay before starting allopurinol?


    I guess to minimize the likelihood of a patient with a severly compromised heart having to bear an acute gout attack…and telling the doctor LOUDLY about it. A two week delay sounds a bit “over-safe” to me but defensive practice seems the medical operative these days.

    “Wait a year and start allopurinol”

    “Don't take colchicne, it will upset your tummy!”

    But then the opposing flip side is: “Here, take this NSAID, it's new and VERY pricey…we're alll excited about it!”

    Why don;t we get good studies about allopurinoll and colchicine? Easy, becasue finding out that allopurinol cures heart disease and cancer won;t make anyone rich. Nobody is interested in mounting a study with cheap generics when they can mount one to sell a pill that nets them $50 a day.

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