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Getting the amount of uric acid in your blood right doesn’t fix gout right away because abnormal amounts of old uric acid can remain in the rest of your body for months or even years after the starting the therapy.

That’s good to hear, actually. And I’m still taking the allopurinol, in case I gave you the impression that I stopped. I was just a bit suspicious that my uric acid levels should have been lowered that much so soon. I guess there is no need to increase the dosage, at least, unless my body develops a tolerance.

I’d say tophaceous gout is unlikely in your situation but it’s the rheumatologist’s opinion which matters, not mine

I figured that’s what it’d have to be, if it lingered even when uric acid levels had reached target levels. Given my present predicament, I am relieved to hear I’m wrong.

I’d give colchicine a try in your situation because it’s slow acting but can put gouty inflammation to rest or at least keep it at a low level without having the same side effects as regular anti-inflammatories.

I’d love to give colchicine a try, but my doctor has been very unaccomodating on that point. “That’s for the rheumatologist to consider” has been the reply when pressed.

I have so far not had any side effects of either voltaren or ibuprofen, though I switched from the former to the latter because I feared the long term effects of voltaren more.

Alternatively, try a higher anti-inflammatory dose before stopping because you want the inflammation to stop completely rather than being merely moderated or there’s a good chance it’ll come back.

When my foot has been really bad, I’ve been at the maximum recommended dose for nearly a week straight. When I was on voltaren, that was 3×50 mg a day, and for ibuprofen it’s been 3×400 mg a day. I do not wish to go above that without a doctor’s go-ahead. And my doctor already thinks I’m taking too much ibuprofen: he says I shouldn’t use it prophylactically, but when and as necessary when I get symptoms. But as that’s pretty much a constant thing, it’s a catch 22.

Something else you could try while the symptoms are very mild (but this works for some joints and not others) is a topical anti-inflammatory instead of a pill.

I have recently started to use Voltaren Forte. I haven’t really been very consistent in using it, as it says to apply at 12 hour intervals – and that’s difficult to manage when I work irregular hours. But it hasn’t had as good an effect as pills.

D deficiency is common in overweight people. Do you have a gallbladder issue as well? Are your liver function numbers good? Both obesity and D deficiency are associated with NAFLD.

My liver values were normal. I don’t know what values from my tests pertain to the gall bladder, but my doctor hasn’t said anything about it.

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Ok, I thought I’d wait until they were done with all things blood related before posting an update.

Good news: I don’t have high blood pressure after all. They had me wear one of those blood pressure monitors for 24 hours, and my average is 126/74.
My kidney function is tip top.
I also don’t have diabetes.

I am, however, vitamin D deficient, and my cholesterol is somewhat high.

And for the uric acid levels, which they didn’t actually test until I nagged them about it:

296 mmol/l, or 4,9 mg/dl.

That’s just after four weeks of 200 mg allopurinol a day. So that certainly sounds good, but my foot isn’t any better. Things that rush to my mind:

1. The first blood test – which revealed high uric acid levels – was taken the day after my foot was at its worst. I was still in agony when they drew blood. Could the elevated levels be explained by the infection, perhaps?

2. I have not been able to identify any food stuffs that trigger an attack. Instead, it comes back as soon as I’m off anti-inflammatories. Just ever so slightly the first day with no drugs, and then just a little bit more on day two, and a lot more on day 3. I am able to prolong this period if I use ice and paracetamol, but only anti-inflammatories have had any success in reducing all the symptoms. But they never go away completely.

3. I’m thinking this may not be gout at all – or if it is, it must surely be tophaceous. When swelling is minimal, there remains a hard swelling of the joint which, but for comparison with the other foot, might look like a normal part of the joint.

What say you?

I have an x-ray scheduled for April 6th, and an appointment to a rheumatologist April 29th.

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They drew more blood today, so we’ll see what it says. The ECG was also “not bad”, according to the nurse who administered it (I didn’t think to ask for actual numbers at the time). My follow-up is on the coming Tuesday, I guess I’ll know more then. But with the quantity of voltarene and lately ibuprofen, I shouldn’t be surprised if that has been a major contributor. My toe was acting up again just yesterday, so I had a hefty dose of 1200 mg ibuprofene (400 at 6 hour intervals).

I tried to press the issue about colchicine, but the doc said he wanted to check with the rheumatologist first.

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I’m actually glad you mentioned climate deniers, Nobody; I had a paragraph about it myself in an earler post but decided to cut it. Climate deniers, while they often claim to cite peer review, they invariably misquote it, quote it out of context, or flat out lie about what’s in it. The peer reviewed climate science itself is pretty solid, and always in stark contradiction to climate deniers’ claims.

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The million dollar question is: Why should I listen to you? I’m not a physician, I have no medical training of any kind. How am I supposed to separate the wheat from the chaff? No one says peer review is perfect, but it’s what we’ve got. Fraud is certainly a problem, but it is hardly rampant. And peer review is still the best we’ve got.

So do I trust peer review? Of course. I have no choice. The alternative is much, much worse. But what does it mean that I trust peer review? Do I take it on faith? Not at all. It means that peer review is statistically more likely to provide good information. And as a layman essentially makes an unqualified guess as to which authority to listen to, it is certainly advisable to go with the ones with the best track record.

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Ah, but isn’t gout a very individual experience? So however much a person may be expert on his own condition, it may be anecdotal to another.

The art of getting research published is the art of being an expert – so long as it is peer reviewed. Publishing outside of peer review (or in phoney peer reviewed journals – such as the infamous paper “Get Me Off Your F-ing Mailing List”) – is not much of an art. Graham Hancock may be a popular and well published author, but none of his output has ever come close to passing muster in academic circles.

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I cannot agree with your assessment of peer review. Peer review is not just one academic agreeing or disagreeing with another; typically several external reviewers are involved (in this particular case, three). It is also not their job to either agree or disagree per se, but to analyse the methodology. Peer review is the cornerstone of science. Sure it has flaws, but it is the best system – perhaps the best possible system – for advancing scientific knowledge. And the history of peer review is also preserved here, so we can read the reviewers’ assesments of the study. It is all very transparent.

Your criticism that the paper in question can be misleading to gout sufferers, however, I can fully agree with. Most people will derive their own conclusions from the conclusions of the paper (“oh, so does this mean that…”), and most researchers do not caution against such pitfalls – they are writing for their own academic community, after all. Usually, scientific papers need to be dumbed down before they can be properly disseminated to the masses – though it often falls on journalists, who aren’t really the right people to do so.

Your last couple of paragraphs echo what I said on this topic, so we are basically in agreement. I just think you mis-characterised peer review a tad.

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This may well be true, and the article you called garbage may well indeed be garbage, but wouldn’t it be irresponsible for me, a layman, to simply take your word for it? If I were to be so trusting, I might end up buying homeopathic remedies from someone who told me the same thing: “don’t listen to the medical community, that’s rubbish. You want something that works, you come to me”.

You may well know better than the researchers of the paper above, but I don’t know that. I can’t know that. I can’t know that you are correct in your statement about peer review, either. Contradiction in peer review isn’t unusual – two contradicting papers can both be sound. The purpose of peer review is to ensure that the methods leading up to the conclusion are good.

Now, I do get the distinct impression that the medical field relies on received knowledge more than it should when it comes to gout, but then I haven’t seen received knowledge peer reviewed. When a paper passes peer review, I wouldn’t accept it even from an authoritative source if they simply dismissed it off-hand. Substance must be refuted with substance. If you say there is no substance, well it looks like substance to me, so where does that leave us?

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If there are objections to an article posted in this thread, surely this would be the appropriate place to elaborate on those objections? I, too, am passionate about research, but I have no qualifications relevant to gout so I wouldn’t presume to lecture anyone on that score – and I would feel it awfully pretentious if I, a newcomer, were to create a thread on academic research in general.

I also did not mean an attack on Nobody – I chose my wording carefully in hopes of avoiding that impression. Of course, I do not know any of you from Adam, but from what I can glean, he possesses a wealth of knowledge and experience. But whether medicus or Adam, when he dismisses peer review in such fashion, it does not give a favourable impression in terms of credibility, I’m afraid.

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BMJ is a respected peer reviewed journal, and the article Clemmens linked to is peer reviewed. I haven’t read the article myself, but I am not myself a medical professional so my opinion on its quality wouldn’t count for much either way. However, it is precisely because I am a layman in this field that I must trust peer review. Someone on the internet simply calling peer review garbage should rightly be dismissed, even if he did qualify his claims – unless he did so by referring to peer reviewed studies himself.

This is Alpha and Omega for anyone wishing to do their own research: if this is not my field, then I am not in a position to decide who qualifies as an expert. I have to rely on whomever is regarded as an expert in the field in question. Sure, there really is a lot of toss bandied about in every field of human endeavour, but even toss may sound like ice cream to the uninitiated. Which is why the layman should never dismiss peer review, nor listen to non-peer reviewed claims that peer reviewed research is “garbage”.

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Just got back from the doctor’s. My blood pressure was 158/100, which is uncomfortably high. Now I wish he had taken my blood pressure before I started allopurinol, because I do not know if my elevated BP is due to either allopurinol, all the NSAIDs I’ve taken, or both. He didn’t mention any conflict with allopurinol today, and I didn’t think to ask (the leaflet in the allo packet lists it as a cautionary note). He cautioned me against NSAIDs, however. I’ve already taken 100 mg allo this morning – I’m thinking about skipping the one for this evening until I’ve checked.

He seemed much more diligent when it came to my blood pressure than he was with my gout – after all, he never booked any follow-up appointments for my gout, they have all been on my initiative. Taking my blood pressure, too, was on my initiative. But with my elevated blood pressure, it seemed like he was more in familiar territory.

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So I’ve been waiting for the summons to my X-ray (or ultrasound) appointment, and started to suspect my doctor had forgotten to book one for me. I called the X-ray wing of the hospital, and sure enough, nothing was booked. So at least I called my doc and booked an appointment to have my blood pressure taken, as well as new blood tests. That’s for Thursday the coming week. If the swelling persists by that time (and I have no reason to believe otherwise), I will ask him to book an appointment then. There may be as much as a 10 week wait to x-ray extremities, so I changed my mind about waiting until after x-ray for my next consultation.

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It could be that gout patients need a higher dose of vit. C for it to be effective, and it could also be that vit. C has effect only a certain time after a flare has subsided. It seems strange that gout patients should be immune to some of the effects of vitamin C, but who knows. There is still a good reason to take vitamin C while on allopurinol regardless, however, as vit. C increases plasma ascorbate, and so reduces the risk of oxidative stress from use of allopurinol. Apparently.

Oxidative Stress from Use of Allopurinol – Is There a Reason for Patients with Gout to Take Vitamin C?

Anyway, yeah… “anything that makes you leak a lot should be avoided.” I’ve never gone to the bathroom so often as after I started taking allopurinol. In the leaflet it stresses the importance of water, 2-3 litres a day, which to me is an extreme amount. I can push myself to 2 litres, but with all the water I’m taking I feel like I’m going to the bathroom all the time. I have found that diet sodas help me retain water better than water. Water seems to be… water purging. If I try to push the 3 litre mark especially, it leaves me feeling bloated and my urine will be crystal clear. Even with 2 litres, my urine is often clear. It is never dark these days. Before gout, I could easily make do with 1 litre of fluid in a day. If I drank more, it was because of my sweet tooth. I’m trying my best to spread the fluid out for the whole day, and to drink less after 8-9 in the evening (to avoid having to get up in the night so much). I am gradually finding a good balance, though. I think 3 litres is probably excessive for my body size, so if I manage 2, I’m satisfied. My food diary has proven essential to help me get all the fluid I need, from all sources.

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Can’t say I’ve really noticed the effect of dairy. I’ve been a fairly big consumer of dairy before my gout (whole milk, fat-free yoghurt, cheeses), to a heavy consumer after (skimmed milk, fat-free yoghurt and cheeses). Skimmed milk makes up a significant portion of my daily fluid intake.

All research I have been able to find re: the effects of dairy on uric acid levels have included healthy subjects only. With respects to vitamin C, there is certainly literature suggesting vit. C helps prevent gout in the first place, but I have found one article that has specifically targeted patients with established gout:

https://onlinelibrary.wiley.com/doi/full/10.1002/art.37925

The sample size was not tremendously huge (40 individuals), but the methodology seems sound enough:

Patients with gout and an SU level >0.36 mmoles/liter (6 mg/dl) were recruited. Twenty patients already taking allopurinol were randomized to receive an increase in the dose of allopurinol or to commence taking vitamin C (500 mg/day). Twenty patients who had not been taking allopurinol were randomized to start receiving either allopurinol (up to 100 mg/day) or vitamin C (500 mg/day). Levels of plasma ascorbate, creatinine, and SU were measured on day 0 and week 8.

As you can see, 10 subjects who had not yet commenced allopurinol were given 500 mg vitamin C in place of it – and it had no effect in the initial 4 weeks. Adding allo after 4 weeks had some effect after the next 4 weeks, but not nearly as much as those who commenced allo and then increased dosage of allo after 4 weeks (fig. 3).

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This is all very good advice. The reason I figured 4 weeks is because I’ve read a second test should be taken 3-4 weeks on the initial dose of allopurinol, to see if an adjustment of the dosage is recommended.

Of course, different sources give me different figures – for just about everything. Some suggest starting with 50-100 mg of allo, others say 100-300 mg for an initial dose. All in all, I was dismayed to learn just how little clinical testing has been done for a disease which has been known since ancient times. A lot seems to be based on received knowledge and anecdotal evidence. We haven’t even properly identified the mechanics by which alcohol hinders uric acid from being excreted, we have just accepted that it does. And the same goes for most dietary recommendations. My heart sank when I read that tomato products were the fourth most commonly reported gout trigger, but it doesn’t seem to have affected me adversely.

And vitamin C and dairy products are supposed to be good for lowering uric acid levels. But wait: that’s just for healthy people. For people with gout, vitamin C apparently has no effect in lowering uric acid. Presumably the same is true for dairy.

I will book another appointment to have additional blood drawn – and I’ll ask to have my blood pressure taken while I’m at it (I have never had my blood pressure taken as an adult). But I’ll wait until after the X-ray – besides, my previous consultation was just over a week ago, I don’t want to be “that” patient.

Thank you kindly for your replies so far.

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Yes, here’s the thing about my prescription of allopurinol:

In my consultation following the results of the blood tests, I was prescribed 200 mg allopurinol a day – and that’s it. No mention of colchicine or anything else to be taken in combination. At that time I still didn’t know much about gout, so I had no reason to question anything my doctor said. When I had my second gout attack, I called my doctor for another consultation. He told me to immediately stop allipurinol because, he said, it had no effect during an attack (maybe he meant because of the other drugs I’d be taking to bring the attack down?). At this time I had been on allopurinol exactly one week.

By my third consultation, a little over a week ago, I had done my homework. This time I was going to suggest colchicine myself, but he beat me to it. However, what he suggested was that I might take colchicine instead of allopurinol. I tried to point out that the two drugs were usually prescribed together, but it is difficult for a layman to argue with an expert. In the end, where we landed, was that I was to resume allopurinol and take ibuprofen if and when I had flares. I asked if I could have a prophylaxis with respects to these flares, and he said, “allopurinol is a prophylaxis.” I said sure, in the long run with respects to uric acid levels, but he insisted it was a prophylaxis for the flares as well.

I tried to tell him I got my information from the Norwegian Medical Association (I’m in Norway), but naturally professional pride will prevent a doctor from conceding the point to a layman – I didn’t expect he would, so I didn’t force it. But hopefully I will have prompted him to do a bit of reading-up for my next consultation. If not, I’ve got print outs from the Medical Association, and if that doesn’t help, I’m seriously considering changing my GP.

I should perhaps add that my doctor is in his 70s, and the notion to halt allopurinol during flares might be an obsolete medical advice from the old days. Since most every source I’ve come across stresses that one should not stop taking it, I get the impression that such is the case.

I have kept a meticulous log of all drugs and dosages I’ve taken, and so far this is how much allopurinol I’ve taken:

Jan 28 – Feb 3 (8 days) (200 mg)
Feb 19 (16 days hence) – present. 11 days and counting. (200 mg)

As for voltaren in the same period, this has been entirely on my own recognizance. Dosage and duration as follows:
Feb 9 – Feb 18 (10 days): 3×50 mg
Gradual improvement until Feb 15th, after which improvement stagnated at a negligible level of discomfort.
Feb 19 – Feb 21 (3 days): 2×50 mg
Discomfort stayed the same in this period. There was certainly no increase.
Feb 22 – Feb 25 (4 days): 50 mg
My foot didn’t get worse during this period, either. The toe joint was only tender under certain exertions of the toe (eg. when taking off my right boot, by pressing down on the boot’s heel with my left toe). It was not tender to the touch, in spite of the (minute) swelling of the joint itself. I figured “this is as good as it’s going to get”, and went off voltaren, because I didn’t want voltaren in my system if and when I started ibuprofen.

Since my adventure with gout commenced a month and a half ago, I have taken:

prednisolone: 17 days (4+5 days 20 mg, 8 days gradually smaller doses)
voltaren: 28 days (5+6+17 days)
ibuprofen: 2 days (started yesterday)
no anti-inflammatories at all: 11 days (3+6+2 days)

Side effects so far: None that I have been able to detect.

My uric acid level per Jan. 15 was 513 mmol/l (should be 8.55 mg/dL by my calculations). I have not had any blood taken since. I am waiting till after my X-ray and/or four weeks of allopurinol (counting from Feb. 19th) to book my next appointment – whichever seems most prudent.

The basis for my initial gout diagnosis was that blood test, following the emergency appointment on Friday 15th. The evening before I was not able to move my big toe at all, neither with its own muscles or with digital manipulation, for unfathomable pain. It didn’t take long for the missus to persuade me to get that doctor’s appointment first thing. Gout was, of course, suspected right off the bat, but it was the blood test that secured the diagnosis. It does run in the family, too, although my father didn’t get it until his 80s (but then he has always been healthier and more active than I). My brother isn’t diagnosed, but he gets what might be gout flares about once a year, in his ankle. But he takes a few pain killers and that’s that.

My apologies for being so verbose. And thank you for your reply.

[Author]

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