1) Gout is no longer the disease of kings, or even of the affluent. It is hitting harder in lower socioeconomic groups.
2) A low purine diet is no longer a strongly recommended intervention. Cutting back on organ meats and alcohol is. Purine rich vegetables, once viewed as triggers, may be safe because of their fiber content.
3) Uric acid crystals are involved in gout, but it is primarily an inflammatory condition. So not everyone with high uric acid gets gout. This is just like how high cholesterol and low inflammatory markers seems safer than average cholesterol and high inflammatory markers. And, heart attacks and strokes are more likely to happen in the months following a gout attack.
4) Colchicine, one of the treatment options for both acute and chronic gout, works without lowering uric acid levels at all. It treats inflammation, just like the commonly used attack medicine indomethacin and my personal choice, prednisone.
5) Allopurinol, which we use to prevent gout attacks by lowering blood uric acid levels, can also cause them. It should never be started during a gout attack. If attacks happen in the beginning of treatment, I give short prednisone bursts to get patients through the initiation phase.
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A Country Doctor Writes: 
Concur with all 5 points, doc!
40 mg prednisone for 3 days
Point 5 is time-honoured wisdom – I was taught it too – but recent trials suggest that it is not true. See for example:
https://pubmed.ncbi.nlm.nih.gov/25807090/
https://pubmed.ncbi.nlm.nih.gov/23098865/
https://pubmed.ncbi.nlm.nih.gov/34406530/
Gout patients and their doctors need to know that a gout flare is the direct result of the chronic intermittent lack of oxygen from sleep apnea. The first manifestation of gout should lead to diagnostic testing for sleep apnea, and then treatment for sleep apnea. It really is a matter of life or death! See the Youtube post “Gout is an Early Warning of Sleep Apnea” for more information.
See: https://www.health.harvard.edu/blog/gout-sleep-apnea-may-raise-your-risk-201511178633
The information in the Harvard blog is inadequate. First, the paper from the UK database reports that the odds ratio for sleep apnea (SA) is 1.5:1. It is actually much higher because the large majority of those with SA have never been diagnosed with it, so they are misplaced in the data base’s noSA category. A different study conducted by rheumatologists found that 89% of their gout cohort were diagnosed with SA, 8:1 odds. Second, the Harvard report is short on describing the physiological reasons: intermittent generation of excess uric acid in every oxygen-starved cell fed into the blood; concurrent increased acidity of the blood due to reduced oxygen so uric acid is more likely to precipitate as urate crystals; and gradual reduction in kidney function which slows the removal of uric acid from the blood. Third, the emphasis of the Harvard report is that SA raises the risk for gout. Since SA has many life-threatening comorbidity consequences, the emphasis should be that gout is a warning to get tested for SA, and then treated for SA if warranted.
Besides the low oxygen level during sleep, there may be an additional reason that SA causes gout – dehydration in the body. One of the known reversible consequences of SA is nocturia, which is getting up frequently from sleep to urinate. That means to me that the bladder is being excessively hydrated, so the rest of the body is dehydrated.