Diagnosis and management of gout
BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7553.1315 (Published 01 June 2006) Cite this as: BMJ 2006;332:1315All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Sir
It's been a long time since I studied physical chemistry but surely
the basic physical processes of crystalisation must be exploited in the
management of acute gout attacks.
Greatly increased water intake and the application of heat to the
affected joint will increase the rate of clearance of the crystalline
solute from the affected joint.
My advice to sufferers is analgesia, colchicine 500mcgm TDS, lots to
drink and soak the foot in a bucket of hot water.
Yours sincerely
Steven Ford
Competing interests:
None declared
Competing interests: No competing interests
Two decades ago, after a prolonged intercontinental flight where at
every meal I helped myself to the free wine, I developed my first attack
of gout.The left big toe was acutely inflamed.Stayed home for a fortnight
till it subsided. Blood reports were unremarkable. Colchicene was
taken.Drank plenty of water.Read lot about food items that can initiate or
exacerbate the misery.
Subsequently, every 12 - 18 months I would be bed ridden with an attack of
gout.It was the same process. Always it was the left big toe. I would hop
around the house with the help of crutches.
During a casual conversation a Rheumatology colleague informed that if at
the first hint of a pain in the big toe, an NSAID is swallowed, the attack
could be aborted. I followed his advice. A miracle it was! No gout attacks
since then, which is 36 months. The NSAID of my choice was Naproxen sodium
220 mgs.- just one oral dose when pain initiates.
I still enjoy an occasional glass of wine.The seventieth birthday was few
months ago. The pair of crutches are collecting dust in the garage.
Why is that gout always visits my left big toe?
Competing interests:
None declared
Competing interests: No competing interests
In my response of 9th June I suggested that Tennis Elbow was due to
gouty elements in the "FLEXOR" origin of the muscles of the forearm.
As every schoolboy knows, this is wrong. It is the "EXTENSOR" origin of
those muscles which is the Gouty lesion.
Competing interests:
None declared
Competing interests: No competing interests
It would not be unusual for Gout to attack unilateraly since, if one
is right-handed then Tennis Elbow will occur in the Right-sided Flexor
origin.
A Right-handed golfer will suffer his Gout in the Left forearm.
All people walk or stand lop-sided so the strains and pressure will
be to one side or the other.
Therefore Left Podagra or Right Podagra for instance.
It is quite true, as Dr. Kuldip P. Anand (8th June) has well pointed
out that a "normal Urate Concentration" does not exclude a diagnosis of
Gout.
It is my opinion that "there is no normal figure". That each of us
has an inherited threshold over which one gets an attack and below it will
be pain-free. That is a personal matter bequeathed by one's parents and
grandparents' parents. Choose them well.
For example, 25 mgm.% may produce no evidence of
Gout or kidney stones in one patient, whereas any higher than 3.2 mgm.% in another could bring on pains in practically every joint.
It would be of interest to know if Dr. Kuldip P. Anand had any
experience of Ayur-vedic prescriptions for arthritic pain. Such as those
containing Ginger, Turmeric, Frankincense and Japanese Wild Cherry? This
seems to work very well and Chinese people will say "Of course we knew
that Ginger was good" for arthritis!
Safer to keep away from long-term use of Diclofenac things and
Indomethacin and Celecoxib in any of their forms. The Spanish and French
will usually prefer them as suppositories.
Colchicine is so much cheaper too. The restrictions in diet will
also save money.
In India patients should avoid eating gourds, if they do, that is.
And many other unkown Oxalate and Urate containing vegetables and fruit
(Durian for instance and Alphonse Mango) and what one knows not what of.
Competing interests:
None declared
Competing interests: No competing interests
Many cases of "arthritis" could well be re-classified as Gout.
The condition is caused by the deposition of Urate crystals on joint
surfaces, in tendon and ligamentous insertions, paricularly when they have
been recently stressed or strained.
Hence Achilles tendonitis, Calcaneal Spur, Golfer's forearm (L),
tennis elbow, olecranon bursitis, carpal tunnel ("mouse") syndrome and
sacro-iliac strain.
To just prescribe for the pain the latest NSAID (Non-Steroidal Anti-
Inflammatory Drug) is too easy. It does not get at the cause, is only
palliative and may have side effects.
The cause lies in the source of that Uric Acid. Though it can and
has come from the breakdown of one's own specialised tissues when
debilitated, as amongst the inmates of Changi Gaol and Camp in the last
War, the origin is more likely in one's own diet.
Such a diet that is rich in DNA (Deoxyribo-Nucleic Acid) which will
of course be found in the highly nucleated tissues of rich meats, and
offal, liver, brain, kidney, tongue, sausage and close-fibred fish and all
shell-fish. Also in the young growing-tips of vegetables as found in
Asparagus and bean-sprouts, and bamboo shoots. All show a similar
histological pattern of closely packed nuclei with little cytoplasm in
proportion.
Hence from this nucleo-protein the enzymes break down that DNA
through Adenine and Guanine to Hypoxanthine to Uric Acid.
It seems wrong therefore to see repeated from time to time the
advertisement that "diet plays little or no part in the causation of
Gout". Which is just a promotion of Allopurinol to be taken for the rest
of one's life.
When Uric Acid cannot be blamed then Oxalic Acid will replace it, and
a watch must be kept on some vegetables, spinach for instance, and fruit
such as Raspberies, Strawberries, Gooseberries, Rhubarb, Apricots,
Persimmons and Peaches. Mango has no Oxalate but in susceptible and
particular people will cause Gout.
The list is long.
Alcohol in any form plays its part by blocking the kidney's ability
to excrete the Uric and Oxalic Acids. All such drinks must be stopped
during any treatment.
An important part of the treatment will be an adequate intake of
water (not iced), enough to produce urination at least six times a day, as
clear as a mountain stream.
Urate excretion can be accelerated, even ridding the kidney of
offending recent stones and crystals, by taking three times a day a soup
of the large white radish (Raphanus Sativus), called "Moolie" in
supermarkets and "Daikon" in Japanese restaurants. Stones will either
dissolve away or be passed in two or three days. It may be mentioned that
this was noted by Nicholas Culpeper in his 17th Century "Herbal". It has
been part of Indonesian family lore for far longer.
Chocolate and coffee are both strong in Oxalates and strongly-brewed
English tea more in Urates, from those growing tips of the tea-bush.
Treatment of Gout then is with the well-tried Colchicine (500 mcg,)
taken as two tablets (1,000 mcg.) to begin and repeat one after an hour.
Four tablets in one day will probably produce bowel looseness and patients
shouod be so warned.
And in combination with Benzbromarone ("Narcaricin"), found more on
the European continent. Two tablets to be taken at night-time followed by
two Colchicine tablets each morning.
In very severe attacks of Gout then recourse must be to intramuscular
injections of Steroids, and then tail them off with tablets on a reducing
daily dosage.
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir,
Congratulations to Dr. Underwood for his excellent review of
Diagnosis & management of Gout [1]. Gout is considered a disease
associated with abundance and overindulgence like old Roman ways. There
seems to be a lack of interest in this disease due to unexplained reasons.
Harrison’s Principles of Internal Medicine devotes only 1½ page to this
disease [2]. However Davidson’s Principles and Practice of Medicine [3]
covers it in 3½ pages. As brought out well by the author, this disease
affecting 1% of the world population is likely to become more common in
future due to increasing affluence. While working in Armed Forces, we are
impressed by large number of cases of gout in Nepali Gorkha soldiers.
Perhaps it is due to their fondness for red meat and alcohol.
Few conditions can be diagnosed with more certainty or treated more
successfully and dramatically than gout. Gout is a prominent member of
‘Club of unilateral diseases’ like Bell’s palsy, Trigeminal Neuralagia,
Herpes Zoster, Migraine, Poliomyelitis, Filariasis, wherein the clinical
features are predominantly unilateral in majority of patients. What is the
cause of unilateralism of clinical features of these diseases is a well
guarded secret of nature, but this fact definitely helps in arriving at
the correct diagnosis of these diseases. Unilateral acute podagra (painful
swelling of great toe) is the usual presenting feature of majority of
cases of Gout. Contrary to common belief, normal serum urate concentration
does not exclude the diagnosis. In fact this situation is pretty common in
clinical practice.
Treatment of acute gouty arthritis is well summed up in the box
‘Patient’s story’ of the article [1]. Colchicine is rarely used in
treatment of acute Gout because of its not easy availability and marked
gastrointestinal side effects. Indomethacin and diclofenac have almost
replaced colchicine because of their equal efficacy and few side effects.
We have never felt the need to use oral or intra-articular corticosteroids
in acute gout.
References :
1. Underwood M. Diagnosis and management of Gout. BMJ 2006; 332:1314-
1319.
2. Reginato AJ. Gout and other crystal arthropathies in Kasper DL,
Braunwald E, Fauci AS et al (Eds) Harrison’s Principles of Internal
Medicine 16th Ed. McGraw-Hill. 2005:P 2046-2050.
3. Doherty M, Lanyon P and Ralston SH. Musculoskeletal disorders. In
Haslett C, Chilvers ER, Boon NA and Colledge NR (Eds). Davidson’s
Principles And Practice of Medicine. 19th Ed Churchill Livingstone.
2002: P 957-1047.
Competing interests:
None declared
Competing interests: No competing interests
The article on diagnosis & management of gout suggests treatment
with NSAI / colchicine or steroids if creatinine is < 167mmol/L.
Are there any suggestions as to the best way to treat when the creatinine
is higher than this? Some of my patients with gout have a significantly
higher creatinene than this.
Competing interests:
None declared
Competing interests: No competing interests
Re: Me and My Gout
I suffered from irregular recurrent attacks of gout (diagnosed by
polarizing microscope examination of aspirated joint fluid) every few
weeks for a period of 15 years. When my sleep apnea was diagnosed and
resolved 3 years ago, my gout attacks ceased immediately and completely.
Through my reading of medical journal literature, I was able to find
the physiological explanation for the connection of gout with sleep apnea.
The intermittent hypoxia from sleep apnea causes the cells to begin a
catabolic process in which the ATP disintegration begins a chain of
chemical transitions, the irreversible end product of which is the excess
generation of uric acid. The hypoxia also results in hypercapnia, causing
acidosis that makes the precipitation of monosodium urate more likely.
Although these processes were well-described over 15 years ago in medical
literature, it appears that no one connected them with gout attacks until
now.
During my fifteen years of suffering, I avoided eating foods with
high purine content. That regimen had little benefit for me. Now the foods
that I used to avoid, I eat with relish, and I have had no attacks. What
matters is not how I eat, but how I sleep.
Competing interests:
None declared
Competing interests: No competing interests