This page is concerned only with what is called properly "secondary gout", or gout which is caused by an agent or drug of some sort, rather than true "classical" gout. There are three types of "gout":

a) True "gout", which is the result of overly high uric acid naturally occurring in the system.

b) Pseudo-gout. This has nothing to do with "gout" as such, but is a symptomatically gout-like condition involving calcium deposits on the bones of the foot.

c) "Secondary Gout", which is a gout condition arising from high uric acid in the blood, but caused by a drug used for another medical purpose. Hence the name "secondary". This is the topic of this discussion.

1) Diuretics like THIAZIDE and a variety of similar drugs, have been used for years as one of the ways to reduce high blood pressure by excreting water from the system. This is a basic process of programming the kidneys to remove water from the blood, it is effective and the use of such "water pills" is widespread.

2) Diuretics are known in the pharmacological literature as causing an increase in uric acid in the system. This produces a situation in which crystalline deposits from the uric acid are liable to be deposited in joints and muscles, especially in the foot and lower limbs, and the resulting condition is well documented in medical textbooks as "secondary gout".

3) If a diuretic is administered without consideration of existing uric acid levels, or the necessity of concomitant use of an anti- uric-acid agent such as allopurinol or probenecid, there is a fair chance that the continued use of the diuretics will produce an attack of the gout. This can be anything from a sore toe, to incapacitating crippling of the foot and ankle.

4) If you are taking a diuretic, your uric acid levels should be checked regularly, but gout can occur even with median level uric acid readings. Often diuretics are prescribed for continued, even life-long use, so you should be completely sure that your blood pressure level really requires this treatment.

5) A drug (allopurinol, probenecid.........) may be required along with the thiazide diuretic to control the uric acid level.


The patient had never had an attack of the gout, his uric acid levels were well within the acceptable range on multiple testings. In check of blood pressure at the doctor's office, his BP was running about l60/95, and although the doctor felt it was probably high because of tension at testing in the office, the patient purchased an electronic tester and verified the readings as continuing in that elevated range.

At that point the doctor prescribed thiazide, which was taken for about one year, during which time there were increasing bouts of swelling and pain in either right or then left foot. After a full year of use of thiazide, a crippling attack in the left foot left him unable to walk more than a few steps without excruciating pain, the turning point at which he realized something had to be done. He turned to a wider range of medical opinion, as follows.

Since this was not typical gout attack of the joint of the big toe, it did not seem clear whether it was gout or an arthritic condition, so other doctors were consulted for further insight. One suggested pseudo-gout, which is a deposit of calcium on the bones of the foot at the joints, but an Xray showed no deposits at all. This ruled out pseudo-gout as well as uric-generated tophi or deposits at the joints, which would be signs of true-gout. Another doctor pointed to an arthritic condition or lupus, which a set of tests did not indicate. An orthopedic examination with Xraysy brought a medical recommendation back as true-gout with suggestion for use of allopurinol.

During this time the patient was doing his own reading in the medical literature, and discovered to his surprise that "secondary gout" was a regular terms for gout-like attacks caused by the widespread use of diuretics to control blood pressure. But none of the four doctors who examined the patient seemed aware of "secondary gout" as a medical term, or of its etiology in high uric acid resulting from a diuretic.

At this point the patient decided to take more active interest in his own medical fate, and went to the medical literature, reading carefully for the facts and also between the lines. First he discontinued to use of the diuretic completely, and on advice of his primary doctor started a normal adult-dosage of allopurinol. At the same time he started to avoid purine producing foods such as red meat, legumes and alcohol, and within two months was able to walk on the bad foot without crutches. In two month more he was largely restored to normal use of the foot.

In answer to the question whether this was true-gout or secondary, drug-induced gout, the patient as a test, resumed his prior use of alcohol (which is always mentioned as a primary trigger in cases of gout), as well as moderate use of red meat and shellfish which are also warned. No gout attack followed over the period of more than a month. Although this was not good scientific procedure, it did establish in his mind the opinion that this was not gout, but actually a "secondary gout" attack he had suffered, and therefore the result of what could ultimately be called thiazide-poisoning.

At this point the patient documented daily his blood pressure readings taken at various times of the day under different stress conditions, and found that the readings stayed in the range of l40/80 normally, a higher systolic only when active, both lower by five more points when fully relaxed. So completing the full circle back to where started, the blood pressure was back to anacceptable level, possibly by diet in part and also by avoiding stressful events in family life. Then it was clear that no medication (diuretic) was required for blood pressure, and continued uric acid tests gave results of middle-to-low readings.

Other background information:

The "patient" is none other than myself, a 72 year old non- medical retired professor with a Ph.D. in Linguistics, who has a developed skill at reading involved documentation carefully while mentally recording and evaluating masses of factual detail. In the past I have relied on my excellent medical experts for advice and treatment, but I have learned that in some dimension the individual has to take responsibility for his own continued well-being. It is critically important to check out on one's own all information available, to learn more about one's own body and its myriad of functions, and to be intelligently critical of all the factors of every medical treatment.

In looking back over the above case, it seems to me remarkable that four skilled and experienced medical men examined my ailment, but not one mentioned the possibility of "secondary gout". Yet this is a term I find commonly used in the Complete Home medical Guide (Columbia University College of Physicians and Surgeons) as well as the AHFS manual (American Hospital Formulary Service).

In these days of complicated medical information, nobody can be expected to know everything, but it should seem a basic caution to advise patents taking a diuretic to have uric acid levels checked frequents, and also (since the levels may not accurately prognose a gout attack) watch for pain or swelling. And if taking a diuretic, why not add an anti-uric agent in maintenance dosage as a precaution against attack?


a) If BP is high, get an instrument and check regularly at home over peak periods of stress as well as at rest. Without full data you really don't know where you are. There is no reason to start drug therapy until you have a bank of data. Checking at the office is not enough since stress may be involved there.

b) If you have high blood pressure, discuss with your doctor the various way of reducing it. There are other drugs than diuretics, which may be more suitable if you have high uric-acid levels to start with.

c) If you do take a diuretic, be sure you doctors knows the danger of increasing uric-levels and knows the term "secondary gout". If he dismisses discussion on these topics, get another doctor, there is no room for pig-headedness in your well- being.

d) If you have a gout-like condition, rule out the possibilities by getting an Xray to see if there are calcium or uric crystal deposits. Check with blood tests for other conditions like rheumatoid arthritis or lupus. Check for prior history of high uric levels, in which case you may have true-gout for which there is regular prescribed treatment. If none of these gives positive results, then look in the direction I have discussed here, which is "secondary gout" as the result of raised uric acid levels resulting possibly from use of a diuretic in a blood-pressure treatment.


When searching the Web under the term "gout" you may wonder why fine Belgian chocolates keep coming up in reply to your search, an odd treatment for a serious medical malady. Then you remember from your high school French classes, that "gout" in French means "taste", and nothing to do with the matter at hand (or foot).

In the 6th century B.C. Pythagoras returned from India and set up a monastic-style center in South Italy for the study of Science and Philosophy. His group feel under suspicion of the locals, who raided the "compound" and destroyed the monastery as such, but as the staff dispersed to the Hellenic world although they were bound to absolute secrecy, word somehow leaked out about their thinking and their findings.

A document does exist which lists some seventy of the "Pythagorean Counsels" which I have translated and furnished with commentary on this website under the "Philosophy" category. But I want to mention here that among these "Counsels", which range from religious notions, ideas about the nature of the world, thinking and understand, to other topic which we do not fully comprehend, there is a set of instructions relating to diet, which fits exactly the recommendations we now list for treatment of gout:

1) Avoid eating the brain (high in almost everything bad...)

2)Do not eat beans (which are notably high in purines, a gout producer)

3) Eat not the heart (organ meat with its purines)

4) Refrain from melanouros (technically catfish, a fish with red meat and a high purine level. In Greece this is the Melanouros Aristotelis, so named by Agassiz in the l9th century, as accurate according to Aristotle's description)

5) Do not eat anything which is split by its nature (another reference to beans and legumes generally, even certain grains e.g. wheat)

Surely this derives from the extensive Indian medical literature which goes back to the Ayur Veda and other ancient medical texts, incorporating centuries of observation and filing of medical findings. Since it is known that Pythagoras spent many years in India, the source of these recommendations can be taken as "clinical" rather than items of an obscure ritual "tabu".

Or if you have a flair for the Latin historical background, the Latin word for gout is "podagra" and the Romans knew it well. The great orator Cicero, in a pained note to a friend (Cicero, Epistulae ad Familiares 7.4) mentions gout in the course of an attack. Or for description and Roman medical treatment, you can confer with Scribonius Largus (De Medicina Sec. 160-2) or the indefatigable Pliny the Elder (Natural History27.63 and 32.110), but Celsus is really the better authority (De medicina 2.8.10). Or for a legal opinion on gout in society, check out Javolenus in the Digest (21.1.53).


When you discuss Gout with your doctor, he will certainly be thinking of the traditionally recognized crystaline deposits which lodge in the joints, especially those of the foot and specifically the large toe. In my Bout with Gout as described above in l998, it was the muscles of the foot and ankle which became swollen, and I recall this happening rather suddenly after exercising the right foot on orders of a physical therapist. The swelling was large, very painful and lasted for several months. My doctor insisted that this was not gout, since it does not manifest itself in muscle tissue.

Recently I came across what my doctor and I think is the answer. When a muscle is exercised strongly, it produces purines and finally at the end of a complicated chemical exchange, uric acid which is absorbed by the blood. This is a normal part of muscle tissue breakdown and when the uric is passed into the blood, it can be excreted with other materials in the urine. But when the serum uric level is high, as the result of use of a diuretic to lower the blood volume for BP control, the blood may not be able to carry away the muscular uric excesses, in which case the muscle becomes suffused with uric acid far beyond its carrying capacity.


This deserves special note, since it explains a muscular distress which only resolves itself after a period in which the serum uric is finally lowered. If gout is defined as joint-related in the normal occurrence, then this could be called Muscular-Gout as a the result muscle esercise and high serum uric levels in the vascular system. Resolution of the muscular distress when the blood uric levels are normalized is the best indication and explanation of this condition.

William Harris
Prof. Em. Middlebury College