What’s the difference between gout and psuedogout? The cause of gout is excess uric acid in the body that may lead to crystals forming around various bodily joints which lead to inflammation and pain.

Psuedogout is similar to gout, but is caused by excess calcium in the blood-stream that may lead to calcium-crystal formation around joints.

Both diseases may lead to the same end results, but it’s understood they have different underlying causes. In particular, it’s thought psuedogout is not related to diet.

Comment:

I like the design, you have worked hard on this gout site. My gout was first diagnosed two years, after an initial diagnosis of psuedogout. Most people can't imagine how many this affects me, the pain is really bad sometimes. I never realised I had gout until I experienced big-toe swelling. Both of my uncles had gout so I think it’s in our family history. I’ll be back – great layout and easy to read. It is a joy to read such a site. Congratulations. Malcolm Bishop, UK

Every one has heard of it, but what is gout? Simply put, it's is a form of arthritis that can be extremely disabling! Its symptoms have been noted for many hundreds of years and even documented in many old books. It primarily affects middle-aged people especially 40-upwards. It can be difficult to treat and often involves tailor-made treatment plans.

It’s caused by uric acid build-up in the body. There may be a number of factors that contribute to this including inadequate kidney-function, excess consumption of specific foods and drinks including shellfish and alcohol, and use of certain medications.

In time, with excess levels of uric acid in the blood, deposits may occur around various bodily joints leading to very painful and often acute gout attacks. Gout is known to affect around 1000 in every 100,000 and seems to affect men more than women, however, menopausal women may be at greater risk of developing it.

How many times have you head people say yeah I've heard of it, but what is gout disease? Now you know!

Why does gout traditionally ‘attack’ the big toe? Although the there’s no direct proof, the reasoning seems scientifically to me. Gout is caused by uric-acid crystal formation around body joints. Therefore it’s reasoned that gout causes big-toe pain because it’s the furthest joint away from the heart, and the area around the heart is the warmest part of the body. So the big toe is joint is likely to be the coolest joint in the body and therefore predisposed for crystal formation.

In other words, it seems heat play a role in preventing crystals of uric acid forming.

I’ve begun to really like this blog because of all the useful information. Learning to live with gout has helped me tremendously – denying it just adds to the stress! Gout affects me strongly. I wonder if any of your visitors have tried drugs and diet for gout – worked for me; especially reducing big toe pain. The cause of gout confused me a lot, none of my relatives have it! Cool stuff here – I like the pics. Keep up the good work! Pol Hansen

If you want to learn about the origins of gout I thoroughly recommend “Getting Rid of Gout” by B. Emmerson. It’s available from Amazon or Barnes and Noble.

Here’s a detailed excerpt from the book:

Gout is an ancient disease. The word gout itself is derived from the Latin gutta meaning a drop, reflecting the medieval belief that the disease originated with a drop of a noxious humour falling into an affected joint. A similar word is used in most western European languages: French, goutte; Italian, gotta; German, gicht Spanish, gota.

From the time of the Greek physicians of the Hippocratic School in the fourth century BC, gout has been recognised as different from all other forms of arthritis. Some characteristic features of gout are recorded in some of the surviving aphorisms of Hippocrates:

Hippocrates also recognised that it was a disease that came and went, of remissions and exacerbations.

Gout has an even longer history than this, although not recorded in written form: urate deposits symptomatic of gout have been found in the skeletons of mummies from Upper Egypt.

Like the Greeks, the Romans recognised gout as a specific disease, but they tended to relate it to the particular joint that was affected. Accordingly, they spoke of podagra when the acute gout affected the bunion joint (the first metatarsopha¬langeal joint, where the big toe joins the foot), as gonagra when the knee was involved, and so on.

The term 'gouty diathesis', referring to an inherited tenden¬cy to gout, was first used by Aretaeus the Cappadocian in the second century Al), who also recognised the frequency with which the great toe was involved and the tendency for com¬plete remissions, of unpredictable length, between the recur-rent acute attacks. He also reported that a person with gout had won the Olympic marathon during an interval between his recurrent attacks of gout.

These descriptions are so characteristic and still so typical that there can be no doubt that the ancient writers recognised and were describing the disease we know as gout. However, during the Dark Ages this distinction became clouded, and it was not until the Age of Enlightenment in the seventeenth cen¬tury that there was any further progress in understanding this disease.

In 1683, the English physician Sydenham published A Treatise of the Gout, which was based on his own extensive and personal experience with the disease. He clearly distinguished the acute attacks of gout in the early stages of the disease from the chronic arthritis which persisted in the later stages. At about this time too, in 1679, needle-shaped crystals from a gouty deposit or tophus were seen and drawn by the discover¬er of the microscope, Leeuwenhoek. Almost one hundred years later, the chemist Scheele identified uric acid in a renal calcu¬lus (kidney stone), and in 1798 Wollaston showed that urate was the major component of the crystals obtained from a tophus. (Unite is a salt of uric acid; both forms occur in the body, but the two forms can he regarded as interchangeable.)
By the middle of the nineteenth century, Garrod had described urate crystals forming on a thread suspended in the plasma of a patient with gout, evidence of high concentrations of urate in the blood. His book The Nature and Treatment of Gout and Rheumatic Gout, published first in 1839 and subsequently in many other editions, summarises the knowledge concerning the nature of gout at that time:

First, in true gout, uric acid, in the form of urate of soda, is invari¬ably present in the blood in abnormal quantities, both prior to and at the period of the seizure, and is essential to its production; but this acid may occasionally exist, at least for a time, in the cir¬culating fluid without the development of inflammatory symp¬toms, as in cases of lead poisoning. Its mere presence, therefore, does not explain the occurrence of the gouty paroxysm (attack).
Secondly, the investigations detailed in the chapter on the Morbid Anatomy of Gout, prove incontestably that true gouty inflammation is ALWAYS accompanied with a deposition of urate of soda in the inflamed part.

Thirdly, the deposit is crystalline and interstitial (in the soft tis¬sues) and when once the cartilages and ligamentous structures become infiltrated, remains for a lengthened time, often through-out life. Fourthly, the deposited urate of soda may be looked upon as the cause, and not the effect, of the gouty inflammation. Fifthly, the inflammation which occurs in the gouty paroxysm tends to the destruction of the urate of soda in the blood of the inflamed part, and consequently of the system generally. Sixthly, the kidneys are implicated in gout, probably in its early, and certainly in its chronic stages; and the renal affection, possibly only functional at first, subsequently becomes structural; the urinary secretion is also altered in composition. Seventhly, the impure state of the blood, arising principally from the presence of urate of soda, is the probable cause of the disturbance which precedes the gouty seizure, and of many of the anomalous symptoms to which sufferers from gout are liable.

Eighthly, the causes which predispose to gout, independently of those connected with individual peculiarity, are either such as produce an increased formation of uric acid in the system, or lead to its retention in the blood. Ninthly, the causes exciting a gouty fit are those which induce a less alkaline condition of the blood; or which greatly augment, for the time, the formation of uric acid; or such as temporarily check the eliminating power of the kidneys.

Tenthly, in no disease but true gout is there deposition of urate of soda in the inflamed tissues. With regard to the fact enumerat¬ed in the first of these propositions, namely, that the blood in gout always contains an abnormal quantity of uric acid during the attacks, sufficient evidence has been already afforded, inasmuch as it has been shown that in fortyseven patients suffering from the disease the blood contained much uric acid, and subsequently to the formation of the table, an examination of the blood of at least a hundred other patients has demonstrated the same truth. That this impregnation occurs prior to an attack is well illustrated in the annexed cases of lead paralysis, in which the patients experi¬enced the first fit of gout when in the hospital.