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Q: gout: Purine-rich food-> precipitation questions ( Answered 4 out of 5 stars,   0 Comments )
Subject: gout: Purine-rich food-> precipitation questions
Category: Health > Medicine
Asked by: eddiezap-ga
List Price: $50.00
Posted: 14 Jun 2005 13:00 PDT
Expires: 14 Jul 2005 13:00 PDT
Question ID: 533292
I have mild gout, or crystalization of uric acid settled in my foot /
toe joints.  Uric acid comes from
1. the breakdown of body tissue
2.  dietary intake of foods containing purines

a. How long after a purine-rich meal will uric acid appear in my bloodstream
b. what controls the rate at which dissolved uric acid will
precipitate out into a joint
c. what controls which joints?
Subject: Re: gout: Purine-rich food-> precipitation questions
Answered By: crabcakes-ga on 14 Jun 2005 20:14 PDT
Rated:4 out of 5 stars
Hello eddiezap-ga,

  As you know, with gout, you may have increased uric acid production,
or decreased excretion of the uric acid. Increased uric acid
production is generally caused by enzyme deficiencies, and diseases
like mono and hemolytic anemia to name a few. When a person has
decreased excretion of uric acid, it may be due to an unknown reason,
genetics, hypothyroidism, high blood pressure, kidney damage, or

  In the absence of genetic disorders, it is not totally clear what
triggers sodium urate crystals to collect in joints and tissues. Gout
is more common in older people,especially men. About 300 people per
100,000 get gout. The rate at which the uric acid crystallizes depends
on the amount in the blood, and is variable. The crystals form when
there is a large amount of uric acid in the blood, when it is
?supersaturated?. Body temperature, as you will read further down in
the answer affects uric acid crystal formation as well.

  There is no definite timing of how quickly uric acid will accumulate
in the joints or bloodstream after a meal. Some patients claim to have
symptoms several hours after a rich meal, and this may be so in some.
In others it may be coincidental ? the person could have had a high
enough level before eating a meal that adds just enough uric acid to
cause symptoms. Whether the person is well hydrated or not can also
affect timing. Dehyrated people will feel symptoms more readily than
folks that don?t consume plenty of water. If  pressed for an
approximate timing after a meal, I?d have to say 8-12 hours.

?The joints of the foot, ankle, knee, wrist, elbow, and hand are other
frequently affected sites. In such cases the condition is known as
polyarticular gout. More than one joint is affected in 10% to 20% of
first attacks. The pain usually occurs in joints on one side of the
body and it usually, although not alway in the lower extremities.
People with polyarticular gout are more likely to have a more gradual
onset of pain and a longer delay between attacks. They also more
likely to experience a low-grade fever, loss of appetite, and a
general feeling of unwellness.

The primary symptom, which usually takes eight to 12 hours to develop,
is severe, sometimes crushing pain at and around the joint. In many
cases the attack occurs late at night or early in the morning and
announces itself by waking the sufferer. Some patients describe it as
resembling a disoclated bone and one writer described it as "like
walking on my eyeballs". Chills and mild fever may follow. The area
can be so tender that walking and even the weight of bedsheets can be
unbearable. Swelling may extend beyond the joint, indicating fluid
build-up within. The skin over the affected area is often red, shiny,
and tense. After a few days it may start to peel. An untreated attack
will typically peak 24 to 48 hours after the initial appearance of
symptoms, and subside after five to seven days, although it can last
only hours to several weeks.?

Uric acid does have a preference for the big toe (then called
podagra)and ankle joints, and can accumulate in the rims of the ears,
as well as tissues and kidneys. This is because the toe, ankle and ear
rim are cooler in temperature than other joints.
?Over time, uric acid in the blood crystallizes and settles in the
joint spaces, causing swelling, inflammation, stiffness, and pain.
Gout usually affects the first metatarsal phalangeal joint of the big
toe (hallux) or the ankle joints.?

?In the bloodstream, uric acid exists predominantly as a dissolved
salt called monosodium urate (MSU). At 37 degrees C (normal body
temperature) and at a uric acid concentration approaching 7 mg/dL, the
blood plasma becomes supersaturated, and needlelike crystals of MSU
form. Crystallization is governed by other factors as well. In joints,
such as the knee and ankle, temperatures are cooler (29 degrees C to
32 degrees C), and MSU crystals are able to form at even lower uric
acid concentrations, which explains why gout favors these joints.?

?Gout can also affect the instep, ankles, heels, knees, wrists,
fingers, and elbows.?

?Uric acid is a substance that results from the breakdown of purines
or waste products in the body. Normally, uric acid is dissolved in the
blood and passes through the kidneys into the urine, where it is
eliminated. If the body increases its production of uric acid or if
the kidneys do not eliminate enough uric acid from the body, levels
build up (a condition called hyperuricemia). Hyperuricemia may also
result when a person eats too many high-purine foods, such as liver,
dried beans and peas, anchovies, and gravies. Hyperuricemia is not a
disease and by itself is not dangerous. However, if excess uric acid
crystals form as a result of hyperuricemia, gout can develop. The
excess crystals build up in the joint spaces, causing inflammation .
Deposits of uric acid, called tophi, can appear as lumps under the
skin around the joints and at the rim of the ear. In addition, uric
acid crystals can also collect in the kidneys and cause kidney

?Gout is one of the most common forms of arthritis (joint
inflammation). It appears as an acute attack often coming on
overnight. Within 12-24 hours there is severe pain and swelling in the
affected joint. The skin over the joint may be red and shiny.

Gout usually affects only one or two joints at a time - most often the
feet and ankles. The ball of the big toe is the commonest site.
Without treatment the attack subsides in a week or so and when
patients first develop gout there may be intervals of many months or
even years between attacks. As time goes by, these tend to become more
frequent and more severe and eventually many joints may be involved,
sometimes all at the same time. At this stage a state of chronic or
continuous joint disease may develop with progressive joint damage,
disability and crippling (chronic gout). Gout affects mostly men and
is very rare in women until after the menopause when it is quite often
seen. Gout is very common in New Zealand and it is particularly common
in Maoris and Pacific Islanders. Some surveys have shown it to be
present in up to 10% of adult males.?
?Uric acid is a chemical which is a natural part of the normal
breaking down and building up of food and body tissues. The level in
the blood can be measured and shows how much there is in the body
overall. The condition of raised blood uric acid is called
hyperuricaemia. When this is present the uric acid which is normally
dissolved in the blood may, from time to time, form microscopic
crystals in the joint. These crystals set up the inflammation which is
called acute gouty arthritis or acute gout.?

·	?Asymptomatic (without symptoms) hyperuricemia--In this stage, a
person has elevated levels of uric acid in the blood but no other
symptoms. A person in this stage does not usually require treatment.
·	Acute gout, or acute gouty arthritis--In this stage, hyperuricemia
has caused the deposit of uric acid crystals in joint spaces. This
leads to a sudden onset of intense pain and swelling in the joints,
which also may be warm and very tender. An acute attack commonly
occurs at night and can be triggered by stressful events, alcohol or
drugs, or the presence of another illness. Early attacks usually
subside within 3 to 10 days, even without treatment, and the next
attack may not occur for months or even years. Over time, however,
attacks can last longer and occur more frequently.
·Interval or intercritical gout--This is the period between acute
attacks. In this stage, a person does not have any symptoms and has
normal joint function.
·Chronic tophaceous gout--This is the most disabling stage of gout and
usually develops over a long period, such as 10 years. In this stage,
the disease has caused permanent damage to the affected joints and
sometimes to the kidneys. With proper treatment, most people with gout
do not progress to this advanced stage.?

?To confirm a gout diagnosis the doctor may want to take a sample of
fluid from the affected joint or from one of the lumps under the skin,
to look for the presence of uric acid crystals under a microscope.
Your doctor may also suggest you have an x-ray of the affected joint.?|fr=|r

?Thus, hyperuricemia should be distinguished from gout, even though
urate supersaturation is necessary for the expression of gout. Uric
acid overproduction and diminished renal uric acid excretion are the
major mechanisms resulting in hyperuricemia, and an understanding of
the basis of hyperuricemia in individual gout patients is an important
step in determining appropriate treatment and in identifying
underlying disorders, offending drugs and toxins, and inherited enzyme
defects, all of which can result in hyperuricemia and gout.?

?The end product of purine catabolism in man is uric acid. Other
mammals have the enzyme urate oxidase and excrete the more soluble
allantoin as the end product. Man does not have this enzyme so urate
is the end product for us. Uric acid is formed primarily in the liver
and excreted by the kidney into the urine.

Urate in the blood could accumulate either through an overproduction
and/or an underexcretion of uric acid. In gouts caused by an
overproduction of uric acid, the defects are in the control mechanisms
governing the production of - not uric acid itself - but of the
nucleotide precursors. The only major control of urate production that
we know so far is the availability of substrates (nucleotides,
nucleosides or free bases).?

?The problems that can results are:
·Acute inflammatory arthritis
·Chronic erosive and deforming arthritis
·Kidney and/or bladder stones
·Chronic renal disease or hypertension.?

The four stages of gout:
1 Asymptomatic hyperuricaemia
Crystals probably take a long time (months or years) to accumulate,
most commonly in peripheral connective tissues in and around synovial
joints, especially in the lower limbs. During this period there may
well be no symptoms whatsoever. About 95% of people with
hyperuricaemia will remain asymptomatic throughout their lives.
2 Acute attacks
A single peripheral joint is almost always involved in all initial
episodes, and most often this is the metatarsalophalangeal joint
between wrist and finger. Typically local irritation and aching
proceeds to tissues becoming swollen, red, hot, shiny and extremely
painful. The pain is often describes as the worst ever experienced. By
24 hours inflammation is maximal, and it then resolves slowly over a
week or so, often with itching and flaking of overlying skin.
3 Intercritical gout
These are asymptomatic periods between attacks. Some never have a
second attack, or perhaps after many years, but in most the second
attack occurs with a year. The frequency of attacks and number of
sites then increase with time, leading eventually to joint damage and
chronic pain, after an average of about 10 years.
4 Chronic tophaceous gout
Large crystal deposits, or tophi, produce irregular firm nodules,
predominantly around the upper surfaces of the fingers and hands, but
other places as well, including forearms or Achilles tendons or ears.
When untreated, these can lead to severe deformity.
?Lifestyle changes in early primary gout involve weight loss,
reduction in alcohol consumption and avoidance of toxins like low-dose
aspirin and lead. With diuretic-induced gout stopping the diuretic may
be possible and be all that is required.
The usual choice for reducing uric acid levels is allopurinol, because
it inhibits xanthine oxidase and can depress new purine synthesis.
Probenecid prevents proximal tubular reabsorption of urate.?

?The increase in blood uric acid results from increased purine intake
(purines are precursors of uric acid), or increased turnover or
production, or from decreased uric acid elimination by the kidneys, or
a combination of all these (Figure 1). Though higher purine intake may
play a part in high blood uric acid levels, excretion by the kidney
should increase to compensate. In most (75%-90%) people with gout,
clearance of uric acid by the kidney is significantly reduced.
Increased uric acid production or decreased renal clearance can be
secondary to other disorders?

?Uric acid passes through the liver, and enters your bloodstream. Most
of it is excreted (removed from your body) in your urine, or passes
through your intestines to regulate "normal" levels.
Normal Uric acid levels are 2.4-6.0 mg/dL (female) and 3.4-7.0 mg/dL
(male).  Normal values will vary from laboratory to laboratory.?

?When we consider the many different roles purines play in our
metabolism, it is not surprising that the diseases of purine
metabolism are as varied, ranging from asymptomatic conditions, which
are only discovered accidentally, to disorders with severe
neurological abnormalities, which are ultimately fatal. As with other
metabolic diseases, each disorder is caused by a defective gene which
results in an enzyme with too little or too much catalytic activity.
The numbered enzymes referred to below are shown in Figure 2. Purine
metabolic diseases include:
Gout. The most common defect of purine metabolism is one of the oldest
known metabolic diseases. Gout was known to the ancient Egyptians, and
was extensively studied by the Roman physician Galen (A.D. 131-200).
We now know that gout is caused by overproduction of uric acid, with a
consequent depositing of uric acid crystals in the joints. Several
different enzyme defects cause gout, notably deficiency of HPRT
(enzyme 21). Gout can be treated successfully by limiting purines in
the diet and by using drugs which inhibit xanthine oxidase (enzyme 27)
and, thereby, the production of uric acid?

Not only joints are affected by gout:

?Kidney Stones. Kidney stones occur in between 10% and 40% of gout
patients, and can occur at any time after the development of
hyperuricemia. Although the stones are usually composed of uric acid,
they may also be mixed with other materials.

Kidney Disease. About 25% of patients with chronic hyperuricemia
develop progressive kidney disease, which sometimes ends in kidney
failure. It should be noted, however, that many experts believe that
chronic hyperuricemia is unlikely to be a common cause of kidney
disease. In most cases, the kidney disease comes first and causes high
concentrations of uric acid.

Gout and Heart Disease 
Gout often accompanies heart problems, including high blood pressure,
coronary artery disease, and congestive heart failure. Hyperuricemia,
in fact, has been associated with a higher risk of death from these
conditions. One 2001 study reported that disease activity in gout may
contribute to unhealthy cholesterol and lipid levels. Some interesting
evidence, however, suggests that hyperuricemia may occur as a response
to inflammatory damage that occur with heart disease and may even be
Other Medical Conditions Associated with Gout 
The following are some conditions that are associated with long-term gout: 
·Dry eye syndrome. 
·Complications in the lungs (in rare cases, uric acid crystals occur
in the lungs).

Protein and Purine metabolism

?Clinical problems associated with nucleotide metabolism in humans are
predominantly the result of abnormal catabolism of the purines. The
clinical consequences of abnormal purine metabolism range from mild to
severe and even fatal disorders. Clinical manifestations of abnormal
purine catabolism arise from the insolubility of the degradation
byproduct, uric acid. Excess accumulation of uric acid leads to
hyperuricemia, more commonly known as gout. This condition results
from the precipitation of sodium urate crystals in the synovial fluid
of the joints, leading to severe inflammation and arthritis.
Most forms of gout are the result of excess purine or of a partial
deficiency in the salvage enzyme, HGPRT. Most forms of gout can be
treated by administering the antimetabolite, allopurinol. This
compound is a structural analog of hypoxanthine that strongly inhibits
xanthine oxidase.?

You can see on the chart on this page, that there are several purine
metabolism defects that cause gout.

?Patients shall maintain ideal bodyweights. Overweighted patients need
to reduce weights slowly by a rate of losing 1kg in 1 month. Fast
weight loss will produce purine in a large amount from tissue and
result in acute syndromes. When acute syndromes occur, any
weight-losing plan must be halted.
Gout patients produce more purine from nuclear protein and harder to
excrete them than normal people. Therefore, they shall avoid eating
too much protein. The ideal intake is about to eat 1g of protein per
1kg of ideal bodyweight.
In acute illness phase, patients shall choose low-purine foods (such
as foods classified as the first category). The best protein source
for them is egg, milk and dairy products.
In non-acute illness phase, patients shall still avoid foods listed in
the third category because they contain purine richly. The second
category foods shall be chosen carefully and watched out in amount.
Dried bean intake shall be reduced. The first category foods produce
low purine and can be adopted in ordinary time.
According to studies: a large amount of lipid will inhibit uric acid
excretion and accelerate gout occurrence.. Therefore, use appropriate
amount of oil when cooking. Try to choose plant oils. Avoid from
cooking food by frying.?

For a more scientific explanation:
?Pyrimidine nucleosides are not extensively cleaved by enzymes of the
intestine, and the ribosylpyrimidines are absorbed intact and utilised
for the synthesis of tissue nucleic acids. The known mammalian
nucleosidases readily cleave inosine (ribosyl-hypoxanthine) and
guanosine. Adenosine is converted by adenosine deaminase to inosine,
and the net result leads to purines
which are extensively catabolised to uric acid. Nucleic phosphorylases
with high activity are responsible for the decomposition to free
bases. A high xanthinoxidase activity in the mucosa of
the small intestine oxidises most of the purine bases to uric acid
[Montag et al., 1989]. Chinsky et al. (1990) found that adenosine
deaminase was one of the most abundant proteins of the epithelial
lining of the alimentary mucosa in mice. Levels were low at birth but
achieved very high levels within the first few weeks of life. Thus
dietary DNA, nucleotides, nucleosides, and bases are readily degraded
in both the gastric and small intestine compartments.?


?Transport of nucleosides into the enterocyte occurs via both
facilitated diffusion and specific Na+- dependent carrier-mediated
mechanisms [Bronk and Hastewell, 1987; Jarvis, 1989]. The upper region
of the small intestine has the greatest absorptive capacity. Once
absorbed, most of the nucleosides and bases are rapidly degraded
within the enterocyte, and catabolic products such as
uric acid are excreted in the urine and intestine [Salati et al., 1984].
Despite extensive catabolism, tracer studies in animals indicate that
only 2?5% of dietary nucleotides are incorporated into tissue pools,
primarily within the small intestine, liver, and skeletal muscle
[Burridge et al., 1976]. Incorporation into tissues is reportedly
increased at younger ages. Extensive salvage of purines and pyrimidine
nucleotides has been demonstrated in
intestinal tissues. Adenine is the most extensively reutilised purine,
particularly during the fasted state. In contrast, other purines are
extensively degraded to uric acid in the gut. Further, up to 20% of
orally administered adenine may be recovered unmetabolised in the
portal vasculature
[Salati et al., 1984]. Schubbert et al. (1994) reported that a portion
of <0.1% of ingested phage M13 DNA was found as fragments (between
<200 and 976 bp) in the blood stream, in liver and in different spleen
cells in mice (i.e. tissues of the immune system).?

Role of Diet

Reduce Foods Containing Purines. Because uric acid levels are only
minimally affected by diet, dietary therapy does not play a large role
in the prevention of gout in the first place. Still, people who have
suffered an attack of gout may benefit from reducing their intake of
purine-rich foods if they habitually eat unusually large quantities of
such foods. (Because purines are found in all protein foods, no one
should eliminate all purines.)

Purine-containing foods include the following: 
·Beer and other alcoholic beverages. 
·Anchovies, sardines (in oil), fish roes, herring. 
·Organ meats (eg, liver, kidneys, sweetbreads). 
·Legumes (eg, dried beans, peas). 
·Meat extracts, consommé, gravies. ( Note: Any meat, fish, or poultry
has moderate amounts of purines. And diets high in protein,
particularly animal protein increase uric acid. No studies have
determined the value of reducing protein in gout patients, however.)
·Mushrooms, spinach, asparagus, and cauliflower. 
Drinking plenty of water and other nonalcoholic beverages helps remove
MSU crystals from the body. Some researchers are studying the
anti-inflammatory properties of green tea, which might have some
benefit for gout. It should be noted, a Japanese study reported a
higher association between gout and tea drinking (although the study
did not describe the type of tea).
Avoid Alcohol 
Alcohol should be avoided, since it promotes purine metabolism and
uric acid production; it also may reduce excretion of uric acid. Heavy
drinking, especially binge drinking of beer or distilled spirits,
should especially be avoided.

Regularly drinking alcohol interferes with the removal of uric acid
from the body and can increase the risk for developing gout. Other
risk factors include the following:
·Exposure to lead in the environment 
·High dietary intake of rich foods that contain purine (e.g., cream
sauces, red meat, sardines, liver, scallops)
·Medications that may interfere with the body?s ability to remove uric
acid (e.g., aspirin, diuretics, levodopa [used to treat Parkinson's
Cyclosporine (e.g., Gengraf®), which is a medication used to suppress
the body's immune system and prevent rejection after organ transplant,
also increases the risk for developing gout.

How to Lower Uric Acid (Hyperuricaemia)
?If in spite of all the measures above the uric acid remains high and
attacks continue or become more frequent, other drugs can be used
which directly lower the blood uric acid. However, it must be
understood that these drugs have no effect on the actual attacks of
acute gout and they must be taken on a continuous and long term basis.
The dose must be adjusted by repeated checks on the blood uric acid
before a permanent maintenance dose can be decided on. Once the uric
acid is down within normal limits, the patient should remain free from
gout provided the drug is continued. Some drugs work by increasing
elimination via the kidneys and others by blocking uric acid
It is also very important for patients beginning such drugs to realize
that for the first few months of treatment, gouty attacks can become
more severe and frequent. This is usually controlled by taking one or
two tablets a day of an additional drug for at least several months
and if any acute attacks do appear they must be treated in the usual
way and the long term medicines continued.?

Here are some illustrations of purine metabolism:

I hope this is the information you were seeking. If anything is
unclear, I?ll gladly offer further assistance, before you rate this

Sincerely, Crabcakes

Search Terms
Purine metabolism
Protein breakdown + gut
Absorption + purines
Uric acid metabolism + liver
Gout metabolism
Gout + joints
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