Hyperuricaemia is a higher than normal blood level of uric acid. There are individuals with high blood uric acid levels and have never had an attack of gout. Are these people at risk of arthritis of the joints and kidney stones from urate crystals deposits? Yes they are.

Firstly the diagnosis of asymptomatic hyperuricaemia is made more frequently because of more screening, and blood tests for insurance purposes. Secondly you can break it down to primary and secondary types. In the primary type there may be a genetic link. In this case there is a deficiency of an important enzyme leading to excess production of uric acid. When this is severe (Lesch-Nyhan Syndrome), there are severe problems.

Secondary hyperuricaemia results from factors affecting the production and/or elimination of uric acid. These include medical conditions, drugs, metabolic conditions, obesity and alcohol consumption.

Sometimes hyperuricaemia is suspected when patients present to the doctor with tophi. These can be acute or chronic. An acute tophus is usually small and later soften when it becomes chronic. They look like small nodules and as they grow bigger, the skin overlying them looks shiny and feels smooth. Sometimes they can ulcerate and release white chalky stuff. If the patient is treated with allopurinol the tophi usually becomes smaller.

Dr. Phil Hariram

Arthritis Guide.

In the days before adequate treatment controlled the blood level of uric acid, chronic gout presented with multiple joint involvement and chronic poly-arthritis. Today this is rare and only found in patients who refuse medication, have poor compliance or unable to take suitable medication.

Here the acute gout attack will become more frequent. Then other joints become involved. The crystals deposited in and around the joints are needle shaped and I suspect this is why acute gout is so painful.

I had an elderly patient who had heart failure and was on large doses of diuretics and ace inhibitors. She developed acute gout. Her medication was looked at and altered. Unfortunately her uric acid level remained very high. She was started on allopurinol.

She developed an allergic rash to allopurinol. In fact everything the consultant prescribed gave her problems. In the end she had no medication and refused any attempt to try anything for her gout because she was worried about side effects.

She was put on a specific diet. Eventually she developed poly-arthritis. Her fingers had big nobbles for joints and she had problems walking around her ground floor flat. Tophi developed first on the ear then elsewhere.

A joint badly damaged by chronic gout will on x-ray show erosions, secondary calcium deposits and soft tissue swelling.

Allopurinol is the drug of choice in chronic gout. By maintaining the blood level of uric acid within the normal range, separation of urate crystals into joints and kidneys are prevented.

Dr. Phil Hariram.

Arthritis Guide.

The first explanation of podagra was in the sixteenth century by Burgamer, a German Physician. He said podagra is a pain in the feet with or without swelling which comes from dampness or drought.

Podagra is acute gout affecting the big toe and typically the first metatarso-phalangeal joint. It is as a result of higher than normal uric acid in the blood. Uric acid is mainly excreted by the kidneys.

Diuretics and other drugs can affect the function of the kidneys and reduce excretion of uric acid. This can cause elevated level of uric acid in the blood and acute gout.

Over indulgence in alcohol can trigger acute gout. Beer is the worse alcoholic beverage for gout. Port was linked to gout in the eighteenth century. At the time, port was stored in lead lined casks and lead diffused into the port.

Lead in the consumed port accumulated in the body and in the kidneys, it affected the ability of the kidneys to excrete uric acid. The imbalance caused high uric acid in the blood. This condition is called Saturine gout.

Sometimes podagra can develop following initiating treatment with allopurinol. Gross over eating especially seafoods and red meat can trigger podagra.

No one knows exactly why podagra is the commonest manifestation of acute gout. Some suggested that the first metatarso-phalangeal is used a lot and takes a lot of the body’s weight when walking.

Dr. Phil Hariram,

Arthritis Guide.

Gout develops when the level of uric acid in the blood stream is higher than normal. When this happens urate crystal are deposited in and around the joints.
There are two types of gout, primary and secondary. The body eliminates uric acid from the blood naturally and most of this (66%) is done by the kidneys. In primary gout the process of elimination is slow and as a result the uric acid level in blood remains higher than normal. This is called hyperuricaemia.

In this condition the level of uric acid in the blood gradually increases over several years and during this time there are no gout symptoms. In addition it is estimated that only 5% of people with high blood level of uric acid develop gout.

Secondary gout is as a result of other diseases or factors that can elevate the level of uric acid. Often it is the case that these diseases or drugs make the body produce uric acid faster than the body can eliminate it.

Drugs that can raise uric acid level are diuretics especially thiazides,low dose aspirin,pyrazinamide and cytotoxic drugs.

Medical conditions that can trigger gout include kidney disease, myxoedema, psoriasis, lead poisoning, sarcoidosis, obesity, myeloproliferative disorders and polycythaemia.

People on very strict (almost starvation) diet can have high uric acid levels. Hyperlipidaemia is associated with high uric acid level.

Urates are eliminated mainly by the kidneys. The renal tubules are the important part of the kidneys for excretion of uric acid. So anything that can affect the efficient functioning of the renal tubules can affect the level of serum uric acid.

Dr. Phil Hariram,

Arthritis Guide

Gout is a form of inflammatory arthritis. In gout, crystals of uric acid is deposited in and around the joints. For this deposit of urate to occur, the circulating level of uric acid in the blood must be higher than normal.

Gout has been recorded through the centuries. Hippocrates wrote about it and urate crystals were found in the big toe of an Egyptian mummy.

Gout is more prevalent in males and high in affluent societies. This may be a dietary factor. In the old days the rich ate the expensive red meat while the poor could only afford grain. Guess who developed gout?
Acute gout is rare in pre-menopausal women and it is predominantly a male disease up to the age of 50. It usually starts after 30 years of age and more commonly between 40 and 50 in males. In women the first attack is usually between 50-60 years.

The first attack of gout is usually in the big toe and this is called Podagra. 70-90% of first attacks present this way.

Pain often develops at night and within a few hours the pain level can escalate to severe and throbbing. The big toe will become red, hot, swollen and very tender to the touch. This acute attack will resolve spontaneously but can take weeks. Medical intervention often shorten this episode.

After this first attack your doctor is not likely to start you off on long term medication because you may not get another attack for years. On the other hand, you could have another attack in days.

Dr. Phil Hariram,

Arthritis Guide.

Gout develops when the level of uric acid in the blood stream is higher than normal. When this happens urate crystal are deposited in and around the joints.
There are two types of gout, primary and secondary. The body eliminates uric acid from the blood naturally and most of this (66%) is done by the kidneys. In primary gout the process of elimination is slow and as a result the uric acid level in blood remains higher than normal. This is called hyperuricaemia.

In this condition the level of uric acid in the blood gradually increases over several years and during this time there are no gout symptoms. In addition it is estimated that only 5% of people with high blood level of uric acid develop gout.

Secondary gout is as a result of other diseases or factors that can elevate the level of uric acid. Often it is the case that these diseases or drugs make the body produce uric acid faster than the body can eliminate it.

Drugs that can raise uric acid level are diuretics especially thiazides, low dose aspirin, pyrazinamide and cytotoxic drugs.

Medical conditions that can trigger gout include kidney disease, myxoedema, psoriasis, lead poisoning, sarcoidosis, obesity, myeloproliferative disorders and polycythaemia.

People on very strict (almost starvation) diet can have high uric acid levels. Hyperlipidaemia is associated with high uric acid level.

Urates are eliminated mainly by the kidneys. The renal tubules are the important part of the kidneys for excretion of uric acid. So anything that can affect the efficient functioning of the renal tubules can affect the level of serum uric acid.

Dr. Phil Hariram,

Arthritis Guide

Gout is a form of inflammatory arthritis. In gout, crystals of uric acid is deposited in and around the joints. For this deposit of urate to occur, the circulating level of uric acid in the blood must be higher than normal.

Gout has been recorded through the centuries. Hippocrates wrote about it and urate crystals were found in the big toe of an Egyptian mummy.

Gout is more prevalent in males and high in affluent societies. This may be a dietary factor. In the old days the rich ate the expensive red meat while the poor could only afford grain. Guess who developed gout?
Acute gout is rare in pre-menopausal women and it is predominantly a male disease up to the age of 50. It usually starts after 30 years of age and more commonly between 40 and 50 in males. In women the first attack is usually between 50-60 years.

The first attack of gout is usually in the big toe and this is called Podagra. 70-90% of first attacks present this way.

Pain often develops at night and within a few hours the pain level can escalate to severe and throbbing. The big toe will become red, hot, swollen and very tender to the touch. This acute attack will resolve spontaneously but can take weeks. Medical intervention often shorten this episode.

After this first attack your doctor is not likely to start you off on long term medication because you may not get another attack for years. On the other hand, you could have another attack in days.

Dr. Phil Hariram,

Arthritis Guide.

Image via Wikipedia

When the level of uric acid in the blood is too high, gout can develop. It was known as the patrician’s malady in the past because it was considered a disease of over indulgence amongst the wealthy.

High purine diet can affect gout and red meat is high in purine. The rich ate red meat while the poor could only afford grain.
Gout is predominantly a male disease up to the age of 50. It usually start around age 30 and the highest incidence is between 40 and 50 years. In pre-menopausal women, it is rare.

Gout can be classified as primary and secondary. In primary gout the body either produces too much uric acid or it cannot excrete it effectively to maintain a normal blood level. These patients benefit significantly from dietary changes.

Secondary gout develops as a result of other factors. Some medical conditions can raise uric acid level and trigger gout. These include renal disease and myeloproliferative disorders. In leukaemia, the imbalance is due to excessive production of uric acid, and in renal disease the excretion of uric acid is impeded.

Drugs can affect blood uric acid levels. These include diuretics especially thiazide diuretics, aspirin and cytotoxic drugs. Gout is also linked to obesity and alcohol.

Hippocrates wrote about gout as a disease of males and post-menopausal women and urate crystals were found in the big toe of an Egyptian mummy.
Acute gout often develops during the night. 70-90% of acute gout develops in the big toe and typically affects the first metatarso-phalangeal joint. This is called podagra. Within hours the pain becomes severe and throbbing. The big toe swells up and can feel hot.

It is extremely painful to the touch and even the touch of the bed sheath can induce excruciating pain. The acute episode resolves on its own but can take over a week. Medication can shorten this time.

Since the introduction in 1951 of probenacid and allopurinol in 1963, chronic gout is rare apart from non-compliant sufferers. Before these drugs were introduced chronic gout caused severe distress. Acute gout was frequent and severe. In addition urate crystals separated out into other joints, kidneys and other organs leading to polyarthritis, kidney stones, heart disease and tophi.

Diet and weight loss has an important role in gout management. A low intake of purine can reduce blood urate level by up to 20%. Foods high in purine are meat especially liver and other organ meat, sausages and other processed meat, seafood, milk, eggs and certain beans. Alcohol increases the possibility of gout. Beer is the worse culprit. It contains guanosine. This chemical is converted by the gut flora into uric acid.

Today, with screening and tests done regularly and even for insurance purpose, we are seeing a group of individuals with high uric acid without any signs of gout.

These people need to be monitored. Once all potential factors that can influence gout are eliminated or reduced and diet and weight loss in place, if the uric acid level remains high, then maintenance therapy in the form of allopurinol is recommended to keep the blood uric acid level within the normal range. This stops urate crystals separating out into important parts of the body.

Dr. Phil Hariram

Arthritis Treatment.