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Beating Gout

A S u f f e r e r ’s G u i d et o L i v i n g P a i n F r e e

V i c t o r K o n s h i n

S e c o n d E d i t i o n

W i l l i a m s v i l l e , N e w Y o r k



Beating Gout A Sufferer’s Guide to Living Pain Free by Victor Konshin

Ayerware Publishing

Post Oce Box 1098 Williamsville, New York [email protected]://www.ayerware.comSAN: 856-1656

All rights reserved. No part o the book may be reproduced or transmitted

in any orm or by any means, electronic or mechanical, including photocopy-ing, recording or by any inormation storage or retrieval system, without written permission rom the author, except or the inclusion o brie quota-tions or a review.

Copyright © 2008, 2009 by Victor Konshin

Edition ISBNs:Sot cover: 978-0-9816624-6-6

Second Edition, First Printing 2009.Printed in the United States o America.

Publisher’s Cataloging-in-Publication(Provided by Quality Books, Inc.)

Konshin, Victor.Beating gout : a suerer’s guide to living pain ree

/ Victor Konshin. -- 2nd ed.p. cm.Includes bibliographical reerences and index.LCCN 2008908821ISBN-13: 978-0-9816624-6-6ISBN-10: 0-9816624-6-3

1. Gout--Popular works. I. Title.

RC629.K66 2009 616.3’999QBI08-600315



T a b l e o f C o n T e n T s

Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .i

Introduction iii

Chapter 1: The Four Stages of Gout 1

Why Do We Get Gout? 1 Asymptomatic Hyperuricemia Acute Attacks Intercritical Periods 7

Advanced Gout

Chapter 2: Treating Gout 11

Part One: Treating Acute Attacks 12Part Two: Managing Hyperuricemia 23Part Three: Prophylaxis 32

An Alternative Treatment Method 34Gout Management at-a-glance 36

Chapter 3: Getting the Right Diagnosis 39Synovial Fluid Diagnosis 39

Tophi Sampling Diagnosis 4Clinical Diagnosis 41Blood Tests 42Urine Tests 43Genetic Tests 43Diagnostic Imaging 44Other Conditions that Look Can Like Gout 46

Chapter 4: Hyperuricemia 49

What is Hyperuricemia? 49Why Does Hyperuricemia Occur? 50Some Causes of Secondary Gout 51Conditions Associated with Hyperuricemia and Gout 53

Chapter 5: Diet and Lifestyle 61Weight and Exercise 61

Alcohol Diet 66Fructose 70Proteins, Dairy and Fats 72Other Lifestyle Factors 74Diet and Lifestyle at-a-glance 76



Chapter 6: Alternative Medicine 79

Alternative Treatments backed by Scientic Evidence 80

Alternative Treatments with Little or no Scientic Evidence 82

Appendix A: Purine Content of Food 87

Appendix B: Additional Medication Information 93

General Information on NSAIDs 93Information on Specic NSAIDs 96

Colchicine 107Uric Acid Lowering Medications 109

Other Uric Acid Lowering Medications 116Other Medications for Acute Attacks 117

Appendix C: For Doctors 119

Glossary 121

References 129

Index 139



Beating Gout



P r e f a C e T o T h e s e C o n d e d i T i o n

Gout has been around or thousands o years, and has been known as a

unique disease or all o recorded medical history. Despite this disease’s long

and oten colorul history, gout is now actually one o the best understood o

all diseases. A furry o gout research and discoveries in the mid-part o the

last century led to the development o several medications and treatments or

suerers o the disease. However, now that the mystery o gout has waned,

it has become a “has been” disease with ew doctors or researchers paying

much attention to it. Unortunately, this neglect has resulted in gout becom-

ing one o the most mismanaged diseases over the past ew decades.

It still amazes me how little most people, whether patients or doctors, know

about this disease and just how much misinormation is out there, particu-larly on the Internet. This book is my eort to change that; to help the mil-

lions o gout suerers around the world to better understand this debilitating

and potentially deadly disease and how to treat it properly. It is also my hope

that this book will inspire more interest and research in the medical com-

munity.

I am thrilled to get letters and comments rom people that have been helped

by this book. My most sincere hope is that my work will help you live a long

lie, ree o the pain o gout.

— Victor [email protected]

Williamsville, NY

December 1, 2008

Beating Gout | i



Beating Gout | iii

i n T r o d u C T i o n

For the whole o human history, people have been suering rom gout.

In ancient times, only kings and noblemen could live the liestyle that pre-

cipitated gout; but in modern times all but the poorest people in the devel-

oped world live much better than those kings and noblemen could ever have

dreamed.

Today, most o us have plentiul access to nearly every kind o ood the world

has to oer. A trip to the grocery store is essentially a trip around the world,

providing a huge variety o oods rom dierent regions and countries. And

while many o us work at jobs that may be stressul or require long hours, it

is ar rom the backbreaking work o our ancestors. Even the nobility o past

centuries would be envious o our climate-controlled oces, our modern

conveniences and, most o all, our medicine.

Cases o gout were rst recorded in ancient times. Yet it was only with the

discovery o the drugs probenecid in 1950 and allopurinol in 1964 that gout

turned rom a constant menace to a condition that could be easily managed.

But even now, almost 60 years later, gout is still mismanaged and mistreated.1 I am always amazed at how oten I hear stories rom gout suerers about how

their doctors have been unable to nd the right treatment or their condition

and how they’re still suering ater many years. The treatments or gout have

changed very little in the past several decades, yet most doctors still have little

understanding o these treatments. As a result, care varies widely.2



iv | Introduction

A Cautionary Tale

One suerer, Gary, had a particularly dicult time getting his gout properly

treated. It started typically, with pain and swelling in the big toe. Convinced

he had an inection in his oot, Gary visited his doctor. The doctor thought

it might be gout and decided an X-ray would be helpul.

When the results o the X-ray came back, the doctor immediately called

Gary and told him to drop whatever he was doing and go directly to the

nearest emergency room. The radiologist who examined the X-ray believedthe infammation he saw to be a potentially deadly inection o the bone

called osteomyelitis. Gary complied, as anyone would in such a situation. He

spent the next ve days in the hospital, being pumped with antibiotics and

subjected to a battery o tests, ater which the doctors determined that Gary

did, in act, have gout.

Unortunately, Gary’s medical mistreatment didn’t end there. Upon being

discharged rom the hospital he was given little inormation on what to do

about his gout – other than a vague warning to stay away rom seaood and

beer.

Gary continued to have periodic gout attacks that requently landed himin the emergency room. Still, none o the doctors he encountered ever

explained to him the basics o gout care, much less how to properly treat

the attack he was having. Even the emergency room treatment he received

varied rom doctor to doctor. Usually, he was sent home with prescriptions

or colchicine and painkillers and told to ollow up with his general practi-

tioner.

Over time, Gary’s attacks became more requent and more severe. He asked

his doctor i there was anything that could be done. The doctor prescribed

a medication called allopurinol, but at the wrong dose. She never explained

that in 2% o patients serious, even lie-threatening side eects can occur.



Beating Gout | v

She also did not properly ollow up on his care, nor did she prescribe the

proper medication to help prevent additional attacks.

Ater a ew weeks o treatment with allopurinol, Gary vomited violently i he drank the slightest amount o alcohol and soon noticed his skin and eyes

turning yellow. Aware that these signs were not good – and were symptoms

o possible liver ailure – he quickly did some research and ound that al-

lopurinol can, in rare cases, cause liver toxicity. He stopped taking the drug

on his own, and his liver quickly recovered.

Gary returned to his doctor and asked, “What else can I do to stop these

attacks?” His doctor picked up the phone and called a pharmacist. The

pharmacist suggested that the doctor prescribe colchicine, once a day. This

treatment would make attacks less likely; but, as Gary later ound out, is

inappropriate by itsel without also treating the underlying cause o gout.

Gary’s attacks became a little less requent, but they still continued.

Ater several months o taking colchicine, Gary noticed that the big toe on

his right oot had a bulge growing around one o the joints. He also started

having more requent attacks in that joint. His doctor did another X-ray and

the radiologist concluded that it was harmless “sot tissue.”

One day Gary elt another gout attack coming on. Ater experiencing dozens

o attacks he could tell almost immediately that it was going to be a bad one.

He immediately headed to the emergency room just as the pain went rom

bad to unbearable. The doctor never actually came in to see Gary, but pre-

scribed painkillers and sent him home.

When he returned home rom the emergency room, he reeled in pain all

night, suering the most intense agony he had ever experienced in his lie.

He took triple doses o the painkillers while downing colchicine and indo-

methacin (an anti-infammatory) in dangerous quantities. He spent the next

three days with severe diarrhea and vomiting requently while his gout raged

in both eet and his right knee.



vi | Introduction

The medications dulled the pain a little but this attack still lasted three ull

weeks. He was very lucky he did not die o an overdose or interaction rom

the medications he was taking. Ater this incident, Gary resolved to get help

rom an expert.

The sad truth is that Gary’s tale, as bad as it was, is all too common.1 It

seems everyone I meet has a story about a riend or a relative that is still su-

ering rom gout. It doesn’t need to be that way.

So, why is gout so often mismanaged?

In 1836, English writer and clergyman Sydney Smith wrote in a letter to a

riend, “I hope you and Lord Gray are well – no easy thing seeing that there

are above 1,500 diseases to which Man is subject.” Today, the number o

diseases known to modern medicine is well above 1,500.* With such a long

list o maladies, including deadly cancers and heart disease, most doctors pay

little attention to “benign” ailments, such as gout.3

The second actor is that gout aects only about 1% to 2% o the general

population in the developed world;** thereore, most general practitioners

see only a ew cases in a typical practice.4 For these reasons, doctors oten

ail to keep up on the latest research, treatment methods and options.1

The truth, however, is that gout and its underlying disorder, hyperuricemia,

are ar rom benign. Beyond the suering that gout causes, hyperuricemia

has been shown to be associated with a host o secondary diseases that can

signicantly shorten your lie.3

* To get a eel or just how many diseases are known to modern medicine go to: http://www.who.int/classications/icd/en/. This reerence lists every known disease at the time o printing and is stag-geringly long.** The incidence o gout has doubled over the past two decades.



Beating Gout | vii

One recent study ound that only 22% received high-quality care or their

gout and hyperuricemia.5 This book is an eort to change that. My goal is

to provide gout suerers with the inormation they need to obtain the cor-

rect treatment and to make sure they do not end up living out a horror story like Gary’s.

Gary eventually learned how to manage his gout and hyperuricemia. The

growth on his big toe has started to shrink. And most importantly, he has

not had a single gout attack since starting the course o treatment described

in this book. He now knows what to do to stop a gout attack in its tracks.He still occasionally eels some discomort, but even this is declining as his

joints heal. His doctor now properly manages his gout, and he is getting the

appropriate ollow-up care.

This book outlines the proper treatment course and provides useul, practi-

cal inormation or the gout suerer. I have let out much o the theoreticalinormation in avor o practical inormation you can use to improve your

health now. I’ve also taken great pains to cite the research used in this book

so that the curious reader can dig deeper into a topic i they are interested or

to share it with his/her doctor.

Over ve hundred research papers and texts were reviewed and studied or

this book; unortunately, however, the empirical evidence in terms o the

best treatment methods is weak all too oten. Frequently the best inorma-

tion available is simply expert opinion based on years o treating gout but not

backed up by scientic evidence. I have tried to indicate where the evidence

is strong and where it is lacking. Fortunately, in the last ve years or so, new

interest by pharmaceutical companies, along with better technology, has re-

sulted in a resurgence o research into the causes and management o gout

and hyperuricemia as well as its associated conditions. Also, the pace o gout

research seems to be accelerating.



viii | Introduction

How to use this book

The key to beating gout is to become educated about the disease, to under-

stand the treatments, learn how to use them and reduce the risks that this

condition presents.4 This book is designed to help you do just that, and I

have worked hard to ensure that it is as accurate as possible. As with all

medical advice, however, it is not intended to replace consultations with

your doctor, and I cannot guarantee that every bit o inormation in this book

is applicable to your individual case o gout. There are situations where the

treatment o gout and hyperuricemia can be very complicated and even dan-gerous – this is not a do-it-yourself book.

This publication is designed to accompany the treatment rom your doctor.

Where your doctor’s treatment diers rom what this book suggests, you

should politely ask why, as it is possible you have medical considerations

your doctor is aware o that contradict what this book suggests. However,i you nd that your doctor is not up-to-date on the latest gout treatments

and research, politely reer him/her to Appendix C o this book. There,

your doctor will nd reerences to several up-to-date and very inormative

review articles on the latest research relating to the management o gout and

hyperuricemia.

Gout and hyperuricemia can be very serious diseases. They can greatly im-

pact your quality o lie, can be crippling and are linked to many other seri-

ous conditions. Improperly treated gout may even shorten your lie. There

is no cure or gout, but it can and should be managed, allowing you to live

a long, pain-ree lie. Tools that may help you achieve this goal also are

available on this book’s companion web site, http://www.beatinggout.com/, where updates, news and new research ndings will be posted.



C h a P T e r o n e

The Four STageS oF gouT

I gout is not treated properly it can become a crippling disease, damaging or

destroying joints and resulting in constant pain along with requent, intense

and long-lasting acute attacks. Beore we discuss how gout is treated, let’stake a look at what causes the disease and how it progresses i untreated.

Gout is a orm o arthritis, more ormally known as acute gouty arthritis or

crystal-related arthropathy. Unlike rheumatoid arthritis, which is caused by the

immune system attacking the joint itsel and eating away at it, gout is caused

by uric acid crystals that orm within the joints.

Why Do We Get Gout?

A long time ago – somewhere between when our ancestors were still swing-

ing in trees and when they started to walk upright on land – something hap-

pened. Nearly every mammal on earth produces an enzyme called uricase.

This enzyme’s unction is to degrade uric acid, the normal by-product o

the metabolization o chemicals called purines.4,6 At some point, while early

humans were taking their rst tentative upright steps on land, a mutation oc-

curred in their genes, and they stopped producing uricase.7

“When I have gout, I feel as if I am walking on my eyeballs”

— Sydney Smith



2 | The Four Stages of Gout

This lack o uricase didn’t seem to cause too much o a problem or early

man. Without any orm o medicine and only limited intelligence, these

early bipeds survived on a sparse diet and were lucky i they made it past

the age o 40. However, as man evolved urther, developing bigger brains,language, agriculture and civilizations, people began living longer and with

more abundance.

As their diet grew richer, their hair grayer and their lives more sedentary,

nature’s omission o the uricase enzyme came back to haunt them. Initially

this omission aected only the wealthy – those who could aord rich oodsand wine. The consumption o these rich oods (which contain higher con-

centrations o purines) resulted in higher levels o uric acid in their blood.

Alcohol and lack o exercise made things even worse. Gout became the dis-

ease o kings and noblemen.

Over time, as the global economy and wealth grew and complex systems ortransporting ood products were developed, even common people were able

to live with the abundance o the kings o past. Gout could strike anyone,

not just the rich. Thus, gout became more common, and the portion o the

population suering rom this disease continues to grow today.

• • •

Gout occurs in our stages. Not all cases progress to the nal stage, but i let

unmanaged, many do.

The Four Stages of Gout:

1. Asymptomatic Hyperuricemia2. Acute Attacks

3. Intercritical Periods

4. Advanced Gout



Beating Gout | 3

Asymptomatic Hyperuricemia

Having high levels o uric acid in your body without experiencing any symp-

toms is called asymptomatic hyperuricemia. Gout will only develop in peo-

ple who have had asymptomatic hyperuricemia or years or even decades.8

Today, somewhere between 5% and 30% o people living in the developed

world are hyperuricemic.6 However, having hyperuricemia does not guaran-

tee that you will get gout; it only predisposes you to it. About 20% o people

with this condition go on to develop gout.2,6,9

Hyperuricemia is sometimes caused by a genetic abnormality in the body’s

metabolic system that causes it to produce more uric acid than normal. Or,

much more commonly, hyperuricemia is caused by a genetic abnormality

that makes the kidneys less able to remove uric acid rom the body. The

kidneys are very good at ltering uric acid, but about 90% o it still gets

reabsorbed back into the blood beore leaving the kidneys.4 Oten peoplecan be both “over-producers” and “under-excretors” o uric acid, resulting

in exceptionally high levels. This makes gout more requent and painul, as

well as more dicult to manage.

This chapter discusses the direct eects o untreated gout, but untreated

hyperuricemia may pose many more health problems. There are a host o disorders associated with hyperuricemia that are much more dangerous than

gout. Researchers are just starting to put the pieces o hyperuricemia and

these other conditions together, and a rightening picture is developing. In

Chapter Four we will discuss hyperuricemia, its causes and the diseases that

scientists are now beginning to link with this condition.




Acute Attacks

Uric acid dissolves in

blood serum (the liquid

part o blood), other

body fuids and sot tis-

sues. In people with

hyperuricemia, uric acid

concentrations rise to a

level where it becomesa super-saturated so-

lution,10 meaning that

more uric acid is dis-

solved in the body than

is normally possible.

An acute gout attack oc-

curs when these body

fuids can no longer

sustain this super-satu-

ration and urate crystals

begin to orm, like ice crystals that orm in reezing water.*

These crystalscan orm anywhere in the body, but during a gout attack they develop in the

synovial fuid - the liquid that lls the gap between the bones o the joints.11

The body’s immune system quickly detects these newly appearing urate crys-

tals and assumes they are diseased cells or inection. In response, white blood

cells are sent in to attack the invaders; but when they try to devour them, thelarge rigid crystals burst the cells, just like popping balloons. As the white

blood cells die, they release proteins telling the immune system that the

* Technically, urate is the salt orm o uric acid. However, uric acid and urate are very oten usedinterchangeably. For the purpose o making things as clear as possible in this book, I will reer touric acid in a dissolved state such as in the blood as uric acid, and will call it urate when it is in acrystal orm.

Photo 1: This photo shows the swelling and red-ness o podagra. ©1972-2004 American College o Rheumatology Clinical Slide Collection. Used withpermission.



Beating Gout | 5

cell has lost its ght with

the invader and reinorce-

ments should be sent in.

The released proteins also

cause an increase in the

acidity o the fuid o the

joint. This makes condi-

tions more avorable or

even more urate crystalsto orm. The immune

system responds by send-

ing in more white blood

cells and by causing in-

fammation. More white

blood cells are killed by the urate crystals, causing

even more proteins to be

released and more crystals

to orm. This process per-

petuates itsel, creating a

runaway infammatory re-

sponse that directly causes

the extreme pain o a gout

attack.12

Most men are stricken with their rst gout attack between the ages o 30-60,

and most women are aected only ater reaching menopause,2,14 with gout

being 5 to 8 times more common in men than women.4 An acute gout at-

tack typically starts with the rapid development o severe pain in the joint

that reaches a peak within 6 to 12 hours. Tenderness, swelling and redness

around the aected joint 18 are also typical symptoms o an attack. In severe

attacks, ever and chills may also be present.1,9,15

Figure 1: The rst metatarsophalangeal joint o theoot (arrow) is the most common joint or early gout attacks. Sixty percent o rst gout attacks strike inthis joint.




A rst attack o gout oten occurs in the middle o the night and usually only

strikes one joint. However, as the disease progresses, attacks may become

more requent and can involve multiple joints.8,15 Eventually the infamma-

tion process o an attack will run its course and the pain subsides on its ownater a ew days, but severe attacks can last weeks.4

The classic and very oten-quoted description o an acute gout attack was

written by the 17th century clinician Thomas Sydenham: “The regular gout

seizes in the ollowing manner – The patient goes to bed and sleeps quietly

until about two in the morning, when he is awakened by a pain which usually seizes the great toe, but sometimes the heel, the cal o the leg or ankle. The

pain resembles that o a dislocated bone… [The pain] grows gradually more

violent every hour, and comes to its height toward evening [and is sometimes

similar to] the gnawing o a dog and sometimes a weight and constriction o the

parts aected, which become so exquisitely painul as not to endure the weight

o the clothes nor the shaking o the room rom a person’s walking…”

Sixty percent o rst gout attacks aect the second joint rom the tip o the big

toe. (This is known as the rst metatarsophalangeal joint; see gure 1). An at-

tack in this joint is also known as podagra*.7 Gout can aect any joint in the

body, but it is most common in the joints in the oot, ollowed by those in

the ankles, hands, wrists, knees and elbows.7,9

Historically, gout o the hips and spine was thought to be rare, but one re-

cent study ound that gout in the spine might be requently misdiagnosed.16

Another interesting nding is that articial joints are not immune to gout

and can be the target o an attack.17

The list o reasons why asymptomatic hyperuricemia develops into gout is

long; it is usually dicult to identiy the exact cause in each case. Regard-

less, once a gout attack has occurred, additional attacks become much more

likely.3 About 60% o people who have had their rst attack will have an-

* Podagra comes rom the Greek word ‘pous’, ‘pod-‘ that means ‘oot’ and ‘agra’ that means ‘seizure.’



Beating Gout | 7

other attack within a year.7 However,

some patients do not have another at-

tack or years ater their rst, while an

even smaller portion never experiencea second attack.4,19

In some people with hyperuricemia,

uric acid may crystallize in the sot

tissues o the body and develop into

what is called a tophus.13

Tophi (plu-ral or tophus) are masses o urate

crystals that can orm anywhere in the

body, even the heart *, but most com-

monly appear around the joints o the

arms and legs and the outer rim (he-

lix) o the ear (See Photo 2).

9

In what is called atypical gout, tophi can occur

without a person ever having a single

gout attack or having experienced at-

tacks with much more mild, diuse

pain. Atypical gout is oten misdiagnosed as other orms o arthritis and is

much more common in women than men.

Intercritical Periods

The time between acute attacks is known as the intercritical period.1 The

individual’s uric acid levels are still high, and another attack can occur at any

time. Even though there are no symptoms, damage may still be occurring.

One study ound that 70% o people with gout had detectable urate crystalsin their joints during these intercritical periods.18 These urate crystals are

like sand in the joints, doing damage with each movement. Another study

ound that 25% o people reported eeling pain or discomort during inter-

critical periods, lowering their quality o lie.20,21

* Though very rare, tophi in the heart can be very dangerous.

Photo 2: A photo o a person with tophion the helixes o the ear, a common loca-tion or tophi. ©1972-2004 AmericanCollege o Rheumatology Clinical SlideCollection. Used with permission.




Over time, the requency, duration and intensity o gout attacks usually in-

creases. Attacks become longer and more painul, while attacks involving

multiple joints become more common.22

During intercritical periods, tophi may be orming. These deposits o urate

crystals can grow to be very large. I tophi are close to the skin or grow large

enough they may eventually break (ulcerate) or kill the skin (necrosis), allow-

ing chalky white or yellow urate crystals to ooze out. These ulcerations may

also become inected, causing additional problems.7,9 Usually tophi orm in

the cooler parts o the body but they can orm anywhere, even in the heart and

other internal organs, potentially resulting in lie-threatening conditions.

As time passes and more gout attacks occur, bony changes called “punch-

out lesions” start to orm around the joint. These lesions usually grow andharden over time, limiting the fexibility o the joint.8 Eventually punch-

out lesions can use together, totally immobilizing the joint. The presence

o large tophi and punch-out lesions is sometimes called intermediate gout.

These changes typically signal a person’s progression to the last stage o gout

known as advanced gout.

Photo 3: A photo o the hands o a person with advanced gout. Note the bulgesaround the joints caused by chronic swelling and tophi. ©1972-2004 American Col-lege o Rheumatology Clinical Slide Collection. Used with permission.



Beating Gout | 9

Advanced Gout

Advanced gout is dened as constant pain stemming rom years o urate crys-

tals degrading the joints. Joints are damaged and even destroyed completely

by these crystal deposits and the accompanying constant infammation andlesions. Along with this come requent, long-lasting and painul multi-joint

gout attacks. Joint damage is clearly visible on X-rays, and there are usu-

ally multiple, large tophi throughout the body.8 At this point, extensive and

permanent damage has occurred and cannot be reversed. Treatment or

advanced gout can only slow additional damage and reduce the occurrence

o additional acute attacks.

• • •

P a i n

A s y

m p t o m a t i c

H y p

e r u r i c e m i a

I n t e r c r i t i c a l P e r i o d

I n t e r c r i t i c a l P e r i o d

Acute Attacks

Advanced Gout

Time

Figure 2: Over a period o years, gout attacks become more requent and painul.

Eventually, once enough damage is done, the pain continues even between attacks.

The Progression of Gout23




As mentioned in the introduction, this was the normal course o the disease

until 1950 and the discovery o the drug probenecid. Despite the act that,

today, gout is still oten mismanaged, the good news is that gout is now a

well-understood disease, and there are many tools or treating it. With athorough understanding o how the disease progresses and what can be done

to stop it, gout dam-

age can be reversed

well beore it reaches

the advanced stage.

I hyperuricemia

is caught early and

properly managed,

any developing to-

phi can actually start

to dissolve back intothe blood as uric

acid, where it will be

removed by the kid-

neys.24 Crystals that

have ormed in the joints also will dissolve, and the damage they caused can

start to heal.19 In the coming chapters, this book will provide you with the

inormation you need to manage hyperuricemia, reduce or eliminate acute

gout attacks, and reverse the progress o this disease.

As mentioned earlier, the dangers o gout do not end here. Unmanaged

hyperuricemia is even more dangerous than gout itsel. Chapter Four will

cover the diseases associated with hyperuricemia and the dangerous health

risks they pose.

Photo 4: A photo o a patient’s hand with advanced gout.

The tophi growing below the skin are starting to destroy the skin above them (a condition known as skin necrosis).This skin opening can easily become inected. ©1972-2004 American College o Rheumatology Clinical SlideCollection. Used with permission.

gout chapter1

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