ENGLISH PAPER

THE CORRELATION BETWEEN OSTEOARTHRITIS AND OBESITY

KHRISNA PARAMAARTHA
030.09.130

FACULTY OF MEDICINE
TRISAKTI UNIVERSITY

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PREFACE

Assalaamualaikum Wr. Wb.

Firstly, I really thanks to God Allah S.W.T. This English paper had been finished at the
perfect time. This assignment had been made as a requirement to pass the English lesson in this
6th semester in Faculty of Medicine Trisakti University.
Second of all, I would like thanks to my parents, my oldest brother and oldest sister for
their love and support and also to dr. Hendarto Natadidjojo, MARS Sp.PD as my supervisor for
his guidance and some critics to my articles so that I can finished it easily. For all my friends, I
really appreciate their great time to accompany me and discuss the materials of the articles as
long as I had difficulties in making this article.
Last but not least, I realize to accomplish this assignment is far away from being perfect
because of lack of my knowledge and grammatically language, so that I really need constructive
critics to make it better. And hopefully this article is worth for all.
Wassalaamualaikum Wr. Wb.

Jakarta, Mei 2012

Khrisna Paramaaratha
030.090.130

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ABSTRACT

Osteoarthritis is usually considered to be a joint disorder the central pathological feature

of which is cartilage destruction. However, this concept has evolved, and today osteoarthritis is
generally regarded as a disease that may affect the whole joint (bone, muscles, ligaments and
synovium). Although the aetiology of osteoarthritis is not established, the main risk factors are
well known and commonly include mechanical, biochemical and genetic factors. Of these risk
factors, obesity is beyond doubt considered a prominent one.
A total of 1854 people aged 2476 years in 1994 participated in a Norwegian study on
musculoskeletal pain in both 1994 and 2004. Participants with OA or rheumatoid arthritis in
1994 and those above 74 years in 1994 were excluded, leaving n = 1675 for the analyses. The
main outcome measure was OA diagnosis at follow-up based on self-report. Obesity was defined
by a body mass index (BMI) of 30 and above.
At 10-years follow-up the incidence rates were 5.8% (CI 4.37.3) for hip OA, 7.3% (CI
5.79.0) for knee OA, and 5.6% (CI 4.27.1) for hand OA. When adjusting for age, gender, work
status and leisure time activities, a high BMI (> 30) was significantly associated with knee OA
(OR 2.81; 95%CI 1.325.96), and a dose-response relationship was found for this association.
Obesity was also significantly associated with hand OA (OR 2.59; 1.086.19), but not with hip
OA (OR 1.11; 0.412.97). There was no statistically significant interaction effect between BMI
and gender, age or any of the other confounding variables.

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Infants and young children are prone to developing upper respiratory tract infections,
which often result in bacterial complications such as acute otitis media. We evaluated 623 upper
respiratory tract infection episodes in 112 children (635 months of age) to determine the
proportion of upper respiratory tract infection episodes that result in acute otitis media. Of all
upper respiratory tract infections, 30% were complicated by acute otitis media. The rate of acute
otitis media after upper respiratory tract infection declined with increasing age (1) .
Children aged < 1 year and those who attended day care centers had a greater risk of
acquiring upper respiratory tract infection and otitis media, compared with older children and
those who were cared for at home (2) . Risk for acute otitis media may be reduced substantially by
avoiding frequent exposure to respiratory viruses (eg,avoidance of day care attendance) in the
first year of life or home care can be provided for children until at least 1 year of age (1) .
Kidney stones are increased in patients with inflammatory bowel disease (IBD),
particularly those who have had resection of part of their gastrointestinal tract. These stones are
usually calcium oxalate, but there is a marked increase in the tendency to form uric acid stones,
as well, particularly in patients with colon resection. These patients all share a tendency to
chronic volume contraction due to loss of water and salt in diarrheal stool, which leads to
decreased urine volumes. They also have decreased absorption, and therefore diminished urinary
excretion, of citrate and magnesium, which normally act as inhibitors of calcium oxalate
crystallization. Patients with colon resection and ileostomy form uric acid stones, as loss of
bicarbonate in the ileostomy effluent leads to formation of an acid urine. This, coupled with low
urine volume, decreases the solubility of uric acid, causing crystallization and stone formation..
Enteric hyperoxaluria (EH) leads to supersaturation of urine with respect to calcium oxalate, in
conjunction with low volume, hypocitraturia and hypomagnesuria. Then another possible role in
kidney stone formation may caused by infrequency of colonization with Oxalobacter formigenes
in IBD.

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TABLE OF CONTENT
Chapter I

: Introduction

Chapter II

: Inflammatory Bowel Disease

II.1

: Definition

. 6

II.2

: Causes

.. 6

II.3

: Symptoms

.. 7

II.4 : Physical Examination

II. 5
Chapter III

.. 8

: Pathophysiology

.. 9

: Kidney stones

. 12

III.1 : Definition

. 12

III.2 : Causes

. 12

III.3 : Symptoms and sign

. 13

III.5 : Diagnosis

14

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Chapter IV

: The Correlation between kidney stones and IBD

16

Chapter V

: Conclusion

20

21

References

INTRODUCTION
Osteoarthritis (OA) is a degenerative joint disease, occurring primarily in older person,
characterized by erosion of the articular cartilage, hypertrohy of bone at the margins,
subchondral sclerosis, and a range of biochemical and morphologic alterations of the synovial
membrane and joint capsule.
Gout occurrences in certain individuals may be attributed to their kidney conditions. Uric acids
found in purines are generally excreted out of the system and are not expected to be totally
absorbed by the body. Their levels are not wholly dependent in the amounts of purine rich food
that body takes in.
It is also dependent on the ability of the kidney to excrete uric acids out of the system.
Failure to excrete may cause them to amass and reach the high-level point when uric acid
crystals form and cause gout pains. Hence, there is an existing relationship between gout and
kidney stones.

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The kidney's ability to excrete is affected by the formation of kidney stones. If the
kidneys become impaired, excretion then poses a problem of retaining too much uric acid in the
blood stream.
As uric acid amasses it will reach a certain level where in they will crystallize and lodge
themselves in an individual's joint where they will not be bothered. Hence, gout and kidney
stones forge a relationship by the failure of the kidney to excrete uric acids and the ability of
them to form into crystals that causes gout.

Chapter I
GOUT
1.1 Definition(1,3)
Gout is a common disorder of uric acid metabolism that can lead to deposition of
monosodium urate (MSU) crystals in soft tissue, recurrent episodes of debilitating joint
inflammation, and, if untreated, joint destruction and renal damage. Gout is definitively
diagnosed based on the demonstration of urate crystals in aspirated synovial fluid.

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Today, the term gout is used to represent a heterogeneous group of diseases found
exclusively in the human species that include:
-

An elevated serum urate concentration (hyperurecemia)

Recurrent attacks of acute arthritis in which monosodium urate crystals are demonstrable
in synovial fluid leukocytes.

Aggregates of sodium urate deposited chiefly in and around joints, which sometimes lead
to deformity and crippling.

Renal disease involving glomerular,tubular, and interstitial tissues and blood vessels

Uric acid neprolithiasis.

1.2 Epidemiology(1,2)
The incidence of gout varies in populations, with an overall prevalence of less than 1 to
15.3 percent and appears to be increasing. The prevalence seems to increase substantially with
age and increasing serum urate concentration. The annual incidence rate of gout is 4.9 percent
for urate levels greater than 9 mg/dL, 0.5 percent for values between 7 and 8.9 mg/dL, and 0.1
percent for values less than 7 mg/dL.

1.3 Etiology(4)
Gout develops in the setting of excessive stores of uric acid in the form of monosodium
urate. Uric acid is an end-stage by-product of purine metabolism. Lacking uricase, humans
remove uric acid primarily by renal excretion. When excretion is insufficient to maintain serum
urate levels below the saturation level of 6.8 mg/dL (with some variability depending on
temperature and pH), hyperuricemia may develop, and urate can crystallize and deposit in soft
tissues. Ninety percent of patients with gout develop excess urate stores due to an inability to
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excrete sufficient amounts of normally produced uric acid in the urine (underexcretion). The
remaining patients either overconsume purines or produce excessive amounts of uric acid
endogenously (overproduction).
The origin of hyperuricemia divided two types
Primary hyperuricemia
A. Increased production of purine

Secondary Hyperuricemia
A. Increased catabolism and turnover of purine

- Idiopathic

- myeloproliferative disorders

- specific enzyme defect (eg lesch nyhan - lymphoproliferative disorders

Syndrome,glycogen storage disease)
- psoriasis
B. Decreased renal clearance of uric acid
B. Decresed renal clearance of uric acid

(idiopathic)

1. Intrinsic kidney disease

2. Functional impairment of tubular transport
- drug induced (thiazide,probenecid)
- hyperlacticacidemia

1.4 Pathophysiology.(5,7)
Although the presence of urate crystals in the soft and synovial tissues is a prerequisite
for a gouty attack, the fact that urate crystals can also be found in synovial fluid in the absence of
joint inflammation suggests that the mere presence of intrasynovial urate crystals is not sufficient
to

cause

flares

of

gouty

arthritis.

One explanation for this may lie in the observation that clumps or microtophi of highly
negatively charged and reactive MSU crystals are normally coated with serum proteins
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(apolipoprotein [apo] E or apo B) that physically inhibit the binding of MSU crystals to cell
receptors. A gout attack may be triggered by either a release of uncoated crystals (eg, due to
partial dissolution of a microtophus caused by changing serum urate levels) or precipitation of
crystals in a supersaturated microenvironment (eg, release of urate due to cellular damage). From
either source, naked urate crystals are then believed to interact with intracellular and surface
receptors of local dendritic cells and macrophages, serving as a danger signal to activate the
innate immune system.
This interaction may be enhanced by immunoglobulin G (IgG) binding. Triggering of
these receptors, including Toll-like receptors, NALP3 inflammasomes, and the triggering
receptors expressed on myeloid cells (TREMs) by MSU, results in the production of interleukin
(IL)1, which in turn initiates the production of a cascade of pro-inflammatory cytokines,
including IL-6, IL-8, neutrophil chemotactic factors, and tumor necrosis factor (TNF)alpha. (6)
Neutrophil phagocytosis leads to another burst of inflammatory mediator production.
Subsidence of an acute gout attack is due to multiple mechanisms, including the clearance of
damaged neutrophils, recoating of urate crystals, and the production of anti-inflammatory
cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)beta.

1.5 Signs and symptoms(3)

In complete development of its natural history,gout passes through four stages.
1. Asymptomatic Hyperuricemia
Asymptomatic hyperuricemia is a situation in which the serum level is high, but gout as
manifested by arthritic symptoms,tophi, or uric acid nephrolithiasis has not appeared.
2. Acute Gouty Arthritis.
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A single joint is involved in about 85 to 90 percent of first attack, with the first
metatarsophalangeal joint being the most commonly affected site. Criteria For the classification
for acute Gouty Arthritis are
More than one attack of acute arthritis.
Unilateral attack involving tarsal joint.
Maximal Inflammation developed within one suspected tophus
day
attack of monoarticular arthritis
Joint redness observed

Hyperuricemia
Asymmetric swelling

within

joint

(radiograph)
First metatarsophalangeal joint painful or Subcortical cysts without erosions (radiograph)
swollen.
Unilateral

attack

involving

metatarsophalangeal joint

first negative

culture

microorganisms

of
during

joint
attack

fluid
of

for
joint

inflammation.
3. Intercritical Gout.
The terms intercritical gout have been applied to the periods between gouty attacks.
Roentgenographic changes may develop during the intercritical period despite no sign of tophi
on physical examination. These changes are more likely in those with more severe hyperuricemia
and more frequent acute attacks.
4. Chronic Tophaceus Gout.
The time from the initial attack to beginning of chronic symptoms or visible tophaceus
involvement highly variable in studies of untreated patients. Tophaceus gout is consequence of
the chronic inability to eliminate urate as rapidly as it is produced. As the urate pool expands,
deposits of urate crystals appear in cartilage, synovial membranes, tendons, soft tissues, and
elsewhere. The rate of tophus formation also increases with the severity of the renal disease.
Tophaceus deposits may produce irregular, asymmetric, moderately discrete tumescence of
fingers, hands, knees or feet. The process of tophaceus are insidiously. The tophi are relatively
painless, acute inflammation can occur around them at times. Extensive destruction of the joints

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and large subcutaneous tophi may lead to grotesque deformities, particularly of the hands and
feet, and to progressive crippling.

1.6 Diagnostic Procedures(4)

A. Sign and Symptom
Acute gouty arthritis is characterized by its sudden onset, frequently nocturnal, either
without apparent precipitating cause or following rapid fluctuations in serum urate levels. The
metatarsohalangeal joint of the great toe is the most susceptible joint (podagra), although others.
The involved joints are swollen, and exquisitely tender and the overlying skin tense, warm, and
dusky red. Fever is common and may reach 39oC. tophi may be found in the external ears, hands,
feet, and olecranon and prepatellar bursae. They usually develop years after the intial attacks of
gout.
Asymptomatic periods of months or years commonly follow the initial acute attack. After
years of recurrent severe monoarthritis attacks of the lower extremities and untreated
hyperuricemia, gout can evolve into a chronic, deforming polyarthritis of upper and lower
extremities that mimics rheumatoid arthritis.
B. Laboratory Findings
The serum uric acid is elevated (> 7.5 mg/dL) in 95% of patients who have serial
measurement during the course of an attack. Identification of sodium urate crystals in joint fluid
or material aspirated from tophus establishes the diagnosis. The crystals, which may be
exracellular or found within neutrophils, are needle like and negatively birefringent when
examined by polarized light microscopy.
C. Imaging
Early in the disease, radiographs show no changes. Later, punched out erosions with an
overhanging rim of cortical bone (rat bite) develop. When these are adjacent to a soft tissue
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tophus, they are diagnostic of

gout.
Plain radiograph showing chronic
tophaceous gouty arthritis in the
hands.

Plain radiograph showing typical changes of gout in the first

metatarsophalangeal joint and fourth interphalangeal joint.

1.7 Treatment(4)
1. Asymptomatic Hyperuricemia
Asymptomatic hyperuricemia should not be treated, uric acid lowering drugs need not be
instituted until arthritis, renal calculi, or tophi become appearent

2. Acute Gouty Arthritis

Arthtiris is treated first and hyperuricemia weeks or month later. The medication for
Acute Gouty arthritis are
-

NSAIDs
These drugs are the treatment of choice for acute gout. Indomethacin has been the most

frequently used agent, but all of the other newer NSAIDs are probably equally effective.
Indomethacin is initiated at dosage of 25-50 mg orally every 8 hours and continued until the
symptoms have resolved. Active peptic ulcer, impaired renal function, and history of allergic
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reaction to NSAIDs are contraindications. For patients at high risk for upper gastrointestinal
bleeding, COX 2 inhibitor may be appropriate first choice for management of an acute gout
attack.
-

Colchicine.
Neiher oral nor intravenous colchicines is any longer recommended for the treatment of

acute gout flares. The use of oral colchicine during intercritical period to prevent gout attacks
is discussed below.
-

Corticosteroids
Corticosteroids often give dramatic symptomatic relief in acute episodes of gout and will

control most attacks. They are most useful in patients with contraindications to the use of
NSAIDs. If the patients gout is monoarticular, intra articular administration (eg
triamcinolone, 10-40 mg depending on the size of the joint) is most effective. For
polyarticular gout, corticosteroids may be given intravenously (eg metylprednisolone, 40
mg/d tapered over 7 days) or orally (eg prednisolone 40-60 mg/d tapered over 7 days).
3. Intercritical Gout
Treatment during symptom free periods is intended to minimize urate deposition in
tissues, which causes chronic tophaceous arthritis, and to reduce the frequency and severity of
reccurences
- Diet
Potentially reversible causes of hyperuricemia are high purine diet. Foods with high
purine content are.

Low purine foods

High purine foods

Refined cereals product, milk products, eggs, All meat, including organ meats and seafood,
fruits, lettuce,tomatoes, water, butter, green yeast, beer, beans, peas, oatmeals, spinach,
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vegetables

(except

spinach, asparagus,cauliflower, mushrooms

asparagus,cauliflower, mushrooms)
A high liquid intake and more importantly, a daily urinary output of 2 L more will aid urate
excretion and minimize urate precipitation in urinary tract.
- Allupurinol
The xanthine oxidase inhibitor allupurinol promptly lowers plasma urate and urinary uric
acid concentrations and facilities tophus mobilization. The initial daily dose of allupurinol is 300
md/d for patients who have normal renal function and who are taking prophylactic colchicine. In
the absence of prophylactic colchicine, the initial dose should be 100 mg/d orally. The dose of
allupurinol can be increased in a week if needed to achieve the desires serum uric acid level
5.0 mg/dL. Successful treatment usually requires a dose of 300-400 mg of allupurinol daily.the
maximum daily dose is 800 mg. allupurinol can be used in renal disease, but the dose must be
reduced to decrease the chance of side effects.
4. Chronic Tophaceus Gout
With rigorous medical compliances, allupurinol shrinks tophi and in time can lead to their
disappearance. Resorption of extensive tophi requires maintaining a serum uric acid below 5
mg/dL, which may be achievable only with concomitant use of allupurinol and a uricosuric
agent. Surgical excision of large tophi offers mechanical improvement in selected deformities

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Chapter II
UROLITHIASIS
2.1 Definition(15)
Urolithiasis are small.hard deposits that form inside the kidneys. Urolithiasis are made of
mineral and acid salts. Urolithiasis have many causes, in common, urolithiasis form when the
urine becomes concentrated, allowing minerals to crystallize and stick together.
2.2 Epidemiology(9)
The lifetime prevalence of urinary tract stone disease in the United States is
approximately 10%. The annual incidence of urinary tract stones in the industrialized world is
estimated to be 0.2%. The likelihood that a white male will develop stone disease by age 70
years is 1 in 8. Stones of the upper urinary tract are more common in the United States than in
the rest of the world. Roughly two million patients present on an outpatient basis with stone
disease each year in the United States, which is a 40% increase from 1994.
2.3 Etiology(15)
Urolithiasis often have no definite, single cause. A number of factors, often in
combination, create the condition in which susceptible people develop urolithiasis. Urolithiasis
form when the components of urine, fluid and various minerals and acids are out of balance.
When this happens, the urine contains more crystal forming substances, such as calcium, oxalate,
and uric acid, than the available fluid can dilute
Most kidney stones contain crystals of more than one type. Types of kidney stones
include:
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- calcium stones
Most kidney stones are calcium stones, usually in the form of calcium oxalate. High
oxalate levels can be found in some fruits and vegetables for example nuts. Dietary factors, high
doses of vitamin D, intestinal bypass surgery and several different metabolic disorders can
increase the concentration of calcium or oxalate in urine. Calcium stones may also occur in the
form of calcium phosphate.
-Struvite stones.
Struvite stones form in response to an infection, such as a urinary tract infection. Struvite
stones can grow quickly and become quite large.
- Uric acid stones
Uric acid stones can form in people who are dehydrated, those who eat a high protein diet
and those with gout. Certain genetic factors and disorders of the blood producing tissues also
may predispose to uric acid stones.
- Cystine stones
These stones represent only in a small percentage of kidney stones. They form in people
with a hereditary disorder that causes the kidneys to excrete excessive amounts of certain amino
acids (cystinuria).
2.4Pathophysiology (8)
The first phenomenon is supersaturation of the urine by stone-forming constituents,
including calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which
ions from the supersaturated urine form microscopic crystalline structures. The overwhelming
majority of renal calculi contain calcium. Uric acid calculi and crystals of uric acid, with or
without other contaminating ions, comprise the bulk of the remaining minority. Other, less
frequent stone types include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and
various rare stones related to precipitation of medications in the urinary tract. This is likely the
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underlying cause of uric and cystine stones, but calcium-based stones (especially calcium oxalate
stones) likely have a more complex etiology.
The second etiology, which is most likely responsible for calcium oxalate stones, is
deposition of stone material on a renal papillary calcium phosphate nidus, typically a Randall
plaque. Evan et al (2007) recently proposed this model based on evidence accumulating from
several laboratories. Calcium phosphate precipitates in the basement membrane of the thin loops
of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal
papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually
erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate
gradually deposit on the substrate to create a urinary calculus. Randall plaques are always
composed of calcium phosphate.
2.5 Sign and symptom(15).
Obstructing urinary stones usually present with colic. Pain usually occurs suddenly. It is
localized to the flank, is usually severe, and may be associated with nausea and vomiting.
Patients are constantly moving, in sharp contrast to those with an acute abdomen. The pain may
occur episodically and may radiate anteriorly over the abdomen. As the stone progresses down to
the ureter, the pain may be referred into ipsilateral testis or labium. If the stone becomes lodged
at the ureterovesicular junction, patients will complain of marked urinary urgency and frequency.
2.6 Diagnostic(15)
The diagnosis of urolithiasis entails several component questions: is a stone present, does
it cause some degree of obstruction, exactly where is located, and is its chemical
composition.once again, the history may furnish what amounts to almost conclusive evidence for
the presence of a renal stone, if it provide the story of typical renal colic, associated perhaps with
dysuria, nausea and vomiting. Once elicited, the story of renal colic is unforgettable and
unmistakable. Fever, chills and leukocytosis represent concomitant infection. The urine may
contain any or all of the following: albumin (usually from trace 2+), red blood cells, white blood
cells and occasionally granular or hyaline casts.

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Physical examination may elicit costovertebral tenderness, especially on local percussion.

During, and even after, an acute attack of renal colic, hyperesthesia of the skin may be detectable
over appropriately reffered area. Exact localization of renal stones is of course best demonstrated
by x ray visualization. More often, however better diagnostic results are obtained both with these
and with radioluscents stones by intravenous injection of radiopaque dyes for intravenous
pyelography(IVP).
Direct chemical analysis of a stone passed spontaneously or obtained at operation offers
conclusive evidence concerning its chemical composition. Thus visualization of stones on an
abdominal scout film suggests that calcium is one of there component, since this is the most
likely, if not the only, radiopaque material found within the kidneys or ureters. Thus, in the case
of stones originating in gout, oxalosis, or cystinosis, appropriate analyses of 24 hours urine will
reveal significantly increased amounts of uris acid, oxalic acid or cystine, respectively.
Determining chemical composition of renal stones serves two main functions:
- it may furnish us with insight into etiological and pathogenic mechanism contributing to their
formation.
- as a corollary, this information may guide us in the management of such cases.
2.7Treatment(15)
In general terms, the management of the patient suffering from renal stones is directed
toward removing, if possible, the underlying cause of their formation, as well as the stones
themselves. Eliminating the underlying cause of stone formation, although we are broadly
familiar with the biochemical mechanism (gout,oxalosis, and cystinosis), we are presently unable
to correct these processes and thus to eliminate the underlying cause of the stone formation.
However some dietary and pharmalogical measures may be helpful. Thus the reduction of uric
acid precursor foods and the use of uricosuric agents may reduce the incidence of urate stones in
gout.
Treatment for renal stones varies, depending on the type of stone and the cause.
1. Treatment for small stones with minimal symptoms
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drinking water as much as 2 to 3 quarts (1.9 to 2.8 liters) a day may help flush out the
urinary system.

Pain relievers, passing a small stone can cause some discomfort. To relieve mild pain, the
doctor recommended pain relievers such as ibuprofen, acetaminophen, or naproxen
sodium
2. Treatment for larger stones and those that cause symptoms.
Kidney stones that cant be treated with conservative measure, either because thay are
too large to pass on their own or because they cause bleeding, kidney damage or ongoing
urinary tract infections, may require more invasive treatment. Procedures include:

using sound waves to break up stones

A procedure called extracorporeal shock wave lithotripsy uses sound waves to create

strong vibrations called shock waves that break the stones into tiny pieces that are then
passed in urine. The procedure creates a loud noise and cause moderate pain, so it may be
under sedation. Extracorporeal shock wave lithotripsy can cause blood in the urine, bruising
on the back or abdomen, bleeding around the kidney and other adjacent organs, and
discomfort as the stone fragments pass through the urinary tract.
- Surgery to remove very large stones in the kidney
A procedure called percutaneous nephrolithotomy involves surgically removing a kidney
stone through a small incision in a back. This surgery may be recommended if extracorporeal
shock wave lithotripsy has been unsuccessful or if the stone is vey large

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Chapter III
THE CORRELATION BETWEEN GOUT AND UROLITHIASIS

Gout is a systemic metabolic disease in which several forms of nephropathy can occur (10).
The most frequent type of gout-related nephropathy

(11,12)

is urolithiasis (10%20%), and its

prevalence is much higher than observed in the general population.

Risk Factors(13)
Uric acid urolithiasis primarily occurs in patients with no obvious abnormality in uric
acid metabolism.however, upon closer examination, many posses a combination of findings that
together favor stone formation. These include relatively high serum uric acid levels,
comparatively low urinary pH, and low fractional excretion of urate

Pathophysiology. (13)
Uric acid results as a relatively insoluble end product of purine metabolism. The
concentration of uric acid in plasma depends on dietary ingestion, de novo purine synthesis and
uric acid elimination by the renal and intestine. Uric acid is a weak acid, with an ionization
constant of acid (pK) of 5.8. at pH levels below pK, uric acid is predominantly found in a
nonionized form. The urate ion is more soluble than the nonionized molecule. Urate ions
(predominant form at a pH level 7.4) are about 5% protein. Urate is filtered at the glomerulus.
The renal tubule can reabsorb (movement of urate from tubule lumen to peritubuler fluid) or
secrete (movement of urate from peritubuler fluid into tubular lumen) urate. When the
concentration of uric acid in urine exceeds its solubility at the urine pH, uric acid changes from a
compound dissolved in solution to an insoluble precipitate. Urate stones are formed by one of

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three general mechanisms: overproduction, increased tubular secretion, or decreased tubular

reabsorption.
Sign and Symptom.(3,15)
Usually uric acid urolithiasis occurred in chronic tophaceus gout stage, which tophaceus
gout is consequence of the chronic inability to eliminate urate as rapidly as it is produced. As the
urate pool expands, deposits of urate crystals appear in cartilage, synovial membranes, tendons,
soft tissues, and elsewhere. The rate of tophus formation also increases with the severity of the
renal disease.
Tophaceus deposits may produce irregular, asymmetric, moderately discrete tumescence
of fingers, hands, knees or feet. The process of tophaceus are insidiously. The tophi are
relatively painless, acute inflammation can occur around them at times. Extensive destruction of
the joints and large subcutaneous tophi may lead to grotesque deformities, particularly of the
hands and feet, and to progressive crippling.
Obstructing urinary stones usually present with colic. Pain usually occurs suddenly. It is
localized to the flank, is usually severe, and may be associated with nausea and vomiting.
Patients are constantly moving, in sharp contrast to those with an acute abdomen. The pain may
occur episodically and may radiate anteriorly over the abdomen. As the stone progresses down to
the ureter, the pain may be referred into ipsilateral testis or labium. If the stone becomes lodged
at the ureterovesicular junction, patients will complain of marked urinary urgency and frequency.

Diagnostic.(14)
Exact localization of renal stones is of course best demonstrated by x ray visualization.
Uric acid stones are nonopaque on radiologic examination. More often, however better
diagnostic results are obtained both with these and with radioluscents stones by intravenous
injection of radiopaque dyes for intravenous pyelography(IVP).

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Treatment.(15)
Increasing the solubility of the various chemicals associated with the stone formation is
accomplished first by forcing the ingestion water, leading to the formation of dilute urine. In
addition, changes in the acidity or alkalinity of the urine are produced by appropriate agents, in
accordance with whether the substance under consideration is more soluble in acid or in alkaline
solution. Sodium bicarbonate can be used as the alkalizing agent, but potassium citrate is usually
preferred because of the availability of slow-release tablets and the avoidance of a high sodium
load. The dosage of the alkalizing agent should be adjusted to maintain the urinary pH between
6.5 and 7.0.
Urinary pH of more than 7.5 should be avoided because of the potential deposition of
calcium phosphate around the uric acid calculus, which would make it undissolvable. Both uric
acid and cystine calculi form in acidic environments.. If the uric acid levels is high, allupurinol
(300 mg/d) may be given. Uric acid urolithiasis can be treated with purine dietary restrictions or
allupurinol therapy (or both).
The primary indications for surgical treatment include pain, infection, and obstruction.
Additionally, certain occupational and health-related reasons exist.

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Chapter IV
CONCLUSION

Gout is a disorder that is related to excess production and deposition of uric acid crystals.
Uric acid is the byproduct of purine nucleotide catabolism. Gout passes through four stages, are
Asymptomatic Hyperuricemia, Acute Gouty Arthritis, Intercritical Gout, Chronic Tophaceus
Gout.
Chronic tophaceous gout results after a number of years in an untreated individual.
Episodes of acute gouty arthritis become more frequent and severe and the intercritical period
may disappear completely. This stage of the disease is characterized by the deposition of solid
urate (tophi) in the articular (cartilage covering the bony ends of the articulating joints) and other
connective tissues. The continued development of tophi results in destructive arthropathy
(disease of a joint).
Aside from gouty arthritis and tophus formation, renal disease is the most frequent
complication of hyperuricemia. Kidney disease in patients with gout is of numerous types. Urate
nephropathy is the result of the deposition of monosodium urate crystals in the renal interstitial
tissue. Uric acid nephropathy is caused by the deposition of uric acid crystals in the collecting
tubules, renal pelvis or the ureter and results in impaired urine flow. Calcium oxalate urolithiasis
also occurs in hyperuricemic patients. Uric acid urolithiasis (uric acid kidney stones) accounts
for approximately 10% of all urinary calculi (stones) in the US.
Urinary pH of more than 7.5 should be avoided because of the potential deposition of
calcium phosphate around the uric acid calculus, which would make it undissolvable. Both uric
acid and cystine calculi form in acidic environments.. If the uric acid levels is high, allupurinol
(300 mg/d) may be given. Uric acid urolithiasis can be treated with purine dietary restrictions or
allupurinol therapy (or both).The primary indications for surgical treatment include pain,
infection, and obstruction. Additionally, certain occupational and health-related reasons exist.

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