CASE PRESENTATION
ON GOUT
PRESENTED BY:
SOFIA TASNEEM
PHARM D III YEAR
170620882027
INTRODUCTION:
DEFINATION:
Gout involves hyperuricemia, recurrent attacks of acute arthritis with monosodium
urate (MSU) crystals in synovial fluid, deposits of MSU crystals in tissues in and
around joints (tophi), interstitial renal disease, and uric acid nephrolithiasis.
Gout is the most common inflammatory joint disease in men and is strongly age
related.The prevalence and burden of gout has increased over recent decades.
It is caused by the deposition of monosodium urate crystals within articular and
periarticular tissue.
PATHOPHYSIOLOGY:
Uric acid is the end product of purine degradation. An increased urate pool in
individuals with gout may result from overproduction or underexcretion.
Overproduction of uric acid may result from abnormalities in enzyme systems that
regulate purine metabolism (eg, increased activity of phosphoribosyl
pyrophosphate [PRPP]synthetase or deficiency of hypoxanthine-guanine
phosphoribosyl transferase [HGPRT]).
Uric acid may be overproduced because of increased breakdown of tissue nucleic
acids. Cytotoxic drugs can result in overproduction of uric acid due to lysis and the
breakdown of cellular matter.
Two thirds of uric acid produced daily is excreted in urine.
The remainder is eliminated through gastrointestinal (GI) tract after degradation by
colonic bacteria. Decline in urinary excretion to a level below rate of production
leads to hyperuricemia and increased pool of sodium urate.
ETIOLOGY: RISK FACTORS:
DIAGNOSIS:
Definitive diagnosis requires aspiration of synovial fluid from the affected joint and
identification of intracellular crystals of MSU monohydrate in synovial fluid
leukocytes.
When joint aspiration is not feasible, a presumptive diagnosis is based on
presence of characteristic signs and symptoms, as well as the response to
treatment.
European League Against Rheumatism (EULAR) recommends a diagnosis based
on the classical features of gout such as podagra, tophi and rapid response to
colchicine.
Modern imaging techniques, such as ultrasound and dual-energy computed
tomography, can also be used to assist in diagnosis. Gout and septic arthritis may
co-exist and to exclude septic arthritis, synovial Fluid is sent for Gram staining and
culture
COURSE OF DISEASE:
The course of gout follows a number of stages; initially, the patient may be
asymptomatic with a raised SUA level.
TREATMENT:
GOALS OF TREATMENT:
TREATMENT FOR ACUTE GOUT:
Nonpharmacologic Therapy :Local ice application is the most effective adjunctive
treatment. Dietary supplements (eg, flaxseed, celery root) are not recommended.
Pharmacologic Therapy:Most patients may be treated successfully with
nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or colchicine.
NSAIDs have excellent efficacy and minimal
toxicity with short-term use. Indomethacin,
naproxen, and sulindac have Food and Drug
Administration (FDA) approval for gout, but
others are likely to be effective.
Corticosteroid efficacy is equivalent to NSAIDs;
they can be used systemically or by
intra-articular (IA) injection. Systemic therapy is
necessary if an attack is polyarticular.
Colchicine is highly effective in relieving acute
gout attacks; when it is started within the first 24
hours of onset, about two thirds of patients
respond within hours. Use only within 36 hours of
attack onset because the likelihood of success
decreases substantially if treatment is delayed.
IL-1β is critically associated with the inlammatory
response induced by monosodium urate crystals
Canakinumab is a fully humanised monoclonal
antibody against IL-1β.
TREATMENT FOR CHRONIC GOUT AND HYPERURICAEMIA CONDITION:
Nonpharmacologic Therapy:
Patient education should address the recurrent nature of gout and the objective of each
lifestyle/dietary modification and medication.
Promote weight loss through caloric restriction and exercise in all patients to enhance renal urate
excretion.
Alcohol restriction is important because consumption correlates with gout attacks. ACR
guidelines recommend limiting alcohol use in all gout patients and avoidance of any alcohol
during periods of frequent gout attacks and in patients with advanced gout under poor control.
Dietary recommendations include limiting consumption of high-fructose corn syrup and
purine-rich foods (organ meats and some seafood) and encouraging consumption of vegetables
and low-fat dairy products.
Evaluate the medication list for potentially unnecessary drugs that may elevate uric acid levels.
Gout is not necessarily a contraindication to use of thiazide diuretics in hypertensive patients.
Low-dose aspirin for cardiovascular prevention should be continued in patients with gout
because aspirin has a negligible effect on elevating serum uric acid.
Pharmacological therapy:
After the first attack of acute gout, prophylactic pharmacotherapy is recommended if
patients have two or more attacks per year, even if serum uric acid is normal or only
minimally elevated. Other indications include presence of tophi, chronic kidney
disease, or history of urolithiasis.
Urate-lowering therapy can be started during an acute attack if anti-inflammatory
prophylaxis has been initiated.The goal of urate-lowering therapy is to achieve and
maintain serum uric acid less than 6 mg/dL (357 µmol/L), and preferably less than 5
mg/dL (297 µmol/L) if signs and symptoms of gout persist.
Urate lowering should be prescribed for long-term use. Serum urate can be reduced
by decreasing synthesis of uric acid (xanthine oxidase inhibitors) or by increasing
renal excretion of uric acid (uricosurics).
Xanthine oxidase inhibitors are recommended first-line therapy; the uricosuric agent
probenecid is recommended as alternative therapy in patients with a contraindication
or intolerance to xanthine oxidase inhibitors.
In refractory cases, combination therapy with a xanthine oxidase inhibitor plus a drug
with uricosuric properties (probenecid, losartan, or fenofibrate) is suggested.
Pegloticase may be used in severe cases in which the patient cannot tolerate or is not
responding to other therapies.
Preventing gout flare when initiating urate lowering therapy:
When prophylactic treatment is commenced, there is a risk of precipitating an acute
gout attack, or ‘mobilisation flare’, for approximately 12 months. Mobilisation flares are
thought to be caused by the rapid decrease in serum urate after the initiation of a
ULT. When ULT therapy is commenced it is very important that additional medicines
are co-prescribed to prevent precipitating an acute flare.
Colchicine is the agent of first choice to prevent the precipitation of a flare when
commencing chronic gout treatment. Low doses of colchicine (500 micrograms orally
twice a day or once a day) should be prescribed and continued for at least 6 months.
NSAIDs If there are no contraindications to the use of NSAIDs, they may be
considered second line to colchicine in patients who are intolerant to colchicine.
NSAIDs should be continued for a maximum of 6 weeks, and gastric protection
should be provided.
Corticosteroids Intramuscular steroid injections (methylprednisolone acetate 80–120
mg) or low-dose oral prednisolone (<10 mg prednisolone/day) may sometimes be
used to prevent the precipitation of a lare on initiation of ULT for gout
SOAP FORMAT:
Subjective data:
The patient, a 45-year-old male, came to the clinic complaining of sudden onset
severe pain and swelling in his right big toe. He reported that the pain started last
night and has progressively worsened since then. He rated the pain as 9/10 on the
pain scale. The patient also reported that he has been feeling generally unwell for
the past few days, with low-grade fever and fatigue.He has no past medical history
and no family history and no known drug allergies are found.patient was found
taking IBUPROFEN for pain relief and PARACETAMOL for fever.
Objective data:
On examination, the patient's right big toe was erythematous, swollen, and tender to touch.
There was no warmth or discharge noted. The range of motion of the joint was limited due to
the pain. The patient's vital signs were within normal limits.the patient right big toe was found
to be erythematous,swollen,tender,no discharge and limited movement was seen.
Abnormalities were found to be:
Abnormality found in Abnormal range Normal range
WBC count 13,000 per m/l 4500-11,000 per m/l
Platelet count 5,00,000 per m/l 1,50,000-4,50,000 per m/l
Neutrophils 65% 40-60%
ESR 18 mm/hr 0-15 mm/hr
CRP 10 mg/dl 0.8-1 mg/dl
Serum uric acid 8.0 mg/dl 3.4-7.2 mg/dl
Assessment:
PAIN and SWELLING: The pain associated with gout is caused by the buildup of uric acid crystals
in the joints. These crystals can cause inflammation and irritation, leading to pain, swelling, and
stiffness in the affected joint(s).
FEVER: temperature of the body rises due to infection.
HIGH WBC COUNT: This is because gout is an inflammatory condition and can cause the body to
produce more white blood cells to fight off the inflammation.
HIGH ESR RATE: This is because gout is an inflammatory condition and can cause the body to
produce more proteins that make red blood cells clump together and settle more quickly in a test
tube.
HIGH CRP LEVELS:This is because gout is an inflammatory condition and can cause the body to
produce more CRP to fight off the inflammation.
HIGH SERUM URIC ACID:Serum uric acid levels can increase due to a variety of factors, including
diet, genetics, medications, and underlying health conditions. Foods that are high in purines, such
as red meat, organ meats, and seafood, can increase uric acid levels in some people.
Based on the objective and subjective data the final diagnosis was found to be
GOUTY ARTHRITIS
Plan :
Brand name Generic ROA Dose Frequency Category Indication
name
Inj PAN Pantoprazole IV 40 mg OD Proton pump Acid reflux
inhibitor disease
Tab CAMBER Cholchicine PO 0.6 mg Every hour Anti gout agent To treat gout
Tab Naproxen PO 500 mg BD NSAID To treat pain
NAPROSYN
Tab Allopurinol PO 100 mg OD Urate lowering To decrease
ZYLOWELL agent serum uric acid
[hyperuricaemia]
Discharge medications:
1. Tab PAN - 40 MG- OD X 5 DAYS
2. Tab COLSHINE - 0.6 MG TID X 5 DAYS
3. Tab NAPROSYN - 500 MG BD X 5 DAYS
4. Tab ZORZOR - 100 MG OD X 5 DAYS
Drug interactions:
1. Cholchicine + naproxen / Allopurinol: gastrointestinal bleeding
2. Pantoprazole + naproxen / allopurinol: may increase risk of kidney damage.
Pharmacist intervention:Prescription was found to be rational. Minor drug interactions were
found but, frequency and dose was adjusted. Definite diagnosis was not performed for gout.
Patient counselling:
About disease: Gout is a type of arthritis that occurs when uric acid crystals accumulate in the
joints, causing pain, swelling, and inflammation. Uric acid is a waste product that is produced by
the body when it breaks down purines, which are naturally occurring substances found in many
foods.
When uric acid levels are too high, the excess uric acid can form crystals that accumulate in
the joints, leading to gout. Gout typically affects the big toe, but it can also affect other joints
such as the ankle, knee, wrist, and elbow.
About medication:
● Pantoprazole should be taken before a meal, usually once daily, as prescribed by
doctor.
● Cholchicine can be taken with or without food, but it's important to take it exactly as
prescribed by doctor.
● Naproxen can be taken with or without food, but it's usually recommended to take it with
food to help prevent stomach upset.
● Allopurinol should be taken with food or immediately after a meal to help reduce the risk
of stomach upset.
● It's important to take these medications at the same time each day to maintain
consistent levels in the body.
Life style modifications:
There are several lifestyle modifications that can help manage gout symptoms and reduce
the risk of future gout attacks.
Maintaining a healthy body weight: Being overweight or obese can increase the risk of
gout, so it's important to maintain a healthy body weight through a balanced diet and
regular exercise.
Limiting alcohol consumption: Alcohol can increase uric acid levels in the blood, so it's
important to limit or avoid alcohol consumption, especially beer and hard liquor.
Drinking plenty of water: Staying hydrated can help flush excess uric acid out of the body,
so it's important to drink plenty of water and other fluids throughout the day.
Eating a balanced diet: A diet rich in fruits, vegetables, whole grains, and lean proteins
can help reduce the risk of gout and promote overall health.
Avoiding high-purine foods: Foods high in purines, such as red meat, organ meats, and
seafood, can increase uric acid levels in the blood, so it's important to limit or avoid these
foods.
Exercising regularly: Regular exercise can help maintain a healthy body weight and
improve overall health, which can help reduce the risk of gout.
Managing stress: Stress can trigger gout attacks, so it's important to manage stress
through relaxation techniques such as deep breathing, meditation, or yoga.
THANKYOU
