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Dr. Lau-Cam slides set 4 Gout
Terms in this set (194)
The disease of the rich and affluent. Disease of the kings
What is gout description
A complex form of chronic arthritic disease having a metabolic basis and characterized by high levels of uric acid (hyperuricemia) in the blood and by inflammation and severe pain in the joints and surrounding tissues
Variably defined as a blood uric acid level greater than 6.0 mg/dL in women and 6.8 mg/dL in men.
Gout and uric acid
In humans it is an end product of the metabolism of compounds known as purines, which is eventually eliminated in the urine.
As pf 2011 there is how many cases of gout
8.3 million cases (4% of population) in USA
What percentage of the population is hyperuricemics
In USA 43.3 million hyperuricemics (21% of population) with men women
Gout is more common in
adult men than in premenopausal women (3.3:1); after menopause incidence gets closer. Prevalence among the black population is 2x of that among the white population
Three major causes of Gout
Increased production of uric acid (UA)
Decreased urinary excretion of UA
Increased production + decreased urinary excretion of UA
Risk factors for gout may include
Family members with gout
Alcohol abuse (hard liquor, beer)
Eating foods rich in purines
Using medicines such as: diuretics, aspirin, cyclosporine, levodopa
Supplementation with niacin.
Meats (beef, fish, chicken, organ)
Co-morbidities (diabetes, hypertension, atherosclerosis, hyperlipidemia, chronic kidney disease)
UA is a
weak acid, with an ionization constant (pKa) of 5.8.
At pH levels below the pKa
UA is found in a nonionized form
Urate ion is more soluble than
the nonionized (UA) molecule
Urate ions (predominant form at a pH of 7.4)
are about 5% protein bound
Urate is filtered by the
glomerulus as part of urine. The renal tubule can reabsorb urate from the tubular lumen into the peritubular fluid or secrete urate from the peritubular fluid into the tubular lumen.
Of the amount of urate passing through the glomerulus
up to 100% is reabsorbed by the proximal tubule.
Of the amount of urate secreted by the tubules
up to ~50% is reabsorbed back into the peritubular fluid, more in acid than alkaline pH (blood levels reflect this difference). Hence, lower renal clearance with acid urine
As a result, 8-12% of urate passing through the kidney is
present in the urine at the end of one day.
At physiological pH, UA
circulates in the body as monosodium urate (MSU)
About 70% of body UA is
excreted by the kidney into the urine ~0.7 g/day
MSU transported from blood into the urine
a) through glomerulus = filtration process or (b) across proximal tubular cells with the help of protein transporters, e.g. UAT, ABCG2, OAT4 = secretion process
URAT1, SLC22A12 and other proteins
can also transport urate back into the blood = reabsorption process, thus regulating blood urate levels
Since UA is not very soluble in water
alkaline urine facilitates its excretion as MSU. Conversely, a low pH urine favors the less soluble UA form. An amount of UA within the tubules exceeding the solubility limit of UA can lead to the precipitation of UA within the tubules as stones.
UA renal stones can clog the tubules
, raise the luminal pressure, and cause mucosal and glomerular damage (bleeding, necrosis, renal failure). Also found in urether and bladder. Generic name for UA stones = urolithiasis. Renal failure due to UA stone = UA nephropathy.
Renal elimination of uric acid
Renal tubular transport systems for urate
Proximal tubule cells
Kidney stones in minor and major calyces of the kidney
kidney stone in the ureter
Renal necrosis in advanced gout
Stages of gout
There is hyperuricemia., there may be tissue deposition of MSU but
no overt symptoms of gout. The deposition of MSU, however, is causing damage
Deposits of MSU crystals in the joint(s) cause acute inflammation. A flare is characterized by pain, redness, swelling, and warmth lasting days to weeks. Pain may be mild or excruciating. Most initial attacks occur in lower extremities. A typical signs is inflammation in the metatarsophalageal joint of the great toe (podagra) , which is presen in~ 50% of people with gout. About 80% of gouty people will get it at some point. UA may be normal in about half of patients with an acute flare. In the elderly there may be many joints affected.
Occur after an acute flare has subsided and the gout becomes clinically inactive until the next flare. Since the hyperuricemia persists, deposition of MSU crystals in tissues continues and may result in damage. Intercritical segment beccome shorter as the disease progresses.
It is characterized by chronic arthritis, with soreness and aching of joints. Person may also get tophi (lumps of urate crystals deposited in soft tissue)—usually in cooler areas of the body (e.g., hand, elbows, ears, distal finger joint, ankle).
Gout one chronic disease best described by 4 stages
Progression of GOUT
Gout pain graph
Acute attack of gout characteristics
rapid onset of joint pain associated with swelling and erythema due to the inflammatory response to the presence of urate crystals in the joint.
Sx of acute attack of gout
peak within 12 - 24 hours after the beginning of an attack.
The majority of people with acute attack of gout will
seek treatment due to pain, however, if untreated, most attacks will spontaneously resolve in 7-10 days.
Some people will go on to have reccurent
acute attacks (flare ups) with an asymptomatic period between attacks (referred to as the intercritical gout).
Untreated frequent gout attacks
can lead to tophus formation, the number increasing with time.
Serum UA levels ideally should not be
measured during an acute attack of gout, as 11-49% of people may have a misleadingly normal level.
Mild chronic tophaceous gouty arthopathy
Severe CTGA example
The inflammatory reaction of gout is a direct
consequence of too much UA in the blood
At physiological pH UA circulates
in an ionized (salt form) known as monosodium urate (MSU).
Neutrophils and macrophages are attracted to a joint (synovium, synovial fluid)
by chemokines, infiltrate the tissue, and start to phagocyte MSU
MSU can activate inflammatory cells (macrophages, neutrophils)
by interacting with surface Toll -like receptors and relaying a signal to activate nuclear transcription factors that will mediate the phagocytosis of MSU as well as the production of proinflammatory agents such as free radicals, H2O2, cytokines (IL-1β, IL-6, IL-10, IL-18, TNF-), PGE2, and nitric oxide (NO), which is is also produced by chondrocytes and synovial cells and released along with chemokines into the synovial surroundings o cause pain, swelling and damage, and to attract new phagocytic leukocytes.
Lysosomes release hydrolases into the cytosol
of the phagocytic cell host cell that further amplify the inflammatory reaction
The spiral of GOut
Immune reaction to gout
Inflammation of the big toe
Individual with gout on side of foot
Needles of monosodium urate (MSU)
Detailed image of the process of gout formation
How gout medications work
Diet and gout
Purine content of common food iteams
Purine content in order of high to moderate
Risk factors for gout diagram
There are 5 classes of drugs according to a specific purpose (or scenario)
prevent new attacks
Treat symptoms (pain, inflammation)
Lower UA production
Promote enzymatic conversion of UA to allantoin
Promote renal elmination of UA
Treat symptoms of pain and inflammation
) -NSAIDs naproxen, ketoprofen, ibuprofen, indomethacin; corticosteroids methylprednisolone, prednisone; and colchicine
Prevent new attacks
lower UA production
xanthine oxidase inhibitor (XOI) allopurinol, febuxostat
Promote enzymatic conversion of UA to allantoin
Promote renal elimination of UA
uricosuric agents specifically approved in USA (probenecid, sulfinpyrazone) or used on an off-label basis due to intrinsic uricosuric action (fenofibrate, losartan)
Patients with frequent flares need to be treated with drugs;
otherwise the pain gets worse, there may be loss of joint function, and eventual joint and soft tissue damage by deposits of MSU.
Treatment of inflammation of gout
NSAIDS = aspirin, naproxen, ketoprofen, indomethacin, ibuprofen, sulindac, celecoxib
Glucocorticoids = hydrocortisone, prednisone, methylprednisolone
Treatment of hyperuricemia of gout
Xanthine oxidase inhibitor = allopurinol, febuxostat Uric acid metabolizer = uricase
Uricosuric = probenecid, sulfinpyrazone, losartan, fenofibrate
Molecular targets for the treatment of gout
An example of a sulfa compound
Probenecid effect of renal excretion
- It can block the tubular secretion of many common drugs, thus increasing their plasma concentration and prolong -ing their action(NSAIDS, methotrexate, penicillin, cephalosporin, sulfas, lorazepam, aciclovir, gancyclovir, zidovudine). Used in penicillin treatment as an adjunct to increase plasma penicillin levels.
- Filtered by the glomerulus, secreted in proximal tubule and reabsorbed in the distal tubule
To treat chronic gout and acute gouty arthritis, to prevent gout attack.
Available as tablets, 250 mg, 500 mg (Benemid®, Probalan®). It may increase frequency of attacks of gout during first 6-12 months of use but eventually it will prevent them. It is recommended to used it in combination with colchicine early in the course of therapy to avoid precipitating an attack of gout, which may occur in up to 20% of gouty people treated with probenecid alone (Colbenemid®, Proben-C®). Drink lots of fluid to minimize risk of renal stones. Take with food or antacid.
Gout 250 mg bid for 1 week, then increase to 500 mg bid to 2-3 g/day maximum; penicillin treatment 500 mg q.i.d. For penicillin/cephalosporin treatment it is usually given at 500 mg q.i.d.
Probenecid side effects
About 5-10% users develop nausea, heartburn, flatulence or constipation. Also mild pruritic rash, drug fever, and renal disturbance.
Effect decreased by high doses of aspirin (>2 g/day) and renal insuffi-ciency. It will increase the plasma levels of indomethacin, ketoprofen, naproxen, ketorolac, methotrexate, penicillin or cephalosporin when used concurrently by lowering their renal clearance.
B) MSU crystals deposited in joints, kidneys and soft tissues,
C) Local inflammation
First line treatment for GOut attack is
A recommended regimen for gout attack is
naproxen 500 mg, repeated after 8 - 12 hours, then twice daily on the following day, tapering the dose as the attack resolves.
Alternative NSAIDS choices for gout attack are:
diclofenac, indometacin, ketoprofen celecoxib, tenoxicam and sulindac.
Use a corticosteroid (CST) if the patient is unable to
to tolerate colchicine, NASAID and joint infection is excluded, only one joint is involved, or NSAIDs or colchcine is inappropriate because of GI bleeding, severe ulcer of kidney disease. Given orally, IV or locally (intrarticularly). Examples are hydrocortisone, dexamethasone, triamcinolone, methylprednisolone, and prednisolone.
A recommended regimen for CST is
oral prednisone 20 - 40 mg daily, gradually reduced over 10 -14 days. Intraarticular injections of CST can be used if one or two joints are affected, e.g. trimcinolone acetonide (Kenacort-A), with the dose dependent on the size of the affected joint.
If a NSAID or corticosteroid is not appropriate for gout attack
low dose colchicine may be used, specially if its is taken early in the attack (within 12 hr).
Toxic plant product, originally extracted from Colchicum
autumnale (the autumn croccus) corms/seeds.
Control of pain and inflammation of acute attacks of gout. No effect on uric acid synthesis or urinary excretion
Available as tablets, 0.5 and 0.6 mg (Colcrys®)
Usual initial dose is 1.0-1.2 mg at first sign, followed by 0.5 -0.6 mg ea. 1 hr or 1.0-1.2 mg ea. 2 hr until pain subsides or feeling of GI discomfort or diarrhea ensues. Maximum dose in 1 hr is 1.8 mg and in 24 hr is 2.5-4.8 mg.
Although pain and swelling abate by 12 hr and disappear by 24 hr, it is not regarded as an analgesic agent like NSAIDs.
Colchicine prophylactic use
Can abort (prevent) an attack if taken at the first sign of the attack. Dose is 0.5-0.6 mg q.d. up to 3-4 times per week (<1 attack/yr). Some may require 2-3 times more. For those 16 yr or older with >1 attack/yr, take 0.5 or 0.6 mg q.d. or b.i.d. throughout the year.
Rapid oral absorption, excreted unchanged in urine and stools. Avoid use if renal creatinine clearance is low (10-30 mL/min).
MOA colchicine on gount exact mechanism
of action has not been established. It may prevent the inflammatory reaction that follows the engulfment of MSU crystals by cells of the innate immune system (neutrophils, macrophages) which eventually release proinflammatory agents like IL-1β, matrix metalloproteinases and NO.
MOA colchicine on gout due to capacity to
block microtubule assembly in neutrophils and other inflammatory cells, it decreases phagocytosis and transport of MSU crystals into the lysosome.
MOA colchicine on gout Also inhibits the release
of chemotactic factors from neutrophils, inhibits the extracellular signal needed for the activation of neutrophils exposed to MSU crystals, and reduces the adhesion and recruitment of neutrophils and macrophages to the inflamed joint
MOA colchicine on gout also approved for use
familial Mediterranean fever (FMF) in children 4 years of age or older and adults. Very rare and hereditary. Symptoms usually begin at 5-15 yrs. There is abdominal, joint and chest pain due to inflammation, along with high fevers that usually peak in 12 to 24 hr. Attacks may vary in severity of symptoms. Patients are usually symptom-free between attacks. Recommended doses for the control of the inflammation or to prevent an attack are:
Children 4-6 years old: 0.3 to 1.8 mg daily; children 6-12 years old: 0.6 to 1.8 mg daily
Adults and adolescents >12 years: 1.2 to 2.4 mg daily
It has a narrow therapeutic index, with no clear-cut distinction between nontoxic, toxic, and lethal doses. High fatality rate was reported after acute ingestions exceeding 0.5 mg/kg. The lowest reported lethal doses of oral colchicine are 7-26 mg. Colchicine's toxicity is an extension of its mechanism of action - binding to tubulin and disrupting the microtubular network. As a result, affected cells experience impaired protein assembly, decreased endocytosis and exocytosis, altered cell morphology, decreased cellular motility, arrest of mitosis, and interrupted cardiac myocyte conduction and contractility. The culmination of these mechanisms leads to multi-organ dysfunction and failure. Colchicine poisoning should be suspected in patients with access to the drug and the typical toxidrome (gastroenteritis, hypotension, lactic acidosis, and prerenal azotemia).
AE of colchine in decreasing oreder of severity
Bone marrow depression with aplastic anemia, granulocytosis, leukopenia or thrombocytopenia if used for a long time. Can increase risk of infection and bleeding
Peripheral neuritis (numbness of fingers or toes), purpura, myopathy (muscle pain, weakness), alopecia, unusual bleeding or bruising, and reversible azoospermia have also been reported.
Vomiting, diarrhea, nausea and stomach pains, especially when maximal doses are used. To avoid more serious toxicity, discontinue its use when these symptoms appear, regardless of whether or not joint pain has been relieved.
Dermatoses have been reported. Hypersensitivity reactions may occur infrequently. Can increase serum liver enzymes.
Use with caution in hepatic, renal or cardiovascular disease
It arrests cell division at mitosis and lowers spermatogenesis in humans and animals.
Pharmacological action decreased by acidifying agents and increased by alkalinizing agents.
Use of a xanthine oxidase inhibitor
They block the last 2 steps in purine metabolism to UA by inhibiting the enzyme xanthine oxidase (XO).
Use of a xanthine oxidase inhibitor Drugs
Allopurinol and febuxostat
Use of a xanthine oxidase inhibitor
To prevent attacks of gout by lowering blood UA levels
xanthine oxidase inhibitor also used when there is
Overproduction of uric acid.
- Frequent gout attacks.
- Presence of tophi
- Failure of other drugs to adequately reduce uric acid levels.
- An allergy to or severe side effects by uricosuric agents
- Poor renal function.
- History of uric acid kidney stones
The dose of xanthine oxidase inhibitors
may need to be lowered for people who have chronic kidney disease.
Purine metabolism to uric acid
Xathine oxidase inhibitors
Purine compound structurally related to hypoxanthine and xanthine:
- Metabolized to oxypurinol by XO within 2 hr of its intake. Both allopurinol and oxypurinol bind to Mo in the Mo-pterin component of XO, thus preventing XO from converting hypoxanthine and xanthine to uric acid.
Allopurinol Other actions
It also blocks enzymes involved in purine synthesis.
Acute attacks of gout, erosive destructive gouty joint disease, tophi, gouty kidney disease, and uric acid stones.
Available as oral tablets ,100 and 300 mg and as powder for injection, 500 mg (Zyloprim®, Aloprim®)
Average dose = 200-300 mg/day for mild cases, 400-600 mg for moderate to severe cases. Doses >300 mg given in divided doses. Minimum dose is 100 mg/day and maximum is 800 mg/day.
Allopurinol treatment approach
- Started at a low dose (100 mg/day)which can be increased weekly by 100 mg to achieve a low serum UA level (5-6 mg/dL). Best taken with food to prevent gastric irritation. Also drink plenty of water/fluids while taking the drug to prevent formation of kidney stones
- Fall in serum UA in 2-3 days, but full effect in 1-3 weeks
Allopurinol side effects
Hypersensitivity syndrome (fever, skin rash, itching, hives)
Swelling of face, lips, mouth, tongue or throat
GI disturbance (upset stomach, nausea, diarrhea, anorexia)
Can increase the blood levels of mercaptopurine, azathio-prine sand theophylline since it prevents their metabolic degradation.
Action of drugs from purine to excretion
MOA of allopurinol diagram
Recomnended treatment algorithm for the dosing of allopinol in patients with gout
Pharmacueical interventions for acute gout
pharmaceutical interventions for chronic gout
Uloric® tablets, 40 and 80 mg
Nonpurine selective inhibitor of XO, used to lower high serum uric acid. Recommended for those not tolerating allopurinol. Can be used along colchicine or NSAIDs.
- Noncompetitive inhibitor of XO directed at the Mo-pterin active site of the enzyme. Stronger affinity for XO than oxypurinol (Kd <0.1 nM vs Kd =0.5 nM).
Febuxostat Advantage over allopurinol
- More potent and more effective in lowering serum UA, but more expensive. No need to adjust dose in those with renal problems. Taken once a day (vs. twice a day with allopurinol).
Average dose 40 or 80 mg/day. Better to start with 40 mg and, if not satisfactory after 2 weeks, then increase to 80 mg
Febuxostat side effects
Nausea, diarrhea, joint pain, headache, gout flares, and rash. It causes a higher incidence of liver function abnormalities than allopurinol
Can increase blood levels of azathioprine, mercaptopurine and theophylline by reducing their metabolic breakdown
Febuxostat vs allopurionl serum urate
Nondrug-related approaches for controlling gout patient
education on diet, lifestyle, treatment objectives,
and management of co-morbidities is a recommended core therapeutic measure in gout.
Nondrug-related approaches for controlling gout Limit consumption
of diet rich in purines, saturated fats, calories
Limit consumption of proteins , which lower urine pH
Life style changes to Nondrug-related approaches for controlling gout
drink 8-16 cups (2-4 L) fluid/day with at least one-half being water to promote renal excretion (pale yellow)
Limit intake of red meats, organs, fish (seafood) and chicken to 4-6 oz (113-170 g)/day
Reduce intake of alcohol, especially beer (rich in purines), in men to 2 drinks/day, in women to 1 drink/day
Lose weight - obesity increases risk of gout
Allopurinol Average dose
100mg intial, 200-300 mg to 400-600mg/day maintenance
Allopurinol oral Bioavailability
allopurinol 1-2 hr
oxypurinol 15-30 hr
Allopurinol Protein binding
1.5 hr allopurinol, 4.5 hour oxypurinol
hepatic 80% to oxypurinol
urine, mostly as oxypurinol;
oxyurinol can undergo tubular reabsorptio like UA feces around 20%
Thiazole average dose
40 or 80mg
Thiazole oral bioavailability
Thiazole Protein binding
mainly conjugation with glucuronic acid;
some bu CYP 450
Urine, mostly as metabolites (49%)
feces mostly as metabolites (45%)
Uricosuric agents type of drug
Lower blood uric acid (UA) by promoting its renal excretion and preventing its tubular reabsorption.
Uricosuric agents MOA
Due to the higher acid nature of probenecid (pKa = 3.4) and sulfinpyrazone (pKa = 2.8) than UA (pKa = 5.8) they bind in preference to UA to organic acid transporters located in the proximal tubule and which reabsorb UA back into the blood [e.g., organic acid transporter (OAT), soluble carrier (SLC) or uric acid transporter (URAT)]. As a result, UA tends to stay in the urine and to decrease in the blood.
Uricosuric agents Importance
Their use has decreased considerably since they are ineffective in patients with poor renal function (creatinine clearance of less than 20-30 mL/min) and are contraindicated in patients with urate nephropathy or who are UA overproducers
A derivative of phenylbutazone, an NSAID, capable of
blocking the proximal tubular reabsorption of uric acid.
To treat chronic gout and acute gouty arthritis, to prevent gout attack.
Filtered by the glomerulus, secreted in proximal tubule and reabsorbed in the distal tubule
Tablets, 100 mg; capsules 200 mg (Anturane®), taken b.i.d. If necessary, the dose can be increased to a maximum of 200 mg b.i.d. Take medication with plenty of fluid to minimize risk of renal stones; and with foods, milk or antacids to minimize GI irritation (can worsen a peptic ulcer). Can be used with colchicine.
Sulfinpyrazone side effects
Similar to those of probenecid
Should not be used in persons with renal impairment or showing a high rate of uric acid excretion. Aspirin in a high dose (>3 g/day) can interfere with its uricosuric effect.
Therapeutically impoortant drug-UA interactions at renal tubules
Role of a high daily dose of aspirin in the renal elimination of uric acid
It is well established that the daily intake of a large dose of aspirin (>3 g/day) can enhance the urinary excretion of uric acid.
Role of daily low doses of aspirin in the renal elimination of uric acid
A study by Caspi et al. (Arthr. Rheum., 2000) examined the effect of low doses of aspirin (<0.5 g/day) and equal to 75, 150 and 325 mg/day. It was determined that at the lowest dose, aspirin caused a 15% reduction in uric acid elimination, an effect that was decreased proportionally to the increase in aspirin dose. In another study in elder patients, a 100 mg dose of aspirin reduced the elimination of uric acid by 4%.
Role of other drugs in the renal elimination of uric acid
All diuretics, ethambutol and pyrazinamide behave like a low dose of aspirin, namely as antiuricosurics
Approved in USA (2010) for use in severe refractory chronic gout (RCG) when other drugs have failed
- It is a porcine-like uricase made by recombinant DNA technology and further modified by the addition of polyethylene glycol (PEG) to increase its half-life from 8 hr to 10-12 days and to decrease its immunogenicity because of its foreign nature.
- It catalyzes the conversion of UA to allantoin, a compound that is 5-10x more soluble than UA and, hence, less likely to precipitate in the body. It can help to eliminate tophi
- Krystexxa® injection (given by IV infusion)
Pegloticase side effects
The most common side effects are gout flare-ups or attacks (usually at beginning of treatment), infusion reactions, nausea, bruising, sore throat, constipation, chest pain, severe allergic reactions (anaphylaxis, 5%), and vomiting.
Recombinant nonglycosylated form of the human IL-1 receptor antagonist (IL-1Ra) modified by the addition of one methionine at its N-terminus.
By acting as a IL-1β receptor antagonist it blocks the binding of IL-1β released by inflammatory cells (neutrophils, monocytes, macrophages) to its receptors, thus preventing the inflammation of gouty arthritis
Prefilled syringes containing 100 mg/0.67 mL (Kineret®). When taken s.c. for 3 days it can suppress the inflammation of gout or chronic tophaceous gout by at least 50% within 48 hr. It can be given at 100 mg s.c. for 2 weeks together with colchicine, probenecid and prednisolone to treat tophaceous gout.
Sulfinpyrazone is a derivative of the antiinflammatory compound phenylbutazone, formerly used to treat gouty arthritis. It works by lowering the amount of UA in the blood, thus preventing gout attacks. The drug does not treat an attack once it has started.
Sulfinpyrazone helps the body get rid of UA in the urine by preventing its tubular reabsorption. This process may sometimes cause kidney stones, particularly in an acidic urine, which can be prevented by drinking 10 to 12 glasses (240 mL each) of fluid each day or drinking enough water to keep the urine with a light yellow color.
Sulfinpyrazone side effects
Sulfinpyrazone may cause side effects: nausea,
vomiting, loss of appetite, joint pain, redness, or swelling
100 mg tablets and 200 mg capsules (Anturane®)
- Human monoclonal antibody specifically targeted at IL-1β (does not interact with IL-1)
Blocks the interaction between IL-1β and its receptor, thus preventing the initiation of an inflammatory response.
Awaiting approval by the FDA as a treatment for reducing the frequency of gout flares (preventive measure).
Already in use in Europe and USA for cryopirin-associated periodic syndrome..
Canakinumab and Rilonacept indication
Reduce frequency of attacks of gouty arthritis unresponsive to or unable to tolerate other drugs.
Canakinumab and Rilonacept MOA
Bind to extracellular IL-1 generated by inflammatory cells (neutrophils, monocytes, macrophages) molecules and prevent this cytokine from binding to surface IL-1 receptors (IL-1R). As a result, IL-1 cannot send a signal promoting pain and inflammation into the cell:
Canakinumab and Rilonacept products
Canakinumab (Ilaris®) and rilonacept (Arcalyst®) for injection
Canakinumab ad rilonacept mechanism diagram
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