crystal arthritis, gout, pseudogout

1. CRYSTAL ARTHRITIS
( gout and pseudogout )
Abdul Waris
Dept: internal medicine

2. DEFINITION/EPIDEMIOLOGY
Gout : is a painful and potentially destructive rheumatic disorder arising in the setting of
Hyperuricemia and sodium urate crystals.

3. DEFINITION/EPIDEMIOLOGY
GOUT
The prevalence of gout is increasing mainly in developed Countries
The prevalence is 1.4% in the UK and 2.7% in the USA.
their diet becomes moreWestern.
Gout develops in men more than women (10 : 1)
Some 85–90% of cases are idiopathic.
Asian populations are more at risk as

4. Urate is the end product of purine
metabolism that occurs in liver

5. URAT1 and GLUT9, are members
of the organic acid transporter
family and have predominant
effects on serum urate level.

6. AETIOLOGY
GOUT:
URATE IMBALANCE >>>>>

7. RISK FACTORS
GOUT
Dietary influences
Chemical composition (Total caloric intake , Triglycerides , Carbohydrates ,Protein
Specific food examples (Red meat , Beer, Liver , Shellfish etc.. )
Associated with lower urate level (Dairy products Vitamin C )
Clinical associations
Age
Male or postmenopausal female gender
Direct causal link ( such as genetic diseases or autoimmune diseases etc..)
etc..)
Associated disorders ( hypertension , hypothyroidism , obesity, renal impairment etc.. )
Acute precipitants ( trauma, surgery , dehydration , shellfish binges etc..)
Drugs
Aspirin , Diuretics, losartan, levodopa , cyclosporine etc..
Alcohol

8. CLINICAL MANIFESTATIONS
GOUT
Gout is presented in three main stages:
1- Asymptomatic hyperuricemia
2-acute intermittent gout
3-advanced gout

10. DIFFERENTIAL DIAGNOSIS

11. INVESTIGATION
GOUT :
The clinical picture is often diagnostic.
1-
2-
3-
Joint fluid microscopy is the most specific and diagnostic test but is technically
Serum uric acid is usually raised (>600 μmol/L)
difficult.
Serum urea, creatinine and eGFR are monitored for signs of renal impairment.
Needle-shaped urate crystals

12. MANAGEMENT
The use of NSAIDs or coxibs in high doses rapidly reduces the pain and swelling. The first
dose should be taken at the first indication of an attack:
1-
2-
3-
4-
5-
Naproxen-750 mg immediately, then 500 mg every 8–12 hours
Diclofenac-75–100 mg immediately, then 50 mg every 6–8 hours
Indometacin-75 mg immediately, then 50 mg every 6–8 hours
Colchicine- 1000 μg immediately, then 500 μg every 6–12 hours
Corticosteroids- oral prednisolone or intramuscular or intra-articular depot
methylprednisolone.
Treatment with agents that reduce serum uric acid levels:
The aim of treatment is to reduce the uric acid level below the 360 μmol/L level; some
guidelines recommend below 300 μmol/L.
Allopurinol, Febuxostat , Pegloticase, Uricosuric agents, Losartan, Anakinra

13. Allopurinol:-
Should only be used when the attacks are frequent and severe , associated with renal
impairment or tophi, or when the patient finds NSAIDs or colchicine difficult to tolerate.
Allopurinol (300– 600 mg) blocks the enzyme xanthine oxidase, which converts
xanthine into uric acid .
It reduces serum uric acid levels rapidly and is relatively non-toxic but should
be used at low doses (50–100 mg) in renal impairment.
Skin rashes and gastrointestinal intolerance are the most common side-effects. A
hypersensitivity reaction is the most serious adverse event. This is rare, as is bone marrow
suppression.

14. Febuxostat (80–120 mg)
Is a non-purine analogue inhibitor of xanthine oxidase but not other enzymes in
the purine and pyrimidine pathway.
It is well tolerated and as effective as allopurinol in trials and is safer in renal
impairment as it is metabolized in the liver and not renally excreted.
It has been approved by the FDA and is helpful in patients who cannot tolerate
allopurinol but there are anxieties that it may increase cardiovascular risks.
At time of writing, most doctors advise trying allopurinol first unless there are
strong contraindications to its use.

15. Pegloticase
a pegylated recombinant uricase given intravenously, lowers urate levels
dramatically but its place in therapy is unclear.

16. Uricosuric agents
also lower the serum uric acid but their use is restricted throughout
Europe by the very rare occurrence of serious hepatotoxicity.
Benzbromarone acts on the
URAT-1 transporter and is well tolerated.
Sulphinpyrazone and probenecid are best avoided in renal impairment.

17. Losartan
is an angiotensin I-receptor antagonist and is uricosuric
in hypertensive patients with gout. I
t may reduce the risk of gout in patients with the
metabolic syndrome.

18. Anakinra
blocks IL-1β and canakinumab is a human monoclonal antibody with
specific cross-reactivity for IL-1β but not other members of the IL-1
family.
Their role in treatment-resistant gout is still subject to trials to
establish when their use is justified in gout which has not responded
to the more conventional agents.

19. Pseudogout
Precipitation of crystals of calcium pyrophosphate dihydrate (CPPD) in
connective tissues which may be asymptomatic or may be associated
with several clinical syndromes

20. CLINICAL MANIFESTATIONS
Pseudogout (pyrophosphate arthropathy)
Calcium pyrophosphate deposits in hyaline and fibrocartilage produce the radiological appearance of
chondrocalcinosis.
Shedding of crystals into a joint precipitates acute synovitis which resembles gout, except that it is more
common in elderly women and usually affects the knee or wrist.
The attacks are often very painful.
In young people it may be associated with haemochromatosis, hyperparathyroidism, or Wilson's disease.

23. INVESTIGATION
PSEUDOGOUT
Central investigations for diagnosis are
1-
fluid and tissue analysis for
2-
plain radiographs.
the presence of CPP crystals
Rhomboid shaped crystal

24. Treatment
Aspiration of the joint reduces the pain dramatically but it is usually
necessary to use an NSAID or colchicine, as for gout.
If infection can be excluded, an intra-articular injection of a corticosteroid
helps.

25. REFERENCES
Kumar & Clark’s clinical medicine 8th edition
Harrison, Tinsley Randolph, and Anthony S. Fauci. Harrison's principles of internal medicine. 14th ed.
New York: McGraw-Hill, Health Professions Division, 1998. Print.
Hochberg, Marc C.. Rheumatology. 5th ed. Philadelphia: Mosby/Elsevier, 2011. Print.