If a high uric acid level leads to gout, the symptoms include inflammation and redness in the joints, combined with intense pain. Gout is a type of arthritis where uric acid in the blood becomes too concentrated and begins to form sharp crystals within the joints, most commonly the joint at the base of the big toe but can be any joint. Normally, uric acid remains dissolved in the blood and is excreted by the kidneys, but when the kidneys don't filter enough or the body produces too much, crystals can form. All it takes is for for crystals to form in one joint and the whole extremity is affected.  

Thanks, could you please let me know what is the level of uric acid that can cause this problem?

for example, if the patient uric acid level is 387 umol/l and the reference range is 154.7-357. Is this level enough to cause crystallization of uric acid in joint (hands only)

Elevated serum level of uric acid is a classic lab symptom of gout, but it may also occur without hyperuricemia. There are also many people with elevated uric acid levels without clinical manifestation of gout. So the diagnostic value of measuring uric acid may be limited. In my opinion, an exact upper level of uric acid for triggering a gout attack is not possible to set.

 Anyway, in the case discussed you have to take into consideration the clinical picture (not typical affect here) and also some other blood tests i.e. rheumatoid factor, ESR, white blood cell count with differential count, CRP, electrolytes, kidney function, urine analysis. I think you have to carry out a serious differential diagnosis ruling out other kinds of rheumatoid arthritis and similar syndromes. A debute of  rheumatoid arthritis is possible  in this patient .

Thanks Prof Panayot

SER and Uric acid are high. liver function is good (ALT, TBIL, DBIL,IBIL)

so the only way to differentiate between gout and RA is by doing blood analysis?

Should the patient take medicine for uric acid or should run the blood analysis before take it?

First diagnostics. Qui bene diagnostic bene curat.

From the clinical pain of view, gout usually debuts as monoarticular disease and later on it takes a polyarticular form. initially, the joints of the lower limbs are predominantly affected.

A noninvasive usefull diagnostic tool is ultrasound, that may display double contour sign in the case of gout and some other elementary lesions in the case of rheumatoid arthritis, psoriatic arthritis or osteoarthritis. Thus, i suggest including ultrasound in the initial diagnostic work-up of this patient. 

Totally agree. Gout is more reliably a clinical diagnosis than a lab diagnosis

 well uric acid level raised which can be simply is due to gout or due to a response of occurence of inflammaion inside the body like ESR and CRP as psoariasis or lymphoproliferative disorders can be associated with high uric acid

you should see the differential diagnosis which can be rheumatoid arthritis or sero negative arthritis

there is now new diagnostic procedures other than blood and urine tests which is US MSK 

in which uric acid can appear in the joints by using US msk

Does gout (high uric acid) lead to rheumatoid arthritis?

or if a patient has rheumatoid arthritis, can this increase the level of uric acid?

dear dr Kahil,

1. For data on the relationship between the serum level of urate and the chance of gout attacks in the coming 5 years, the article by Roddy et al. Gout. Epidemiology of gout, Arthritis research & therapy 2010, is informative.  It contains a nice graphic on the 5-year incidence of gout in relation to the serum level of urate.

2. deposition of urate crystal takes place before the first attack, and ultrasound can be very helpfull, as stated by dr Pineda, in identifiyng deposition on cartilage and in soft tissue. it can also aid in obtaining synovial fluid from joints which are difficult to approach

3. the clinical problem you present is not typical of gout, but gout can sometimes have a very atypical presentation, depending, amongst others, on phenotypical differences in urate handling and cellular responses to crystal formation.

hope this is helpfull

Thanks Dr Flendrie and others

your comments are very helpful to me. 

Chronic hyperuricemia is a requirement to develop gout; however, the level of uric acid varies from individual to individual, and the clinical expression of gout is likely related more to genetic predisposition than just absolute levels of serum uric acid. The phenomenon of crystal deposition in the form of a salt, monosodium urate or MSU crystals in tissue is temperature dependent. All the symptoms you mentioned above can be present in gouty arthritis, being mild in certain patients and more severe in others, depending on the length of time, the level or degree of hyperuricemia, renal function, diet, certain medications like diuretics, etc. 

Dear Dr. Khalil,

I agree with the opinions provided by the other colleagues. On your question about gout and rheumatoid arthritis, there is no known relationship  between these conditions. In late-stage uncontrolled gout, you may have persistent polyarticular involvement that resembles rheumatoid arthritis, but the presence of tophi, laboratorial work-up and especially the x-ray findings help you distinguish the two. Rheumatoid arthritis does not usually elevate uric acid levels.

Regards,

Filipe Araújo

The above is correct; here, chronic polyarticular tophaceous gout clinically mimics rheumatoid arthritis (RA), 

Thanks Drs, so this means that chronic gout can shows the same symptoms as RA. and the only way to distinguish between them is by doing more analyses

but when can gout described as chronic? as this patient has only 20 units over the maximum reference range.

No, you are not understanding it correctly. Forget the uric acid levels of your patient and look at the clinical history. The distinction between the RA and gout is, above all, clinical. RA usually starts as a symmetrical arthritis involving hands, wrists, elbows, shoulders, knees, ankles and feet, with prolonged morning stiffness, high ESR and CRP, and may have positive rheumatoid factor and ACPA. It´s chronic and persistent, meaning that lasts at least 6 weeks. In gout, the disease usually starts as self-limited monoarticular arthritis of feet, ankle or knees, lasting usually 1-2 weeks, and if the hyperuricaemia is not treated, the patient will have further flares in the future, and more joints will be affected, and after several years it may resemble RA. But it's usually clinically easy to distinguish the two as there are tophi in gout, the x-ray destruction is different and rheumatoid factor and ACPA are negative.

The complaints you describe in your patient don't resemble gout, regardless of uric acid levels.

Thanks Dr Araújo, it's more clear now to me

Yes, clinically, chronic tophaceous gout may be polyarticular, mimicking RA. What I am saying is that in early gout, and this may last several years, the disease is characterized by episodic, monoarticular, intermittent, self-limiting attacks, with pain-free periods in between. In late gout, usually tophaceous in nature, the disease becomes polyarticular, hurting most of the time, without pain-free periods anymore, the reason it begins to mimic RA. The subcutaneous nodules may be tophi or true RA nodules. The gout patients will likely have hyperuricemia, while RA patients will display a positive RA factor, and a positive anti-CCP antibody. Radiographically, both diseases would look different from each other as well. Finally, occasionally, you may have a patient who has both, RA and gout although this is relatively uncommon,  

Following the advices mentioned, RF, CRP & SER analyses has been done.

RF is very high (104.9 KIU / L; Ref:

The patient should be sent to a Rheumatology appoiment as soon as possible as the differential diagnosis and appropriate therapy should be performed by a specialist.

Best regards,

Filipe Araújo 

Thanks Dr Araújo

How do you rate this level of RF? 

Is it high level "advanced stage of RA" or this is a beginning stage of RA?

Thanks

The stages of RA are not defined by the degree of elevation of the RA factor. Rather by the degree of joint inflammation, CRP elevation, duration of morning stiffness, and number of joints involved, not to mention the functional abilities (or lack thereof) of the patient. The patient should be referred to a rheumatologist. Is the anti-CCP also positive? If not, I would also order a hepatitis C antibody since hepatitis C infection can present with polyarthralgias/itis, and a positive RA factor; in addition, other autoimmune diseases can present with polyarthritis and a positive RA factor, e.g., Sjogren's syndrome, lupus, etc.,