Introduction
The diagnosis of gout is usually based on a careful history and physical examination. A raised blood uric acid confirms the diagnosis. But suppose the uric acid is normal?
Crystal deposits in the joint cavities are found in gout, pseudogout, and osteoarthritic cartilage degeneration. The actual aggregates responsible in each case are monosodium urate, calcium pyrophosphate dihydrate (CPPD), and basic calcium phosphate (carbonate-substituted hydroxyapatite and octacalcium phosphate), respectively. Osteoarthritis is usually clearly distinguished, but differentiating between gout and pseudogout (calcium pyrophosphate microcrystalline arthritis) can present difficulty, in some cases. Two years ago, physicians at the University of Ferrara, Italy, made a retrospective analysis of the seasonal incidence of gout and pseudogout, at the same time providing data on further distinguishing characteristics of the two conditions.
Method
All case records of suspected microcrystalline acute arthritis seen at St Anna Hospital, Ferrara, during an 8-year period were examined. Diagnosis was based on history, examination, and microscopic examination of synovial fluid under polarized light. Intracellular monosodium urate crystals and a leukocyte count of >2,000 mm3 in the synovial fluid was diagnostic of gout, while the presence of intracellular calcium pyrophosphate crystals and the same leukocyte count determined the presence of pseudogout. The day and month of each event were categorized into four 3-month seasonal periods, and into 12 1-month periods. Distributions were analyzed using chi-square tests for goodness of fit, and partial Fourier series for rhythmicity.
Results
Over the 8-year period 210 acute gout attacks were recorded - 93% in men (mean age 56 years), and 7% in women (mean age 68 years). During the same period, 179 acute pseudogout events were reported - 32% in males (mean age 67), and 68% in females (mean age 72).
Gout attacks were more common in the spring, as shown in this table:
|
|
Number of Attacks
|
Winter %
|
Spring %
|
Summer %
|
Fall %
|
Fit p value
|
|
GOUT
|
|
|
Total
|
210
|
27
|
36
|
20
|
16
|
<0.001
|
|
Male
|
196
|
28
|
36
|
20
|
16
|
<0.001
|
|
Female
|
14
|
21
|
36
|
29
|
14
|
0.699
|
|
PSEUDOGOUT
|
|
|
Total
|
179
|
25
|
21
|
25
|
29
|
0.531
|
|
Male
|
58
|
33
|
21
|
17
|
29
|
0.302
|
|
Female
|
121
|
21
|
22
|
29
|
29
|
0.392
|
Although fewer in number, women with gout showed the same increased frequency in the spring as men, albeit without statistical significance. Pseudogout, on the other hand, was distributed evenly among the seasons, with only a trend towards a non-significantly increased frequency in the fall.
Comment
As the mean age of the population increases, crystalline arthritis will be encountered more often. Gender and the season of occurrence may be additional clues to diagnosis, which, however, will still depend on uric acid determination and microscopy of the joint aspirate. Radiography shows CPPD crystals as radio-opaque, which may be an added criterion.
Is the spring increase in gout frequency readily explicable? Atmospheric variables (temperature, humidity) do not seem to provide the answer. The authors of the Italian study suggest that the formation or presence of intracellular microcrystals is not the stimulus for an attack, but that seasonal biochemical or hormonal changes are responsible. As dietary indiscretions are so often blamed for an attack of gout, seasonal changes in eating or drinking habits are sometimes held responsible, but there is little evidence for this.
The results of the study summarized here indicate that pseudogout is almost as common as gout (179 vs. 210 events during the same period). Although no significant seasonal changes in incidence were detected here, there is one published report suggesting a causal connection with fluctuations of the geomagnetic field, such as during solar rotation and lunar cycles.1The cause of pseudogout is unknown, although it is seen in people with hyperparathyroidism (increased serum calcium), hemochromatosis (increased iron in the tissues), and hypomagnesemia. Treatment, therefore, is of any such known cause, as well as symptomatic treatment along the same lines as for gout. Ultrasound therapy may improve symptoms of chronic calcific tendonitis, and might possibly, therefore, be expected to improve pseudogout. However, the classical dietary modification often recommended for gout victims is unlikely to be helpful.
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