GoutPal Interactive

That doesn't surprise me in the least. Uric acid as an end product of purine and nucleic acid  degradation is a defect in man's metabolism. Although gout is the most overwhelmingly OBVIOUS manifestation of the defect, it would be unreasonable to assume it is the ONLY one.

There is good science implicating hyperuricemia in heart disease, primarily in men.

I have seen some good theory relating it to back pain as well. In fact one man made a distinguished career out of curing “bad backs” with colchicine injections.

I SUSPECT that UA is involved in many many arthritic diseases, not just the ones where joints are filled with crystals. After all, even in gout, the pain presents LONG before lasting crystallization becomes evident.

Thus I have no doubt that one's eczema reacting favorably to allopurinol is more than coincidence.

Though gout is typified by uric acid crystals forming in the joints where they cause the inevitable painful swelling, crystals can also form in the skin tissue causing psoriasis. I have had this in varying degrees, and I can see how it might viewed as eczema.

Goldman, in “Uric acid in the etiology of psoriasis” writes:

The potential etiologic relationship between uric acid in its microcrystalline monosodium urate form and psoriasis was examined by 1) substantiating the reported correlation between hyperuricemia and psoriasis using the phosphotungstate method; 2) examining psoriatic tissue samples for the presence of urates under a microscope using polarized light and a compensator; 3) attempting to induce psoriasis-like symptoms in laboratory animals with purine-to-uric acid metabolism by increasing serum uric acid level; and 4) observing psoriasis-hyperuricemic patients following treatment for their hyperuricemia with Allopurinol. As expected, both men and women psoriatics had higher uric acid levels than did their counterparts in a control group. Monosodium urate crystals were found in samples from psoriatic plaques by both methods used. They were clustered particularly around sweat pores and Munro abscesses, but were found only occasionally in epidermal tissue taken from nonpsoriatics. Psoriasis-like symptoms were induced in laboratory animals (the South American boa, Constrictor constrictor) when they were fed doses of uric acid. Patients with psoriasis and hyperuricemia showed marked improvement in psoriasis when treated for their hyperuricemia. Psoriasis, like gout, may be, at least partly, a result of disorder of purine metabolism and monosodium urate crystals may be responsible for the cell proliferation that is characteristic of psoriatic plaques. Monosodium urate crystals were found by the author to be strikingly segmented. This structure may result in ease of fragmentation, thus increasing the difficulty in identifying urates in any tissue.