[Hyperuricemia is frequent and its prevalence is increasing as it correlates with obesity and metabolic syndrome by several different mechanisms. Furthermore, recently several data are available for the cardiovascular and renal protective effect of allopurinol in the treatment of hyperuricemia and gout. The new European EULAR guidelines suggested treat to target principle in urat lowering therapy of gout. The uric acid target is below 360 µmol/l in mild to moderate gout. The guidelines unequivocally stated, that allopurinol is the first line uric acid lowering drug. Allopurinol treatment should be started immediately at the diagnosis and should be continued lifelong.]

[In medical practice there are a number of “truths etched in stone” that are passed on from textbook to textbook and learned by generations before they become obsolete. This short study aims to eliminate a misbelief from the diagnosis of gout that is related to the histological detectability of urate deposits. According to the generally accepted thesis, urate crystals obtained from patients with gout are dissolved in formalin solution, therefore, tissue samples should be fixated in alcohol. The authors have found that urate crystals can be detected on conventionally mounted, native (unstained) sections, despite formalin fixation, whereas the great majority of urate crystals are dissolved during haematoxylin-eosin staining. Therefore, for the detection of urate crystals the tissue samples should be examined on native, unstained sections.]

[The authors studied the solubility of urate crystals in alcohol, in an 8% aqueous solution of formaldehyde and in acetone, respectively. The urate crystals were least soluble in alcohol. In comparison, the amount of urate crystals decreased in the aqueous solution of formaldehyde, which confirmed the suggestion of our predecessors that tissues suspected to contain urate crystals should be fixed in alcohol. Urate crystals dissolved in greatest amounts in acetone. Acetone is widely used by histological laboratories for dehydration of tissue blocks before embedding them in paraffin, which, in case of fixation in aqueous formaldehyde, contributes to the dissolution of urate crystals. In our earlier studies, we found that dissolution of urate crystals from haematoxylineosin stained sections is caused by the staining of nuclei in haematoxylin, therefore urate crystals are preferably demonstrated in unstained tissue sections.]

[In our previous study we refuted the thesis that sodium urate crystals are not, or only rarely detectable in formalin-fixed histological samples because they dissolve in the aqueous formalin solution. Our observations indicate that dissolution of urate crystals is primarily caused by haematoxylineosin staining. Undeniably, however, urate crystals are partially dissolved in the aqueous solution of formaldehyde, and thus a small amount of urate deposits may totally dissolve from tissue samples. The aim of the present study was to identify those steps of the staining procedure that are responsible for the dissolution of urate crystals. We found that the dissolution of urate crystals during the course of staining was caused by the combined effects of haematoxylin staining, treatment with 1% aqueous lithium carbonate solution and dehydration with acetone. As the simplest histological method for the detection of urate crystals, we recommend examining unstained sections (mounted with Canada balsam) of formalin-fixed, paraffin-embedded tissue samples in polarised light. According to our previous study, about two thirds of urate crystals remain detectable on unstaied sections, whereas haematoxylin-eosin stained sections of the same tissue samples (derived from patients with gout) did not contain urate crystals. In the samples where urate crystals could be detected in haematoxylin- eosin stained sections using polarised light, the unstained sections contained much more crystals, which shows that dissolution is greatly decreased on unstained sections.]

[The prevalence of hyperuricemia is is increasing as it is related by several different mechanisms to obesity and metabolic syndrome spreading epidemically worldwide. Several beneficial cardiovascular and renorotective effects of the xanthin-oxydase inhibitor allopurinol, administered in the treatment of hyperuricemia and gout, have been found out recently. The newest European EULAR guidelines for the treatment of gout recommended the treat-to target principle. A target value of ≤360 umol/l in patients with mild-to moderate gout and ≤300 umol/l in more serious cases has been suggested. The guidelines took an unequivocal commitment, that allopurinol is the first-line treatment. The hypouricemic therapy should be started as soon as possible after the diagnosis and should be continued lifelong in patients with gout.]