By N. Zöllner (auth.), Privatdozentin Dr. Ursula Gresser, Professor Dr. Nepomuk Zöllner (eds.)
One individual in 4 within the industrialized international locations suffers from hyperuricemia and is accordingly vulnerable to constructing gouty arthritis, nephrolithiasis, or any of the opposite results of urate deposition. at the moment, a long way too little is understood approximately urate deposition and the mechanisms during which it happens, in addition to approximately its scientific effects, which come with formation of toph; over the helix of the ear or in bones as regards to joints that experience by no means exhibited an assault, improvement of bursitis, persistent tendovaginitis resulting in carpal tunnel syndrome, and gouty paraplegia. info on those concerns is required to estimate the hazards of hyperuricemia and to figure out while healing intervention is indicated. The contributions and discussions during this e-book, because of a world symposium held in December 1990 within the Medizinische Poliklinik in Munich, offer an updated resource of present wisdom approximately hyperuricemia in guy and its scientific consequences.
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Additional info for Urate Deposition in Man and its Clinical Consequences
L. SCHMIDT Wehave heard from Dr. Scott that urate tophi never can be observed in muscle. However, in severe cases of CPPD-deposition disease we can see calcifications in the adductor muscles of the legs. What is the biochemical reason for this discrepancy between the behaviour of urate and CPPD crystals? MOHR In histological tissue sections, mon os odium urate crystals appear as collections of negative birefringent, needle-like deposits (Fig. 1 a, b). Their electron microseopie equivalent is crystals with a focal parallel arrangement of their long axes (Fig.
The morphological changes of the hyaline cartilage are also well-known. In advanced cases, the surface of the cartilage is covered by urate (Kersley et al. 1950). Histological changes consist of superficial deposits of urate in the cartilaginous matrix (Fig. 12) as described by Garrod (1859) and Brogsitter (1926). The surface of the cartilage often exhibits a fine granular eosinophilic appearance (Fig. 12c, d), indicating that crystals have been dissolved by the staining method from these areas.
As pointed out by Beck , most of these patients also suffered from coronary artery disease, heart failure, or hypertension other than from severe gout; in addition, minimal clinical evidence of renal impairment was present in a few patients with severe tophaceous gout . Later, Barlow and Beilin performed biopsies in 25 patients with primary gout; they concluded that needlelike urate crystals in the medullary interstitial tissue surrounded by inflammatory cells are the most specific findings in gout nephropathy.
Urate Deposition in Man and its Clinical Consequences by N. Zöllner (auth.), Privatdozentin Dr. Ursula Gresser, Professor Dr. Nepomuk Zöllner (eds.)