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R W Stephens

Publications and source records attributed to R W Stephens.

79 records · Page 5Linked to original sources

The characterisation and function of the polysaccharidases of human synovial fluid in rheumatoid and osteoarthritis.

A potential enzymic mechanism for the degradation of glycosaminogly cans was characterised using enzymes found in rheumatoid synovial fluid from the knee joint. This mechanism involves a true hyluronidase together with the concerted action of beta-glucuronidase and beta-N-acetylhexosaminidase. The contribution of the exopolysaccharidases to hyaluronate degradation was demonstrated by the use of specific inhibitors, while the distinct identity of a true hyaluronidase was shown by ammonium sulphate and agarose gel column fractionations. Only the hyluronidase fraction was capable of degrading high molecular weight hyaluronate. The exopolysaccharidase activities were shown to be markedly elevated in rheumatoid as compared to osteoarthritic synovial fluid and also normal serum. On the other hand, hyluronidase was similarly active in rheumatoid and osteoarthritic synovial fluids; both these levels were lower than that of normal human serum. Hyaluronidase in synovial fluid may thus be derived by diffusion from serum, since it is of relatively low molecular weight (60 000). The pH requirements of this enzyme system and the strong inhibition of hyaluronidase by synovial fluid make it unlikely that the mechanism operates extracellularly. It is proposed that as a lysosomal mechanism, however, it is an important contributing factor in the chronic erosion process characteristic of rheumatoid arthritis.

Acetates↗

The origins and relative distribution of polysaccharidases in rheumatoid and osteoarthritic fluids.

Three lysosomal polysaccharidases were measured in synovial fluid (SF) and serum from rheumatoid (RA) patients, SF from osteoarthritic (OA) patients, and serum from healthy volunteers. (1) There was no correlation between the enzyme levels and white cell counts in the SF. (2) beta-glucuronidase and beta-N-acetylglucosaminidase were markedly elevated in the SF of RA as compared to OA. (3) beta-glucuronidase and beta-N-acetylglucosaminidase levels in the SF of RA correlated well with each other but not with hyaluronidase. (4) beta-glucuronidase and beta-N-acetylglucosaminidase levels were higher in the SF of RA than in the corresponding serum, while the converse was true for hyaluronidase. (5) Hyaluronidase levels were significantly higher in RA serum than in normal serum. These results suggest that the synovial membrane may be the source of beta-glucuronidase and beta-N-acetylglucosaminidase, while hyaluronidase is derived from a source remote from the joint via the serum. This source of hyaluronidase may be the liver. (J Rheumatol 2: 393-400, 1975).

Acetylglucosaminidase↗

Congenital tracheoesophageal fistulas in adults.

Congenital tracheoesophageal fistula without esophageal atresia is commonly known as "H" type. This is an extremely rare anomaly in infants and accounts for approximately 1 1/2-4% of all congenital tracheoesophageal malformations. An anomaly should be described by its anatomical defect, not by a number or letter. There are five main anatomical categories with 85-95% being of the esophageal atresia and distal tracheoesophageal fistula type. About 1 1/2% are of the "H" type. Although today tracheoesophageal fistula is a well-recognized entity, a few of the "H" type have passed through the pediatric period without diagnosis. Those undetected fistulas have successfully masqueraded as chronic lung disease of unknown etiology. Congenital "H" type tracheoesophageal fistulas assume an oblique orientation with the growth of the host to adulthood. This helps to explain the difficulty in diagnosis plus the ability of the host to survive to adult life. Treatment is surgical, consisting of simple ligation via cervical or thoracic approach depending upon location. The 12 previously reported cases in the English literature are reviewed, and a 13th case has been added.

Adult↗