Plasma phosphatase was first determined by Martland (1925) and then by Kay (1930), using glycerophosphate and estimating the inorganic phosphate liberated at 370 C. at a specified pH and in a given time.

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This paper describes a comparison of the recently developed substrate 2-methoxy-4-(2′-nitrovinyl)-phenyl-2-acetamido-2-deoxy-β-d-glucopyranoside (MNP-GlcNAc) and the corresponding 4-methylumbelliferyl substrate (4-MU-GlcNAc) for the determination of urinary NAG. A good correlation ( r = 0·977) was found between NAG activities in 366 urine samples from renal transplant patients determined by either the fluorimetric method or the colorimetric procedure. The colorimetric method may be used with confidence as an alternative to the fluorimetric assay and does have the advantage that colorimetry is widely used in clinical chemistry laboratories. Sample blanks are not normally required unless there is blood contamination in the urine which can easily be identified visually. The incorporation of the MNP-GlcNAc substrate into a kit suitable for the assay of urinary NAG using a simple battery-operated miniphotometer is also described. The presence of elevated NAG levels in urine can be detected rapidly and this procedure is suitable for routine monitoring of renal patients in the laboratory and may prove to be suitable for use by non-laboratory personnel in clinics or on the ward.

SUMMARY Raised serum alkaline phosphatase (AP) levels were found in 13 of 76 patients (17 %) with ankylosing spondylitis (AS), and 1 1 of these 13 underwent further investigation to determine the origin of the increased enzyme activity. Three had levels within the normal reference range on re-estimation, and, of the remaining 8, AP isoenzyme studies indicated an increased liver fraction in 6. Serum gamma-glutamyl transpeptidase (GGT) was raised in only 3 patients. Increased AP activity did not appear to be directly related to disease activity or to drug therapy. These findings confirm the occurrence of increased serum AP activity in AS but challenge a previously reported suggestion that bone is the source of the increased enzyme.The serum level of alkaline phosphatase (AP) may rise in a variety of inflammatory rheumatic diseases.' 2 The source of the increased enzyme activity is usually the liver,`-4 but it has been suggested that it arises from bone in ankylosing spondylitis (AS).' We have investigated the prevalence of raised AP in AS and attempted to determine the origin of the increased enzyme activity by isoenzyme studies and by reference to other liver enzymes, specifically alanine transaminase (ALT) and gamma-glutamyl transpeptidase (GGT). Patients and methodsSixty-seven men and 9 women, aged 18-71 years, with AS as defined by the New York criteria, were assessed clinically, haematologically, and biochemically. Five had associated psoriasis, 2 Reiter's disease, and 4 chronic inflammatory bowel disease. The mean duration of spondylitic symptoms was 14-9 years.The initial laboratory investigations included haemoglobin, full blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and a serum biochemical screen for calcium, phosphate, AP, total protein, albumin, bilirubin, and ALT. Repeats of these tests with additional AP isoenzyme studies and estimation of GGT were performed on patients found to have AP levels above 13 King-