It is crucially important to detect subarachnoid haemorrhage (SAH) in all patients in whom it has occurred to select patients for angiography and preventative surgery. A computerized tomography (CT) scan is positive in up to 98% of patients with SAH presenting within 12 h, but is positive in only 50% of those presenting within one week. Cerebrospinal fluid (CSF) bilirubin spectrophotometry can be used to determine the need for angiography in those few CT-negative patients in whom clinical suspicion of SAH remains high; it may remain positive up to two weeks after the event. A lumbar puncture (LP) should only be performed .12 h after the onset of presenting symptoms. Whenever possible collect sequential specimens. Always ensure that the least blood-stained CSF sample taken (usually the last) is sent for bilirubin analysis. Protect the CSF from light and avoid vacuum tube transport systems, if possible. Always use spectrophotometry in preference to visual inspection. All CSF specimens are precious and should always be analysed unless insufficient sample is received. Centrifuge the specimen at .2000 rpm for 5 min as soon as possible after receipt in the laboratory. Store the supernatant at 48C in the dark until analysis. An increase in CSF bilirubin is the key finding, which supports the occurrence of SAH but is not specific for this. In most positive cases, bilirubin will occur with oxyhaemoglobin.

This study compares the lipid peroxidation marker urinary thiobarbituric acid reactive substances (TBARS) and antioxidants including plasma alpha-tocopherol (vitamin E), plasma (P-GSH-Px) and erythrocyte glutathione peroxidase (E-GSH-Px) activities, and plasma selenium levels in two groups of type 2 diabetic subjects (both n=20) with a disease duration of < or =2 (GP1) and 4-6 years (GP2), and non-diabetic age and gender-matched control subjects (CG, n=20). The mean (standard deviation [SD]) age of the groups was similar at 41(10) years. Fasting blood and midstream urine samples were obtained from diabetic and non-diabetic subjects attending the diabetic clinic and HbAlc, fructosamine, urine TBARS, total antioxidant (TAS) levels, P-GSH-Px, E-GSHPx and plasma selenium and vitamin E concentrations were measured. HbA1c (%) and fructosamine levels in the GP1 and GP2 diabetic subjects and the controls were 5.75 (0.67), 11.43 (2.01) and 4.33 (0.47), and 3.09 (0.57), 6.09 (1.15) and 1.67 (0.31), respectively (GP1 vs. GP2, GP1 vs. GC and GP2 vs. CG, all P < 0.001). Elevated urinary TBARS (micromol/mmol urinary creatinine) in the GP1, GP2 and GC groups were 2.47 (0.37), 3.73 (0.93) and 1.18 (0.24), respectively (GP1 vs. GP2, GP1 vs. GC and GP2 vs. CG, all P < 0.001). A significant correlation between HbA1c and TBARS was also noted (r2 = 0.894, P < 0.001) but only in the GP2 subjects. TAS levels were only decreased in the GP2 group compared to control values (0.59 [0.18] vs. 1.74 [0.21], P < 0.001). Plasma vitamin E concentrations (micromol/L) of 34.11 (3.31), 9.57 (2.20) and 39.01 (2.91) were observed in the GP1, GP2 and GC groups, respectively (GP1 vs. CG, P < 0.05 and GP1 vs. GP2 and GP vs. CG, both P < 0.001). E-GSH-Px (U/g Hb) and P-GSH-Px (U/L) activities in GP1, GP2 and CG groups were also decreased at 57.04 (4.31), 24.0 (8.94) and 67.6 (4.29), and 6.16 (1.56), 2.67 (0.47) and 8.72 (0.31), respectively (E-GSH-Px: CG vs. GP1, P < 0.01, CG vs. GP2 and GP1 vs. GP2, both P < 0.001; P-GSH-Px: CG vs. GP1, CG vs. GP2 and GP1 vs. GP2, all P < 0.001). Plasma selenium levels (miromol/L) were only significantly decreased in GP2 compared to both GP1 and CG values (0.49 [0.29] vs. 1.67 [0.80] vs. 1.79 [0.26], both P < 0.001). These observations support the suggestion that chronic hyperglycaemia can influence the generation of free radicals, which may lead ultimately to increased lipid peroxidation and depletion of antioxidants, and thereby enhanced oxidative stress in subjects with type 2 diabetes mellitus.

No abstract

SUMMARY Faecal a-l-antitrypsin and 51Cr-albumin losses in 42 patients with either gastrointestinal or hepatic disease were compared. The reference range was derived from measurements in 20 controls without gastrointestinal disease.Alpha-l-antitrypsin excretion was increased in patients with excessive 5"Cr-albumin loss, and correlations were found between a-1-antitrypsin clearance and 51Cr-albumin excretion. Because of the considerable overlap of faecal a-l-antitrypsin excretion between controls and patients, sensitivity and specificity of the test were only 58% and 80%, respectively. This poor reliability could not be explained by sampling error or temporal variations in a-l-antitrypsin excretion.These results show that although faecal a-l-antitrypsin excretion correlates with 5"Cr-albumin excretion when whole groups of patients are studied, its poor sensitivity makes it an unreliable measure of enteric protein loss.Gastrointestinal protein loss is traditionally measured by estimating faecal excretion of 51Cr-albumin.'Because this test requires the use of a radioisotope and a minimum five day faecal collection, measurement of ac-l-antitrypsin excretion has been proposed as a less troublesome and equally reliable alternative. Alpha-i -antitrypsin is a broad spectrum protease inhibitor that is synthesised in the liver and is resistant to proteolytic degradation within intestinal secretions and faeces2; its intestinal clearance is thought to parallel that of albumin.Only two groups of workers have attempted to val idate a-I -antitrypsin excretion as a measure of enteric protein loss by direct comparison with 5tCr-albumin excretion. Florent et al3 found a highly significant correlation between the two methods, but Haeney et at4 did not. Despite this disagreement ac-l-antitrypsin excretion has since been adopted by several investigators as the method of choice in measuring faecal protein loss.5 -7We therefore set out to compare a-1 -antitrypsin and 51Cr-albumin excretion in patients with a wide range of gastrointestinal diseases, and we also sought to examine the possibility that the discrepant results of previous studies might be due to differences or errors in the methods used to estimate a-1 -antitrypsin excretion.

This study investigates the association between serum cystatin C, serum creatinine concentrations, N-acetyl-beta-D-glucosaminidase (NAG enzymuria), urine alpha1-microglobulin (alpha1-MG) and beta2-microglobulin (beta2-MG) levels in subjects with type 2 diabetes (n=40, 20M/20F, age range 25-65 years; duration of diabetes 8-10 years) and age- and gender-matched healthy controls (n= 20). Exclusion criteria were absence of gross proteinuria, hypertension, dyslipidaemia or cardiovascular disease. Fasting blood samples and mid-stream specimen of urine (MSSU) were collected and serum creatinine, cystatin C, urine creatinine, NAG enzymuria, alpha1-MG and beta2-MG were measured. Diabetic subjects were separated into two groups based on albumin:creatinine concentration ratio. Group A: <3.5 (mg/mmol creatinine), group B: 3.5-35 (mg/mmol creatinine). While serum creatinine concentrations remained within the laboratory reference range for all groups, serum cystatin C concentration (mg/L) was significantly increased in group B (1.79 +/- 0.42 [mean +/- SD] compared to both control [0.81 +/- 0.10] and group A values [0.95 +/- 0.10]; both P<0.001). NAG enzymuria (units/mmol creatinine) was increased in both diabetic groups compared to control values (group B: 122 +/- 7, group A: 70 +/- 5, controls 27 +/- 2, all P<0.001). alpha1-microglobulin (microg/mmol creatinine) concentrations, similar in both the control group and group A diabetics at 1.10 +/- 0.10 and 1.11 +/- 0.21, respectively, were significantly elevated in group B at 2.10 +/- 0.41 (both P<0.01). Similarly, elevated beta2-MG (microg/mmol creatinine) levels were also observed in group B compared to both group A and control values (3.20 +/- 0.21 vs. 1.80 +/- 0.51 and 0.91 +/- 0.11, respectively; both P<0.001). In addition, group B levels were significantly higher than group A (P<0.001). These observations suggest that serum cystatin C is a more appropriate and effective biomarker for the overall estimation of GFR than serum creatinine values. In addition, increased serum cystatin C values were also associated with early renal tubular insult in subjects with type 2 diabetes, as characterised by increased NAG enzymuria, alpha1- and beta2-microglobulin excretion.