The prevalence of microalbuminuria was assessed in 149 consecutive, newly-diagnosed and untreated patients with Type 2 diabetes, 129 of whom were followed up for 1 year, with at least three urine specimens being obtained during this period. At initial presentation, 39 (26%) patients had a urinary albumin to creatinine ratio (ACR) of greater than 2.5 mg mmol-1 and compared with patients who had a normal ACR, they were older (64 (11) (SD) vs 58 (11) yr, p less than 0.002), with higher random blood glucose (14.4 (4.5) vs 12.3 (4.4) mmol l-1, p less than 0.02) and glycosylated haemoglobin (13.0 (3.1) vs 11.3 (2.7)%, p less than 0.01) concentrations. An elevated ACR was also associated with a higher systolic blood pressure (149 (22) vs 140 (22), p less than 0.05) and the presence of macrovascular disease, particularly peripheral vascular disease (p less than 0.001), with this association persisting after adjustment for the effect of age. Ten patients reverted to normal albumin excretion on improving blood glucose control, this group having a significantly higher glycosylated haemoglobin concentration at initial presentation than the group with a persistently elevated ACR (14.4 (2.5) vs 12.0 (3.0)%, p less than 0.05). The 21 (16%) patients with a persistently elevated ACR from diagnosis of Type 2 diabetes were older than those with normal albumin excretion throughout (64 (7) vs 58 (10) yr, p less than 0.02) and it is probable that these patients have abnormal albumin excretion secondary to established renal pathology.

A cross-sectional study to assess home glucose monitoring practices was conducted in 200 non-insulin-treated diabetic patients consecutively attending our hospital clinic. Of the 200, 97 (48%) patients (Group 1) regularly monitored urine (n = 74), blood (n = 19) or both (n = 4); 103 (52%) patients (Group 2) performed no home monitoring. The two groups were similar in terms of age, sex, duration of diabetes and type of treatment. The prevalence of diabetic complications was also closely comparable and only peripheral neuropathy differed between the groups, being more common in Group 1 (n = 12) than Group 2 (n = 4); p < 0.05. There was also no significant difference between the HbA1 concentration (mean +/- SD) in Group 1 (9.7 +/- 2.2%) and Group 2 (9.4 +/- 2.0%). The mean frequency of home monitoring was four tests weekly, but only 21 (22%) kept a written record and 60 (62%) would never alter their treatment on the basis of their results. Almost a third of patients could not interpret the results of monitoring or give the normal range of values. Home glucose monitoring, particularly of urine, is widely practised in Type 2 diabetes, at considerable overall expense. However, convincing evidence of its value in helping patients improve their blood glucose control or preventing the complications of the disease is lacking.

Insulin-induced hypoglycaemia in humans is associated with the rapid mobilization of leucocytes in peripheral blood. The aim of the present study was to determine whether neutrophil activation, manifested in plasma by neutrophil elastase concentration, occurs in response to insulin-induced hypoglycaemia. Acute hypoglycaemia (mean blood glucose 1.3 +/- 0.2 mmol l-1; mean +/- SD) was induced with intravenous insulin in 15 normal human subjects, and provoked an increase in the neutrophil count from 3.4 (range 1.9-6.5) to 10.7 (9.4-16.3) X 10(9) l-1 (p less than 0.001), and in the total leucocyte counts from 5.7 (4.1-8.1) to 12.8 (11.3-18.6) X 10(9) l-1 (p less than 0.001), with associated elevations in plasma neutrophil elastase concentration from 21 (12-34) to 29 (14-70) micrograms l-1 (p less than 0.05), and in total neutrophil elastase concentration from 5.90 (3.13-8.20) to 25.20 (23.00-52.00) mg l-1 (p less than 0.001). As neutrophil elastase is implicated in the development of vascular disease, this rise in response to hypoglycaemia may be of pathological importance in insulin-treated diabetic patients.

SummaryOne hundred insulin-dependent diabetic patients (age < 45 years, 53 smokers) were foliowed for six years. The age, duration of diabetes and mean glycated haemoglobin levels, were comparable between the smokers and non-smokers. Microvascular complications (retinopathy and increased urine albumin excretion) were commoner and more severe in the smoking group at six years, particularly in heavy smokers. Of the 45 original smokers reviewed at six years, 12 (27%) had stopped, six of whom had developed microvascular complications. Only two of the 'heavy' initial smokers, likely to be at most risk, had stopped smoking, and three original nonsmokers had started smoking.Keywords: insulin-dependent diabetes, diabetic nephropathy, diabetic retinopathy, smoking, ischaemic heart disease A diabetic patient who smokes has a 4-6 fold increased risk of developing ischaemic heart disease compared with a non-smoking, nondiabetic subject." 2 Smoking may also promote the development and progression of diabetic microvascular disease, particularly diabetic nephropathy.""4 Unfortunately, many young people with diabetes start smoking,5 and smoking prevalence amongst diabetic patients is similar to the non-diabetic population.6 Anti-smoking counselling has little initial impact on smoking habits, although long-term data is lacking.7'8This study followed the smoking habits and the development of microvascular complications over six years in a cohort of young adult smokers with insulin-dependent diabetes mellitus (IDDM). The degree of nicotine dependence was measured by urine cotinine, a metabolite of nicotine. Patients and methodsFifty-three smokers with IDDM were recruited consecutively into a programme of anti-smoking counselling.7 None stopped smoking following this. During the same period, 47 patients who had never smoked were identified as a control group. At recruitment the two groups were comparable for age, duration of diabetes, and glycated haemoglobin (HbAl) concentration (table 1).In all patients urine cotinine was measured as an objective assessment of the smoking load over the previous 24 hours.9 All non-smokers had a cotinine:creatine ratio (COT:CR) < 1.5 jug/mg. The smoking group was subdivided into 29 'light' smokers (COT:CR<7 ug/mg) and 24 'heavy' smokers (COT:CR> 7 p,g/mg).Six years later, the two groups of patients were followed-up. Background retinopathy was defined as microaneurysms, haemorrhages or hard exudates in one or both eyes; proliferative retinopathy by the presence of soft exudates (cotton wool spots), active neovascularisation, or previous photocoagulation therapy. Nephropathy was identified by the measurement of urinary albumin excretion (Beckman rate nephelometric analyser) in at least two early morning urine specimens over a six-month period. A timed overnight urine sample confirmed the presence of microalbuminuria (urinary albumin excretion rate of 20-200 pig/min). Macroproteinuria (albustix positive) was confirmed by a 24 h urinary protein excretion of > 500 mg. Results are given as mean (SD) o...

The relationship between clinic-measured random blood glucose and glycated haemoglobin was investigated in 204 non-insulin-dependent diabetic patients to determine the value of random blood glucose on management decisions in these patients. Treatment was with diet alone in 104 patients (51%: Group 1), and diet and oral hypoglycaemic agents in 100 patients (49%: Group 2). Random blood glucose and glycated haemoglobin were lower in Group 1 than Group 2 (10.9 +/- 4.0 vs 13.0 +/- 4.0 mmol l-1, p < 0.001, and 8.5 (7.8-10.2) vs 9.6 (8.1-11.0)%, p < 0.01, respectively), and there was a positive correlation between random blood glucose and glycated haemoglobin in both groups (rGroup1 = 0.76, and rGroup2 = 0.54, both p < 0.001). In Group 1, 48 (46%) patients had a random blood glucose < 10 mmol l-1 and all but 2 of these had a glycated haemoglobin of < 10%. Thus, random blood glucose < 10 mmol l-1 was 96% sensitive for glycated haemoglobin < 10%. In Group 2 the same sensitivity was 92%. These data suggest that clinic-measured random blood glucose levels below 10.0 mmol l-1 predict acceptable overall glycaemic control in non-insulin-dependent diabetic patients, particularly in those on diet alone. However, a clinic-measured random blood glucose above 10 mmol l-1 was of limited value in predicting glycated haemoglobin values above 10% and a blood glucose cut-off of 14 mmol l-1 appeared more useful. Where resources are limited, clinic random blood glucose estimation may allow clinicians to use glycated haemoglobin measurements more discriminately.