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In a group of 149 maturity-onset type diabetic patients followed from diagnosis, 55 (37%) had retinopathy on colour photography 7 years later. Those patients with retinopathy had significantly greater glycaemia, as shown by higher fasting plasma glucose levels at diagnosis, larger mean values for fasting glucose 1, 3 and 5 years later, and higher random glucose and haemoglobin A1c at ophthalmic review (p = 0.001, 0.002, 0.007 and 0.001, respectively). Substantial retinopathy, as measured by greater than 5 microaneurysms, also correlated significantly with each index of glycaemic control.

Seventy-one Type 2 (non-insulin-dependent) diabetic patients showed only a slight deterioration in mean vibration sensory threshold (measured biothesiometrically) on the feet during the 5 years from diagnosis. However, multiple linear regression analysis of the wide range of individual changes in this threshold showed as significant independent associated factors the initial sensory threshold (p less than 0.001), age, gender, and both the mean fasting blood glucose and failure to become thinner under treatment (p less than 0.05 for all). The relationship with fasting glucose was stronger if the pre-treatment value was included in calculation of the mean (p less than 0.001). Mean fasting blood glucose under treatment accounted for only a small fraction of the total variance of the deterioration of the vibration sensory threshold, but represented one-twelfth of that attributable to identified factors, and one-third of the variance ascribable to factors subject to therapy. Interim values revealed the persistent effect of hyperglycaemia over the 5 years. An increase of 1 mmol/l in mean fasting blood glucose has an equivalent effect on the sensory threshold to an extra 5 years of age.

Forty-three diabetic patients on maintenance chlorpropamide (100-750 mg daily) drank 0.2 ml/kg 90% ethanol after equilibration in a room controlled at 20 degrees C. Twenty-five patients had already noted marked alcohol flushing since starting chlorpropamide therapy (group A), while 13 had not observed this (group B). The remainder were teetotal or unsure of their reaction. Cheek temperature rise correlated with plasma chlorpropamide concentration (r = 0.6, p less than 0.001) in all patients and was inversely related to basal cheek temperature (r = -0.35, p less than 0.02). Plasma chlorpropamide correlated with daily chlorpropamide dose (r = 0.8, p less than 0.001) but not with basal cheek temperature. The correlation between chlorpropamide level and cheek temperature rise was strengthened on analysis of group A alone (r = 0.7, p less than 0.001) and absent in group B (r = 0.2, p greater than 0.3) who tended to have lower chlorpropamide levels and cheek temperature rise than group A.

Further progress can depend only on standardised testing to determine the response precisely, after consideration of known interacting factors (e. g. initial cheek temperature, plasma chlorpropamide concentration). Until liver biopsy to identify the alcohol dehydrogenase isoenzymes becomes harmless, further studies will perhaps reveal more about the extra-pancreatic effects of one sulphonylurea than about the aetiology of Type 2 diabetes and its complications.