The effect of simultaneous pancreas and kidney transplantation on diabetic retinopathy was studied in a prospective study with 30 patients (57 eyes) and 15 control subjects (26 eyes), patients who lost the pancreas, but preserved kidney function. There was no significant difference between the groups after a mean observation time of more than 35 months (a range of 12 to 96 months). Both populations had a stable retinopathy during follow-up. This seems to be a consequence of the far advanced retinopathy (mean duration of type 1 diabetes was 22 years) and the high percentage of coagulated eyes (81% and 85%, respectively), but is not related to the organ transplantation. A closer look at the few patients who did not receive laser coagulation (14 patient and 6 control eyes), produced a different result. Four control eyes experienced a significant deterioration of the retinopathy which had been stable before rejection. It is the most important and so far never mentioned aspect of this study, that periods of destabilisation are a definite threat for the retinopathy. Nevertheless, it seems questionable whether we will ever be able to make a definite statement on the pancreas-eye relation, as long as the transplantation must be restricted to carefully selected late-stage diabetic subjects.

Summary. Long-term normalization of glucose metabolism is necessary to prevent or ameliorate diabetic complications. Although pancreatic grafting is able to restore normal blood glucose and glycated haemoglobin, the degree of normalization of the deranged diabetic metabolism after pancreas transplantation is still questionable. Consequently glucose, insulin, C-peptide, glucagon, and pancreatic polypeptide responses to oral glucose and i.v. arginine were measured in 36 Type 1 (insulin-dependen0 diabetic recipients of pancreas and kidney aUografts and compared to ten healthy control subjects. Despite normal HbA1 (7.2_+0.2%; normal <8%) glucose disposal was norreal only in 44% and impaired in 56% of the graft recipients, Normalization of glucose tolerance was achieved at the expense of hyperinsulinaemia in 52% of the subjects. C-peptide and glucagon were normal, while pancreatic polypeptide was significantly higher in the graft recipients, Intravenous glucose tolerance (n=21) was normal in 67% and borderline in 23%. Biphasic insulin release was seen in patients with normal glucose tolerance. Glucose tolerance did not deteriorate up to 7 years post-transplant. In addition, stress hormone release (cortisol, growth hormone, prolactin, glucagon, catecholamines) to insulininduced hypoglycaemia was examined in 20 graft recipients and compared to eight healthy subjects. Reduced blood glucose decline indicates insulin resistance, but glucose recovery was normal, despite markedly reduced catecholamine and glucagon release. These data demonstrate the effectiveness of pancreatic grafting in normalizing glucose metabolism, although hyperinsulinaemia and deranged counterregulatory hormone response are observed frequently.

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Twenty-seven patients with successful transplantation and a control group of 14 patients with early rejection of the pancreas graft but functioning kidney graft were examined in a prospective study for 3 yr. Before transplantation, all patients had long-standing type I diabetes with advanced secondary complications, including end-stage diabetic nephropathy. After transplantation in the patients of both groups, kidney function was almost normal. Mean HbA1 levels were normal in the group with pancreas graft survival. In the control group, HbA1 levels were, on average, 1.5% higher compared with the group with pancreas survival (P = 0.00005). After 3 yr, the patients with functioning pancreas graft showed fewer symptoms (mean difference 1.0 in a symptom score ranging from 0 to 16, P = 0.004) compared with the control group. No statistically significant difference between both groups concerning clinical signs of polyneuropathy could be observed. In the pancreas and kidney transplantation group, peroneal and median nerve conduction velocities increased 7.2 m/s (P < 0.01) and 3.5 m/s (P < 0.05), respectively, whereas no increase was registered in the control group. The change of median and sural sensory nerve conduction velocities, peroneal and median compound muscle action potentials, and sural and median sensory action potentials was insignificant. In conclusion, although the improvement of clinical symptoms and neurophysiological signs of polyneuropathy was modest in the pancreas and kidney transplantation group, our data suggest that successful pancreas transplantation is able not only to halt the progression of diabetic polyneuropathy but also to improve it to some extent even at a far advanced stage.

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