Panretinal photocoagulation (PRP) effectively retards the progress of proliferative diabetic retinopathy. However, after PRP, more than a few retinopathy patients have complained of loss of visual function. Fifty-eight diabetic subjects who had undergone PRP and 58 age and sex matched non-diabetic subjects were surveyed using the qestionnaire originally developed by Russel et al. to determine the visual difficulties they experienced. In diabetic subjects before PRP, the frequencies of complaints that were significantly higher compared with non-diabetic subjects were loss of visual acuity, trouble in sorting dark colors, difficulty adjusting to bright light, difficulty judging distances and visual field loss. Visual acuity was significantly worsened 1 to 15 years after PRP, and the most frequent items that worsened 1 month to 3 years after PRP were difficulty recognizing scenes at a distance, difficulty adjusting to dim and bright lighting, difficulty judging distances, and blurry vision in reading (20-30%). Frequency of visual field loss increased in 20% after PRP. It was shown that after PRP visual functions, such as visual acuity, dark adaptation, judging distances and visual field, were worsened at high rates of frequency.

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Clinical data obtained from diabetic patients associated with acromegaly, Cushing's syndrome, pheochromocytoma, or primary aldosteronism were analyzed. In acromegaly, the incidence of accompanying diabetes (39.6%) and the plasma glucose level in 75 g OGTT were the highest among the four diseases. Although 38.5% of patients with Cushing's syndrome had accompanying diabetes, their fasting plasma glucose concentrations were almost normal. Hyperinsulinemia was observed in these two diseases, and age, family history of diabetes, degree of hormonal abnormality, and weight gain in these patients were regarded as pathognomonic for diabetes. In pheochromocytoma and primary aldosteronism, diabetes was observed in 27.8 and 17.9%, respectively, with relatively high fasting plasma glucose concentrations. The suppression of insulin secretion, degree of hormonal abnormality, and weight loss in these patients, in addition to abnormalities of electrolytes in patients with primary aldosteronism, were considered pathognomonic for diabetes in these diseases.

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Hyperglycemia and the impairment of the Na⁺/K⁺ pump have been reported to be associated with the development of diabetic neuropathy. To elucidate the implications of high glucose for nerve dysfunction and the associated changs in Na⁺/K⁺ pump activity, we investigated membrane current using the voltage clamp technique in single myelinated nerve fibers, which were dissected from rat sciatic nerves. An external application of 30 mM D-glucose caused a transient decrease in action potential with a fall in inward Na⁺ current followed by a rise in Na⁺ current which gradually returned to the control level in amplitude. Similar but larger changes in Na+ current were oserved when L-glucose or sucrose was added to the experimental solution. In the presence of 0.1 mM ouabain, no recovery in Na⁺ current was observed in a 30 mM glucose solution. These findings indicated that the Na⁺/K⁺ pump plays an important role in the process of recovery to the control state from the state of high intracellular Na⁺ concentration induced by the high osmolarity of external solution.

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Hyperinsulinemia is recognized as a major coronary risk factor, however, no standardized index for identifying hyperinsulinemia simple enough to be used in outpatient clinics has yet been developed. In the present study, we tried to develop suitable insulinemic measures based on the results of a 75 g oral glucose load. Two hundred fifty-two individuals, 138 males and 114 females, all aged over 30, were divided into 9 subgroups using the obesity index (<+10, +10<+20, +20≤) and glucose telerance (normal, borderline, diabetic).Insulinemic measures, fasting IRI (FIRI), 0.5, 1 and 2h IRI, ΣIRI, FIRI/FPG, ΔIRI/ΔPG, ΣIRI/ΣPG, were then selected and examined for their efficacy. Assuming that the value of the mean+2SD of individuals with normal body weight and normal glucose tolerance was the upper limit for each measure, and that those with insulinemic measures exceeding the limits could be classified as hyperinsulinemic, hyperinsulinemia was judged to occur in a higher percentage using FIRI, ΣIRI, FIRI/FPG andΣIRI/ΣPG. Furthermore, the incidence of hypertension and/or hypertriglyceridemia, but not hypercholesterolemia, was found to be significantly higher in those classified an hyperinsulinemic by this method. Among the above 4 measures, FIRI and FIRI/FPG values were found to be useful based on their higher hyperinsulinemia detection rates even in routine examinations without any loading. These values may therefore provide more concrete information regarding hyperinsulinemia and related atherosclerosis.

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The extrapancreatic effect of glimepiride on hepatic glucose disposal was quantitatively investigated in seven healthy dogs using a euglycemic hyperinsulinemic clamp combined with the hepatic venous catheterization technique. Euglycemic clamping (EC) was performed by peripheral infusion of somatostatin and glucose and intraportal infusion of insulin for 180 minutes, prior to and after 7 day admisistration of glimepiride (0.1 mg/kg/day). During the latter half of each clamp, glucose was simultaneously infused intraportally at a rate of 7 mg/kg · min. After glimepiride treatment, 1) fasting plasma IRI levels increased significantly, and plasma glucose concentrations decreased significantly (p<0.05), 2) during the first 90 min of the EC, systemic glucose utilization significantly increased (8.2±0.7 vs. 11.6±1.3 mg/kg·min, mean±SEM, p<0.05), but there was no change in hepatic glucose uptake, 3) during the second 90 min of the EC, there was a remakable increase in the hepatic glucose disposal (net hepatic glucose balance, 2.2±0.5 vs. 5.8±1.0 mg/kg·min, p<0.05).
These data indicate that insulin-stimulated hepatic glucose disposal is markedly augmented by 7 day glimepiride treatment when glucose is loaded via a physiological route.

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A patient with chronic hepatitis C associated with NIDDM was treated with interferon. His ICA changed to positive and transtition to IDDM with a marked increase in blood sugar was found.
This patient was a 35-year-old man who was found to have liver dysfunction and diabetes at the age of 33. In October 1992, he was hospitalized with anorexia and reduced body weight as his chief complaints. After dietary therapy and transitional insulin therapy, he was administered an oral antidiabetic agent (40 mg/day ofgliclazide). When his blood sugar was well controlled, a liver biopsy was performed and interferon treatment was started. From the 3rd day of interferon administration, marked increases in urinary sugar excretion and blood sugar level were observed. Furthermore, insulin secretion was reduced, and ICA, which was not seen before interferon administration, appeared.
This case suggests there is a possibility that blood sugar will increase through the mechanism of appearance of ICA when interferon is administered to patients with chronic active hepatitis C associated with or without glucose tolerance disorders, and that special attention should be given to patients with glucose tolerance disorders.

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It is well known that hypophosphatemia often occurs during insulin therapy of diabetic ketoacidosis. However, tha necessity and efficacy of phosphate replacement is still controversial. We encountered a fresh case of IDDM in which acute respiratory failure and myocardial dysfunction with severe hypophosphatemia developed in the course of insulin therapy of ketoacidosis. Intravenous administration of phoshate rapidly improved the respiratory and cardiac condition, suggesting the importance of phosphate supply. Monitoring and adequate replacement of phosphate appears to be necessary, especially in patients with severe acidosis.

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A diabetic woman aged 71 years was admitted to our hospital with complaints of left backache, chills and vomiting. A diagnosis of acute pyelonephritis was made, and the patient was treated with ampicillin, but died of septic shock and disseminated intravascular coagulation (DIC) on the 13th hospital day. An echogram on her first hospital day showed two round, low-echo, abnormalities measuring 1.0 cm, in diameter each, surrounded by the sinus echoes of the left kidney. Autopsy revealed renal papillary necrosis of the left kidney compatible with the findings on the echogram. In this case, echogram findings useful in detecting the lesions had been obtained on the first hospital day. Vesicoureteral reflux due to atonic bladder was presumed responsible for her rapidly progressive course to sepsis and DIC.

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