Recently, a genetic predisposition to susceptibility to diabetic nephropathy has been suggested. In 1994 Marre et al reported that a Deletion (D)/Insertion (I) polymorphism in the angiotensin I converting enzyme (ACE) gene is related to the development of diabetic nephropathy in insulindependent diabetes mellitus. This theory has been questioned by Schmidt and others, and a consistent conclusion has not been reached. The reason for these contradictory results are thought to be due to the different clinical states of patients tested, especially with respect to blood sugar control.
In this study we examined the relationship between the D/I polymorphism of the ACE gene and diabetic nephropathy in non-insulin-dependent diabetic patients with proliferative retinopathy (n=45), who were thought to have been exposed to a hyperglycemic state long enough to suffer from microangiopathy. They were divided into two subgroups: 24 patients with nephropathy (albumin excretion rate: AER≥20μg/min) and 21 patients without nephropathy (AER<20μg/min). There was no difference between these subgroups in the duration of diabetes, the level of HbA1c, or average blood pressure in the latest year, nor in other clinical characteristics. However, patients without nephropathy had the I allele more often than those with nephropathy (P=0.025). AER was lowest in the II genotype and highest in the DD genotype but the difference was not significant (P=0.07).
From the findings of the present study, it was concluded that the II genotype of the ACE gene is a marker for reduced risk for diabetic nephropathy.

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We investigated the long-term effect of an a-glucosidase inhibitor (Acarbose) on metabolic control in patients with insulin-dependent diabetes mellitus (IDDM) with or without an eating disorder. The subjects were 21 IDDM patients, 14 female and 7 male, aged 11-62 years, with poor metabolic control. Acarbose at 150mg/day was administered for three months. Acarbose was considered effective if the improvement of mean HbA_1c was more than 5%, which was calculated by the difference between the mean HbA_1c of three months before and after the administration. It was effective in 8 patients (group A) and not effective in 13 patients (group B). Six patients in group B had binge eating disorder; their mean age was 23 years, 5 were female and 1 was male. Acarbose had no effect on any of them with binge eating disorder. Otherwise there were no differences between group A and group B with respect to insulin dose, BMI, baseline HbA_1c values and microvascular complications. None of patients had severe side effects. We suggest that Acarbose may be effective for a long-term metabolic control in IDDM patients without eating disorder, and is worth continuing.

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Measurement of levels of HbA1c and glycated proteins, such as glycated albumin (GA) and fructosamine, is the most reliable method of assessing long-term glycemic control in diabetic patients. However, little is known about GA in patients with associated uremia. In order to clarify the effects of impaired renal function on GA levels, we measured blood glucose, HbA_1c, GA, serum albumin and blood urea nitrogen in patients with and without chronic renal failure (CRF). Each group was divided into normal glucose tolerance, borderline glucose tolerance and diabetic subgroups. There was no difference in GA levels between those with and without CRF in either the normal or the borderline glucose tolerance groups. HbA_1c levels in the CRF group were significantly lower in the patients taking erythropoietin than in the patients not taking erythropoietin. Multivariate regression analysis revealed that neither the serum albumin nor the blood urea nitrogen level independently influenced GA levels. Fasting blood glucose and age were variables that independently influenced GA levels. In contrast, HbA_1c was strongly influenced by both erythropoietin dosage and fasting blood glucose. In conclusion, GA is a more useful indicator of glycemic control than HbA_1c in diabetic patients with end-stage renal disease.

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Establishment of a simple and reliable test to assess cardiovascular autonomic nerve function is important since impairment of these nerves is associated with high mortality in diabetic patients. In the present study, we examined heart rate changes during standing and squatting to evaluate the integrity of parasympathetic and sympathetic nerves in a series of tests and compared the results with those of other reflex tests widely used to diagnose autonomic neuropathy: coefficient of variation of R-R intervals (CV_RR) at rest, blood pressure changes after standing (OH), and analysis of heart rate variability on 24-h ECG recordings. In the squatting test, each subject stood still for 3 min, squatted for Lmin and then stood up for 1 min. The squatting test vagal (SqTv) and sympathetic (SqTs) ratios were calculated in 72 healthy subjects and 39 diabetics over 40 years of age. The reproducibility of the SqTv and SqTs ratios was less 6%. Because the SqTv ratio increased with age in healthy subjects and the SqTs ratio decreased, reference ranges of means±SD were obtained in 10-year intervals. Thirty-eight of 39 diabetics diagnosed as having autonomic dysfunction based on positive, findings on either CV_RR or OH, or both, also had an abnormal SqTv and/or SqTs ratio, and those who were classified as having autonomic dysfunction by the squatting test though negative on CV_RR and OH had abnormalities on their 24-h ECG recordings alone. The squatting test is a useful tool to simultaneously parasympathetic and sympathetic regulatory identifydys function at a relatively early stage of diabetic autonomic neuropathy.

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A 70-year-old man, diagnosed as having pancreatic diabetes, was admitted in December 1993 with the complaint of a mass in the right lower quadrant of the abdomen. Abdominal arteriography was performed and a saccular aneurysm of the right common iliac artery was found. He was treated surgically and the operation showed the aneurysm adherent to a surrounding retroperitoneal abscess. Culture of specimen from it yielded Candida albicans. Histological examination of the excised aneurysm showed severe atherosclerosis and no active inflammation. In this case the aneurysm was assumed to be a result of the retroperitoneal abscess on the basis, of the severe atheroscrelotic change in the right common iliac artery. The retroperitoneal abscess was presumed to be a complication of candidal infection acquired during intravenous hyperalimenta. tion at a gastorectomy in 1989. The cell-mediated immune deficiency resulting from his diabetes was presumed responsible for recurrence of the candidal infection.

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A 28-year-old woman with insulin-dependent diabetes mellitus was hospitalized after referral from a local hospital on October 16, 1994. Lowered consciousness and hypothermia were noted. The plasma glucose level was 633mg/dl, arterial blood gas analysis revealed pH 6.898, PaCO2 7.2mmHg, PaO₂ 112.7 mmHg, indicating hyperglycemia and metabolic acidosis. Under a diagnosis of diabetic ketoacidosis (DKA), she was immediately transfused with fluid, insulin and antibiotics. Cough, foamy sputum, and dyspnea followed by hypoxemia and pulmonary edema developed about 14 hours after the initiation of treatment. Oxygen inhalation was started, but her general condition deteriorated rapidly and apnea and shock appeared 20 hours after hospitalization. Respiratory management was started immediately under cardiac massage, then hydrocortisone and urinastatin were administered. Her blood pressure was barely maintained by life-support treatment, but PaO₂ was 15-17mmHg, indicating an extremely hypoxic state that persisted for about 6 hours. During that period, the patient was apprehensive of severe disturbance in the central nervous system. However, the PaO₂ gradually increased, and her consciousness eventually improved. Respiratory management was continued by using a respirator with positive end-expiratory pressure (PEEP) for 8 days, resulting in survival without neurological damage. Our experience with this patient suggested that respiratory management using PEEP, acute administration of a corticosteroid, and a protease inhibitor are important in treating adult respiratory distress syndrome associated with DKA.

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