Myocardial distribution of¹²³I-MIBG was examined in 43 NIDDM patients (33 men, 10 women, age58.9±15.9years) using single-photon emission tomography. According to the defect pattern of¹²³I-MIBG imaging, the patients were divided into three groups. The study groups consisted of group N with normal¹²³I-MIBG uptake (n=18), group I with normal¹²³I-MIBG uptake at15min and a perfusion defect of the inferior wall at180min after injection (n=15), and group II with a clear perfusion defect to the inferior wall at both 15min and 180min after injection (n=10). Diabetic duration of group I and II was significantly longer than group N (N 4.6 years vs. I 10.4 years, II 15.0 years) and fasting plasma glucose and HbAic of I and II groups tended to be higher than for group N (HbAic N 6.5%vs. I 7.5%, II 7.6%). Patients with diabetic retinopathy, nephropathy or neuropathy were more frequent in group II than in either group N or group I. Six of ten patients in group II had retinopathy, and three of these, had B stage retinopathy, but groups N and I included no retinopathy patients. Patients with diabetic nephropathy were seven of ten in group II, but no patients in group N had nephropathy. Nerve conduction velocity in group II was significantly slower than in group N (N52.6m/sec vs. II 41.5m/sec), CV_{R_R}was remarkably smaller than in group N (N 3.18% vs. II 1.71%) and washout rate of¹²³I-MIBG from 15min to 180 min after injection was significantly accelerated in group II (N 10.4% vs. II 24.9%). Every group included 20-30% of patients with hypertension and cardiomegaly. In regards to blood pressure and cardiothoracic ratio no significant differences were found among the three groups. In group II, two patients had atrial fibrillation.

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A study was made of 107 cases of non-insulin-dependent diabetes mellitus. These cases were measured continuously over 9 years, from 1986 to 1995, using as an indicator the albumin-creatinine ratio (A/C) of random urine samples.These cases were divided into 4 groups according to the degree of A/C (mg/g.crea.) in the first year: A (<30) B (31-00), C (101-300) and D>301). The change in A/C was observed over the 9 years, revealing that 23 out of the 85 cases in groups A and B deteriorated into group D, and 13 out of 14 in group C.On the other hand, 7 out of 24 cases in group B improved into group A, while no cases in group C or D showed any improvement.It was only after deteriorating to group D that some cases died of vascular complication.The cases were divided into a stable group (A→A.B→A, B) and a worsening group (A, B→C, D.C→D) by the A/C measurement in the last year, and blood pressure and glycemic controls were compared between these groups yearly intervals.In the worsening group, systolic blood pressure remained high throughout the 9 years, diastolic blood pressure became high from the fourth year, and serum creatinine became high from the seventh year.The prevalence rate of hypertension was apparentlyhigh throughout the 9 years.On the other hand, the mean values of fasting blood glucose (FBG) and 2 h post prandial blood glucose (2 hBG), and the prevalence rate of hyperglycemia, were all significantly high in the first 4 years, while there was no difference between the stable group and the worsening group in these measures during the subsequent 5 years.
The point of no return for A/C was in the stage where th e A/C is under 100 mg/g.crea. It is apparent that hypertension throughout the 9 years, and hyperglycemia in the frist 4 of the 9 years, were involved in the deterioration of diabetic nephropathy.

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To evaluate methods of blood glucose control affecting the retinopathy of NIDDM patients without Achilles'tendon reflex (ATR), in those cases with a high incidence of retinopathy deterioratation when rapid blood glucose control (RBC) was performed, 84 patients were studied. All subjects were hospitalized for 2-4 weeks for a checkup. FBG was measured every day and followed up for one year. HbA_1c was measured every 3 months. A retinal examination was performed on admission and again after one year. Deterioration in retinopathy was defined as either a progressionof NDR to SDR, or of preproliferative retinopathy (PPDR) and SDR to PPDR.
The rate of change of HbAic after 3 months and of FBG after 2 weeks was employed in the index of blood glucose control. Mean HbAic of one year was defined as mean HbA_1c 3 months after admission. The retinopathy condition deteriorated in 27cases. The rate of change of HbA_1c after 3 months (RCH) and of FBG after 2 weeks (RCF) was correlated significantly (r=0.71p<0.0001), and retinopathy deteriorated significantly more when RCH and RCF was more than 30%.The rate of deterioration in retinopathy was highest (77%) when RCH was more than 30% and mean HbAic was above 8%, and deterio ration was lowest (7%) when RCH was less than 30% and mean HbAic was below 8%. These results indicate that blood glucose control in admission must be handled conservatively and mean HbA_1c of one year must be below 8% in NIDDM patients without ATR.

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We often observe hypoglycemic symptoms to occur at a wide glycemic range. Some patients feel hypoglycemic symptoms at 90 mg/dl, while other patients don't feel them even as low as 40 mg/dl. To elucidate this diversity, we determined glycemic thresholds for counterregulatory hormone secretion and hypoglycemic symptoms by using an artificial pancreas. Twenty-six variously controlled diabetic patients, 1insulinoma patient, and9healthy controls were analyzed. Diabetics with recent episods of hypoglycemia had significantly lower thresholds for epinephrine than subjects without hypoglycemia. Diabetics had several glycemic thresholds for epinephrine at a wide glycemic range (30-110 mg/dl). The high-glycemic threshold group (more than mean±2 SD of healthy controls) had significantly higher HbA1c, 13.0±3.0%, than did the low-threshold group (less than mean-2SD). 7.8%.
In general, glycemic thresholds for epinephrine secretion parallel HbA1c, but hypoglycemic episods change this tendency. A lowered threshold for epinephrine in the insulinoma patient elevated toward the normal range after pancreatectomy. To the contrary, the glycemic threshold of a very poorly/controlled IDDM woman were elevated. Intensive insulin therapy for 1 month lowered it toward the normal range. In conclusion, continuous hyperglycemia may elevate the glycemic threshold for epinephrine secretion and autonomic symptoms, but episods of hypoglycemia may lower them. Avoiding hyperglycemia or hypoglycemia normalized abnormal glycemic thresholds.

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A 52-year-old female with non-insulin-dependent diabetes mellitus (NIDDM) was admitted to our hospital on January5, 1997, because of high fever and macrohematuria. Laboratory examination showed massive hematuria, prolonged erythrocyte sedimentation rate, positive CRP, thrombocytopenia and renal dysfunction. E. coli and Klebsiella were detected in urine and blood cultures. A plain abdominal roentgenogram revealed a “radiolucent ring” suggesting gas filled intramucus of the bladder wall. Despite treatment with antibiotics and pressor agents for about 5 hours, she suddenly died of septic shock. On autopsy, macroscopic examination showed no vesicular formation in the kidney or bladder mucosa, however, microscopic examination showed the appearance of vacuoles by a pool of gas, which existed in the external circumferense of the tubular basement membrane in the cortex of the kidney, and there was evidence of vacuolation with aerogenesis in the tunica mucosa ventriculi and submucosa of the bladder. These findings confirmed emphysematous cystitis, which is a rare disease frequently complicated by diabetes mellitus. In this patient, the poorly controlled diabetes may have been related to the cause of the disease and death.

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We describe a rare autopsy case of IDDM with Cogan's syndrome reported previously. A 42-year-old man who was treated with insulin for15years and with glucocorticoid and β-blocker for 11years was admitted to the hospital because of anorexia. He had been diagnosed as IDDM at the age of 27 and subsequently as Cogan's syndrome with deafness and blindness at the age of 31. Microalbuminuria appeared at35years old and develoed into nephrotic syndrome at 41 years old. He died of progressive uremia with pyuria. For these 15 years, HbAic was8-10%, indicating that his blood glucose levels were constnantly high because he often stopped taking the injection of insulin. Also, he had sustained high blood pressure and hyperlipidemia because of refusing to take the medication continuously.
The pathological findings at autopsy showed a decrease inβcells without hyalinosis in Langerhans islets, advanced diabetic nephropathy with papillary necrosis of the left kidney, severe atherosclerosis of the aorta and systemic arteies without evidence of arteritis, and concentric hypertrophy of the cardiac left ventricle with fibrinous pericarditis. Since Cogan's syndrome is a subtype of polyarteritis nodosa caused by autoimmunity, the severity of the atherosclerosis may be increased by the immunological factor in the pathogenesis of Cogan's syndrome.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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