Eun Sasaki

Postprandial hypotension in patients with non-insulin-dependent diabetes mellitus

This study attempted to determine whether postprandial hypotension (PPH) is associated with diabetes mellitus by 24-h ambulatory blood pressure monitoring (24-h ABPM) and by monitoring blood pressure during 75-g oral glucose tolerance test (75-g OGTT) in 15 normal subjects and 35 patients with non-insulin-dependent diabetes mellitus. When we defined PPH as a postprandial decrease in systolic blood pressure of greater than 20 mmHg, the incidence of PPH in diabetics was 37% by 24-h ABPM and 20% by 75-g OGTT. The incidence of proliferative retinopathy and proteinuria was greater in diabetics with PPH than in those without PPH. All of the patients with PPH had somatic and autonomic neuropathy. The C-peptide response was lower in diabetics with PPH than in those without PPH. We revealed the presence of PPH in diabetics, and found that PPH was closely related to disease severity, especially diabetic autonomic neuropathy.

Acarbose improved severe postprandial hypotension in a patient with diabetes mellitus.

Postprandial hypotension (PPH) is defined as a decrease of systolic blood pressure by more than 20 mmHg after meals. Severe PPH is a troublesome diabetic complication, which has no established means of treatment. We encountered a patient who had diabetes mellitus complicated by severe PPH and attempted to treat this problem using several medications (octreotide, midodrine hydrochloride, and acarbose). A 58-year-old male with diabetic triopathy complained of orthostatic dizziness and vertigo after meals. The blood pressure was monitored for 24 h with an ambulatory blood pressure monitor, revealing that the systolic blood pressure decreased markedly after breakfast and dinner by 45 and 50 mmHg, respectively. PPH was not improved by a subcutaneous injection of octreotide. Administration of midodrine hydrochloride reduced the frequency of hypotensive episodes from twice to once daily, but the magnitude of the postprandial fall in blood pressure was still around 30 mmHg. After the patient started to receive acarbose therapy, the postprandial fall in blood pressure was diminished to 18 mmHg and his symptoms largely disappeared. For the treatment of PPH in diabetic patients, our experience suggests that it may be appropriate to try first on alpha-glucosidase inhibitor like acarbose.

Cerebrovascular Disease in Type 2 Diabetic Patients Without Hypertension

To the Editor: The close relationship between diabetes mellitus and arteriosclerosis of the cerebral arteries has recently been reported. However, in these studies, the subjects included older patients with hypertension, which itself is a significant risk factor for arteriosclerosis of the cerebral arteries.1–3 Thus, previous studies on the effect of diabetes on the development of sclerosis were confounded by hypertension and aging. Therefore, we examined relatively young patients with diabetes mellitus who did not have hypertension in order to clarify the influence of diabetes mellitus itself on the development of sclerosis of the cerebral arteries. The subjects included 30 patients with type 2 diabetes mellitus (DM). The subjects with DM did not have hypertension (systolic blood pressure <140 mm Hg, diastolic blood pressure <90 mm Hg) and had no history of cerebral infarction, diabetic retinopathy, diabetic neuropathy, or diabetic nephropathy. Among the 30 diabetic patients, 4 were being treated with insulin injections, 10 with oral hypoglycemic agents, and 16 with dietary therapy alone. The control group (C) consisted of 20 healthy adults without a history of diabetes, hypertension, or cerebral infarction. There were no significant differences in age (DM: 50.1±7.0 years versus C: 49.7±6.7 years), sex (DM: 21/9 versus C: 11/9 [M/F]), systolic blood pressure (DM: 120±11 mm Hg versus C: 117±10 mm Hg) between the …

Differences in heart rate variability in non-hypertensive diabetic patients correlate with the presence of underlying cerebrovascular disease

We previously showed that diabetes contributes to the development of sclerotic lesions in cerebral arteries. In this study, we attempted to clarify whether differences in heart rate variability in non‐hypertensive diabetic patients were dependent on the presence or absence of underlying cerebrovascular disease. Thirty diabetic subjects between 40 and 59 years of age and who had no prior history of hypertension were used in this study. Lacunar lesions (LA) were detected with magnetic resonance imaging and atherosclerotic lesions (AS) were detected using intra‐ and extracranial magnetic resonance angiography, and by ultrasonographic scanning of the carotid artery. Patients underwent a full clinical laboratory screening and a power spectrum analysis of their heart rate variability. Subjects were divided into two groups: those with and without LA. The low frequency/high frequency ratio (LF/HF ratio) was found to be significantly increased (P<0·01) in subjects with LA (2·2 ± 0·3) compared to those without LA (1·3 ± 0·1). When subjects were divided into groups based on their presence or absence of AS, high‐frequency power was found to be significantly reduced (P<0·05) in the subjects with AS (12·8 ± 3·4 ms) compared to those without AS (19·4 ± 1·7 ms). The LF/HF ratio was found to be significantly increased (P<0·05) in the subjects with AS (2·2 ± 0·3) compared to those without AS (1·4 ± 0·1). Our data suggested that atherosclerotic lesions in cerebrovascular diseased linked to decrease of vagal nerve activity in non‐hypertensive diabetic patients.

A patient with diabetes mellitus, cardiomyopathy, and a mitochondrial gene mutation: confirmation of a gene mutation in cardiac muscle

A 44-year-old woman with diabetes mellitus, cardiomyopathy, and a mitochondrial gene mutation, was reported. She was diagnosed as having diabetes at 33 years of age and was treated with insulin. However, she stopped treatment 6 months later and had no medical care until she developed diabetic ketoacidosis at 41 years of age. She had diabetic foot, diabetic retinopathy, and nephropathy with low insulin secretory capacity, leading to insulin treatment. A point mutation of the mitochondrial tRNA(Leu(UUR)) gene was identified in peripheral leukocytes at 43 years of age, and sensorineural hearing impairment was detected at the same time. Her mother also suffered from diabetes mellitus with deafness and her son, who was not diabetic at age 19, had the same mitochondrial DNA (mtDNA) mutation. At 44 years of age, she developed congestive heart failure due to cardiomyopathy, and the same mtDNA mutation was identified in the cardiac muscle. Thus, it is very likely that in this patient, diabetes and cardiomyopathy was caused by the same abnormality, the point mutation of mitochondrial tRNA(Leu(UUR)) gene.

Insulin-dependent diabetes mellitus in which glycemic control was improved during pregnancy but deteriorated after delivery with the occurrence of postpartum thyrotoxicosis: a case report

We report a patient, a twin, with diabetes mellitus whose hyperglycemic state fluctuated during the course of the pregnancy and the subsequent delivery. She was diagnosed as having slowly progressive IDDM because of her clinical course and the findings of serum positive ICA/CF, positive HLA-DR4 and disconcordance of diabetes mellitus with her identical twin. Insulin therapy was not initially needed in the first two years because the endogenous insulin secretion was not completely reduced. After two years of insulin therapy the patient became pregnant. Her glycemic control was remarkably improved without changes in dietary intake and insulin dosage. After delivery glycemic control deteriorated after delivery with the occurrence of postpartum thyroiditis. Urinary excretion of CPR was increased during pregnancy but decreased after delivery. ICA/CF in serum were persistently detected in the whole observation period. It seems that the improved glycemic control during pregnancy was caused by the reduction in the autoimmune reaction and the deterioration in glycemic control during the postpartum period was induced by the acceleration of the autoimmune reaction by the same mechanism of postpartum autoimmune thyroiditis.