To clarify the relationship between arteriosclerosis of carotid artery and DC 36 antigen activation in peripheral blood monocytes in type 2 diabetes, we analyzed the activation of CD 36 by histogram using flow cytometry for 106 cases of type 2 diabetes divided into 3 groups: Group I, low activation; Group II, intermediate activation; and Group III, high activation.
A comparison of intimamediathickness (IMT) in carotid arteries for the 3 groups should no significant difference between them. The frequency of atheromatous plaque formation for Group I was 43%, for Group II 63%, and for Group III 92%, indicating that the frequency of plaque formation significantly higher (p<0.05) with increasingly activate CD 36 in peripheral blood monocytes. CD 36 activation of peripheral blood monocytes thus appears to be correlated with plaque formation in carotid arteries in type 2 diabetic patients.

View full abstract

Imagawa et al. defined rapid-onset type 1 diabetes with pancreatic exocrine dysfunction as nonautoimmune fulminant type 1 diabetes mellitus based on clinical and histological studies. We studied 5 patients suspected of nonautoimmune fulminant type 1 diabetes mellitus. They did not have antibodies against glutamic acid decarboxylase, IA-2, thyroid, gastric wall, adrenal cortex, or pituitary. Of the 5 patients, 4 were women, in whom 3, the onset of nonautoimmune fulminant type 1 diabetes mellitus was associated with pregnancy or delivery. Three of the 5 patients had HLA DRB 1*0405, DQB 1*0401, as haplotype susceptible to type 1 diabetes in Japanese. Another patient had both susceptible and protective haplotypes, but the other had none of these. We suggest nonautoimmune fulminant type 1 diabetes mellitus may be related to pregnancy or the HLA DRB 1*0405, DQB 1*0401 haplotype.

View full abstract

To characterize the secondary failure of troglitazone, we retrospectively examined type 2 diabetic patients treated with troglitazone, whose HbA_1c levels improved by≥1% within 6 months. Afterwards, HbA_1c of 17 patients remained reliably controlled at≤0.5% fluctuation for 24 months (steady group) and that of 14 other patients increased by≥1%(deteriorated group). Fasting plasma insulin (IRI) and the homeostasis model assessment index (HOMA-R) declined significantly in troglitazone treatment of both groups but returned to pretreatment levels in the deteriorated group as glycemic control worsened. The deteriorated group had significantly lower pretreatment IRI and HOMA-R compared to the steady group. Multiple logistic regression analysis showed that significant predictors for deteriorating glycemic control were pretreatment HOMA-R and a body weight increase in the first 6 months. HOMA-R was a predictive factor in patients whose glycemic control deteriorated before 12 months and body weight increase was a factor in other patients with deterioration after 12 months. These results indicate that low insulin resistance may lead to early-onset secondary failure of troglitazone, while rapid body weight increase may lead to late-onset secondary failure.

View full abstract

To assess the relationship between diabetic nephropathy and coagulation factors, we divided 73 patients with type 2 diabetes mellitus into 3 groups-normoalbuminuria [normo] with urinary albumin excretion [UAE]<30mg/day, microalbuminuria [micro] with [UAE] from 30-300, and macroalbuminuria [macro] with [UAE]>300. Their D dimer, prothrombin fragments F 1+2 (F 1+2), and fibrinogen were measured. D dimer was significantly higher in the micro group than in the normo group, and was significantly higher in the macro group than in the micro group. F 1+2 was significantly higher in the micro and macro groups than in the normo group. Fibrinogen was significantly higher in the macro group than in the normo and micro groups. Thrombin activation may occur from the early stages of diabetic nephropathy, and may progress as nephropathy progresses.

View full abstract

A26-year-old woman was diagnosed with moderate acute pancreatitis based on abdominal pain, elevated serum amylase, and pancreatic swelling. Plasma glucose on admission was 60mg/dl. Her pancreatids was treated conservatively with a good clinical course in 3 weeks. One week after leaving hospital, she was readmitted due to severe thirst and high plasma glucose (417mg/dl). HbA_1c was 10.1% and her urinary and blood ketone levels were extremely high. These findings and blood gas analysis (pH7.212) revealed that she had diabetic ketoacidosis. Anti-GAD antibodies and ICA were both negative. HLA locus was DR-4, DR-9. Urinary CPR excretion was 5.2μg/day and a glucagon test showed no response of serum CPR with lowest basal CPR. On first admission, the IgM antibody of the Herpes simplex viruses (HSV) was posidve. During first and second admission, IgM antibody titer declined gradually with converse elevation of the HSV IgG antibody titer. After admission, her blood glucose was controlled by intensive insulin therapy. None of the 3 major complications of diabetes mellitus was detected. These findings strongly suggest that HSV infection seriously damages the exocdne and endocrine glands of the pancreas, especially pancreadc B cells, and diabetes inthis case was not due to acute pancreatitis. Clinical similarities exist between our case and nonimmune fulminant type 1 diabetes reported by Imagawa et al. To distinguish them correctly, it is important to check for evidence of viral infection.

View full abstract

We determined the prevalence of so-called diabetic foot by a detailed questionnaire given to diabetic patients and their attending physicians recruited from 7 hospitals in southern Okayama. Prevalence of symptoms suggestive of diabetic peripheral neuropathy was 36.5%, a prevalence that increased with the duration from diabetes diagnosis. Among all patients, 26.6% were suggestively diagnosed as having diabetic neuropathy by attending physicians. Apart from these patients symptoms possively related to vascular disease of the lower limbs were present in 15.7% of patients and possively related to radiculopathy in 13.2%. Foot lesions associated with non-diabetes in diagnosis by attending physicians, were present in 24.9%. The frequency of symptoms related to diabetic neuropathy was relatively high but differed from the frequency of diagnosis by attending physicians. In the diagnosis of diabetic foot, the possibility remains that patients with nondiabetic foot lesions may be included among the patients.

View full abstract

[in Japanese]

View full abstract

[in Japanese]

View full abstract