It is extremely important in preventive medicine to screen for postprandial hyperglycemia (PPHG), which is considered to be a risk factor for diabetes and macroangiopathy. We devised a screening method in which gender-segregated cutoff values for 1,5-anhydroglucitol (1,5-AG) were set and the 1,5-AG level was combined with the fasting plasma glucose (FPG) level in cases that fell close to the 1,5-AG threshold. We called this method the KKC method. Using the KKC method, we obtained a sensitivity of 83.3% and a positive predictive value (PPV) of 71.4% when screening for PPHG. The screening results for FPG (using a 95 mg/dl cutoff value) were also 83.3% for sensitivity but had a much lower PPV. The KKC method appears to be an efficient screening method for PPHG during the fasting state. We have efficiently discovered 10-20 new subjects with PPHG every year in a community of 1,500 people using the KKC method.

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The Melbin observational research (MORE) study assessed the efficacy and safelty in Japanese type 2 diabetic patients treated with conventional metformin therapy. A total of 1,197 patients who received metformin therapy for the first time at 74 medical institutions, were enrolled in 2002. Mean HbA_1C and fasting plasma glucose (FPG) values measured at 0, 3, 6 and 12 months of treatment. Mean HbA_1C measured 8.2, 7.3, 7.3, and 7.3% and FPG 168.9, 146.6, 150.4, and 145.2 mg/dl, indicating significantly improved glycemic control during treatment. Body weight was significantly reduced, and no meaningful effect was observed on lipid metabolism. Similar effects were observed in patients treated with metformin alone. HbA_1C improved significantly in 40 cases where the daily dose of metformin was increased from 500 mg to 750 mg. The incidence of adverse drug reactions was 10.0% (118/1,175 cases) and no lactic acidosis was observed. These results demonstrate a significant usefulness of current metformin therapy in Japanese type 2 diabetes mellitus. Results also suggest that an appropriate increment in the daily dose of metformin is required to obtain desirable HbA_1C in patients whose glycemic control would otherwise not be acceptable.

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[in Japanese]

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Peroneal nerve palsy is a type of diabetic mononeuropathy that usually results in self-limited symptoms. We experienced a type 2 diabetic patient who suffered from peroneal nerve palsy for more than one year, resulting in crus muscle atrophy. The patient was a 55-year-old Japanese man who had no remarkable past medical history except for a habit of drinking 720 ml of sake a day for 30 years. He was diagnosed as having diabetes mellitus in 1994, but he did not receive regular treatments. Although he started to take an oral hypoglycemic agent in 1998, his glycohemoglobin (HbA_1C) level remained at 9-10%. In 1999, the patient was pointed out diabetic retinopathy for the first time. Since then, he started medical nutrition therapy. His HbA_1C immediately fell to 7-8%. He suddenly felt paresthesia and a pricking in his right femoral region, and right crus numbness, hypersthenia and drop foot soon appeared thereafter. He visited our hospital in May 2004 and was admitted for further examinations for peroneal nerve palsy. On admission, his HbA_1C was 5-6%, deep reflexes were absent or reduced, and pallanesthesia and numbness in limbs, a Tinnel sign for the right peroneal nerve, atrophy in the anterior tibial muscle, and right drop foot were observed. A nerve conduction study (NCS) revealed right peroneal nerve palsy. Although his HbA_1C level was maintained within 5-6% for 6 months after discharge, nerve conduction studies performed at 3 and 6 months after discharge showed that his peroneal nerve palsy had only slightly recovered. Peroneal nerve palsy may have persisted for a long period, resulting in muscle atrophy, in the present patient because of the presence of not only diabetic mononeuropathy, but possible alcoholic neuropathy and proximal diabetic neuropathy.

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A 64-year-old man with a history of diabetic coma was admitted for loss of consciousness and convulsions with chronic alcohol abuse, and recent binge drinking followed by abrupt cessation of alcohol and loss of appetite. Previously diabetic ketoacidosis was suspected because of his history of diabetic coma. His metabolic acidosis was corrected quickly by hydration and administration of insulin without sodium bicarbonate. Based on mild elevation of blood glucose and HbA_1C, and increasing serum ketone bodies with elevation of the ratio of β-hydroxybutyric acid to acetoacetic acid, we diagnosed his case as alcoholic ketoacidosis (AKA) with type 2 diabetes mellitus. Pathophysiologically, ethanol abuse, acute starvation, and dehydration directly cause AKA. Decreased NAD and glycogen by excessive alcohol intake and suppressed glycogenesis suppress insulin secretion. β oxidation stimulation by low insulin causes increasing levels of ketone bodies and progression of metabolic acidosis. Hydration with electrolytes and administration of glucose are the basic treatment for AKA patients without diabetes. AKA with delay in treatment or marked metabolic acidosis is frequently fatal. AKA is thus an important differential diagnosis among diabetes patients with a history of chronic alcohol abuse and metabolic acidosis.

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A 58-year-old woman with type 2 diabetes mellitus had interrupted medical treatment for five years. She suffered from right otitis externa and media by pseudomonas aerginosa after injury to the external acoustic meatus, and recovered by antibiotics for a month with sequela of deafness. Multiple cranial neuropathy (right II, III, IV, V₁, VI, VII, IX, and X cranial nerve) progressed acutely four month later, and she was diagnosed with Garcin's syndrome. Pseudomonas aerginosa was detected by cultivation of otorrhea. It became clear by contrast-enhanced MRI with fat suppression that inflammation extended from the right middle ear to the skull base. Contrast-enhanced MRI with fat suppression is useful for detecting osteomyelitis of the skull base. The clinical course in our case indicated that susceptibility of infection in diabetes sometimes led to critical condition.

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[in Japanese]

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Not only postprandial hyperglycemia, but also postprandial hyperlipidemia contributes to the development of atherosclerosis. International standards for test meals used to assess both postprandial hyperglycemia and hyperlipidemia simultaneously must now be established. In this report, we prepared a “test meal A” containing a total energy of 450 kcal with 51.4% from carbohydrates, 33.3% from fats and 15.3% from proteins. Eighteen diabetics, 12 IGTs and 29 subjects with normal glucose tolerance, were enrolled in this study. An oral glucose tolerance test was performed one week after the test meal load. There was a close relationship between blood glucose values at 2 hours after glucose loading and at 2 hours after test meal loading. The blood glucose value of 200 mg/dl at 2 hours after glucose loading corresponded to 150 mg/dl at the same sampling point after test meal loading, and the blood glucose value of 140 mg/dl at 2 hours after glucose loading corresponded to 110 mg/dl at the same sampling point after test meal loading. A significant elevation in plasma triglyceride was found in normotriglyceridemic subjects after the test meal load. Thus, the “test meal A”, which we demonstrated here, could be used as a pilot model for the assessment of both postprandial hyperglycemia and hyperlipidemia simultaneously in diabetic subjects.

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