Malnutrition-related diabetes mellitus, classified by WHO in 1985, is attracting attention in addition to Type 1 and Type 2 diabetes.We studied the effects of low-protein feeding on pancreatic endocrine function. Female Wistar rats were divided into 2 groups, 1 fed regular chow (C-1, Prot.25%) and the other a low-protein diet (P-1, Prot.19.5%).These rats had neonates (C-1-1, P-1-1) after 12 weeks. Adults and neonates were sacrificed immediately after birth, and blood glucose and serum insulin were determined. The pancreas head of adults and the total pancreas of neonates were used for insulin and glucagon assay. Half of the neonates (C-1-1, P-1-1) were fed and the same procedures done (C-2, P-2, C-2-1, P-2-1).
Body weight and tissue content IRI of those fed with low-protein diet (P-1, P-2, P-1-1, P-2-1) were lower than that of controls, but not significant. The tissue content of IRI of P-2-1 was significantly lower than that of P-1-1. These results suggest that a long-term low-protein diet probably decreases pancreatic endocrine function in neonates and may cause future glucose intolerance.

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Since measurement of serum C-peptide (CPR) is important in assessing insulin secretion, several serum CPR assay kits have become commercially available for measurement.To evaluate the correlation between kits, we undertook linearity and cross-reactivity experiments using the highly sensitive IRMA kit (Eiken)(kit E), C-peptide kit III (TFB)(kit T), and C-peptide RIA Shionogi II (Shionogi)(kit S). In normal CPR concentration, linearity and recovery showed permeable results and an appropriate correlation between kits. In low CPR concentration, however, no linearity was seen in CPR kits using polyclonal antibody and they tended to show higher titer than the kit using monoclonal antibody, making it necessary to consider kit accuracy when measuring low CPR concentration.

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A 23-year-old nurse admitted for acute-onset visual impairment had undergone annual health checkups including postprandial urine glucose testing but had never glucosuria detected. Her fundus occuli showed marked neovascularization and fluorescein leakage compatible with proliferative diabetic retinopathy, necessitatinglaser photocoagulation and vitrectomy.Her blood concentration of vascular endothelial growth factor (VEGF) was within normal ranges.Although the present case is considered rare, clinicians should be alert for possible advanced diabetic chronic complications in young patients with new-onset type 2 diabetes mellitus.

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The degree of concordance for NIDDM is higher than that for IDDM even though twins are almost always living apart when diabetes is diagnosed. We report a case of anti-GAD discordance in identical twin sisters with aged onset diabetes.
A 78-year-old woman seen in June 14, 1999, was diagnosed with diabetes mellitus (DM) and treated with oral hypoglycemic agent (OHA). Her blood glucose control recovered slightly and her HbAic fell from 10.4 % to 8.3%.Despite the relatively high 01-IA dose of 3.75mg/day of glibenclamide, HbAic rose to 10.3%, showing high anti-GAD titer of 748.0U/ml. We were informed then that she had an elder identical twin sister.Insulin treatment was started and her HbAic fell to 6.8%.The elder sister, living in Hiroshima, had been diagnosed with DM 10 years ago and treated with OHA.Her HbAic was 7.4% and her anti-GAD negative when she was seen at 80 years of age.These patients had HLA DRB 1*1101-DQA 1*0505-DQB 1* 0301, a well-known protective haplotype for type 1 diabetes.No mitochondrial DNA A 3243 G mutation was detected in either twin.

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Soft drink ketosis is thought to be a subset of type 2 diabetes characterized by acute ketotic onset following excessive ingestion of soft drinks by obese people.We treated an obese 12-year-old girl hospitalized with hyperglycemia and ketosis. Although clinical features in the early course were coincidental with soft drink ketosis, she was IA-2 antibody-positive on admission, suggesting the association with autoimmune β cell destruction in the pathogenesis of her diabetes. After eventual insulin therapy, her diabetes was initially well controlled with metformin alone several months after admission. Fasting plasma glucose increased and IA-2 antibody titer increased, possibly reflecting the progression of β cell destruction, so small doses of insulin therapy were initiated. She was diagnosed with slowly progressive type 1 diabetes. Although she is non-insulin-dependent, she may show a progressive decrease in endogenous insulin secretion.

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We report a case of diabetes complicated by a femoral subcutaneous abscess secondary to septic trochanteric bursitis. A66-year-old woman with a17-year history of untreated diabetes mellitus admitted for severe left leg pain was found in laboratory examination on admission to have leukocytosis and high serum CRP. Despite intensive insulin treatment with antibiotics and hyperbolic oxygen therapy, leg swelling and pain continued and worsened. Computed tomography (CT) showed a large abscess around the thighbone. On hospital day26, the abscess was curettaged and drained. She was diagnosed with trochanteric bursitis by radiography using a contrast medium during surgery. After the operation, she improved rapidly. Septic trochanteric bursitis is rare as a complication of diabetes mellitus. In this patient, poorly controlled diabetes was thought to have caused septic trochanteric bursitis and the femoral subcutaneous abscess.

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A 78-year-old man with type 2 diabetes mellitus admitted for fever and muscular weakness had elevated serum creatine kinase (CK) and myoglobin. Chest radiography showed right upper lobe infiltrates. We diagnosed this as rhabdomyolysis following pneumonia. He was immediately treated with cefotaxime and rehydration. CK progressively rose, peaking at 5549 IU/l on hospital day 6 and decreasing thereafter to a normal level as pneumonia improved. He recovered well without renal failure. Pathogenic bacteria were not determined. Rhabdomyolysis may be seen following viral infections, and has rarely been reported in cases of bacterial pneumonia. Bacterial pneumonia is common in elderly diabetic patients, and precipitates dehydration, hyperglycemia, and electrolyte disturbance. Diabetes is known to predispose patients with hyperosmolarity to rhabdomyolysis, but our case shows that diabetic patients with bacterial infections are also at risk for rhabdomyolysis.

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Only 1 previous case has been reported of a patient successfully resuscitated after cardiac arrest for diabetic ketoacidosis (DKA). We report a second patient suffering cardiac arrest due to ketoacidosis who was also treated successfully. A 36-year-old woman had been healthy until she became thirsty on July 16, 2000. A general practitioner initially diagnosed her as having a cold on the evening of July 18. Dyspnea occurred at 5: 00 on July 19, and she was brought to our hospital by ambulance unconscious and with ventricular tachycardia. Cardiac arrest occurred, but she responded to cardiopulmonary resuscitation. Laboratory data was as follows: blood glucose, 2, 069 mg/dl;total ketone bodies, 11, 070μmol/l; pH, 6.8; HCO3, 3.8 mmol/l; and K, 7.0mmEg l findings of DKA. HbA1c was 6.6%, while GAD antibody was negative. A glucagonloading test showed that insulin secretion was severely reduced. Her diabetes was controlled by administration of 42 units day insulin. The clinical course suggested that our patient had fulminant type 1 diabetes. reat care is needed to recognize the occasional patient with type 1 diabetes among those with cold-like symptoms.

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[in Japanese]

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