Dr. Imagawa's group proposed the concept of non-autoimmune fulminant type 1 diabetes citing cases which developed through ketoacidosis, and in which the patient's HbA1c was normal or increased only slightly at the time of outbreak, the auto-antibodies of the pancreatic beta cells were negative and the ability of insulin secretion was markedly lower. At our hospital, over several years, we studied the clinical picture and insulin secretion ability of 7 cases, which met this screening outline of non-autoimmune fulminant type 1 diabetes using glucagon loading tests
In 5 cases in whom glucagon loading tests given during outbreak were examined, the serum CPR of glucagon loading after 6 minutes was below 0.1ng/ml and suggested the complete destruction of pancreatic beta cells at the time of outbreak. Furthermore, glucagon loading tests were administered about every six months after onset and the insulin secretion ability was examined over several years, the longest case being 7 years. In all 6 cases the serum CPR of glucagon loading after 6 minutes was below 0.1ng/ml, and in no case was recognizable recovery of insulin secretion ability seen.

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We studied pancreatic endocrine function following simultaneous pancreas-kidney transplantation in three Japanese patients after the passing of the transplantation law. Patient 1 was a 39-year-old female. The first phase of insulin secretion in response to intravenous glucose was seen at 12 days after the transplantation but not at 6 days. She was totally free from insulin treatment after 103 days. Patient 2 was a 29-yearold female. Insulin treatment became unnecessary immediately after the transplantation. Insulin secretion was supernormal in the intravenous glucose tolerance test at 6 days. Patient 3 was a 36-year-old female. A non-beating heart donation was performed. Insulin secretion was profoundly suppressed immediately after the transplantation, but recovered after 7 days in accordance with the increase in urinary amylase excretion. Insulin secretion was modest in the first phase but evident in the second phase of insulin secretion at 31 days, and insulin treatment was withdrawn at 30 days. Hyperproinsulinemia was detected in patient 3, whereas pasma glucagon levels were elevated in all three cases. Renal graft functions were equally normalized, but the clinical courses of pancreatic endocrine function varied between the three recipients during the early phase after the simultaneous kidney-pancreas transplantation.

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[in Japanese]

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We report our treatment of siblings with hereditary hemochromatosis with diabetes mellitus. Case 1: A 51-year-old man with diabetes mellitus admitted for acute heart failure was confirmed in biopsy of the myocardium to have hemochromatosis. Heart failure adversely affected venesection, treatment. He died four months after admission. His HLA typing was A 24, 52; B 44, 52, w 4. Case 2: A 50 year old woman, the younger sister of case 1, was treated for diabetes mellitus for 6 months. Liver biopsy confirmed the diagnosis of hemochromatosis. Venesection resulted in increased well-being. Her HLA typing was A 24; B 46, 52. Mutations in HFE genes (C 282 Y/H 63 D) were not seen in either case. We measured serum ferritin in 958 patients with diabetes mellitus, but found no hemochromatosis. In Japanese, most cases of hereditary hemochromatosis have no specific HLA typing or HFE genes. Fewer patients with hemochromatosis are reported in Japanese than in Caucasians. Early venesection is effective. Diagnosis depends on a high degree of suspicion and should be considered as a rare cause of diabetes mellitus. J. Japan Diab. Soc. 46 (3): 235-240, 2003

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We report a rare case of dose-related glibenclamide-induced liver toxicity. A 55-year-old man first diagnosed with type 2 diabetes in 1993 was treated with glibenclamide, 1.25mg day, from November 1995. Since diabetes mellitus control became poor, we increased the dosage from 2.5 to 5mg in February 1999. After 1 month, he was hospitalized for systemic jaundice and liver dysfunction (GOT 930 IU l, GPT 1560 IU l, T. Bil 26.3mg dl). Liver dysfunction improved after interruption of glibenclamide therapy for 2 months. We treated him again with glibenclamide again and liver function worsened. When glibenclamide was withdrawn, liver function returned to normal. Extrahepatic biliary obstruction, infectious hepatitis, primary liver disease, and exposure to other drugs were all excluded as a cause of liver dysfunction in this case.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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