Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 48, Issue 3
Displaying 1-7 of 7 articles from this issue
Original Article
  • Toru Matsudaira, Rimei Nishimura, Hironari Sano, Tsuyoshi Isaka, Futos ...
    2005 Volume 48 Issue 3 Pages 159-164
    Published: 2005
    Released on J-STAGE: April 11, 2008
    JOURNAL FREE ACCESS
    Appropriate glimepiride dosage when switching from widely used sulfonylureas (SU) to glimepiride is not well documented, so we studied the glimepiride dosage and change in HbA1c among type 2 diabetic patients who were on glibenclamide (2.5-5.0 mg) or gliclazide (40-80 mg). We stratified patients into 4 groups based on previous regimens and set the glimepiride dosage as follows : group A : glibenclamide 2.5 mg to glimepiride 2 mg daily ; group B : glibenclamide 5.0 mg to glimepiride 3 or 4 mg daily ; group C : gliclazide 40 mg to glimepiride 1 mg daily ; group D : gliclazide 80 mg to glimepiride 2 mg daily. Clinical data were examined before and after 6 months of observation. The glimepiride dosage was adjusted by physicians. Glimepiride dosages were increased in all groups, and significantly so in groups B and C. We concluded that the initial dosage of glimepiride to be substituted for previously used SU to maintain similar HbA1c may not be enough.
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Case Reports
  • K. Fujisawa, N. Okada, K. Sakai, K. Yamaguchi
    2005 Volume 48 Issue 3 Pages 165-170
    Published: 2005
    Released on J-STAGE: April 11, 2008
    JOURNAL FREE ACCESS
  • Masaharu Morohoshi, Motoki Tagami, Takako Arai, Isao Uchimura, Yukio H ...
    2005 Volume 48 Issue 3 Pages 171-176
    Published: 2005
    Released on J-STAGE: April 11, 2008
    JOURNAL FREE ACCESS
    A 65-year-old woman with polymyalgia rheumatica and chronic thyroiditis admitted to hospital due to coma from hyperglycemia and ketoacidosis had a clinical history and laboratory data consistent with a diagnosis of fulminant type 1 diabetes. Proteinuria had not, however developed. After she was discharged, proteinuria occurred with hypoalbuminemia, leading to a diagnosis of nephrosis-like syndrome. She was treated with a protein-restricted diet, prednisone (15 mg) and ACE inhibitor. Membranous nephropathy was diagnosed by histological examination in renal biopsy. Proteinuria improved over the year. Diabetic nephropathy commonly progresses based on diabetes duration and glycemic control, but in this atypical case, the early development of proteinuria appeared to be associated with fluminant type 1 diabetes onset.
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  • Norimasa Sato, Mikiko Okamoto, Shigeo Totsuzaki, Ichiro Kawai, Eri Shi ...
    2005 Volume 48 Issue 3 Pages 177-181
    Published: 2005
    Released on J-STAGE: April 11, 2008
    JOURNAL FREE ACCESS
    A 29-year-old woman admitted for diabetic ketoacidosis (pH=7.272) had suffered fever and abdominal pain 5 days before admission and developed thirst 2 days before. Despite high plasma blood glucose (642 mg/dl), her HbA1c was 4.9%, within normal range. Serum and urinary C-peptide were low, under normal detection (0.1 ng/ml) and 3.3 μg/day. Both serum amylase (242 IU/l) and urinary amylase (754 IU/l) were elevated. No signs of acute or chronic pancreatitis were detected. After starting insulin therapy, metabolic glucose impairment was immediately improved, but insulin therapy had to be continued (HbA1c=6.8%, insulin dose ; 0.6 Unit/kg/day). After 2 years, no C-peptide response to arginine or glucagon was detected, but glucagon response to arginine was. Neither islet cell antibody (ICA) nor antiislet antigen 2 was detected. Anti-GAD antibody, which was checked every 6 months from the onset of overt diabetes, remains negative. These findings suggest that she had fulminant type 1 diabetes as proposed by Imagawa et al. Her HLA haplotypes were presumed to be A2-B54-DRB1*0405-DQB1*0401 and A33-B44-DRB1*1302-DQB1*0604. So far, anti nuclear antibody, low complement and autoantibodies against carbonic anhydrase II and lactoferrin have been detected, unlike in previous fulminant type 1 diabetes patients. It is thus important to observe whether autoimmune disease will develop in this case.
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Report
  • Atsushi Suzuki, Hiroshi Sobajima, Tetsuo Hayakawa
    2005 Volume 48 Issue 3 Pages 183-187
    Published: 2005
    Released on J-STAGE: April 11, 2008
    JOURNAL FREE ACCESS
    Case : A 59-year-old man undergoing total pancreatectomy for multiple intraductal papillary tumor and then transferred to our hospital for management of elevated blood glucose, had, on admission, completely defective pancreatic endocrine function and hyperglycemia without any decrease in blood glucose despite bolus administration of 6 units of rapid-acting insulin given before each meal. When 6 units of NPH insulin were given additionally before bedtime and administration was changed to bolus-basal (4 times), hypoglycemia was observed frequently from midnight to early morning. When NPH was reduced to 2 units before bedtime, hypoglycemia at night disappeared but blood glucose was elevated again from before dinner. When supplemental basal secretion was changed from NPH to long-acting human insulin analog glargine, blood glucose was stabilized by treatment with 2 units before bedtime. In diabetes after total pancreatectomy, the insulin requirement at midnight was extremely low, and the supplement of physiological basal secretion was difficult in conventional insulin therapy, but since blood glucose can be safely stabilized by long-acting insulin, undernutrition and complications can be prevented.
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