Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 39, Issue 12
Displaying 1-5 of 5 articles from this issue
  • Hiroaki Seino, Hiroshi Yamaguchi, Akihiko Hirata, Toshirou Yamazaki, H ...
    1996 Volume 39 Issue 12 Pages 893-899
    Published: December 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    Autoantibodies to glutamic acid decarboxylase (GAD), previously reported to be the 64, 000-Mr (64K) islet cell protein, were measured by a radioimmunoassay using purified pig brain GAD in 53 patients with slowly progressive insulin-dependent diabetes mellitus (SPIDDM). When the level in a sample was higher than 5u/m/ in this method, the serum was considered to be positive. The rate of positive GAD-Ab in SPIDDM patients was 66%(35/53). Patients with SPIDDM were divided into two groups, GAD-Ab positive and negative. We compared the HLA phenotype in these two groups, HLA B44, DR13, DQ1 were significantly more common in GAD-Ab-negative-subjects than in GAD-Ab-positive-patients. The production of GAD-Ab in patients with SPIDDM may be related to their HLA phenotype.
    HLA-A24 is reported to be associated with complete abolishment of β-cell function in acute onset IDDM. We estimated the β-cell function in patients with SPIDDM with the capacity of releasing insulin by loading glucagon. When the level of insulin after loading glucagon was below 0.1 ng/ml, the β-cell was thought to be complete destroyed. Therefore we compared the HLA phenotype in the two groups to determine whether theβ-cells completely destroyed or not, complete destruction of the β-cell in SPIDDM was not associated with HLA-A24 in this study.
    GAD-Ab is a useful means of screening for patients with SPIDDM.
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  • Prospective Follow-up Study for 8 years
    Tomoko Nakagami, Reiko Kawahara, Sadao Hori, Yasue Omori
    1996 Volume 39 Issue 12 Pages 901-906
    Published: December 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    To determine the optimum (HbA1c) value for preventing retinopathy, the progression of retinopathy and HbA1c values in patients with non-insulin-dependent diabetes mellitus (NIDDM) were followed for 8 years. We examined 176 patients first diagnosed with NIDDM, aged 30-65 years, diabetic duration less than 3 years and without retinopathy. The appearance and progression of retinopathy were assessed at least annually. The mean HbA1c value for each patient was calculated by using data of every month except the data at registration. Multiple logistic regression analysis for the mean HbA1c value, onset age, sex, blood pressure, and ΔBMI (Max BMI-BMI at registration) with retinopathy at the end point as dependent variables, showed a significant impact of the mean HbA1c value and ΔBMI. In the group with HbA1c values below 6%, no patients had retinopathy. Patients with HbA1c values above 8% had a prevalence rate 4 times higher than patients with HbA1c values below 8%. The prevalence of retinopathy increased with the increase in the mean HbA1c values over 8 years (trend P<0.05). The data suggest that an HbA1c value below 6% should be effective in preventing diabetic retinopathy in patients with NIDDM.
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  • Akira Kasuga, Taro Maruyama, Yukako Ozawa, Toshihide Ishihara, Shin Am ...
    1996 Volume 39 Issue 12 Pages 907-912
    Published: December 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    To investigate the accuracy of a commercial RIA kit for GAD antibody (RIA kit) compared to a sensitive radioligand binding assay (RBA), we tested sera from 78 patients with insulin-dependent diabetes mellitus (IDDM) and 78 control subjects using the receiver operating characteristic (ROC) plot.
    The titers of the two tests were significantly correlated (r=0.857). The ROC plot showed that RIA was less accurate than RBA, since the highest accuracy of the RIA kit was 80.8%(cutoff 2.5 U, sensitivity 78%, specificity 83%), which was significantly lower than that of RBA (89.7%, p<0.001). Among the 78 healthy subjects, 77 were judged as negative for GAD antibody in both assays (specificity 99%). However, the RIA kit showed lower sensitivity (51%; 40 out of 78 IDDM sera were judged as positive in contrast with RBA [69%, 54/78, p<0.001]). Sera with a lower GAD65 antibody titer (less than 80 ng of MICA3 per ml) were frequently negative by the RIA kit. In conclusion, the RIA kit for pig brain GAD was less sensitive than RBA using recombinant human GAD65. Since sera with low antibody levels became falsely negative, we should test sera with border-line titers (e. g. 2.5-8 U by the RIA kit) with other sensitive assays.
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  • Yukio Ikeda, Tomoko Mimoto, Kiyoshi Tahara, Takahide Yorioka, Kazumasa ...
    1996 Volume 39 Issue 12 Pages 913-918
    Published: December 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    X-ray films of a 61-year-old man with diabetes mellitus under treatment showed migrating pulmonary infiltrates that did not respond to antibiotics. Chest CT scanning revealed a mixture of parenchymal and interstitial lesions. Histological examination after transbronchial lung biopsy showed organizing pneumonia accompanied by alveolitis. Based on these findings together with clinical findings, a diagnosis of bronchiolitis obliterans organizing pneumonia (BOOP) was made. Though steroid therapy was markedly effective, its discontinuation resulted in relapse. In patients with diabetes mellitus, an infectious lung disease often persists because of impaired mechanisms for healing airway infection caused by decreased neutrophil function, and cellular immunity, neuropathy, and microangiopathy. However, when pulmonary infiltrate shadows do not show a responce to antibiotics, early histological examination should be performed, considering the possibility of BOOP.
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  • Keiki Yoshida, Susumu Kajihara, Mitsuaki Motomura, Yoichi Setoguchi, T ...
    1996 Volume 39 Issue 12 Pages 919-923
    Published: December 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A44-year-old man had been admitted in 1989 for polyuria and polydipsia. His serum ADH levels were low, but his blood sugar levels were within the normal rang. A diagnosis of idiopathic diabetes Insipidus was made, but the patient refused treatment. In October 1994 he began to drink 8 liters of cooling beverages a day. In January 1995, he was brought to the hospital because of a consciousness disturbance. His urine volume was 7 to 8 liters/day and his blood glucose, blood pH and urinary ketone body values were 1025mg/dl, 7.193 and 3+ respectively. The patient was given saline and insulin, and his blood glucose level became normal, but the polyuria and polydipsia failed to improve. His serum C-peptide level gradually improved, and insulin therapy was no longer needed 2 weeks after his admission. A glucose tolerance test showed impaired glucose tolerance6 weeks after his admission. The polyuria and polydipsia improved in response to nasal inhalation of deamino-D-arginine vasopressin (DDAVP). We believe that the transient failure of insulin secretion and diabetic ketoacidosis were due to glucose toxicity caused by the excess glucose intake and severe dehydration that accompanied the water diuresis secondary to diabetes insipidus.
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