All issues
Volume 40, Issue 5
Displaying 1-9 of 9 articles from this issue
- |<
- <
- 1
- >
- >|
-
[in Japanese], [in Japanese]1997 Volume 40 Issue 5 Pages 273-275
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSDownload PDF (366K) -
[in Japanese]1997 Volume 40 Issue 5 Pages 277-279
Published: May 30, 1997
Released on J-STAGE: August 04, 2011
JOURNAL FREE ACCESSDownload PDF (415K) -
[in Japanese]1997 Volume 40 Issue 5 Pages 281-284
Published: May 30, 1997
Released on J-STAGE: August 04, 2011
JOURNAL FREE ACCESSDownload PDF (574K) -
Wataru Okumura, Toshihiro Utsugi, Chikara Ishii, Tatsuo Suga, Hideki S ...1997 Volume 40 Issue 5 Pages 285-291
Published: May 30, 1997
Released on J-STAGE: August 04, 2011
JOURNAL FREE ACCESSA 34-year old woman was admitted to our hospital because of hypoglycemic attacks that occurred at the age of 32 years during her second pregnancy. Hyperinsulinemia was not observed in the fasting state, and the plasma insulin responses to glucagon and a 75g OGTT were normal. After fastig for 18 hours, the plasma glucose level decreased to 40 mg/dl, but the plasma insulin level was not suppressed despite the hypoglycemia, suggesting unusual regulation of insulin secretion by pancreatic βcells. Abdominal CT and selective angiography revealed a tumor in the tail of the pancreas, and distal pancreateotomy was performed. The diameter of the three tumors found ranged from 1 to 3 cm. In immunohistochemical studies, the tumor cells were partially positive for insulin staining, and a few cells stained with anti-glucagon or anti-somatostati.No hypoglycemic attacks have occurred since the operation, and a repeat prolonged fasting test showed a normal insulin secretion response.View full abstractDownload PDF (5024K) -
Kuniaki Yoshimori, Michiaki Fukui, Mitsuhiro Fujii, Hirohumi Shigeta, ...1997 Volume 40 Issue 5 Pages 293-297
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe report the case of a 17-year-old woman with NIDDM with an unusually high GAD-Ab level and Graves'disease. The patient was born with a chromosome aberration and cardiac anomaly, and at the age of 9 years, she was found to have 46, XX, add (18)(q23). In Apri11995, she was admitted to a hospital because of polyuria and thirst. On admission, her fasting plasma glucose level was 165 mg/dl, her HbA1c level was 8.2%, and a thyroid function revealed hyperthyroidism. Her urinary C-peptide concentration was 110μg/gCr, and the maximum response level to glucagon loading 3.3ng/ml, dispite poor glycemic control. A diagnosis of NIDDM and Graves'disease was made. GAD-Ab and autoantibodies to thyroidgland were positive, but islet-cell antibodies (ICA), mitochondria Ab and pituitary Ab were negative. Her GAD-Ab level rose as high as 750U/ml, although its ordinary levelin GAD-Ab-positive NIDDM is11-120U/ml, mean range25.4U/ml (positive range>11U/ml). We suspect that the association with autoimmune thyroid disease and chromosome aberration may be one main cause of this.View full abstractDownload PDF (1994K) -
Yoshihiko Suzuki, Kazuhiro Hosokawa, Yoshito Atsumi, Takayuki Asahina, ...1997 Volume 40 Issue 5 Pages 299-303
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe encountered two patients with diabetes mellitus who developed drug-induced parkinsonism. Patient1was a60-year-old female with mitochondrial diabetes associated with 3243 mitochondrial tRNA mutation. She was the mother of a child with MELAS, and had depression. After being treated with sulpiride, she developed oral dyskinesia and rigidity. Patient 2 was 58-year-old female who developed rigidity after taking metoclopramide, and the concentration of metoclopramide and symptoms of extrapyramidal sign were found to be correlated. After withdrawal of the metoclopramide, the rigidity resolved.
Both patients had maternal inheritance of diabetes, and had younger onset diabetes, with no history of obesity, hearing loss, or brain atrophy. Patient 2 was suspected of having a mitochondrial DNA defect because of bilateral abducens nerve paralysis and a history of posttreatment neuropathy.
In conclusion, because mitochondrial dysfunction causes diabetes and parkinsonism, drug-induced parkinsonism in diabetes may be related to the underlyig mitochondrial DNA defects or some unknown neuromuscular disorders related to mitochondrial dysfunction. Under these conditions, the symptoms of parkinsonism may be triggered by increased serum concentrations of metoclopramide or sulpiride. Thus, the two cases reported here provide insights into the pathophysiology of druginduced parkinsonism in patients with diabetes mellitus.View full abstractDownload PDF (2186K) -
Hiroaki Seino, Toshio Yamazaki, Akiyo Karita, Nobuko Arawaka, Hiroaki ...1997 Volume 40 Issue 5 Pages 305-308
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSAdhesion of leukocytes to the endothelium, an early step in atherogenesis, is mediated by celladhesion molecules. In this study, we evaluated the concentration of soluble adhesion molecules andthe levels of carotid arterial wall thickening in NIDDM patients. Carotid arterial wall thickness wasdetermined as intimal and medial thickness (IMT) and the plaque thickness by ultrasound highresolutionB-mode imaging.
Soluble adhesion molecules (ELAM-1, VCAM-1, ICAM-1) were measured in the serum of26NIDDM patients. We compared soluble adhesion molecule levels in the patients with plaquesdetected in the carotid artery and without plaques in the carotid artery.
Elevated levels of ICAM-1were found in the NIDDM patients with carotid artery plaquescompared with hose without plaques (P<0.05). Plaque thickness was determined in additionthickness of the intimal and medial complex, (IMT). The concentration of plasma ICAM-1waspositively correated with arterial wall thickness in the26patients with diabetes (γ=0.485, P<0.05).However, ICAM-1, VCAM-1 and ELAM-1 failed to correlate with glycemic control.
Our findings suggest that soluble forms of ICAM-1 icrease in the serum of diabetic patients withahterosclerosis and that increased expression of cell membrane ICAM-1accelerates the progressionof athe: osclerosis in the carotid arteries of NIDDM patients.View full abstractDownload PDF (681K) -
1997 Volume 40 Issue 5 Pages 309-320
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSDownload PDF (2941K) -
Kenji Shima, Jiro Endo, Munetada Oimomi, Yasue Omori, Yoshiaki Katayam ...1997 Volume 40 Issue 5 Pages 321-326
Published: May 30, 1997
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe Glycohemoglobin (GHb) StaUardization Comittee conducted the fourth external quality assessment to evaluate the interlaboratory variation of GHb values measured by various methods incluing HPLC, various kinds of immunoassay (IMA) and affinity chromatographic methods in 1, 879 institutes throughout the country using four samples (2concentrated whole blood and 2 lyophilized hemolysate).
We got the following results,
1) The CVs as indices of the interlaboratory variation ranged from 6.0% to 8.6% when all data were combined. It was different depeuing on an analytical method used: HPLC, 3.3%-5.4%; IMA, 6.2%-7.7%; Affinity, 7.0%-7.9%.
2) The rneans of the measured values were different depending on a method used. The value measured by the affinity chromatographic method was significantly higher than the others.
The value of a lyophilized hemolysate measured by turbidimetric inhibition immunoassay was remarkably lower than the othes.
When these exceptional values were excluded, the CVs ranging from 4.6% to 6.2% were good enough from a clinical point of view.
3) The CVs among the GHb value corrected with the assigned values of Japan Diabetes Society (JDS) calibrators ranging from 5.8% to 6.2%, were much smaller than those corrected with other calibrators or without correction, 6.4% to 11.9%.
4) Percent distributions of participants classified by the upper value of their reference interval for GHb were as follows:≤5.8%, 62.7%; 5.9%-6.0%, 17.7% and ≥6.1%, 19.7%.
In conclusion, the interlaboratory difference in GHb measurement was reduced to a clinically permissible level, when the values measured by a certain kinds of method were exclued from calculation. These exceptional values should be properly corrected with the assigned values of an improved calibrator.View full abstractDownload PDF (1003K)
- |<
- <
- 1
- >
- >|