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January 1, 1996Internal Medicine7 citationsOpen Access

Evaluation of Cardiac Sympathetic Nervous Function by 123I-Metaiodobenzylguanidine Scintigraphy in Insulin-Treated Non-Insulin Dependent Diabetics with Hypoglycemia Unawareness.

TOTomio OhnoTTTakuji ToyamaHHHiroshi Hoshizaki

Structured PICO

Is the lack of adrenergic symptoms during hypoglycemia associated with cardiac sympathetic nervous dysfunction assessed by 123I-MIBG scintigraphy in insulin-treated NIDDM patients?

P
Population
n=12 insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients with no evidence of heart disease.
I
Intervention
123I-metaiodobenzylguanidine (MIBG) scintigraphy
C
Comparator
Comparison between patients with (group A) and without (group B) adrenergic symptoms during hypoglycemia
O
Outcome
Myocardial 123I-MIBG accumulation (heart/mediastinum ratio and scintigraphic defect)surrogate

Hypoglycemia unawareness in insulin-treated NIDDM patients is associated with cardiac sympathetic denervation as evidenced by 123I-MIBG scintigraphy.

Abstract

The association between the lack of adrenergic symptoms during hypoglycemia and myocardial 123I-metaiodobenzylguanidine (MIBG) accumulation was investigated in 12 insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients who had no evidence of heart disease. These patients were divided into 2 groups according to the presence (group A) or absence (group B) of adrenergic symptoms during hypoglycemia. Autonomic function tests revealed significantly severe autonomic dysfunction in group B compared to that in group A. Insulin infusion test indicated no significant difference in the catecholamine response between the two groups. 123I-MIBG scintigraphy showed that the heart/mediastinum ratio of MIBG uptake was significantly lower, and scintigraphic defect was greater in group B than in group A. There were no significant differences in the washout rate between the two groups. These results suggested that the lack of adrenergic symptoms during hypoglycemia may be associated with cardiac sympathetic nervous dysfunction in insulin-treated NIDDM patients, and this dysfunction is mainly due to cardiac sympathetic denervation.

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Cite This Study

Ohno et al. (1996) studied this question.

synapsesocial.com/papers/6a7e4d41bf2fd941fe8f4972https://doi.org/10.2169/internalmedicine.35.94
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