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DOI 10.1111/j.1365-2265.2008.03395.x

Медицинская библиотека · Clinical endocrinology · 2008

Insulin resistance in subjects with a history of thyrotoxic periodic paralysis (TPP).

Soonthornpun Supamai, Setasuban Worawong, Thamprasit Atchara

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND

Hyperinsulinaemia has been suggested as an important factor for developing hypokalaemic paralysis in patients with thyrotoxic periodic paralysis (TPP). Since hyperinsulinaemia is a common feature of insulin resistance, there may be a causal relationship between insulin resistance and TPP.

OBJECTIVE

To compare insulin sensitivity between subjects with a history of TPP and others with a history of thyrotoxicosis without periodic paralysis.

METHODS

Insulin sensitivity measured by euglycaemic hyperinsulinaemic clamp and 75-g oral glucose tolerance test (OGTT) were performed nonselectively in 10 subjects with a history of TPP (TPP group) and 10 age- and sex-matched subjects with a history of simple thyrotoxicosis (control group). All participants had euthyroidism and fasting plasma glucose of < 5.55 mmol/l at the time of the study.

RESULTS

Body mass index and waist circumference of the TPP group were higher than that of the control group. One of 10 (10%) subjects in the TPP group and 6 of 10 (60%) in the control group had BMI of < 23 kg/m2. Areas under the curve (AUC) of plasma glucose after OGTT were comparable, while the AUC of serum insulin of the TPP group was higher than in the control group. The TPP group had lower insulin sensitivity than the control group.

CONCLUSION

The subjects with a history of TPP were more obese and had lower insulin sensitivity than those with a history of simple thyrotoxicosis. Insulin resistance with compensatory hyperinsulinaemia may be a key feature of the pathogenesis of TPP.

Для цитирования: Soonthornpun Supamai, Setasuban Worawong, Thamprasit Atchara. Insulin resistance in subjects with a history of thyrotoxic periodic paralysis (TPP).. Clinical endocrinology. 2008. DOI: 10.1111/j.1365-2265.2008.03395.x.

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