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致残性体位性低血压并发糖尿病自主神经病变。

Disabling postural hypotension complicating diabetic autonomic neuropathy.

作者信息

Stevens M J, Edmonds M E, Mathias C J, Watkins P J

机构信息

Department of Diabetes, Kings College Hospital, London, UK.

出版信息

Diabet Med. 1991 Nov;8(9):870-4. doi: 10.1111/j.1464-5491.1991.tb02127.x.

Abstract

A 35-year-old Type 1 diabetic man with severe disabling postural hypotension was studied for physiological abnormalities, precipitating factors, and effect of current treatment. A 24-h blood pressure profile indicated a diurnal variation in systolic blood pressure with the lowest values recorded between 0100 and 0600 h, during which the patient often lost consciousness on standing (mean standing systolic pressure 78 mmHg at night vs 105 mmHg in the afternoon, p less than 0.001). Food induced a profound fall in systolic pressure, both while supine and while standing erect. The systolic pressure fall during euglycaemia was 49 mmHg vs 3 mmHg during hypoglycaemia. Plasma noradrenaline and adrenaline levels were low during euglycaemia, but increased during hypoglycaemia. Therapeutic manoeuvres aimed at increasing heart rate (by atrial tachypacing) and reducing the peripheral pooling of blood (vasoconstricting drugs and gravity suit), together with the somatostatin analogue octreotide, proved ineffective. These observations demonstrate the phenomenon of post-prandial exacerbation of postural hypotension in a Type 1 diabetic patient, and indicate that despite failure of conventional methods of treatment, hypoglycaemia increased plasma catecholamines and was effective in abolishing the blood pressure fall on standing.

摘要

对一名35岁的1型糖尿病男性患者进行了研究,该患者患有严重致残性体位性低血压,研究内容包括生理异常、诱发因素及当前治疗的效果。24小时血压监测显示收缩压存在昼夜变化,最低值出现在01:00至06:00之间,在此期间患者站立时经常失去意识(夜间平均站立收缩压为78 mmHg,下午为105 mmHg,p<0.001)。进食后,无论是仰卧位还是直立位,收缩压都会显著下降。血糖正常时收缩压下降49 mmHg,而低血糖时下降3 mmHg。血糖正常时血浆去甲肾上腺素和肾上腺素水平较低,但低血糖时升高。旨在增加心率(通过心房快速起搏)和减少外周血液淤积(血管收缩药物和重力服)的治疗措施,以及生长抑素类似物奥曲肽,均被证明无效。这些观察结果证明了1型糖尿病患者餐后体位性低血压加重的现象,并表明尽管传统治疗方法无效,但低血糖会增加血浆儿茶酚胺,并有效消除站立时的血压下降。

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