Man in 't Veld A J, Boomsma F, Moleman P, Schalekamp M A
Lancet. 1987 Jan 24;1(8526):183-8. doi: 10.1016/s0140-6736(87)90002-x.
A woman was referred with severe orthostatic hypotension at the age of 21. Ptosis, skeletal muscle hypotonia, and recurrent hypoglycaemia had been noticed in early childhood. There was noradrenergic denervation and adrenomedullary failure but baroreflex afferents, cholinergic innervation, and adrenocortical function were intact. Noradrenaline and adrenaline were undetectable in plasma, urine, and cerebrospinal fluid (CSF), but dopamine was 7-fold to 12-fold normal in plasma, 4-fold normal in urine, and 20-fold normal in CSF. Measurements of catecholamine metabolites showed further evidence for impairment of noradrenaline and adrenaline biosynthesis due to deficient dopamine-beta-hydroxylation. Dopamine-beta-hydroxylase was undetectable in plasma and CSF. Physiological and pharmacological stimuli of sympathetic neurotransmitter release caused increases in plasma dopamine rather than plasma noradrenaline.
一名21岁女性因严重直立性低血压前来就诊。自幼便发现有上睑下垂、骨骼肌张力减退和反复低血糖。存在去甲肾上腺素能神经支配缺失和肾上腺髓质功能衰竭,但压力反射传入神经、胆碱能神经支配和肾上腺皮质功能完好。血浆、尿液和脑脊液(CSF)中检测不到去甲肾上腺素和肾上腺素,但多巴胺在血浆中是正常水平的7至12倍,在尿液中是正常水平的4倍,在脑脊液中是正常水平的20倍。儿茶酚胺代谢产物的测量进一步证明,由于多巴胺-β-羟化酶缺乏,去甲肾上腺素和肾上腺素的生物合成受到损害。血浆和脑脊液中检测不到多巴胺-β-羟化酶。交感神经递质释放的生理和药理刺激导致血浆多巴胺增加,而非血浆去甲肾上腺素增加。