Sjaastad O, Sjaastad O V
J Neurol. 1977 Sep 12;216(2):91-104. doi: 10.1007/BF00312943.
Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The excretion was significantly higher on attack days than on attack free days. With migraine, increased excretion was found in 5 of 31 patients on days of an attack, whereas the corresponding figure for headache free days was 7 of 24 patients. Three patients showed increased histamine excretion during, as well as between, attacks. The excretion on attack days was not significantly different from that on attack free days. In cluster headache patients, L-histdine administration on attack days did not indicate that an increased histamine formation took place under such circumstances. The underlying mechanism behind the increased histamine output with cluster headache may be increased formation or liberation or altered catabolism. Histamine is more likely to be a consequence than the cause of an attack of cluster headache.
在所谓的血管性头痛患者中,研究了组胺的尿排泄情况以及静脉注射L-组氨酸负荷后的组胺尿。结果发现,在22例丛集性头痛患者中,有7例在一次或多次情况下组胺尿排泄增加。发作日的排泄量明显高于无发作日。对于偏头痛,31例患者中有5例在发作日排泄增加,而在无头痛日,24例患者中有7例排泄增加。3例患者在发作期间及发作之间组胺排泄增加。发作日的排泄量与无发作日的排泄量无显著差异。在丛集性头痛患者中,在发作日给予L-组氨酸并未表明在这种情况下组胺形成增加。丛集性头痛时组胺排出量增加的潜在机制可能是形成增加、释放增加或分解代谢改变。组胺更可能是丛集性头痛发作的结果而非原因。