Johnsen T
Acta Neurol Scand. 1977 Dec;56(6):525-32. doi: 10.1111/j.1600-0404.1977.tb01457.x.
Five patients suffering from familial periodic paralysis with hypokalemia (FPP) were exposed to standard paralysis induction trials which elicited total paralyysis and hypokalemia. In all cases the serum potassium fell to or below 2.6 mmol/1. After being pre-treated with diazoxide for 72 h, the same five patients were exposed to the same standardized paralysis induction procedure. None of them developed any demonstrable symptoms or signs of paralysis. In one the serum potassium dropped to 3.2 mmol/1, but in all the others the levels were higher. The serum glucose level was significant higher (P less than 0.01), the serum insulin level was significant lower (P less than 0.01) when induction of paralysis was attempted under diazoxide cover than during the untreated stimulation phase. Three patients were put on prophylactic diazoxide medication. After a few months, without paralytic episodes or other prophylactic drugs, adaptation to the diazoxide occurred and the previous, frequent paralytic episodes returned in unchanged severity. This experimental prophylactic effect of diazoxide supports the hypothesis that the glucose deposition in muscles is a major step in eliciting the parese attacks in FPP.
五名患有家族性低钾性周期性麻痹（FPP）的患者接受了标准的麻痹诱导试验，试验引发了全身麻痹和低钾血症。在所有病例中，血清钾降至或低于2.6 mmol/L。在用二氮嗪预处理72小时后，这五名患者接受了相同的标准化麻痹诱导程序。他们中没有人出现任何可证实的麻痹症状或体征。其中一人血清钾降至3.2 mmol/L，但其他所有人的血钾水平更高。与未治疗的刺激阶段相比，在二氮嗪掩护下尝试诱导麻痹时，血清葡萄糖水平显著升高（P小于0.01），血清胰岛素水平显著降低（P小于0.01）。三名患者接受了预防性二氮嗪治疗。几个月后，在没有麻痹发作或其他预防性药物的情况下，出现了对二氮嗪的适应性，先前频繁的麻痹发作以不变的严重程度再次出现。二氮嗪的这种实验性预防作用支持了这样一种假设，即肌肉中的葡萄糖沉积是引发FPP中麻痹发作的一个主要步骤。
