Comi G, Testa D, Cornelio F, Comola M, Canal N
Muscle Nerve. 1985 Jan;8(1):17-21. doi: 10.1002/mus.880080104.
Acute myopathy in conditions associated with endogenous or drug-induced potassium loss has been reported. We describe six patients with potassium depletion myopathy (P-DM). The clinical picture included flaccid muscle weakness without sensory loss, myalgia, polyuria, and polydipsia. All the cases had markedly increased serum creatine kinase (CK) levels. The most consistent pathological characteristics were phagocytosis of degenerating muscle fibers plus fiber regeneration. Atrophy of type 2 fibers was observed. Vacuoles and vesicular elements originating from T-tubules were also encountered. The clinical manifestations and morphological changes had reversed after potassium repletion. Both constriction of vascular smooth muscle and cellular energy failure may be pathogenetic factors in P-DM.
已有报道称，在内源性或药物性钾丢失相关的情况下会发生急性肌病。我们描述了6例低钾性肌病（P-DM）患者。临床表现包括弛缓性肌无力，无感觉丧失、肌痛、多尿和烦渴。所有病例的血清肌酸激酶（CK）水平均显著升高。最一致的病理特征是变性肌纤维的吞噬作用以及纤维再生。观察到2型纤维萎缩。还发现了源自横管的空泡和囊泡成分。补钾后临床表现和形态学改变均已逆转。血管平滑肌收缩和细胞能量衰竭可能都是P-DM的发病因素。
