Gabow P A, Moore S, Schrier R W
Ann Intern Med. 1979 Mar;90(3):338-40. doi: 10.7326/0003-4819-90-3-338.
Six patients with alcoholic cirrhosis developed a reversible metabolic acidosis during treatment with the aldosterone antagonist spironolactone. Mean serum bicarbonate concentration decreased significantly with spironolactone therapy (100 to 200 mg/day) from 18.2 +/- 4.5 to 10.9 +/- 3.2 meq/litre (P less than 0.001). Upon withdrawal of spironolactone, serum bicarbonate concentration increased from 10.9 +/- 3.2 to 18.1 +/- 3.5 meq/litre (P less than 0.001). During the development of this hyperchloremic metabolic acidosis, serum potassium concentration rose from 3.7 +/- 0.5 to 5.0 +/- 0.8 meq/litre (P less than 0.005); this reversed after cessation of spironolactone therapy. These effects of spironolactone treatment were not associated with significant alterations in serum creatinine or sodium concentration. Thus, even though an aldosterone antagonist in the treatment of sodium and water retention in cirrhotic patients may prevent hypokalemia and rapid diuresis, it may also induce or worsen another complication: hyperchloremic metabolic acidosis.
6例酒精性肝硬化患者在使用醛固酮拮抗剂螺内酯治疗期间发生了可逆性代谢性酸中毒。使用螺内酯治疗（100至200毫克/天）期间，血清碳酸氢盐平均浓度显著下降，从18.2±4.5降至10.9±3.2毫当量/升（P<0.001）。停用螺内酯后，血清碳酸氢盐浓度从10.9±3.2升至18.1±3.5毫当量/升（P<0.001）。在这种高氯性代谢性酸中毒发生过程中，血清钾浓度从3.7±0.5升至5.0±0.8毫当量/升（P<0.005）；停用螺内酯治疗后这种情况逆转。螺内酯治疗的这些效应与血清肌酐或钠浓度的显著改变无关。因此，尽管醛固酮拮抗剂在治疗肝硬化患者的钠水潴留时可能预防低钾血症和快速利尿，但它也可能诱发或加重另一种并发症：高氯性代谢性酸中毒。
