Korsten S, Reis H E
Abteilung I, Krankenhaus Maria Hilf, Mönchengladbach.
Dtsch Med Wochenschr. 1992 Mar 13;117(11):419-24. doi: 10.1055/s-2008-1062328.
Three patients with an acute exacerbation of ulcerative colitis (a 40-year-old and a 31-year-old man and a 30-year-old woman) developed a protein C deficiency (serum protein C activity between 32 and 48%). In the two men the protein C deficiency was diagnosed only after the onset of severe thromboembolic complications (cavernous sinus thrombosis; pulmonary embolism) during heparin treatment. But in the woman protein C activity was measured immediately after hospital admission (in the knowledge of the first two cases) even before heparin administration was started. All three patients received treatment with sulphasalazine (3 g daily) and fluocortolone (60 mg daily), as well as full heparinization (22,500-36,000 IU daily). Protein C activity returned to normal on remission of the ulcerative colitis (in one case only after subtotal colectomy). These case reports show that acquired protein C deficiency can be reversed by rigorous treatment of the underlying disease.
三名溃疡性结肠炎急性加重患者（一名40岁男性、一名31岁男性和一名30岁女性）出现蛋白C缺乏（血清蛋白C活性在32%至48%之间）。在两名男性中，蛋白C缺乏是在肝素治疗期间出现严重血栓栓塞并发症（海绵窦血栓形成；肺栓塞）后才被诊断出来的。但在该女性患者中（鉴于前两例情况），甚至在开始使用肝素之前，入院后立即就检测了蛋白C活性。所有三名患者均接受了柳氮磺胺吡啶（每日3克）和氟轻松（每日60毫克）治疗，以及充分的肝素化治疗（每日22,500 - 36,000国际单位）。溃疡性结肠炎缓解后，蛋白C活性恢复正常（其中一例仅在次全结肠切除术后恢复正常）。这些病例报告表明，通过对基础疾病进行严格治疗，获得性蛋白C缺乏是可以逆转的。
