背景:巨细胞病毒感染作为一种机会性病原体在溃疡性结肠炎恶化中的作用及其对治疗的反应仍然是一个持续争论的话题。临床医生遇到许多挑战,包括区分急性溃疡性结肠炎发作和真正的巨细胞病毒性结肠炎的标准,巨细胞病毒性结肠炎的诊断试验,并确定启动抗病毒治疗的适当时机。
方法:一名28岁的叙利亚女性,有7年的泛结肠炎病史,表现为不断恶化的血性腹泻,腹痛,和里急后重,尽管正在用硫唑嘌呤治疗,美沙拉嗪,和泼尼松龙。尽管最近完成了在中度至重度溃疡性结肠炎前四周开始的两次英夫利昔单抗(5mg/kg)诱导剂量,但她经历了急性重度溃疡性结肠炎的新发作。她之前没有手术史。她的症状包括水汪汪,每天发生九到十次血性腹泻,腹痛,和里内重.最初的实验室检查显示贫血,白细胞增多,升高的C反应蛋白(CRP)和粪便钙卫蛋白水平,CMVIgG阳性。粪便文化,艰难梭菌毒素,大肠杆菌和隐孢子虫的检测,卵和寄生虫的显微镜检查均为阴性。乙状结肠镜检查显示许多突出的红斑区域,自发性出血。活检显示CMV包涵体经免疫组织化学证实,尽管以前的活检是阴性的。我们减量泼尼松龙和硫唑嘌呤,并以5mg/kg的剂量开始更昔洛韦10天,随后服用伐更昔洛韦450mg,每日两次,持续三周。一个月后,她表现出明显的进步,CRP和粪便钙卫蛋白水平恢复正常。她在Mayo的部分得分上得了1分。第三个诱导剂量的英夫利昔单抗按计划给药,硫唑嘌呤恢复了。
结论:炎症性肠病患者并发巨细胞病毒感染由于其相关的发病率和死亡率而提出了重大的临床挑战。诊断和管理这种情况特别困难,特别是关于开始或继续免疫抑制疗法。
BACKGROUND: The role of cytomegalovirus infection as an opportunistic pathogen in exacerbating ulcerative colitis and its response to treatment remain a topic of ongoing debate. Clinicians encounter numerous challenges, including the criteria for differentiating between an acute ulcerative colitis flare and true cytomegalovirus colitis, the diagnostic tests for identifying cytomegalovirus colitis, and determining the appropriate timing for initiating antiviral therapy.
METHODS: A 28-year-old Syrian female with a seven-year history of pancolitis presented with worsening bloody diarrhea, abdominal pain, and tenesmus despite ongoing treatment with azathioprine, mesalazine, and prednisolone. She experienced a new flare of acute severe ulcerative colitis despite recently completing two induction doses of infliximab (5 mg/kg) initiated four weeks prior for moderate-to-severe ulcerative colitis. She had no prior surgical history. Her symptoms included watery, bloody diarrhea occurring nine to ten times per day, abdominal pain, and tenesmus. Initial laboratory tests indicated anemia, leukocytosis, elevated C-reactive protein (CRP) and fecal calprotectin levels, and positive CMV IgG. Stool cultures, Clostridium difficile toxin, testing for Escherichia coli and Cryptosporidium, and microscopy for ova and parasites were all negative. Sigmoidoscopy revealed numerous prominent erythematous area with spontaneous bleeding. Biopsies demonstrated CMV inclusions confirmed by immunohistochemistry, although prior biopsies were negative. We tapered prednisolone and azathioprine and initiated ganciclovir at 5 mg/kg for ten days, followed by valganciclovir at 450 mg twice daily for three weeks. After one month, she showed marked improvement, with CRP and fecal calprotectin levels returning to normal. She scored one point on the partial Mayo score. The third induction dose of infliximab was administered on schedule, and azathioprine was resumed.
CONCLUSIONS: Concurrent cytomegalovirus infection in patients with inflammatory bowel disease presents a significant clinical challenge due to its associated morbidity and mortality. Diagnosing and managing this condition is particularly difficult, especially regarding the initiation or continuation of immunosuppressive therapies.