Severe Ulcerative Colitis With Cytomegalovirus Colitis Treated by Early Surgery: A Case Report

ABSTRACT

Acute severe ulcerative colitis complicated by cytomegalovirus infection requires individualized management, and timely surgical intervention should be considered in carefully selected high‐risk patients who are unlikely to benefit from further medical therapy.

1. Introduction

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by relapsing inflammation of the colonic mucosa. A subset of patients develop acute severe ulcerative colitis (ASUC), a life‐threatening condition requiring prompt and intensive management [1]. Cytomegalovirus (CMV) colitis is a recognized complication in patients with severe UC and is associated with steroid‐refractory disease and poor clinical outcomes [2, 3, 4, 5]. Accumulating evidence suggests that CMV reactivation is not merely an incidental finding but an important prognostic factor associated with increased disease severity, prolonged hospitalization, and a higher risk of colectomy [4]. The incidence of elderly‐onset UC has been increasing worldwide, and its management is often challenging due to comorbidities, frailty, and increased susceptibility to treatment‐related adverse events. In such patients, careful therapeutic decision‐making with particular attention to safety is essential. We report a case of ASUC complicated by CMV colitis in an elderly patient with functional immunodeficiency and multiple comorbidities. Despite antiviral therapy and intensive supportive care, the patient experienced rapid clinical deterioration. Given the high risk associated with immunosuppressive therapy and poor prognostic indicators, early surgical intervention was performed, resulting in a favorable outcome. This case highlights the importance of individualized treatment strategies and timely surgical decision‐making in high‐risk patients with ASUC.

2. Case History/Examination

A 71‐year‐old man with a history of atherosclerotic cerebral infarction, resulting in right hemiparesis and epilepsy, presented with hematochezia at a local clinic in November 2024. Initial management at the clinic was conservative; however, his symptoms progressively worsened over the following months. By February 2025, he developed frequent bloody diarrhea (6–8 times per day) and progressive fatigue, necessitating emergency admission to a nearby secondary hospital. Infectious colitis was initially suspected and probiotic therapy was initiated, but clinical improvement was not observed. In March 2025, he was transferred to our institution for further evaluation. On admission, his vital signs were as follows: temperature 37.9°C, heart rate 92 bpm, blood pressure 91/71 mmHg, and respiratory rate 16/min. His body weight was 77 kg, with a body mass index of 28 kg/m², and oxygen saturation was 98% on room air. Peripheral edema was present. Laboratory findings showed leukocytosis (9500/μL), an elevated erythrocyte sedimentation rate (32 mm/h), and increased C‐reactive protein (CRP) levels (5.0 mg/dL), indicating systemic inflammation. Serum albumin was markedly decreased (1.8 g/dL), reflecting severe malnutrition. CMV antigenemia was detected (6 positive cells/50,000 leukocytes).

3. Differential Diagnosis, Investigations, and Treatment

Abdominal CT images showed edematous wall thickening of the cecum and ascending colon, as well as mural thickening extending from the transverse colon to the descending colon (Figure 1a). In addition, edematous thickening of the sigmoid colon was observed (Figure 1b). Colonoscopy revealed a continuous granular fragile mucosa with spontaneous bleeding and loss of vascular pattern extending from the ascending colon to the rectum (Figure 2a–f). Multiple erosions and deep, punched‐out ulcers were observed in the cecum and ascending colon (Figure 2a–c). A histopathological examination of biopsy specimens obtained from the ulcer margins and rough mucosa revealed marked chronic inflammatory cell infiltration, crypt abscesses, and architectural distortion with glandular loss, all of which were consistent with ulcerative colitis (Figure 3a). In addition, CMV nuclear and cytoplasmic inclusion bodies were identified (Figure 3b). The patient was diagnosed with ASUC complicated by CMV infection. Intravenous ganciclovir and total parenteral nutrition were initiated on hospital day 4. Intravenous corticosteroids were not administered due to concerns regarding advanced age, severe malnutrition, marked hypoalbuminemia, poor performance status (ECOG 3), and the potential risk of exacerbating CMV infection under further immunosuppression. Despite antiviral therapy, the patient continued to have frequent diarrhea with progressive fatigue and clinical deterioration. Notably, the patient had experienced a 10‐kg weight loss prior to admission during the clinical course at the referring hospital. Despite antiviral therapy and supportive care, his condition progressively deteriorated after admission, with worsening malnutrition and electrolyte imbalance. Given the poor response to medical therapy, he was transferred to a tertiary care center, where emergency subtotal colectomy with ileostomy was performed on hospital day 7.

FIGURE 1.

Abdominal CT images show edematous wall thickening of the cecum and ascending colon (a, red arrows), as well as mural thickening extending from the transverse colon to the descending colon (a, yellow arrows). In addition, edematous thickening of the sigmoid colon is observed (b, blue arrows).

FIGURE 2.

Endoscopic findings. Colonoscopy revealed continuous granular and friable mucosa with spontaneous bleeding and loss of vascular pattern extending from the cecum to the rectum. Multiple erosions and deep, punched‐out ulcers were predominantly observed in the cecum and ascending colon. Representative endoscopic images are shown as follows: (a) Ulcers in the cecum and proximal ascending colon; (b) punched‐out ulcers in the ascending colon; (c) friable mucosa with easy bleeding in the ascending colon; (d) friable mucosa with easy bleeding in the transverse colon; (e) friable mucosa with easy bleeding in the sigmoid colon; (f) relatively preserved mucosa in the rectum.

FIGURE 3.

Histopathological findings. (a) Biopsy specimens from the ulcer margins showed marked chronic inflammatory infiltrates, crypt abscesses, and architectural distortion, consistent with ulcerative colitis (hematoxylin and eosin [H&E] staining, ×40). (b) Immunohistochemical staining for cytomegalovirus revealed viral inclusion bodies within the cytoplasm of endothelial cells (yellow arrows, ×200).

4. Conclusion and Results (Outcome and Follow‐Up)

The surgical specimen revealed irregular ulcers and erosions extending from the cecum to the distal colon (Figure 4a). Histologically, dense inflammatory infiltrates extending from the mucosa were observed, consistent with ulcerative colitis (Figure 4b,c), and CMV inclusion bodies were identified at the ulcer bases (Figure 4d). After 2 weeks of continued ganciclovir therapy, CMV antigenemia converted to negative. The postoperative course was uneventful. The patient's clinical condition improved, with normalization of CRP and recovery of serum albumin levels. He was discharged to a rehabilitation facility on postoperative day 22 and subsequently discharged home on day 40. During follow‐up, the patient was treated with topical 5‐aminosalicylic acid suppositories, and his residual proctitis remained stable for a period. However, the proctitis later worsened, and the treatment regimen was switched to an anti‐interleukin‐23 monoclonal antibody, which successfully induced and maintained long‐term remission.

FIGURE 4.

Gross and histopathological findings of the surgical specimen. (a) The resected specimen showed irregular ulcers and erosions extending from the cecum to the distal colon. (b) Histopathology demonstrated dense mucosal inflammatory infiltrates (H&E staining, ×10). (c) Higher magnification of the red boxed area in panel (b), showing chronic inflammatory infiltrates, crypt abscesses, and architectural glandular distortion, consistent with ulcerative colitis (H&E staining, ×40). (d) Immunohistochemical staining for cytomegalovirus revealed viral inclusion bodies within the cytoplasm of endothelial cells (yellow arrows, ×200).

5. Discussion

CMV infection is a recognized complication in severe UC and is associated with steroid‐refractory disease and an increased risk of colectomy [2, 3, 4, 5, 6, 7]. While the clinical significance of CMV was previously debated as to whether it represented a true pathogen or a bystander reactivation, recent literature has increasingly recognized CMV colitis as an important contributor to disease exacerbation, steroid refractoriness, and poor clinical outcomes in severe UC [4]. In the present case, although CMV antigenemia was relatively low, histopathological examination confirmed CMV inclusion bodies, suggesting active infection. Current guidelines from the British Society of Gastroenterology (BSG) recommend tissue‐based diagnostic methods, including immunohistochemistry and quantitative polymerase chain reaction (PCR), for the diagnosis of CMV colitis [6]. Quantitative PCR is increasingly used because of its high sensitivity and ability to assess viral burden. The absence of CMV DNA PCR is a limitation, as it may have provided a more precise assessment of viral activity. CMV antigenemia was used in our institution because it remains routinely available in daily clinical practice; however, we acknowledge that tissue PCR would have provided a more accurate assessment of local CMV involvement.

The management of ASUC complicated by CMV infection presents a therapeutic dilemma. Intravenous corticosteroids are generally recommended as first‐line therapy [1]; however, their use in elderly or immunocompromised patients may increase the risk of infectious complications [8, 9]. Current guidelines from the BSG recommend antiviral therapy with intravenous ganciclovir for patients with confirmed CMV colitis, particularly in steroid‐refractory or severe cases, which has been reported to reduce colectomy rates and may restore responsiveness to immunosuppressive treatment in selected patients [6]. In this case, corticosteroids and second‐line immunosuppressive therapies were avoided because of advanced age, severe malnutrition, hypoalbuminemia, poor performance status, and rapid clinical deterioration, all of which suggested a low likelihood of response to medical therapy and a high risk of treatment‐related adverse events. Although antiviral therapy was initiated, the patient's condition continued to deteriorate, indicating that medical treatment alone had failed to achieve disease control. Several predictors of colectomy in ASUC have been reported, including extensive colitis, hypoalbuminemia, elevated inflammatory markers, and failure of medical therapy [10]. Furthermore, a high CMV‐positive cell burden has been associated with steroid‐refractory disease and an increased risk of colectomy [11, 12, 13], and CMV‐associated ASUC has been reported to be associated with higher colectomy rates, particularly in patients with a high CMV burden and poor host condition [7]. Identifying these high‐risk features before irreversible clinical deterioration occurs is an essential component of ASUC management. In the present case, the combination of advanced age, severe malnutrition, poor performance status, extensive disease, histologically confirmed CMV colitis, and ongoing clinical deterioration despite antiviral therapy suggested a low probability of successful medical rescue therapy and a substantial risk of treatment‐related complications. Accordingly, timely surgical intervention was considered the most appropriate therapeutic strategy.

Importantly, the optimal management of CMV‐associated ASUC in elderly or medically frail patients remains insufficiently defined. Although antiviral therapy is recommended by current guidelines and may prevent colectomy in selected patients, some individuals exhibit multiple unfavorable prognostic factors and continue to deteriorate despite appropriate medical treatment. In such circumstances, timely surgical intervention should be considered before irreversible clinical deterioration occurs.

This case does not propose early colectomy as a novel treatment strategy. Rather, it illustrates the importance of individualized decision‐making in patients with CMV‐associated ASUC by integrating disease severity, host vulnerability, and expected response to medical therapy. Emergency subtotal colectomy effectively controlled the severe inflammatory and ischemic colonic lesions, likely preventing further clinical deterioration. Given the patient's performance status and activities of daily living, permanent ileostomy without reconstructive surgery was selected. Although standardized guidelines for surveillance of the retained rectal stump are lacking, regular endoscopic monitoring is generally recommended because of the risks of persistent inflammation and malignancy [14]. Total parenteral nutrition was used solely as supportive therapy for severe malnutrition and not as a primary treatment for ASUC.

In conclusion, appropriate antiviral therapy should be considered in patients with CMV‐positive ASUC; however, timely surgical intervention remains crucial when severe disease, unfavorable host factors, and poor prognostic indicators suggest that medical therapy is unlikely to be effective. Rather than advocating colectomy solely because of CMV positivity, this case emphasizes that CMV‐associated ASUC should be assessed comprehensively and that surgery should not be unnecessarily delayed in carefully selected high‐risk patients [7, 15]. We believe that this case contributes to the limited literature regarding surgical decision‐making in high‐risk patients with CMV‐associated ASUC and highlights the need for further studies to better define the optimal therapeutic strategy for this vulnerable patient population.

Author Contributions

Hiroyuki Fujimura: conceptualization, writing – original draft, methodology, writing – review and editing. Atsushi Goto: data curation, validation, writing – review and editing. Hiroshi Itoh: validation, visualization. Takenaka Kazuyuki: funding acquisition, data curation, writing – review and editing. Taro Takami: conceptualization, supervision, writing – review and editing.

Funding

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.