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  Table of Contents  
LETTER TO THE EDITOR
Year : 2015  |  Volume : 52  |  Issue : 3  |  Page : 280-281
 

Symptomatic Cytomegalovirus reactivation related to chemoradiotherapy for adenocarcinoma of lower third esophagus and gastro-esophageal junction cancer


Department of Medical Oncology, Tata Memorial Hospital, Mumbai, Maharashtra, India

Date of Web Publication18-Feb-2016

Correspondence Address:
A Joshi
Department of Medical Oncology, Tata Memorial Hospital, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.176920

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How to cite this article:
Ishi S V, Joshi A, Noronha V, Prabhash K. Symptomatic Cytomegalovirus reactivation related to chemoradiotherapy for adenocarcinoma of lower third esophagus and gastro-esophageal junction cancer. Indian J Cancer 2015;52:280-1

How to cite this URL:
Ishi S V, Joshi A, Noronha V, Prabhash K. Symptomatic Cytomegalovirus reactivation related to chemoradiotherapy for adenocarcinoma of lower third esophagus and gastro-esophageal junction cancer. Indian J Cancer [serial online] 2015 [cited 2019 Aug 18];52:280-1. Available from: http://www.indianjcancer.com/text.asp?2015/52/3/280/176920


Sir

Cytomegalovirus (CMV) reactivation is a common problem in organ transplant recipients and also in patients of hematological malignancies receiving chemotherapy, but it is an uncommon complication of chemotherapeutic treatments in patients with solid tumor malignancies.

Here we present a rare case of a patient with locally advanced esophageal adenocarcinoma who experienced reactivation of latent CMV infection after starting concurrent chemoradiotherapy. To the best of our knowledge, there have been only two similar case reports in published literature.

A 47-year-old female, in good performance status, with no co-morbidities except well controlled hypothyroidism, presented to our institution in March 2013 with progressive dysphagia to solids, with upper abdominal pain and early satiety since 3 months. Upper gastrointestinal scopy showed polypoidal lesion in the lower esophagus, esopho-gastric junction and fundus of stomach.

Histology revealed poorly differentiated adenocarcinoma. Positron emission tomography computed tomography (PET-CT) further revealed fludeoxyglucose avid enhancing soft tissue wall thickening involving the cardia, gastro-esophageal junction and lesser curvature of the stomach with multiple retroperitoneal nodes. She was planned for neoadjuvant chemotherapy (NACT), followed by reassessment for consolidation with concomitant chemoradiotherapy (CTRT). She received 3 cycles of chemotherapy (epirubicin 50 mg/m 2, oxaliplatin 130 mg/m 2 and capacitabine 625 mg/m 2 PO BD), after which response assessment PET-CT was suggestive of stable disease. She was started on concurrent chemoradiotherapy with weekly cisplatin at a dose of 30 mg/m 2. After completing 20 fractions of radiation and 3 cycles of cisplatin, she reported a 3 days history of fever and extreme fatigue. She was noted to have mild thrombocytopenia (platelet - 116,000) and fever 99.8°F. The remainder of her lab profile, including electrolytes and liver function tests, were normal. She was empirically started on intravenous cefoperazone + sulbactum and levofloxacin on out-patient department basis. After 3 days of antibiotics, patient had a persistent high-grade fever, Blood investigations revealed pancytopenia, Hemoglobin was 9.1 g%, white blood cell count 1.2 X 10e9/L with absolute neutrophil count 0.9 X 10e9/L and platelet count 23 X 10e9/L. She was admitted in the hospital for further evaluation and management. Antibiotics were escalated to meropenem and fluconazole was added. Evaluation for malaria and dengue serology was also negative. CT thorax did not reveal any evidence of infection. Blood and urine cultures were sterile. Despite the appropriate antibiotic coverage, the patient continued to have high-grade continuous fever spikes of >102°F. Antibiotic coverage was expanded to include teicoplanin and colstin with anti-fungal voriconazole and addition of filgrastim support. She also received 3 units of packed Red blood cell and single donor platelet transfusions each, during the course of admission. Repeat liver function tests revealed mildly elevated transaminases (alanine aminotransferase 137, aspartate aminotransferase 69). In view of persistent fever and pancytopenia without any obvious focus, her CMV DNA viral load was measured and found to be 1590 copies/mL. She was diagnosed to have CMV reactivation resulting from immunosuppression induced by chemoradiotherapy and was initiated on intravenous gancyclovir. The patient showed progressive subjective improvement, along with improvement in complete blood count. Subsequent CMV polymerase chain reaction test was negative. She received 10 days of intravenous gancyclovir and was then discharged in a clinically stable condition on oral valgancyclovir for next 7 days.
Table 1: Complete blood count and viral load before and after starting gancyclovir

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Cytomegalovirus infection though common, usually remains silent and latent. Once infected, an individual generally becomes a carrier for a lifetime. Though CMV infection is common in developing countries, but no epidemiological data are available for India. CMV is spread by repeated or prolonged intimate exposure with infected body fluids, and the majority of infections are subclinical and asymptomatic.[1]

Several prospective studies have evaluated CMV reactivation in populations of patients with hematologic malignancies.[2] Han had studied epidemiologic features of reactivated CMV antigenemia among 4,382 cancer patients and found that antigenemia occurred in 9.3% of patients with non-SCT (n: 2511), 12.0% with autologous SCT (n: 582), and 39.1% with allogeneic SCT (n: 1289). Non-SCT patients with lymphoid tumors had a significantly higher rate of antigenemia than those with myeloid tumors (13.6% vs. 3.9%). Non-SCT patients with solid tumors had a tested CMV antigenemia rate of 8.5%; however, most patients with solid tumors did not have severe complications or immune suppression.

A case series reported by Kuo et al.,[3] including 15 cancer patients, 14 with solid tumors (11 had head and neck cancers, two had lung cancers, and one had rectal cancer) and one lymphoma noted that the incidence of CMV reactivation in patients receiving conventional chemotherapy is high (14 out of 15 patients experienced CMV reactivation). Reactivation though asymptomatic, was self-limiting in most of these cases. Symptomatology was directly correlated with CMV viral loads. As the viral load increased, the patients experienced more symptoms and showed more abnormal laboratory tests, the highest CMV DNA loads were found in patients who died (median 26,790 copies/mL), while lower CMV loads were associated with patients who survived (median 1540 copies/mL).

Our patient received initial neoadjuvant chemotherapy followed by 20 fractions of radiation treatment and three doses of concurrent cisplatin. She had no prior history of CMV infection. Consistent with the findings by Kuo et al., our patient, though febrile, had only a moderate viremia and demonstrated minimal end-organ (hepatic) dysfunction but severe pancytopenia. She had normalization of her transaminases and her blood count also improved after initiating gancyclovir.

Viruses like hepatitis B virus (HBV), CMV human herpesvirus-6, and Epstein–Barr virus are commonly reactivated in patients who become immunosuppressed from chemotherapy and should be considered in appropriate clinical setting.

In hepatitis B surface antigen positive breast cancer patients, prechemotherapy HBV DNA high viral loads (>3 × 105 copies/mL) were significantly associated with the HBV reactivation.[4]

Screening for latent CMV infection in patients with solid tumor malignancies is not routine, and there are only few prior cases reported of CMV reactivation in solid tumor malignancies. However, persistent fever despite appropriate antibiotic and anti-fungal coverage should prompt a more thorough evaluation for pathogens, including viruses, which may have been reactivated as a result of cytotoxic interventions for the primary malignancy.

 
  References Top

1.
Bate SL, Dollard SC, Cannon MJ. Cytomegalovirus seroprevalence in the United States: the national health and nutrition examination surveys, 1988-2004. Clin Infect Dis 2010;50:1439-47.  Back to cited text no. 1
    
2.
Han XY. Epidemiologic analysis of reactivated Cytomegalovirus antigenemia in patients with cancer. J Clin Microbiol 2007;45:1126-32.  Back to cited text no. 2
    
3.
Kuo CP, Wu CL, Ho HT, Chen CG, Liu SI, Lu YT. Detection of Cytomegalovirus reactivation in cancer patients receiving chemotherapy. Clin Microbiol Infect 2008;14:221-7.  Back to cited text no. 3
    
4.
Zhong S, Yeo W, Schroder C, Chan PK, Wong WL, Ho WM, et al. High hepatitis B virus (HBV) DNA viral load is an important risk factor for HBV reactivation in breast cancer patients undergoing cytotoxic chemotherapy. J Viral Hepat 2004;11:55-9.  Back to cited text no. 4
    



 
 
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