Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
LETTER TO THE EDITOR
Year : 2012  |  Volume : 8  |  Issue : 3  |  Page : 462-463

Pericardial effusion and the unsuspected culprit


Department of Medical Oncology, Cancer Institute,Amrita Institute of Medical Sciences, AIMS Ponekkara post, Edappally, Kochi, Kerala, India

Date of Web Publication17-Nov-2012

Correspondence Address:
Palaniappan Muthu
Department of Medical Oncology,Cancer Institute, Amrita Institute of Medical Sciences, AIMS Ponekkara post, Edappally, Kochi - 682041, Kerala
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.103538

Rights and Permissions

How to cite this article:
Thomas B, Muthu P, Karichala A, Keechilat P. Pericardial effusion and the unsuspected culprit. J Can Res Ther 2012;8:462-3

How to cite this URL:
Thomas B, Muthu P, Karichala A, Keechilat P. Pericardial effusion and the unsuspected culprit. J Can Res Ther [serial online] 2012 [cited 2019 Nov 12];8:462-3. Available from: http://www.cancerjournal.net/text.asp?2012/8/3/462/103538

Sir,

A seven-year-old boy, a case of T-cell lymphoblastic lymphoma, was subjected to chemotherapy with BFM protocol. After the first cycle of high dose methotrexate in M phase, he presented with chest discomfort and low-grade fever. Chest X-ray was normal except for mild cardiomegaly and the subsequent 2D-echocardiogram revealed pericardial effusion. Since the effusion was minimal, it could not be drained. Mantoux was negative. Anti-inflammatory agents were initiated and he was put on close follow up. The child became asymptomatic with serial echocardiogram showing gradual resolution of effusion.

Before the second cycle of high dose methotrexate, chest X-ray and 2D-echocardiogram were repeated and they showed no effusion. Hence it was decided to proceed with the second cycle. However, during the leucovorin rescue phase, he again developed the same symptoms. Chest X-ray showed significant cardiomegaly [Figure 1] and 2D-echocardiogram confirmed a significant pericardial effusion with impending tamponade. A pig-tail catheter was inserted and approximately 400 ml of serous fluid was removed. Fluid was paucicellular with scattered inflammatory cells, and showed a glucose level of 107.6 mg/dl, protein level of 6.27 g/dl and adenosine deaminase level of 25 U/L. The fluid was negative for malignant cells, and culture and polymerase chain reaction for tuberculosis. In view of the temporal relationship between methotrexate administration and onset of pericardial effusion as well as the negative results for other possible etiologies, methotrexate-induced pericarditis was attributed to the development of pericardial effusion in our patient.
Figure 1: Chest X-ray showing pericardial effusion

Click here to view


Methotrexate is a commonly used drug in oncology. Its dose varies depending on the type of malignancy and route of administration (from 12.5 mg for intrathecal methotrexate to 12 g/m 2 , for high-dose methotrexate). The route of administration can be oral, intramuscular, intravenous or intrathecal. The most commonly encountered toxicities following methotrexate administration are nausea, vomiting and mucositis. Methotrexate-induced pleurisy and pneumonitis with or without pericardial involvement are very rare, [1] where the pathologic mechanism is thought to be immune-mediated serositis. [2]

Isolated pericardial effusion as a toxic effect of methotrexate is extremely rare. Only two cases have been reported in the literature. The first reported case was in a 22-year-old woman with hydatidiform mole who received low-dose methotrexate (total dose over nine courses was 1.8 g) [3] and the second patient was a case of psoriasis treated with very small dose of methotrexate (dose ranges from 7.5 to 25 mg per week). [4] Our patient experienced the toxicity following high-dose methotrexate for malignancy (5 g/m 2 per cycle). We believe it to be immune-mediated as the fluid was protein-rich, paucicellular with inflammatory cells, and negative for malignancy and tuberculosis. Even in a country where tuberculosis is common, the possibility of drug-induced pericardial effusion should be considered in patients receiving methotrexate.

 
 > References Top

1.Sheridan E, Hancock B, Smith S, Dorreen M, Neal F, Pennington G, et al. Gestational trophoblastic disease: experience of the Sheffield (United Kingdom) supraregional screening and treatment service (Review). Int J Oncol 1993;3:149-55.  Back to cited text no. 1
    
2.Akoun GM, Mayaud CM, Touboul JL, Denis MF, Milleron BJ, Perrot JY. Use of bronchoalveolar lavage in the evaluation of methotrexate lung disease. Thorax 1987;42:652-5.  Back to cited text no. 2
[PUBMED]    
3.Forbat LN, Hancock BW, Gershlick AH. Methotrexate-induced pericarditis and pericardial effusion; first reported case. Postgrad Med J 1995;71:244-5.  Back to cited text no. 3
[PUBMED]    
4.Palungwachira P, Palungwachira P, Laohathai P. Methotrexate induced pericarditis and pericardial effusion in psoriatic patient. J Med Assoc Thai 1998;81:141-5.  Back to cited text no. 4
[PUBMED]    


    Figures

  [Figure 1]


This article has been cited by
1 Methotrexate
Reactions Weekly. 2013; 1457(1): 27
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  >Article Figures
  In this article
>References

 Article Access Statistics
    Viewed2567    
    Printed52    
    Emailed0    
    PDF Downloaded119    
    Comments [Add]    
    Cited by others 1    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]