Annals of Tropical Medicine and Public Health
Home About us Ahead Of Print Instructions Submission Subscribe Advertise Contact e-Alerts Editorial Board Login 
Users Online:160
  Print this page  Email this page Small font sizeDefault font sizeIncrease font size
 


 
Table of Contents   
CASE REPORT  
Year : 2013  |  Volume : 6  |  Issue : 3  |  Page : 339-342
Tropical pulmonary eosinophilia presenting as severe pulmonary arterial hypertension


1 Department of Pulmonary Medicine, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Cardiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Click here for correspondence address and email

Date of Web Publication7-Nov-2013
 

   Abstract 

Tropical pulmonary eosinophilia (TPE) is an easily diagnosed and treatable disease. Patients with TPE usually present with respiratory symptoms that include paroxysmal cough, breathlessness, wheeze and chest pain, often misdiagnosed as bronchial asthma. This case highlights one of the unusual presentations of TPE and discusses the association between TPE and pulmonary hypertension.

Keywords: Cor-pulmonale, eosinophilia, pulmonary hypertension, tropical pulmonary eosinophilia

How to cite this article:
Jindal S, Nath A, Patra JK, Kumar S. Tropical pulmonary eosinophilia presenting as severe pulmonary arterial hypertension. Ann Trop Med Public Health 2013;6:339-42

How to cite this URL:
Jindal S, Nath A, Patra JK, Kumar S. Tropical pulmonary eosinophilia presenting as severe pulmonary arterial hypertension. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Sep 23];6:339-42. Available from: http://www.atmph.org/text.asp?2013/6/3/339/121001

   Introduction Top


Tropical pulmonary eosinophilia (TPE) is prevalent in filarial endemic regions of the world especially India, South-East Asia, and Africa. It is characterized by cough, dyspnea, and nocturnal wheezing with diffuse reticulonodular infiltrates in chest radiographs and marked peripheral blood eosinophilia. [1] Long-term sequelae are pulmonary fibrosis with chronic respiratory failure. [2] Pulmonary hypertension can develop if TPE is not timely diagnosed and treated. Therefore, prompt clinical suspicion and early treatment can prevent cardiopulmonary morbidity.


   Case Report Top


An 8-year-old boy from District Hardoi, Uttar Pradesh presented in the Cardiology Outpatient Department in our institute on 10 th July, 2010 with complains of cough with expectoration, intermittent fever, progressive breathlessness, generalized swelling, loss of appetite, and fatigue for the past 5 months. Cough was worse during the night and early morning, often accompanied by wheezing. Breathlessness was modified medical research council (MMRC) grade 5 at presentation. There was no history of orthopnea, paroxysmal nocturnal dyspnea, chest pain, abdominal distension, or decreased urine output. Past history was suggestive of reactive airways disease since early childhood for which he was being treated at local hospital as and when required.

On examination, he was tachypneic; pulse rate was 120/min, regular. Blood pressure was 114/80 mmHg. Jugular venous pressure was raised and ankle edema was present. Cardiac impulse was right ventricular in type. Pulmonary second sound was loud and palpable. A soft, grade 2/6 pansystolic murmur was heard over the tricuspid area. There were inspiratory fine crepitations and rhonchi all over the chest. The liver was palpable 2 cm below right costal margin. Electrocardiogram recorded sinus rhythm with right axis deviation and right ventricular hypertrophy. 2D-echocardiography (ECHO) revealed massive dilated right ventricle and atrium with dysfunction with right ventricular systolic pressure (RVSP) of 72 mmHg and also had moderate tricuspid regurgitation. Simultaneously, pulmonary medicine consultation was sought for further work up. Chest X-ray showed cardiomegaly with bulging of pulmonary conus and bilateral perihilar and paracardiacreticulo-nodular shadows. There were increased reticular markings throughout both lung fields [Figure 1]. Blood count showed hemoglobin of 13.8 g/dl; total white blood cell count was 19,700/mm 3 of which 27% were neutrophils, 23% lymphocytes, and 50% eosinophils. Absolute eosinophil count (by Dunger's method) was 9550/mm 3 . Erythrocyte sedimentation rate was 120 mm in the 1 st h. Serum IgE was 2500 U/ml. Stool microscopy was negative for ova or cyst. No microfilaria was seen in peripheral smear. Antigen detection for filariasis(by BinaxNOW) was positive. Pulmonary function test (PFT) revealed moderate obstruction with significant bronchodilator response with superimposed restriction. Computed tomography of thorax showed bilateral randomly distributed miliary nodules in both lung fields predominately in lower lobes [Figure 2], [Figure 3] and [Figure 4]. A diagnosis of TPE was made based on above information and he was started on diethyl-carbamazine (DEC) (6 mg/kg/day), low dose diuretics, inhaled corticosteroids and bronchodilators. After three weeks of treatment he had marked improvement in his symptoms and his exercise capacity also improved. Absolute eosinophil count dropped from 9550 to 1976/mm 3 and serum IgE decreased to 285U/ml. Repeat ECHO revealed moderate pulmonary arterial hypertension with RVSP of 60 mmHg. Repeat high resolution computed tomography (HRCT) thorax showed prominent main pulmonary artery with mild cardiomegaly with normal lung parenchyma [Figure 5] and [Figure 6]. In view of persistent symptoms, oral prednisolone (0.5 mg/kg/day) was given for 6 weeks along with inhaled bronchodilators, inhaled corticosteroids and low dose diuretics for another three months. A follow-up ECHO at 6 months showed decrease in pulmonary artery pressures to 40 mmHg and there was also a decrease in right ventricular mass. Repeat PFT was normal. Patient is presently on low dose of inhaled steroids and low dose of diuretics.
Figure 1: Chest X-ray posteroanterior shows cardiomegaly with bulging of pulmonary conus and bilateral perihilar and paracardia creticulonodular shadows

Click here to view
Figure 2: Computed tomography of thorax (mediastinal widow): Enlarged mean pulmonary artery (November 2010)

Click here to view
Figure 3: Computed tomography of thorax (November 2010) shows bilateral randomly distributed miliary nodules in both lung fields predominately in lower lobes

Click here to view
Figure 4: Computed tomography of thorax (November 2010) shows bilateral randomly distributed miliary nodules in both lung fields predominately in lower lobes

Click here to view
Figure 5: Computed tomography of thorax (March 2011): Normal lung parenchyma with cardiomegaly

Click here to view
Figure 6: Computed tomography of thorax (March 2011): Normal lung parenchyma with cardiomegaly

Click here to view



   Discussion Top


TPE is one of the important entities in the differential diagnosis of pulmonary infiltrates with eosinophilia. It is caused by immunologic hyper-responsiveness to the human filarial parasites, Wuchereria bancrofti and Brugia malayi. It is prevalent in filarial endemic regions of the world especially India, South-East Asia, and Africa. In India, majority of cases are reported from Uttar Pradesh, Orissa, Bihar, and some areas of south India. [3],[4] It is notable that TPE is seen in only less than 1% of filarial infections. [2]

The following diagnostic criteria has been proposed for the diagnosis of TPE: (a) Appropriate exposure history (mosquito bite) in an endemic area of filariasis, (b) a history of paroxysmal nocturnal cough and breathlessness, (c) chest radiographic evidence of pulmonary infiltrations, (d) leucocytosis in blood, (e)peripheral blood eosinophils more than 3000 cells per cumm, (f) elevated serum IgE levels, (g) elevated serum antifilarial antibodies (IgG and/or IgE), and (h) a clinical response to DEC. [5] Our patient fulfilled the above criteria and diagnosed as a case of TPE. The most biologically plausible concept of the pathogenesis of TPE suggests that it results from lung parenchymal inflammation in individuals immunologically sensitized to filarial parasites. Eosinophils located in the lung, as a response to the presence of filarial parasite in the pulmonary circulation, degranulate and lead to the production of toxic oxygen radicals that contribute to a chronic pulmonary inflammatory process. Ongoing chronic inflammatory process may lead to development of pulmonary fibrosis and chronic respiratory failure. [6] These restrictive pulmonary function deficits may result in pulmonary hypertension that subsequently contributes to cor-pulmonale. It has also been postulated that pulmonary hypertension may result from destruction of the microfilariae and their continued embolization in the lung capillaries. [7] Although most textbooks do not mention TPE as a cause of pulmonary hypertension and isolated heart failure, but literature does suggest that some TPE patients may develop pulmonary hypertension if not timely diagnosed. [8] Development of pulmonary hypertension usually confers to a poor prognosis in patients with lung disease because majority of times it is irreversible. But this case highlights the fact that TPE is one of the few causes of cor-pulmonale which are partially or completely reversible with proper and adequate treatment. The treatment of choice recommended by the WHO is the oral antifilarial drug, DEC for 3 weeks. [9] In addition, these patients have persistent eosinophilic alveolitis and the lower respiratory tract inflammatory cells spontaneously release exaggerated amounts of superoxide (O 2 ) and hydrogen peroxide (H 2 O 2 ). Thus, following a standard 3-week course of DEC therapy, most patients show improvement, but not complete resolution of TPE; many are left with chronic respiratory tract inflammation and a mild form of interstitial lung disease. Treatment with prednisolone significantly reduces the lower respiratory tract inflammation and release of oxidants but still more clinical trials are needed to know the optimum dose and duration of DEC therapy with or without steroids. [2]

In conclusion, TPE is an easily curable disease. Cor-pulmonale in young age secondary to eosinophilic lung diseases of known etiology may be reversible with timely diagnosis and prompt treatment. Furthermore, TPE evaluation may be included in the work up of pulmonary hypertension especially in patients residing in endemic areas.

 
   References Top

1.Udwadia FE, Joshi VV. A study of tropical eosinophilia. Thorax 1964;19:548-54.  Back to cited text no. 1
    
2.Vijayan VK. Tropical parasitic lung diseases. Indian J Chest Dis Allied Sci 2008;50:49-66.  Back to cited text no. 2
    
3.Ray D, Abel R, Selvaraj KG. Epidemiology of pulmonary eosinophilia in rural south India - A prospective study, 1981-86. J Epidemiol Community Health 1993;47:469-74.  Back to cited text no. 3
    
4.Kar SK, Mania J. Tropical pulmonary eosinophilia in an Orissa village. Natl Med J India 1993;6:64-7.  Back to cited text no. 4
    
5.Ottesen EA, Nutman TB. Tropical pulmonary eosinophilia. Annu Rev Med 1992;43:417-24.  Back to cited text no. 5
    
6.Boggild AK, Keystone JS, Kain KC. Tropical pulmonary eosinophilia: A case series in a setting of nonendemicity. Clin Infect Dis 2004;39:1123-8.  Back to cited text no. 6
    
7.Obeyesekere I, Peiris D. Pulmonary hypertension and filariasis. Br Heart J 1974;36:676-81.  Back to cited text no. 7
    
8.Quah BS, Anuar AK, Rowani MR, Pennie RA. Corpulmonale: An unusual presentation of tropical eosinophilia. Ann Trop Paediatr 1997;17:77-81.  Back to cited text no. 8
    
9.World Health Organization. Final report: Joint WPRO/SEARO Working Group on BrugianFilariasis. Manila: WHO; 1979. p. 1-47.  Back to cited text no. 9
    

Top
Correspondence Address:
Shikha Jindal
MRA-A-98, SGPGIMS Campus, Raebrailey Road, Lucknow-226014, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.121001

Rights and Permissions


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *


    Abstract
   Introduction
   Case Report
   Discussion
    References
    Article Figures

 Article Access Statistics
    Viewed6940    
    Printed88    
    Emailed0    
    PDF Downloaded14    
    Comments [Add]    

Recommend this journal