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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 11  |  Issue : 2  |  Page : 112-116

Clinicodemographic Profile of Tropical Pulmonary Eosinophilia in a Tertiary Care Institute of Bihar


Department of Pulmonary Medicine, Indira Gandhi Institute of Medical Sciences, Patna, Bihar, India

Date of Submission09-Nov-2021
Date of Decision18-Jan-2022
Date of Acceptance19-Jan-2022
Date of Web Publication08-Apr-2022

Correspondence Address:
Dr. Md Arshad Ejazi
Department of Pulmonary Medicine, Indira Gandhi Institute of Medical Sciences, Sheikhpura, Patna - 800 014, Bihar
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijrc.ijrc_138_21

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  Abstract 


Background: Tropical pulmonary eosinophilia (TPE) is a type of eosinophilic lung disease, and it is associated with a hypersensitivity response to Wuchereria bancrofti and Brugia malayi's microfilariae. Any systemic data regarding its clinical, demographic, and radiological profile in patients of this part of the world are sparse. This study aimed to study the clinical and demographic profile of TPE patients in this geographical area. Materials and Methods: This is a prospective observational study done over 1 year period in patients with TPE-like features in a tertiary care center of Bihar. After appropriate clinical and blood examination, absolute eosinophil count (AEC), serum total immunoglobulin E (IgE), spirometry, filarial antigen, and filarial antibody and chest radiology were done. Results: Among 77 cases of TPE, 54 were male (70.1%) and 23 were female (29.9%), in a ratio of 2.35:1. The majority of cases 43 (55.9%) were found in age less than 30 years. Most of our participants were students 28 (36.4%), homemakers 19 (24.7%), and farmers 17 (22.1%). The most common clinical feature was cough 77 (100%). Filarial antibody was raised in all (100%) while antigen was positive in 96.1%. Chest radiology was normal in 71.4%. Mean AEC and IgE ± standard deviation were 6730.71 + 4671.12 and 7983.14 ± 7279.60 kU/L, respectively. Spirometric findings were mild restriction 25 (32.5%). Conclusion: The prevalence of TPE is supposed to be higher in endemic areas. The patient should be evaluated in detail if having raised eosinophil count (>3000/mm3) with increased IgE level (>1000 kU/L) along with suggestive clinical features. Timely diagnosis and treatment can cure the disease and prevent its complications.

Keywords: Absolute eosinophil count, filarial antigen, immunoglobulin E, tropical pulmonary eosinophilia


How to cite this article:
Shankar M, Ejazi MA, Choubey S, Kumar D. Clinicodemographic Profile of Tropical Pulmonary Eosinophilia in a Tertiary Care Institute of Bihar. Indian J Respir Care 2022;11:112-6

How to cite this URL:
Shankar M, Ejazi MA, Choubey S, Kumar D. Clinicodemographic Profile of Tropical Pulmonary Eosinophilia in a Tertiary Care Institute of Bihar. Indian J Respir Care [serial online] 2022 [cited 2022 May 25];11:112-6. Available from: http://www.ijrc.in/text.asp?2022/11/2/112/342780




  Background Top


Tropical pulmonary eosinophilia (TPE) is a hypersensitivity reaction to the Wuchereria bancrofti and Brugia malayi's microfilariae trapped in the pulmonary microcirculation.[1],[2] Mosquitoes are a vector for Lymphatic filariasis. TPE is endemic in the tropical and subtropical parts of countries such as Africa, Asia, South America, and Oceania.[1],[2],[3]

It has been reported from the coastal regions of India from West Bengal to Tamil Nadu and Maharashtra to Kerala.[4] The disease prevalence also varied from 9.9% among jail inmates in Patna[5] to 0.5% among children of Tamil Nadu.[6] The term TPE was coined in India for a group of clinical features consisting of cough, fever, wheezing, eosinophilia, and bilateral lung mottling on chest radiograph by Weingarten in 1943.[7]

Less than 1% of patients with lymphatic filariasis develop TPE. The disease is more common in the age group of 15–40 years, with a male-to-female ratio of 4:1.[4],[8] It predominantly affects the lungs, but few studies reported about 7% of patients showed nonpulmonary manifestations.[4],[9]

Cough is the predominant clinical feature followed by wheezing, dyspnea, and chest pain. Symptoms are primarily at night but may present during the day.[4],[10] On examination, wheeze and crackles are predominant findings.[4]

Laboratory findings consist of marked eosinophilia >3000/μm, rising to 80,000/μm.[10],[11],[12] Elevated values of erythrocyte sedimentation rate and raised filarial-specific immunoglobulin E (IgE) and immunoglobulin G (IgG) and serum IgE were also found in TPE.[13],[14],[15] Chest radiograph may be normal (20%) or have reticulonodular opacity predominantly in mid to lower zones or miliary mottling.[4],[16],[17] Computerized tomography scan findings are miliary mottling and interstitial shadows, bronchiectasis, cavitation, consolidation, air trapping, or pleural effusions.[18] Spirometry of TPE was reported to be obstructive, mixed, restrictive.[4] Another study reported decreased transfer factor for carbon monoxide (TLCO).[19] This study aimed to study the clinical and demographic profile of TPE patients in this geographical area.


  Materials and Methods Top


The study was a cross-sectional observational study of prospective type. Ethical clearance was taken from the Institutional ethics committee. Patients of TPE presented to pulmonary medicine outpatient department and inpatient department between June 2020 and May 2021 were included after informed consent.

After taking detailed clinical history (like any history of cough, shortness of breath, chest pain, and fever) and demographic data, patients were clinically examined (like any presence of crepitations and wheezing) and subjected to routine blood biochemistry, chest X-Ray/high-resolution computed tomography thorax, and spirometry. The data of all variables of interest were collected.

Inclusion criteria:

  1. Patient age >10 years
  2. History of cough, wheezing, and dyspnea
  3. Chest radiograph showing reticulonodular opacity or miliary mottling
  4. Absolute eosinophil count (AEC) >3000/mm3
  5. Elevated serum IgE (>1000 kU/L)
  6. Positive filarial specific IgG and IgE
  7. Positive filarial antigen.


Exclusion criteria:

  1. Pregnancy
  2. Age <10 years
  3. History of having received DEC during the past 6 months, allergic reaction to drugs, and/or systemic steroid intake for more than 5 days in the previous 4 weeks
  4. History of worm infestation, pulmonary tuberculosis, pneumonia, bronchial asthma, and chronic obstructive pulmonary disease.


Any patient with a history and clinical examinations suggestive of TPE were subjected to spirometry, AEC, total IgE, filarial antigen, and filarial antibody. Total IgE levels were calculated by fluoroenzyme immunoassay method, filarial antigen by immunochromatography, and filarial antibody by immunochromatography.

Data were analyzed using the SPSS software for Microsoft Windows (version 2021; SPSS Inc.; IBM, USA.) Descriptive analysis was done using mean with standard deviation (SD), median with range, or number (percentage). The differences between variables were analyzed using the Kruskal–Wallis test where required.


  Observation and Results Top


Among 77 cases of TPE, 54 were male (70.1%) and 23 were female (29.9%) in a ratio of 2.35:1. The majority of cases 43 (55.9%) were <30 years of age (male cases [35.1%] and female cases [15.6%]). Out of 77 cases, 46 (59.7%) lived in villages, while 31 (40.3%) lived in cities. Most of our subjects were students 28 (36.4%), followed by homemakers 19 (24.7%) and farmers 17 (22.1%) [Table 1].
Table 1: Epidemiological profile of study population

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Most common symptoms were cough 77 (100%), productive in 10 (13%) and nonproductive nocturnal in 67 (87%) followed by dyspnea 73 (94.8%). The most common finding on physical examination was wheeze 70 (90.0%) [Table 2] and [Figure 1].
Table 2: Clinical features of study population

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Figure 1: Clinical features of study population (P-Present A-Absent)

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Filarial antibody was raised in all patients (100%), whereas filarial antigen was positive in 74 (96.1%) patients. Chest radiology was normal in 55 (71.4%), interstitial pattern 10 (13%) nodular 10 (13%), and bronchiectasis in 2 (2.6%) [Table 3] and [Figure 2].
Table 3: Laboratory parameter of study population

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Figure 2: Chest radiology finding of study population

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Mean AEC 6730.71 ± 4671.12 (male 6866.30 ± 4688.70 female 6412.39 ± 4718.44) [Table 3] and [Figure 3]. The mean IgE ± SD of total cases was 7983.14 ± 7279.60 kU/L (range 1023–44567) (male 7989.39 ± 7772.19 female 7968.48 ± 6126.9). 55% of these cases had IgE levels above 5000 kU/L [Table 3] and [Figure 4]. Spirometric findings were mild restriction 25 (32.5%) followed by mild 18 (23.4%) and moderate 13 (16.9%) obstruction [Table 3] and [Figure 5]. The mean ± SD. of forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and FEV1/FVC of all cases were 2.02 ± 0.84; 2.71 ± 0.87, and 73.6 ± 12.08, respectively [Figure 6].
Figure 3: Absolute eosinophil count of the study population

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Figure 4: Total IgE level of the study population

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Figure 5: Spirometry category of the study population

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Figure 6: Spirometric parameter of the study population

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  Discussion Top


This study was intended to assess the clinicodemographic profile of filarial TPE. In our study, 77 cases of TPE were enrolled, 54 were male (70.1%) and 23 were female (29.9%) (male: female = 2.35:1). Similar results were seen in other studies.[2],[18],[20],[21],[22]

In our study, the mean age ± SD of cases was 33.38 ± 15.13 (range14–69 years).69% of total cases (41 [76%] males and 12 [52%] females) were <30 years, and five (6.5%) patients were more than 60 years. The mean age was 31.31 ± 14.79 for males and 38.22 ± 15.21 for female cases. The findings of our study show similarities to previous studies.[20],[21],[22],[23] In our study, the most common clinical features were cough in 100% cases (dry 87% and productive, 13%) followed by shortness of breath (94.8%), wheezing (90.1%), chest pain (9.1%), and fever (10.4%). The frequency of symptoms showed a similar correlation with other studies.[2],[20],[22],[23]

The mean AEC ± SD of cases was 730.71 ± 4671.12/mm3 (range 3010–24718) in this study. In 56% of patients AEC level was more than 5000/mm3. Similar result of mean AEC ± SD was found by Kumar and Mourya 9,829.64 ± 12,690.18/mm3 (range 2550–26,488),[20] Vijayan et al. 9.18 ± 0.66 × 109/L (range 3010–23,500),[23] Sandhu et al. 9,401 ± 8,556/mm3 (range 2500–30,750),[18] and Sharma et al. 14,880 ± 18,710/mm3 (range 8142–21,618)[24] in their studies. Vijayan et al. also found the AEC level more than 5000/mm3 in 90% of their cases,[23] which is similar to our study.

In the present study, chest radiology was normal in 55 (71.4%), interstitial pattern 10 (13%) nodular 10 (13%), and bronchiectasis in 2 (2.6%).[4] Our finding is in correlation with previous studies.[4],[18],[25]

Spirometric findings were mild restriction 25 (32.5%) followed by mild 18 (23.4%) and moderate 13 (16.9%) obstruction. The finding of this study is similar to Udwadia and Herzog[4] Mean ± S. D. of FEV1/FVC, FEV1and FVC of patients was 73.6 ± 12.08, 2.71 ± 0.87, and 2.02 ± 0.84, respectively. Similar results were seen by Kumar and Mourya the mean ± S. D. of FEV1/FVC, FEV1, and FVC were 79.69 ± 12.41, 2.31 ± 0.75, and 2.95 ± 0.91, respectively.[20] The maximum mean ± S. D. of FEV1 and FVC was found in the age group of 31–40 years, and the maximum mean ± S. D. of FEV1/FVC was seen in 10–20 years of age group. Kumar and Mourya found similar findings in their study. The maximum mean values of FVC and FEV1 were seen in the 21–30 years of age group, and the maximum mean value of FEV1/FVC was between 10 and 20 years of age.[20]

Limitations of study

The study's limitations were single-centered study, a small sample size, and filarial antigen detection by the alere filariasis test strip. It is a qualitative test that detects circulating filarial antigen of Wuchereria bancrofti, not brugia malayia.


  Conclusion Top


The prevalence of TPE is supposed to be higher in endemic areas. Since our locality is a filarial endemic area, TPE should always be considered if the patient presents with dyspnea or wheezing and cough. We found 70% male and 30% females in a ratio of 2.35:1. The majority of the cases were <30 years of age and living in villages. Most of them were students, followed by homemakers and farmers. Predominant clinical features were cough, followed by dyspnea and wheeze.

Clinicians should evaluate the patient in detail if they have raised AEC, increased IgE level, and clinical features of TPE. The wide availability of serological tests will result in a timely diagnosis. If treatment is started on time, we can cure the disease and prevent its complications. Spirometry would help us assess lung function and response to treatment.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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2.
World Health Organization. Lymphatic filariasis: Diagnosis and pathogenesis. WHO expert committee on filariasis. Bull World Health Organ 1993;71:135-41.  Back to cited text no. 2
    
3.
Michael E, Bundy DA. Global mapping of lymphatic filariasis. Parasitol Today 1997;13:472-6.  Back to cited text no. 3
    
4.
Udwadia FE. Herzog H, editor. Tropical eosinophilia. In: Pulmonary Eosinophilia: Progress in Pulmonary Research. Vol. 7. Basel: S Karger; 1975. p. 35-155.  Back to cited text no. 4
    
5.
Viswanathan R, Prasad M, Prasad S, Saran R, Sinha TR, Sinha SP. Morbidity survey of jail population. I. Incidence of certain chronic respiratory diseases, with special reference to pulmonary eosinophilosis. Indian J Chest Dis 1965;7:142-5.  Back to cited text no. 5
    
6.
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. 6
    
7.
Weingarten RJ. Tropical eosinophilia. Lancet 1943;1:103-5.  Back to cited text no. 7
    
8.
Islam N, Haq AQ. Eosinophilic lung abscess – A new entity. Br Med J 1962;1:1810-1.  Back to cited text no. 8
    
9.
Dreyer G, Dreyer P, Piessens WF. Extralymphatic disease due to bancroftian filariasis. Braz J Med Biol Res 1999;32:1467-72.  Back to cited text no. 9
    
10.
Vijayan VK. Immunopathogenesis and treatment of eosinophilic lung diseases in the tropics. In: Sharma OP, editor. Lung Biology in Health and Disease: Tropical Lung Disease. 2nd ed. New York: Taylor and Francis; 2006. p. 195-239.  Back to cited text no. 10
    
11.
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12.
Ottesen EA, Nutman TB. Tropical pulmonary eosinophilia. Annu Rev Med 1992;43:417-24.  Back to cited text no. 12
    
13.
Neva FA, Ottesen EA. Tropical (filarial) eosinophilia. N Engl J Med 1978;298:1129-31.  Back to cited text no. 13
    
14.
Ottesen EA. Immunological aspects of lymphatic filariasis and onchocerciasis in man. Trans R Soc Trop Med Hyg 1984;78 Suppl: 9-18.  Back to cited text no. 14
    
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Spry CJ, Kumaraswami V. Tropical eosinophilia. Semin Hematol 1982;19:107-15.  Back to cited text no. 15
    
16.
Islam N, Huque KS. Radiological features of tropical eosinophilia. J Trop Med Hyg 1965;68:177-80.  Back to cited text no. 16
    
17.
Khoo FY, Danaraj TJ. The roentgenographic appearance of eosinophilic lung (tropical eosinophilia). Am J Roentgenol Radium Ther Nucl Med 1960;83:251-9.  Back to cited text no. 17
    
18.
Sandhu M, Mukhopadhyay S, Sharma SK. Tropical pulmonary eosinophilia: A comparative evaluation of plain chest radiography and computed tomography. Australas Radiol 1996;40:32-7.  Back to cited text no. 18
    
19.
Vijayan V, Kuppurao KV, Venkatesan P, Sankaran K, Prabhakar R. Pulmonary membrane diffusing capacity and capillary blood volume in tropical eosinophilia. Chest 1990;97:1386-9.  Back to cited text no. 19
    
20.
Kumar R, Mourya S. Pulmonary function test in tropical pulmonary eosinophilia. Int J Med Res Rev 2014;2:283-90.  Back to cited text no. 20
    
21.
Vijayan VK, Kuppu Rao KV, Sankaran K, Venkatesan P, Prabhakar R. Diffusing capacity in acute untreated tropical eosinophilia. Indian J Chest Dis Allied Sci 1988;30:71-7.  Back to cited text no. 21
    
22.
Rom WN, Vijayan VK, Cornelius MJ, Kumaraswami V, Prabhakar R, Ottesen EA, et al. Persistent lower respiratory tract inflammation associated with interstitial lung disease in patients with tropical pulmonary eosinophilia following conventional treatment with diethylcarbamazine. Am Rev Respir Dis 1990;142:1088-92.  Back to cited text no. 22
    
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Vijayan VK, Rao KV, Sankaran K, Venkatesan P, Prabhakar R. Tropical eosinophilia: Clinical and physiological response to diethylcarbamazine. Respir Med 1991;85:17-20.  Back to cited text no. 23
    
24.
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25.
Angirish B, Jankharia B, Sanghavi P. The role of HRCT in tropical pulmonary eosinophilia. Eur J Radiol 2020;131:109207.  Back to cited text no. 25
    


    Figures

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

  [Table 1], [Table 2], [Table 3]



 

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