|Year : 2007 | Volume
| Issue : 3 | Page : 94-96
Asthma, tuberculosis or eosinophilic pneumonia?
Subhra Mitra, Somenath Kundu
Department of Respiratory Medicine, Institute of Postgraduate Medical Education & Research and S.S.K.M. Hospital, Kolkata-700020., India
701 Auroville Apartments, 10, Mandeville Gardens, Kolkata 700019.
Source of Support: None, Conflict of Interest: None
| Abstract|| |
A 45 year-old male presented with cough and expectoration for 8 months, shortness of breath and wheeze for 3 months, and fever for 1 month. He remained symptomatic despite repeated courses of antibiotics with partial relief on oral and inhaled bronchodilators. Despite several sputum examinations being negative for acid fast bacilli (AFB), he was put on anti-tubercular drugs (ATD) because of bilateral infiltrates on his chest radiographs. A mildly raised blood eosinophil count, eosinophilia in broncho-alveolar lavage (BAL) fluid and eosinophilic infiltration on CT guided FNAC from his lung lesion raised the suspicion and the dramatic clinicoradiological improvement with oral corticosteroids clinched the diagnosis of CEP.
Keywords: Chronic Eosinophilic Pneumonia, Blood Eosinophilia, Eosinophilic Lung Disease
|How to cite this article:|
Mitra S, Kundu S. Asthma, tuberculosis or eosinophilic pneumonia?. Lung India 2007;24:94-6
| Introduction|| |
Chronic eosinophilic pneumonia (CEP) is an uncommon disorder that has a more protracted clinical and radiological course than simple pulmonary eosinophilia (Loeffler's syndrome). Although etiology and pathogenesis are unclear, a regain (IgE) mediated hypersensitivity pneumonitis has been strongly implicated.
We report here a case of CEP in a 45 year - old man who presented with cough, shortness of breath, fever, weight loss and an unexplained multifocal consolidation.
| Case Report|| |
A 45-year-old male presenting with cough and expectoration for 8 months, shortness of breath for 5 months and fever for 1 month was admitted for evaluation.
He was apparently well till about 8 months back when he started having cough with sputum production. Cough was more common in the early morning and expectoration, mucoid and sometimes mucopurulent, varied from ˝ to 1 cup per day. There was no foul odour or blood streaking of the sputum. The symptoms persisted despite coughmedicines and repeated courses of antibiotics.
After three months of his illness he started having episodes of shortness of breath with wheeze that showed only partial relief on oral and inhaled bronchodilators and oral steroids for 10 days. There was no history of orthopnoea or paroxysmal nocturnal dyspnoea. One month prior to his admission he developed a low grade, intermittent fever with temperature ranging between 99 0 and 101 0 F, night sweats but no chills or rigors.
He was prescribed anti-tubercular drugs elsewhere, based on his chest radiographs [Figure 1] & [Figure 2]. The patient complained of weakness and anorexia during the last three months of his illness and had lost weight more than 10 kgs.
The patient gave no history of diabetes, hypertension, asthma, skin rash, arthritis, sinusitis, dysuria, haematuria, or contact with tuberculosis and pet birds or any risk factor for HIV infection. He was a smoker for 15 years before quitting about 14 years ago. He is an accountant in a packaging firm with history of exposure to water-based varnish coating.
On physical examination the patient looked ill and toxic. There was no clubbing, edema cyanosis, lymphadenopathy or skin lesion. His temperature was 99 0 F, pulse 108/min., respiration 24/min, BP 130/80 and JVP was not raised. There were bilateral scattered rhonchi and a few inspiratory crackles. Other findings were within normal limits. On admission he was put on IV antibiotics, inhaled bronchodilators and ATDs were discontinued.
His chest radiographs (cxr) showed
Haemoglobin 13.2 gm/dl, Platelet count 290,000/mm 3 , WBC: 12,900/mm 3 , Neutrophil: 77% Capymphocyte: 15% Monocyte: 1% Eosinophils: 7% (abs count 903/mm 3 ), absolute Basophil: 0%, ESR: 101mm. A peripheral blood smear done 4 months prior to admission showed WBC 11,200 with eosinophils 14% and another done 1 month prior to admission showed WBC 8,600 with eosinophils 5% and ESR 105mm.
Blood sugar, urea, serum creatinine, and liver function tests, urine microscopy were normal. Sputum for AFB was negative on smear and culture. HIV serology was negative, USG abdomen was normal.
Spirometry showed mixed obstructive and restrictive ventilatory defect. C-ANCA & p-ANCA: Negative IgE: 241.09 kIU/L (<120 kIU/L) C.T. scan of thorax [Figure 4]: bilateral confluent alveolar opacities with air bronchograms.
BAL fluid: 960 cells/mm3 with eosinophil 20%. Stains for AFB and fungus were negative. Malignant cells were not found.
CT-guided FNAC from Rt Lung showed many scattered eosinophils, polymorphs along with degenerated cells. Charcot-Leyden crystals were noticed. Stain for AFB was negative. Findings were consistent with eosinophilic pneumonia.
The patient was put on oral prednisolone 40mg/day and IV antibiotics were discontinued.
He was afebrile on the 2nd day. Cough and expectoration diminished (sputum 10-15 ml/day). His appetite improved and he gained 3 kg. His CXR [Figure 5] 2 weeks after starting oral steroids showed near-complete radiological resolution.
Oral prednisolone 40 mg/day was continued for 2 weeks; then gradually tapered off over a period of 9 months. He is now asymptomatic, off oral steroids but on inhaled corticosteroids and is attending for follow-up for more than a year.
| Discussion|| |
The term chronic eosinophilic pneumonia was coined by Carrington and colleagues  in 1968 to describe a condition characterized by presence of blood eosinophilia and pulmonary eosinophilic infiltration for which no cause is found. CEP usually occurs in middle aged women but can occur at any age in either sex  . Cough with mucoid or no sputum, dyspnoea, weight loss, malaise, wheezing and night sweats are the main symptoms 2 . Asthma is present in half of the cases and tends to be of recent onset  .
Our patient had asthma-like symptoms of recent onset for which he was managed elsewhere before a more definite diagnosis of CEP was made in this department. Blood eosinophilia though typical may be absent  . Only mild peripheral eosinophilia was documented on two occasions in our patient. ESR and serum IgE are raised in most patients but may be normal  .
The classical radiologic features of peripheral pulmonary infiltrates - "reverse pulmonary oedema pattern" - was not present in our case but the serial radiographs suggested that the infiltrates were changing. So with the more common conditions like tuberculosis and necrotizing pneumonia, we considered some largely immunologic conditions like allergic bronchonulmonary aspergillosis (ABPA), Wegeners' granulomatosis, BOOP and CEP. However, compared to the fleeting nature of consolidations in simple pulmonary eosinophilia, the lesions in CEP tend to persist unchanged over days  or be partially fixed and partially evanescent. CT confirms the peripheral distribution of the consolidation  as in our patient.
BAL eosinophilia is a reliable clue to presence of eosinophil-related disorders of the lung and closely co-relates with presence of tissue eosinophilia on lung biopsy. BAL fluid often contains > 20% eosinophils in acute phase of CEP  . Open lung biopsy may be required if there is diagnostic doubt  but because of associated perioperative morbidity we opted for CT-guided FNAC  of the lung consolidation which showed eosinophilic infiltrates and Charcot-Leyden crystals.
Swift clinico-radiological improvement with corticosteroids is a characteristic feature of CEP rarely observed with other inflammatory lung disorders, and may help to confirm a suspected case. ,, Our patient showed considerable symptomatic improvement by the second day of oral steroids with radiologic clearance in two weeks. The corticosteroid dosage is tapered off over 12-18 months , as recurrence is common with rapid weaning off steroids. Our patient is on follow-up for more than a year and is off oral steroids for 3 months.
A diagnosis of CEP requires a high index of suspicion. CEP may mimic common lung disorders like tuberculosis. Migrating infiltrates on serial radiographs are a clue to immunologic disorders. Dramatic response to corticosteroid therapy is an important aid to the diagnosis often helping to confirm suspected case.[Figure 3]
| References|| |
|1.||Carrington CB, Addington WW, Goff AM, et al: Chronic eosinophilic pneumonia. N Engl J Med 1969; 280:787-798. |
|2.||Goetzl Ej, Luce JM. Eosinophilic Lung Diseases. In Murray JF, Nadel JA (ed): Textbook of Respiratory Medicine, 3rd Ed, WB Saunders 2000: 1757-1773. |
|3.||Fox B, Seed W: Chronic eosinophilic pneumonia. Thorax 1980;35: 570-580. |
|4.||Fraser RS, Muller NL, Colman N, Pare PD. Eosinophilic Lung Disease. In Diagnosis of Diseases of the Chest, 4th Ed, WB Saunders 1999; 1743-1756. |
|5.||Kroegel C, Reissig A, Mock B. Eosinophilic pneumonia. In Gibson Gj, Geddes DM, Strek Pj, Costable U, Corrin B (ed): Respiratory Medicine, 3rd Ed, Saunders 2003: 1643-1659. |
|6.||Ramzy I, Geraghty R, Lefcoe MS, et al: Chronic eosinophilic pneumonia. Diagnosis by fine needle aspiration. Acta Cytol 1978;22: 366. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]