The document discusses pulmonary eosinophilias, which are a heterogeneous group of disorders characterized by varying degrees of pulmonary or blood eosinophilia. It classifies the main types as Loeffler's syndrome, drug and toxin induced eosinophilic pneumonia, tropical pulmonary eosinophilia, and allergic bronchopulmonary aspergillosis. Loeffler's syndrome is characterized by transient pulmonary infiltrates associated with eosinophilia caused by parasites. Tropical pulmonary eosinophilia is caused by a hypersensitivity reaction to filarial parasites. Allergic bronchopulmonary aspergillosis involves a hypersensitivity response to inhaled fungal antigens like Aspergillus.

1. PULMONARY EOSINOPHILIAS
Presenter : Dr. Ashutosh Date : 15/06/2017

2. INTRODUCTION
In 1932, Loeffler first identified the association between pulmonary infiltrates
and eosinophilia.
Subsequently, Crofton separated the eosinophilic pneumonias into five groups
on the basis of clinical criteria:
Loeffler’s syndrome,
Prolonged pulmonary eosinophilia,
pulmonary eosinophilia associated with asthma,
tropical eosinophilia, and
Periarteritis nodosa.

3. In 1952, Reeder and Goodrich coined the term pulmonary infiltrates
with eosinophilia (PIE syndrome) to refer to these disorders.
However, it was subsequently appreciated that pulmonary infiltration
With eosinophils can occur in the absence of peripheral blood
eosinophilia.
As a result, in 1969, Liebow and Carrington broadened the description
of the term eosinophilic pneumonia to include all disorders
characterized by infiltration of the lungs with eosinophils, with or
without an excess of eosinophils in the peripheral blood.

4. • Definition: Eosinophilic pneumonias are defined as a heterogeneous group
of disorders characterized by varying degrees of pulmonary parenchymal or
blood eosinophilia.
• Also called pulmonary infiltrates with eosinophilia or eosinophilic pneumonia
• The precise role of eosinophils in the pathogenesis of the eosinophilic
pneumonias is not clear
• However
• Initiation
• Perpetuation
• Amplification of tissue inflammation
• Injury
have been attributed to eosinophils

5. CLASSIFICATION

7. 1. LOEFFLER’S SYNDROME
• Also called as Simple Pulmonary Eosinophila
• In 1932 Loffler first described it as a clinical syndrome characterized by
• Mild respiratory symptoms
• Peripheral blood eosinophilia
• Transient, migratory pulmonary infiltrates
• Immune hypersensitivity to Ascaris lumbricoides and other parasites
• Affects people of all ages
• Clinical features
• Low-grade fever
• Nonproductive cough
• Dyspnea (mild to severe)
• Occasional hemoptysis

8. • The pulmonary manifestations begin approximately 9 to 12 days following
ingestion and occur during the migration of larvae through the lung.
• Respiratory manifestations are self limited, resolving in 1 to 2 wks
• Peripheral blood from patients reveals moderate to extreme eosinophilia.
• Expectorated sputum, if present, frequently contains eosinophils
• Chest X ray shows
• Transient, migratory, nonsegmental interstitial & alveolar infiltrates(often
peripheral or pleural based)
• Pulmonary function evaluation typically reveals a mild to moderate
restrictive ventilatory defect with a reduced diffusing capacity for carbon
monoxide (DlCO).

9. • Ascaris larvae may be identified in sputum or gastric aspirates
• Stool examination for ova and parasites is typically negative until 8
weeks after the onset of the respiratory syndrome.
• Lung histology shows striking eosinophilic infiltration of
interstitium and alveolar-capillary units

10. LOEFFLER’S SYNDROME

11. TREATMENT
• Since Loeffler’s syndrome may be induced by a variety of exposures, a search
for an etiologic agent should be undertaken.
• Bronchodilators and rarely corticosteroids may be used for alleviation of
Pulmonary symptoms, although these are usually self-limited.
• In cases due to Ascaris, treatment with oral mebendazole (100 mg twice a
day for 3 days) should be given to prevent late GI manifestations of Ascaris
infestation, which may include malnutrition, diarrhea, abdominal pain, and/or
intestinal obstruction typically 8 weeks or more after onset of respiratory
symptoms.
Since stool specimens are negative for ova and parasites early in the illness,
clinical follow-up over a 2- to 3-month period is indicated.

12. 2. DRUG AND
TOXIN
INDUCED
EOSINOPHILIC
PNEUMONIA

13. • Several drugs have been implicated, many are commonly used
Acetylsalicylic acid L-Tryptophan
Amiodarone Methotrexate
Bleomycin Minocycline
Captopril Nitrofurantoin
Carbamazepine Penicillamin
Propylthiouracil Phenytoin
Sulfasalazine Gold salts

14. Other causes are
• Radiation therapy for breast cancer
• Iodinated contrast agents
• Heroin (inhaled)
DRUG AND TOXIN INDUCED
EOSINOPHILIC PNEUMONIA

15. • Have an acute or subacute onset and are not always related to either the
cumulative dose of drug used or the duration of treatment.
• Respiratory symptoms vary widely in severity, from a mild Loeffler’s-like
symptoms(dyspnea, cough & fever) to severe fulminant respiratory failure.
• Wheezing may be present, but obstructive physiology is not common on
pulmonary function testing.

16. • A diagnosis of drug- or toxin-induced eosinophilic pneumonia is based upon
a careful review of drug and other exposures (including nonprescription
drugs, herbal preparations, street drugs, and environmental exposures).
• Other causes of eosinophilic lung disease should be excluded.
• A concomitant skin rash and pleural effusion can support the diagnosis of
drug-induced eosinophilic pneumonia.
• Although radiographic findings are not specific, interstitial or alveolar
infiltrates are typically evident on chest radiograph and common high-
resolution chest computed tomographic (HRCT) findings include bilateral
consolidation and ground-glass opacities, both of which are frequently
peripherally located.

18. • The prognosis is favorable in most cases.
• Elimination of exposure to the drug or other toxin - resolution of
symptoms, eosinophilia, pulmonary infiltrates, and normalization
of lung function within a month.
• Supplemental therapy with corticosteroids is not universally
required, but it may hasten recovery in patients who are severely
ill.

19. 3. TROPICAL PULMONARY
EOSINOPHILIA
• Tropical pulmonary eosinophilia (TPE) was first described in the early 1940s
by Weingarten, in India
• Characteristic symptoms are
• Malaise, anorexia, weight loss,
• Paroxysmal dry cough with dyspnea or wheezing,
• Marked peripheral blood eosinophilia,
• Spontaneous resolution over several weeks
• The illness is seen mainly in India and South-east Asia, as well as in Africa

20. • It is a rare manifestation of parasitic infection, TPE occurs in less than 1
percent of patients infected with lymphatic filariae.
• It is a hypersensitivity reaction to microfilariae from Wuchereria bancrofti
and Brugia malayi
• Approximately 4 times more common in men, most patients with TPE
manifest the disease between the age of 25 and 40 years, although children
and older adults may also be affected.

21. • It is a syndrome of immunological hyper-responsiveness to microfilariae in
the lungs.
• Males > Females
Clinical features – apart from symptoms mentioned
• Cough and wheeze that is worse at night
• Presentation can be similar to status asthmaticus
• Chest pain,
• Muscle tenderness,
• Pericardial and CNS involvement
• Rarely, patients remain asymptomatic.
• On Physical examination Coarse crackles, rhonchi
• Generalized lymphadenopathy & hepatosplenomegaly may be present

22. Laboratory findings
• Extreme peripheral blood eosinophilia (>3000 cells/mm3 )
• Serum IgE >1000 U/ml
• high titers of filarial-specific IgE and IgG, measured by complement fixation or
hemagglutination techniques,
• BAL may reveal intense eosinophilic alveolitis
Microfilariae are not found in blood or sputum, and examination of stool or urine for
Ova and parasites is negative (although patients from endemic countries may be
simultaneously infected with other parasites).
In contrast, microfilariae have been identified in lung and lymph node tissue,
especially when lymphadenopathy is present.

23. • Pulmonary function tests reveal an obstructive ventilatory defect in up to 30
percent of patients, particularly when symptoms have been present less
than 1 month.
• A restrictive ventilatory defect and reduced DlCO, with or without a
concomitant obstructive defect, are typical of long-standing disease.
• Lymph node biopsies may reveal degenerating microfilariae or adult worms,
surrounded by aggregates of eosinophils, their granule products,and giant
cells.

24. Radiological findings
• Bilateral indefinite mottling
uniformly distributed in both lung
fields - middle and lower zones
• Increased broncho-vascular
markings
• Cavitation and pleural effusion

25. TROPICAL PULMONARY
EOSINOPHILIA
Treatment
• Diethylcarbamazine in a dose of 2mg/kg orally three times a day for
14–21 days or for as long as 4 weeks
• It is directly filaricidal to both adult worms and microfilariae.
• It can also enhance the binding of granulocytes, macrophages,
antibodies, and complement to the surface of microfilariae.
• Clinical improvement is dramatic within 7 days of administration.
• Acute relapses - in up to 20 % of patients and they require 2-4mg/kg
for 21-30 days

26. • Alternative antifilarial drugs (e.g., ivermectin) or a trial of
corticosteroids may be useful therapies for the chronic variant of
the disease, although controlled studies of these agents are
lacking.
• Although seldom fatal, untreated TPE often leads to the
development of chronic interstitial lung disease.

27. 4. ALLERGIC BRONCHOPULMONARY
ASPERGILLOSIS (MYCOSIS)
• It is a disorder caused by a complex hypersensitivity (I and III) response to
inhaled fungal antigens.
• Most commonly by Aspergillus species (Aspergillus fumigatus)
• When induced by non-Aspergillus species, the syndrome is called allergic
broncho pulmonary mycosis.
• Other cases may be due to
• Candida
• Pseudomonas aeruginosa
• Aspergillus terreus
• Helminthosporium
• Curvularia lunata

28. Greenberger and Patterson
have proposed five minimal
essential criteria needed to
establish the diagnosis,
including

29. ALLERGIC BRONCHOPULMONARY
ASPERGILLOSIS (MYCOSIS)
Clinical features
• Typically nonspecific
• Dyspnea, wheezing, poor asthma control,
• Cough (commonly productive of thick, brown mucus plugs),
• Malaise, low-grade fever, hemoptysis (occasionally)
• Antecedent history of recurrent asthma, other atopic conditions
• ABPA can complicate asthma and cystic fibrosis
• 5 clinical stages have been identified

30. ALLERGIC BRONCHOPULMONARY
ASPERGILLOSIS (MYCOSIS)
Clinical Stages

31. Radiological findings
• Typical findings are parenchymal infiltrates
and bronchiectasis
• They have a predilection for upper lobes
• “finger-in-glove opacities”
• “tramline shadows”
• “toothpaste shadows”
• “ring shadows”
• lobar consolidation
Extensive infiltrates with tubular configuration
and ‘‘gloved finger” appearance

32. Highresolution CT scan image of impacted bronchus (arrow) and
chronic inflammatory changes

33. High-resolution chest CT image, showing moderate bronchiectasis,
with areas of mucoid impaction and atelectasis of the right middle lobe.

34. Treatment goals
Controlling
symptoms
Preventing
exacerbations
Preserving
normal lung
function

35. • Systemic corticosteroids are the mainstay of therapy
• Therapy
Prednisone 0.5-1 mg/kg a day for 2weeks, followed by 0.5
mg/kg every other day for 6 to 8 weeks.
• A subsequent taper (by 5 to 10 mg every 2 weeks) over 3 months
can then be tried.
• A low maintenance dose (~7.5 mg/day) may be required long term
to prevent recurrences
• IgE levels monitored 1 - 2 months of an acute exacerbation and
followed every 2 months thereafter since levels may rise.
• Escalation of steroids if IgE >100%
• CXR should be monitored every 3 months
• Inhaled corticosteroids - bronchospasm
• Steroid-sparing agent for symptomatic exacerbations and
pulmonary infiltrates

36. • Itraconazole 200 mg bid for 16 weeks – shown benefit despite
ABPA not being a fungal ‘infection’
• Especially useful in steroid resistant ABPA
• Also demonstrated utility in ABPA associated with Cystic Fibrosis
• The efficacy of itraconazole in ABPA is lower in patients on proton
pump inhibitors
• Nystatin, Amphotericin B, Miconazole, Clotrimazole, Natamycin,
are generally ineffective in controlling ABPA.

37. Complications
• Chronic or recurrent lobar
atelectasis
• Allergic Aspergillus sinusitis
• Aspergillus tissue invasion
• Aspergilloma (rarely)

38. 5. IDIOPATHIC ACUTE
EOSINOPHILIC PNEUMONIA
• Acute eosinophilic pneumonia (AEP) has been recognized as a distinct clinical
entity.
• More common in younger men, with a mean age of approximately 30 years.
• History of atopy is not essential.
• Occurs in recently commenced smokers and who have been involved in
activities with unusual exposures(such as cave exploration, plant repotting,
woodpile moving, and indoor renovations).
• No definite seasonal variation has been identified, (more in summer).
• It presents as an acute illness with fever, myalgias, cough, dyspnea, pleuritic
chest pain with diffuse crackles & hypoxemia
• Symptoms may lasts upto 30 days with avg. of 3 days

39. • Moderate Leucocytosis is typical but blood eosinophil count may
be normal
• Serum IgE elevated and BAL fluid will contain eosinophils (25-
50%).
• Pulmonary function tests reveal a restrictive ventilatory defect
with a reduced DLCO.

40. Radiological findings
Diffuse bilateral alveolar and
interstitial infiltrates on chest X ray
Diffuse parenchymal ground-glass
opacity and consolidation on CT

41. • Small to moderate bilateral pleural effusions are common.
• Fluid analysis typically reveals a high pH and marked eosinophilia.
• Light microscopic examination of lung tissue reveals prominent eosinophil
infiltration in alveolar spaces, bronchial walls, and, to a lesser degree, the
interstitium.
• The pathological pattern of diffuse alveolar damage with eosinophilic
infiltrates should suggest the possibility of AEP.

42. • Idiopathic AEP is a diagnosis of exclusion & considered in patients
with ALI or ARDS without a typical antecedent illness.
• Methylprednisolone 60 to 125 mg 6th hourly in respiratory failure
• Thereafter, oral prednisone 40 -60 mg per day for 2 -4weeks and
tapered over weeks.
• Prognosis is generally good

43. 6.CHRONIC EOSINOPHILLIC
PNEUMONIA
• First described as a clinical entity by Carrington and coworkers in 1969
• Women > Men, usually Caucasians.
• 30 to 40 years of age
• 33-50% patients have history of atopy, allergic rhinitis, or nasal polyps.
• Subacute presentation, with symptoms over several months
• low-grade fevers
• wheeze
• drenching night sweats
• Moderate weight loss
• Cough (dry mucoid)
• May develop dyspnea and lead to ARDS

44. • Rarely ,patient may develop, arthralgias, skin rash, pericarditis or
unexplained heart failure
• Patients with CEP frequently manifest a moderate leukocytosis.
• The majority (66 to 95 percent) have peripheral blood eosinophilia, with
eosinophils constituting more than 6 percent of their leukocyte differential. (
till 90% eosinophils have been documented)
• A moderate normochromic, normocytic anemia and thrombocytosis may be
present.
• The ESR is typically elevated (greater than 20mm/hour), and IgE levels are
elevated in up to one-half of cases.
• Analysis of BAL fluid reveals increased eosinophils, typically accounting for
40 percent or more of the white blood cell (WBC) differential.
• Blood and sputum cultures routinely fail to identify an infectious etiology in
these patients.

45. Carrington and colleagues described three radiographic features that are
characteristic for CEP:
(1) peripherally based, progressive dense infiltrates;
(2) rapid resolution of infiltrates following corticosteroid treatment, with
recurrences in identical locations; and
(3) The appearance of infiltrates as the “photographic negative of pulmonary
edema.

46. Radiographic appearance of chronic
eosinophilic pneumonia (CEP).
Variable computed tomography
appearance of infiltrates in two patients
with chronic eosinophilic pneumonia.
Peripheral upper-lobe predominant
infiltrates may have a
ground-glass appearance (A) or
may appear as regions of dense
consolidation or nodular opacity (B).

47. Radiological findings
• Infiltrates are bilateral, mid- to upper lung zones, and may mimic loculated
pleural fluid.
• The areas of consolidation are patchy and dense and can have ill-defined
margins.
• The characteristic “photographic negative of pulmonary edema” appearance
(which occurs in less than 50 percent of cases) results if extensive infiltrates
surround major portions of or the entire lung.
• Common CT scan findings include ground-glass opacities without clear
consolidation.
• Mediastinal lymphadenopathy may be present.

48. Treatment
• Corticosteroids are the mainstay of therapy for CEP.
• Even patients presenting with severe respiratory failure may respond well to
steroid treatment.
• Dramatic clinical, radiographic, and physiological improvement occurs with
steroid treatment.
• In most cases, treatment with steroids leads to
defervescence within 6 hours,
reduced dyspnea, cough, and blood eosinophilia within 24 to 48 hours,
resolution of hypoxia in 2 to 3 days,
radiographic improvementwithin 1 to 2weeks,
complete resolution of symptoms within 2 to 3 weeks, and
Normalization of the chest radiograph within 2 months.

49. • Prednisolone 40-60mg/day, continued until 2 weeks after resolution of
symptoms and radiographic abnormalities.
then tapered and stopped.
• Treatment is usually maintained for at least 3 months and optimally for 6 to
9 months.
• The prognosis of CEP is generally favorable.
• Clinical, hematological, or radiographic evidence of relapse occurs in
approximately one-third to one-half of patients when steroids are tapered or
discontinued.
• The reinstitution of steroids generally leads to improvement, and relapses do
not appear to indicate a worse prognosis, increased likelihood of treatment
failure, or increased morbidity.

50. 7. CHURG-STRAUSS
SYNDROME
• The histopathology and clinical features associated with this disease entity
were first described in 1951 by Churg and Strauss, as a
• Form of Necrotizing vasculitis in several organs
• Associated with eosinophilic tissue inflammation and extravascular
granulomas
• Occurring in asthmatics
• With associated fever and peripheral hypereosinophilia
• Also called allergic angiitis or allergic granulomatosis.
• Develops most commonly in patients between the ages of 38 to 50.
• CSS tends to follow a subacute course, with symptoms ranging over months
to years.

51. • Asthma: History of wheezing or diffuse high-pitched expiratory rhonchi.
• Eosinophilia: Eosinophilia >10% on differential white blood cell count.
• Mono- or polyneuropathy: Development of mononeuropathy,
multiple mononeuropathies, or polyneuropathy attributable to systemic
vasculitis.
• Pulmonary infiltrates, non-fixed: Migratory or transitory pulmonary
infiltrates attributable to vasculitis.
• Paranasal sinus abnormality: History of acute or chronic paranasal sinus
pain or tenderness or radiographic opacification of
the paranasal sinuses.
• Extravascular eosinophils: Biopsy including artery, arteriole
or venule showing accumulations of eosinophils in extravascular areas.
ACR diagnostic criteria

52. Prodromal
Phase
• Late onset (2nd & 3rd
decade) allergic
rhinitis and atopy*
• Lasting for >10
years
Eosinophilic phase
• Marked blood
eosinophilia
• Eosinophillic
infiltration of lung,
GI tract or skin
Vasculitic phase
• Vasculitis of the
small and medium
vessels
• Vascular and
extravascular
granulomas
• Constitutional
symptoms including
fever, malaise,
weight loss, and
increased allergic or
asthmatic
symptoms.
3 Clinical phases

53. • Most of the respiratory manifestations of CSS occur in the prodromal and
eosinophilic phases of the disease.
• Nearly all patients have asthma at some point in the illness.
• Upper airway allergic disease, including sinusitis, rhinitis, and polyposis, is
seen in 75 to 85 percent of patients and may be the presenting symptom.
• Spirometry may reveal an obstructive ventilatory defect.

54. • Cardiac manifestations :
not present on initial presentation of CSS.
• However, they typically occur during the vasculitic phase of the disease and
are a major source of morbidity and the principal cause of death (in up to 50
percent of cases) from the disorder.
• Progressive congestive heart failure (CHF) occurs in 47 percent of cases
because of myocardial infiltration by eosinophils or ischemic cardiomyopathy
resulting from necrotizing vasculitis of the coronary arteries.
• Others causes being.
Acute pericarditis
cardiac tamponade
Constrictive pericarditis

55. • CNS Manifestations :
Mono- or polyneuropathy (most notably mononeuritis multiplex) is present in 69 to
75 percent of cases.
other include cranial nerve impairment (especially optic neuritis),
seizure, subarachnoid hemorrhage, and cerebral infarction.
Cerebral hemorrhage and infarction are common causes of patient death.
• Skin findings :
localized crops.
nonthrombocytopenic purpura, tender cutaneous or subcutaneous nodules
(which may ulcerate), urticaria, a maculopapular rash, petechiae, ecchymoses, or
livedo reticularis.
• GI manifestations :
Eosinophilic gastroenteritis or vasculitis that can lead to diarrhea, abdominal
pain, intestinal obstruction, cholecystitis, pancreatitis, bleeding, liver function test
abnormalities, and bowel perforation.

56. • Renal manifestations:
Interstitial nephritis, focal segmental glomerulonephritis (oftenwith
necrotizing features), hematuria, and albuminuria are common.

57. • CSS have a striking but fluctuating degree of peripheral blood eosinophilia
(20 to 90 percent of the WBC differential), generally greater than that seen
with asthma alone.
• Serum total IgE levels are typically elevated (range, 500 to 1000 U/ml)
• Most patients have a normochromic, normocytic anemia and moderate
elevation of their ESR.
• 70 to 75 percent of patients have positive antinuclear cytoplasmic antibody
with a perinuclear staining pattern (pANCA).
• RA factor may be positive.
• Laboratory examination of pleural fluid, if present, reveals an acidotic
eosinophilic exudate with low glucose levels.
• Pleural biopsy shows chronic pleuritis with eosinophilic infiltration.
• BAL reveals an increased percentage of eosinophils.

58. • Chest findings are of asthma, with
transient, migratory nonlobar,
nonsegmental, often peripheral
pulmonary infiltrates, with no
regional predilection.
High-resolution CT scanning has demonstrated patchy peribronchial thickening,
pulmonary artery enlargement (in comparison to the corresponding bronchi),
irregular stellate configuration of some vessels, areas of septal thickening, and
scattered patchy parenchymal opacities with ground-glass or consolidated
appearance.

59. Pathological appearance of small arteriole in
Churg-Strauss vasculitis.
Intense perivascular inflammation with
Eosinophilia.

60. • Prednisone 60 mg/day for 6 to 12 weeks, aiming to eliminate constitutional
symptoms and cardiac, renal, neurological, or other vasculitic manifestations.
• Once the vasculitic phase is controlled, steroids may be tapered
• Low dose steroids for a year
• azathioprine, cyclophosphamide, high-dose methylprednisolone, or
chlorambucil if initial treatment fails
• Untreated patients have a poor prognosis; up to 50 percent die within 3
months after the onset of vasculitis.

61. 8. IDIOPATHIC HYPER-
EOSINOPHILIC SYNDROME
• This rare syndrome is characterized by marked peripheral blood
eosinophilia and by eosinophilic infiltration of many organs in the
absence of a known cause
• The three principal clinical features defining it
• (1) persistent blood eosinophilia greater than 1500/μl for > 6 months
• (2) symptoms and signs of end-organ dysfunction
• (3) no other identifiable underlying cause of eosinophilia.
• Symptoms are similar to AEP - fever, night sweats, anorexia,
malaise, weight loss, pruritus and cough.
• Blood eosinophilia and high IgE levels

62. • Respiratory involvement (40%)
• Nocturnal, minimally productive cough and wheeze
• Pulmonary hypertension, ARDS, and pleural effusions can occur
• Chest radiograph may reveal transient focal or diffuse pulmonary
infiltrates
• Cardiac disease – major cause for morbidity and mortality
• Manifest as progressive CHF due to eosinophilic myocarditis and
endocarditis, intracardiac thrombi, and endocardial fibrosis.
• Bacterial endocarditis has also been noted
• Echocardiographic follow-up at 6-month intervals – recommended
• Neuropsychiatric dysfunction (60%)
include encephalopathy with neuropsychiatric dysfunction, memory
loss, gait disturbances with or without signs of upper motor neuron injury,
visual changes, hemiparesis.
Peripheral neuropathy with sensory and/or motor axonal loss (no
vasculitic or eosinophilic infiltration) is extremely common in IHS

63. • Laboratory findings associated with IHS include an elevated total serum IgE
(25 to 38 percent), hypergammaglobulinemia, circulating immune complexes
(32 to 50 percent), and an ESR above 15 mm/h (68 percent).
• Elevated serum B12 and leukocyte alkaline phosphatase levels are also
noted.

64. Treatment
• Prednisolone 1mg/kg/day for several weeks followed by tapered
• Hydroxyurea 0.5 to 1.5 g per day may be added to the regimen if there is
evidence of further disease progression, with the aim of reducing the
peripheral leukocyte count to the range of 5000 to 10,000.
• Vincristine, etoposide, cyclosporine and chlorambucil have been used

65. Approaching
eosinophilic
pneumonias

66. REFERENCES
• Fishman's Pulmonary Diseases and Disorders – 4th edition
• Harrison's Principles of Internal Medicine - 19th edition
• Crofton and Douglas's Respiratory Diseases – 5th edition

70. TAKE HOME MESSAGES
• A complete occupational and exposure history is vital
• Elimination of the provocative agent is extremely important
• Early evaluation of patients with mild to moderate respiratory
symptoms with absolute eosinophil count and seum IgE levels
can point at eosinophila syndromes