Allergic Bronchopulmonary Aspergillosis (ABPA) is an allergic pulmonary disorder caused by a hypersensitivity reaction to the fungus Aspergillus fumigatus. It occurs most commonly in people with asthma or cystic fibrosis. The pathogenesis involves an immune response to Aspergillus colonization in the airways leading to mucus plugging, bronchiectasis, and lung fibrosis. Diagnosis is based on criteria including asthma, positive skin test or serum IgE to Aspergillus, eosinophilia, elevated total serum IgE, and central bronchiectasis on chest imaging. Treatment involves systemic corticosteroids to suppress the immune response along with antifungal agents
New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
The global Type 2 Diabetes (T2D) market is estimated to be $31.3 billion in 2014 and is expected to grow at a CAGR of mid-range single digit from 2015 to 2021 to reach $46.7 billion by 2021
51 Beginner Cycling Tips From Experienced CyclistsCycling Tips HQ
CyclingTipsHQ.com brings you 51 amazing cycling tips for beginners from cyclists and bloggers across the web. Also contains link to free 'Beginner Cycling Tools' guide.
Differential diagnoses of bronchial asthmaKoktongTan3
Differential diagnoses of bronchial asthma are diverse. Not all patients with wheezing or coughing are having bronchial asthma. In this presentation, I discussed about different case scenarios to broaden our knowledge to think out of the black box.
Clinical features and investigations of asthma is explained in very simple wording and style. Easy to remember and present due to interesting pictures. Helpful for medical students, patients with asthma and knowledge seekers.
Asthma is the most frequent chronic illness in children and is a common noncommunicable disease (NCD) that affects both adults and children. Coughing, wheezing, chest tightness, and shortness of breath are among the symptoms. This presentation target therapies for Asthma including its clinical use, etc. For more information, please contact us: 9779030507.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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3. Definition allergic pulmonary disorder caused by hypersensitivity to Aspergillusfumigatus1 Occurs in asthma or cystic fibrosis2 result of immune response to Aspergillus colonization of airway and poor clearance of mucus secretions subsequent bronchiectasis, pulmonary fibrosis, and compromise of pulmonary function first described by Hinson et al in 1952 in UK 1.CHEST 2009; 135:805–826. 2. Middleton’s Allergy, Principle&Practice 7th edition.
4. Epidemiology 1–2% of patients with chronic asthma 1 2–15% of patients with cystic fibrosis 2 Meta-analysis, prevalence of AH and ABPA in asthma of 28% and 12.9%,respectively3 Prevalence of AH ID test(28.7%) VS SPT (24.8%) (p=0.002)3 prevalence of ABPA in acute severe asthma admitted in ICU, AH (51%) and ABPA (39%) in patients with acute asthma (39%) compared to outpatient bronchial asthma ( 21%) Greenberger PA et al. J Allergy ClinImmunol1988;82:164–70. Stevens D, et al. Clin Infect Dis 2003;37(suppl 3):S225–64. Int J Tuberc Lung Dis 2009
5. Studies Describing Prevalence of AH and/or ABPA in Patients with Bronchial Asthma Over the Last Two Decades (43%) (6%) (18%) (25%) (23%) (16%) (22%) (28%) (7%) (38%) (20%) (30%) (7%) CHEST 2009; 135:805–826
6. Pathophysiology of ABPA. From Aspergillus adherence and penetration of the bronchial mucosa to the B and T cell response Allergy 2005: 60: 1004–1013
7. Genetic Factors Involved in Pathogenesis of ABPA HLA associations: HLA-DR molecules (DR2, DR5, and possibly, DR4 or DR7) associated with susceptibility HLA-DQ2 molecules associated with resistance Pulmonary surfactant protein A gene polymorphisms CFTR (cystic fibrosis transmembrane conductor regulatorgene) mutation Other IL-4 receptor polymorphisms IL-10 promoter polymorphisms IL-13 polymorphisms IL-15 polymorphisms TNF-α polymorphisms Toll-like receptor gene polymorphisms CHEST 2009; 135:805–826.
8. Animal model GM-CSF, IL-4 and IL-5 positive cells was higher in ABPA murine models than in controls Allergy 2005: 60: 1004–1013
9. Human model sIL-2R elevated in ABPA sera compared with sera from asthma without ABPA and nonatopicpatients high numbers of CD3+ HLA DP, DQ, and DR+ T cells or CD19CD23+ B cells levels of IgE and IgA-Aspergillus-specific Abwere higher in BAL than in blood bronchiectasis formation occurs in ABPA as consequence of local influx of N& E IL-8 gene expression and protein levels in sputum were higher in ABPA than controls IL8 may be key mediator of tissue damage in ABPA Allergy 2005: 60: 1004–1013
10. Pathology not necessary for diagnosis bronchial tree was dilated and filled with mucus plugs containing macrophages, eosinophils, Charcot–Leyden crystals and sometimes hyphae or hyphal fragments Bronchial walls were infiltrated with inflammatory cells (E, Land plasma cells), and thickening of basement membrane and epithelial abrasion Allergy 2005: 60: 1004–1013
14. Laboratory Findings Aspergillus Skin Test Type I and III reaction SPT and intradermal test (if SPT negative ) locally prepared or commercial Ag : no difference Total Serum IgE Levels most useful test for diagnosis and follow-up of ABPA Exclude ABPA ( if not steroid used) 35 to 50% decrease : criteria for remission Doubling of baseline IgE levels : relapse of ABPA CHEST 2009; 135:805–826
15. Laboratory Findings Serum IgE and IgG Antibodies Specific to A. fumigatus Hallmark of ABPA cutoff value of IgG/IgE> twice pooled serum samples from AH can help in differentiation of ABPA from other conditions Serum Precipitins Against A. fumigatus Precipitating IgGAb using double gel diffusion technique present in other pulmonary disorders Peripheral Eosinophilia AEC >1,000 cells/μL (major criteria) low eosinophil count not exclude ABPA CHEST 2009; 135:805–826
16. Laboratory Findings Sputum Cultures for A fumigatus supportive ,but not diagnostic grown in other pulmonary diseases rarely perform for diagnosis of ABPA Pulmonary Function Tests Categorize severity, no diagnostic value usual finding is obstructive defect Role of Specific Aspergillus Antigens Further studies are required CHEST 2009; 135:805–826
17. Radiologic Investigations Chest radiographic findings Transient changes Patchy areas of consolidation Radiologic infiltrates: toothpaste and gloved finger shadows due to mucoid impaction in dilated bronchi Collapse: lobar or segmental Permanent changes Parallel-line shadows representing bronchial widening Ring-shadows 1–2 cm in diameter representing dilated bronchi en face Pulmonary fibrosis: fibrotic scarred upper lobes with cavitation HRCT findings Centralbronchiectasis Mucus plugging with bronchoceles Consolidation Centrilobular nodules with tree-in-bud opacities Bronchial wall thickening Areas of atelectasis Mosaic perfusion with air trapping on expiration CHEST 2009; 135:805–826
18.
19. Chest x-ray in a patient with ABPA: ring shadows (long arrows) represent bronchiectatic airways seen in cross-section; tram lines (short arrow) seen longitudinally
24. Diagnosis and Diagnostic Criteria Rosenberg-Patterson criteria Major criteria ( ARTEPICS ) A = Asthma R = Roentgenographic fleeting pulmonary opacities T = Skin test positive for Aspergillus(type I) E = Eosinophilia P = Precipitating Abs (IgG) in serum I = IgE in serum elevated ( > 1,000 IU/mL) C = Central bronchiectasis S = Serums A fumigatus-specific IgG and IgE (more than twice the value of pooled serum samples from patients with asthma who have Aspergillus hypersensitivity) Minor criteria Presence of Aspergillus in sputum Expectoration of brownish black mucus plugs Delayed skin reaction to AspergillusAg (type III ) presence of 6 of 8 major criteria makes diagnosis almost certain; disease is further classified as ABPA-S or ABPA-CB CHEST 2009; 135:805–826
25. Diagnosis and Diagnostic Criteria(Minimal diagnostic criteria for ABPA) Minimal ABPA-CB Asthma Immediate cutaneoushyperreactivity to Aspergillus antigens Elevated IgE Raised A fumigatus-specific IgG and IgE Central bronchiectasis Minimal ABPA-S Asthma Immediate cutaneoushyperreactivity to Aspergillus antigens Elevated IgE Raised A fumigatus-specific IgG and IgE Transient pulmonary infiltrates on chest radiograph CHEST 2009; 135:805–826
29. Differential Diagnosis Aspergillus hypersensitive bronchial asthma pulmonary tuberculosis in endemic areas community-acquired pneumonia (especially acute presentations) other inflammatory pulmonary disorders eg. eosinophilic pneumonia, bronchocentricgranulomatosis, and Churg- Strauss syndrome CHEST 2009; 135:805–826
30. Complication recurrent asthma exacerbations development of bronchiectasis subsequent pulmonary hypertension Respiratory failure CHEST 2009; 135:805–826
31. Management 2 important aspects: glucocorticoids to control immunologic activity and close monitoring for detection of relapses antifungal agents to attenuate fungal burden secondary to fungal colonization in airways CHEST 2009; 135:805–826
32. Management Systemic Glucocorticoid Therapy treatment of choice for ABPA Suppress immune hyperfunction & antiinflammatory Long term therapy not recommended Regimen 1 (relapse /steroid dependence 45%) Prednisolone, 0.5 mg/kg/d, for 1–2 wk, then on AD for 6–8 wk. Then taper by 5–10 mg every 2 wk and discontinue Repeat total serum IgE and chest radiograph in 6 to 8 wk Regimen 2 (steroid dependence 13.5%) Prednisolone, 0.75 mg/kg/d, for 6 wk, 0.5 mg/kg for 6 wk, then tapered by 5 mg every 6 wk to continue for total duration of at least 6 to 12 mo. total IgE levels are repeated every 6 to 8 wk for 1 yr to determine baseline IgE CHEST 2009; 135:805–826
33. Management Follow-up and monitoring Hx and PE , chest radiograph, and total IgE every 6 wk to demonstrate decline in IgE levels and clearing of chest radiograph 35% decline in IgE level signifies satisfactory response to therapy Doubling of baseline IgE : silent ABPA exacerbation If cannot be tapered off prednisolone, disease has evolved into stage IV. Management should be attempted with alternate-day prednisone with least possible dose Monitor for adverse effects (eg, HT, secondary DM) Prophylaxis for osteoporosis: oral calcium and bisphosphonates CHEST 2009; 135:805–826
34. Management Oral itraconazole Dose: 200 mg bid for 16 wk then once a day for 16 wk Indication: First relapse of ABPA or glucocorticoid-dependent ABPA Follow-up and monitoring Monitor for adverse effects (eg, nausea, vomiting, diarrhea,and elevated liver enzymes) Monitor for drug–drug interactions Monitor clinical response based on clinical course,radiography, and total IgE levels CHEST 2009; 135:805–826
36. Fall in total serum IgE by 25% or more after treatment with itraconazole Respiratory Medicine (2004) 98, 915–923
37. Improvement in lung function tests by 25% or more after treatment with itraconazole Respiratory Medicine (2004) 98, 915–923
38. Treatment with itraconazole reduces immune activation in ABPA improves short-term symptoms Reduces frequency of exacerbations that require use of oral corticosteroids Not shown improvement in lung function may exacerbate adrenal suppression seen with regular corticosteroid use Respiratory Medicine (2004) 98, 915–923
39. Management Inhaled Corticosteroids DBPC multicenter (32 pts.) no superiority over placebo Use only for control of asthma once oral prednisolone dose is reduced to 10 mg/d Other Therapies other antifungal agents (e.g. amphotericin B, ketoconazole, clitromazole, nystatin and natamycin) severe adverse effects and no significant beneficial effects Omalizumab (case report) CHEST 2009; 135:805–826
40. ABPA in Special Situations ABPA Complicating CF first reported in 1965 associated with deterioration of lung function, higher rates of microbial colonization, pneumothorax, massive hemoptysis, and poorer nutritional status immunopathogenesis may be exposure to high levels of allergens due to abnormal mucus properties Recognition can be difficult because ABPA shares many clinical characteristics with CF CHEST 2009; 135:805–826
41. ABPA in Special Situations ABPA Complicating CF prevalence of AH in CF 29- 53% and ABPA 1-15% Atopy : important risk factor Atopic (22%) nonatopic (2%) treatment of ABPA in CF is not very different from ABPA in bronchial asthma recommendation :CF should be screened for ABPA age >6 yrs. , yearly or clinical suggestions of ABPA CHEST 2009; 135:805–826
42. Consensus Conference Proposed Diagnostic Criteria for ABPA in CF Classic diagnostic criteria Acute or subacute clinical deterioration not explained by another etiology total IgE > 1,000 IU/mL Immediate cutaneous reactivity to Aspergillus or presence of serum IgE to A fumigatus Precipitating Abto A fumigatus or serum IgGto A fumigatus New or recent abnormalities on chest radiograph or chest CT scan that not cleared with ATB and standard physiotherapy Minimal diagnostic criteria Acute or subacute clinical deterioration not explained by another etiology Total IgE> 500 IU/mL. If total IgE200–500 IU/mL, repeat testing in 1–3 mo is recommended Immediate cutaneous reactivity to Aspergillus or presence of serum IgEto A fumigatus One of following: (1) precipitins to A fumigatus or demonstration of IgGto A fumigatus; or (2) new or recent abnormalities on chest radiography or chest CT scan that not cleared with ATB and standard physiotherapy CHEST 2009; 135:805–826
43. ABPA in Special Situations ABPA Without Bronchial Asthma: 36 cases reported across the globe mistaken initially for TB or CA ABPA Complicating Other Conditions (case report): idiopathic bronchiectasis, post-tubercular bronchiectasis, bronchiectasis secondary to Kartagener syndrome, COPD, and in patients with CGD and hyper IgE syndrome CHEST 2009; 135:805–826
44. Conclusion ABPA is common manifestation in chronic allergic asthma and cystic fibrosis Th2 cytokine mediated Diagnostic criteria Asthma pulmonary opacities Skin test positive for Aspergillus Eosinophilia Precipitating Abs (IgG) in serum IgE> 1,000 IU/mL Central bronchiectasis Serums A fumigatus-specific IgG and IgE
45. Conclusion Treatment Corticosteroid : drug of choice Itraconazole : adjunctive therapy