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Aspergillus & ABPA.

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Presentation on theme: "Aspergillus & ABPA."— Presentation transcript:

1 Aspergillus & ABPA

2 Disease spectrum IPA Invasive pulmonary aspergillosis

3 ABPA

4 ABPA – pathophysiology
conidia of Aspergillus trapped in mucous and narrowed airways of asthmatics/CF  germinate to form hyphae  release of soluble/particulate antigens  airway inflammation  epithelial damage  Antigen diffuses into interstitium  inflammatory mediators released  influx of inflammatory cells esp. E & Ag presented to Th2 cells  IL-4, IL-5 & IL-13 cytokines synthesized and secreted  IgE synthesis  mast cell degranulation  tissue injury  bronchial obstruction, inflammation, mucous plugging  bronchiectasis  fibrosis  respiratory failure

5

6 Diagnostic algorithm

7 Clinical Presentation
Asymptomatic patient with or without pulmonary infiltrates OR Poorly controlled asthmatic patient (more common) Low-grade fever Wheezing Bronchial hyperactivity Haemoptysis Weight loss & malaise Productive cough (often w/ expectoration of brownish black sputum) Severe uncontrolled asthma  with/out central bronchiectasis  pulmonary fibrosis  pulmonary hypertension  Type 2 respiratory failure

8 Physical Exam Normal Other findings include: Polyphonic wheezing
Clubbing (16%) Coarse crackles (15%) Sx of pulmonary HTN and/or respiratory failure

9 Differential Diagnosis of ABPA

10 Asthma vs. ABPA vs. AH

11 Immunological Findings
Cutaneous hypersensitivity Intradermal test > Skin prick test Type 1 immediate +ve & Type 3 delayed +ve positive in virtually all ABPA 40% of asthmatics without ABPA also +ve

12 Immunological Findings
Total IgE Cutoff >1000 IU/mL With Rx Reduction of often > 35% = REMISSION levels do NOT reach normal values repeated measurements needed to determine ‘new baseline’ Doubling of baseline = relapse

13 Radiographic Features - CXR
Parenchymal infiltrates (generally of upper lobes) Transient vs. fixed Atelectasis due to mucous plugging Findings consistent with bronchiectasis “Tram line” shadows d/t thickened non-dilated bronchial walls “Parallel lines” d/t ectactic bronchi Ring shadows d/t mucous filled bronchi or small abscesses “Toothpaste shadows” d/t mucous plugging in 2nd to 4th order bronchi “Gloved finger shadows” (branched tubular radiodensities, 2-3 cm long, 5-8 cm wide, extending from the hilum) d/t intrabronchial exudates w/ bronchial wall thickening

14 Radiographic Findings - HRCT
Widespread proximal cylindrical bronchiectasis (mostly of upper lobes) Bronchial wall thickening Mucous plugging Atelectasis Peripheral airspace consolidation Ground-glass attenuation Mosaic perfusion Air trapping

15 Diagnosis of ABPA

16 Diagnostic algorithm

17

18 Diagnosis 6/8 criteria If not confirmed i.e. less than full compliment of dx criteria FU with 6/52 IgE  if increasing or >1000 IU/ml  Rx ABPA-S (mild) vs. APBA-CB (moderate) vs. ABPA-CB-ORF Recurrent episodes of remissions and relapses

19 Staging of ABPA

20 Remission No established definition Reduction of often >35%
Usually, by end of 6-9 months with a significant fall in IgE, patient said to be in remission i.e. Stage II (Remission) ‘Complete remission’ if no exacerbation for next 03 months after stopping Rx FU with IgE every 6 months for 1st year, then annually

21 Tx - Goals 1) Early control of immunologic activity / inflammation to try to prevent progression to bronchiectasis and fibrosis 2) Monitoring for response and early detection of relapses 3) ?? Decrease fungal burden in airways

22 Tx - Steroids Doses vary depending on stage and prescriber preference. Higher dosages for longer durations may be more effective for tx’g flares. Stages 1 & 3 – Prednisone mg/kg Qday x 14 days, then QOD x 6- 8 wks, then taper by 5-10 mg q 2 weeks until d/c’d Should see resolution of infiltrates and 35-50% dec in serum total IgE (measured q1-2 months during acute treatment) Stage 2 – Steroids not needed. Monitor IgE q6 months x 1 year then q 1- 2 years. Doubling of baseline IgE indicates relapse (stage 3) Stage 4 – Steroid dependent. Aim for lowest possible dose Stage 5 – Steroids not helpful Steroid “prophylaxis” – Ca, Vit D, bisphosphonate

23

24 Regime 1 Regime 2 Dose Calculated dose Duration 0.5 mg/kg/day mg/day
2/52 0.5 mg/kg/alternate days mg/alternate days 6-8/52 Reduce by 5mg Every 2/52 FU every 6/52 with CXR & IgE Total duration of treatment 6 – 12 months Regime 1 Dose Calculated dose Duration 0.75 mg/kg/day mg/day 6/52 0.5 mg/kg/day Reduce by 5mg Every 6/52 FU every 6/52 with CXR & IgE Total duration of treatment 6 – 12 months Regime 2

25 Total IgE levels Date Description Load IU/ml

26 Tx - Itraconazole Decreases antigenic stimulus for bronchial inflammation, possibly by decreasing specific Aspergillus IgG Decreased metabolism of steroids, so may be able to use lower dosages 16 week course + steroids  significant increased likelihood of clinical response (46 vs 19%) 200 TID x 3 days, then 200 BID x 16 wks, +/- once day x 16 wks LFTs: Twice weekly for 3 months  Monthly

27

28 Miscellaneous

29 SAM The presence of concomitant allergic fungal sinusitis (AFS) and allergic bronchopulmonary mycosis in the same patient represents an expression of the same process of fungal hypersensitivity in the upper and lower airways. SAM syndrome: an acronym for sinobronchial allergic mycosis

30 Diagnostic Criteria chronic sinusitis involving multiple sinuses
asthma total serum IgE levels are usually elevated as well immediate cutaneous reactivity to fungal allergens peripheral eosinophilia radiographic evidence of bronchiectasis. variety of chest radiographic abnormalities may occur: ranging from mass lesions to diffuse pulmonary infiltrates and even normal findings on chest radiographs. 


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