Mukhopadhyay S et al

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					                             PULMONARY PATHOLOGY JOURNAL CLUB
                                     (March 2010 articles)
                                        April 26, 2010

                                                  Table of Contents
Discussion articles
Page 1    Katzenstein A-L et al. “Clinically occult interstitial fibrosis in smokers: classification and significance of a
          surprisingly common finding in lobectomy specimens” Hum Pathol 41 (3): 316-25
Page 2    Shigemitsu H et al. “Chronic interstitial pneumonitis in end-stage sarcoidosis” Eur Resp J 35: 695-97
Page 3    Sverzellati N et al. “Biopsy-proven idiopathic pulmonary fibrosis: spectrum of nondiagnostic thin-section CT
          diagnoses” Radiology 254: 957-964
Page 4    Liote H et al. “Rituximab-induced lung disease: a systematic literature review” Eur Resp J 35: 681-87
Page 5    Klebe S et al. “Sarcomatoid mesothelioma: a clinical-pathologic correlation of 326 cases” Mod Pathol 23: 470-
          79
Articles for notation
Neoplastic diseases
Page 6     Voss J et al. “Fluorescence in situ hybridization testing algorithm improves lung cancer detection in bronchial
           brushing specimens” Am J Respir Crit Care Med 181: 478-485
           Schreiber D et al. “Survival outcomes with the use of surgery in limited-stage small cell lung cancer: Should its
           role be re-evaluated?” Cancer 116 (5): 1350-57.
Page 7     Lin P-Y et al. “Tumor size matters differently in pulmonary adenocarcinoma and squamous cell carcinoma.”
           Lung Cancer 67 (3): 296-300
           Wang T et al. “Five-year lung cancer survival: which advanced stage nonsmall cell lung cancer patients attain
           long-term survival?” Cancer 116 (6) 1518-25.
Page 8     Nagano T et al. “Structural and biological properties of a papillary component generating a micropapillary
           component in lung adenocarcinoma” Lung Cancer 67 (3): 282-89
           Hollevoet K et al. “Diagnostic performance of soluble mesothelin and megakaryocyte potentiating factor in
           mesothelioma” Am J Respir Crit Care Med 181: 620-625
Page 9     Richards WG et al. “Proposed adjustments to pathologic staging of epithelial malignant pleural mesothelioma
           based on analysis of 354 cases” Cancer 116 (6) 1510-17.
           Itami H et al. “Pleural malignant mesothelioma with osteoclast-like giant cells” Pathology International 60 (3):
           217-221.
Non-neoplastic diseases
Page 10 Yi JE, Aubry M-C. “Pulmonary Pseudoneoplasms” Archives Pathol Lab Med 134 (3): 417-426.
          Schneider F et al. “Asbestos fiber content of lungs with diffuse interstitial fibrosis: an analytical scanning
          electron microscopic analysis of 249 cases.” Arch Pathol Lab Med 134(3): 457-61
          Roggli V et al. “Pathology of asbestosis—an update of the diagnostic criteria: report of the asbestosis
          committee of the college of American pathologists and pulmonary pathology society.” Arch Pathol Lab Med
          134 (3) 462-80.
Page 11 Mukhopadhyay S et al. “Pathologic findings in novel influenza A (H1N1) virus (“Swine flu”) infection” Am J
          Clin Pathol 133: 380-387
          Jeon EJ et al. “Acute eosinophilic pneumonia associated with 2009 influenza A (H1N1)” Thorax 65: 268-70
          Hage CA et al. “Diagnosis of histoplasmosis by antigen detection in BAL fluid” Chest 137: 623-28
Page 12 Leo F et al. “Structural lung damage after chemotherapy: fact or fiction?” Lung Cancer 67 (3): 306-10
PulmPathRev, April 2010 – Schmidt and Myers                                                              1



I. DISCUSSION ARTICLES
Katzenstein A-L et al. “Clinically occult interstitial fibrosis in smokers: classification and
significance of a surprisingly common finding in lobectomy specimens” Hum Pathol 41 (3): 316-
25
• Purpose: Assess frequency and significance of lung fibrosis in cigarette smokers.

•    Methods
    – n = 23 consecutive lobectomies for malignant neoplasms
    – radiology reports and follow-up from clinical records
    – smoking history obtained from patients prior to surgery
    – 27 sections/“segments” (not anatomical segments) per case; 9 vertical regions, each subdivided
      into 3 segments from medial to lateral
    – recorded 1) interstitial fibrosis (“alveolar septal thickening readily recognizable at low
      magnification”; “minimal or subtle fibrosis associated with emphysema was excluded”), 2)
      fibroblast foci, 3) peribronchiolar metaplasia, 4) honeycomb change, 5) emphysema, 6)
      respiratory bronchiolitis
    – for interstitial fibrosis and emphysema, significant ≥8 slides, extensive ≥ 20 slides

•       Results
                                                                          Smokers (20)                 Non-smokers
                                                All         Currrent (10)      Ex-smokers (10)               (3)
                  men:women                    8:15               2:8                  6:4                   0:3
               age (mean ± STD)            65.4 ± 7.4 yrs   62.8 ± 6.1 yrs       66.1 ± 7.2 yrs        71.7 ± 10.1 yrs
          pack-years (mean ± STD)                           39.3 ± 14.5 yrs     36.6 ± 22.5 yrs               0
                   UL - # (%)                18 (78%)          8 (80%)              8 (80%)               2 (67%)
        signif emphysema - # (sig/ext)        13 (4/9)          7 (1/6)              6 (3/3)                  0
           signif fibrosis - # (sig/ext)      12 (6/6)          6 (2/4)              6 (4/2)                  0
                      SRIF                       9                 5                   4*                     0
                      other                                    LCH (1)       UIP (1), asbestosis (1)
    –     adca (10), sqcc (6), adenosq (1), sm cell ca (2), LCNEC (1), typical (2) & atypical carcinoid (1)
    –     significant fibrosis in 12 cases (all smokers) that was extensive in 6
                subpleural and peribronchiolar (“centrilobular”)
                in association with and away from emphysema
                2 looked like old LCH but no active lesions (and therefore called SRIF*)
                3 had honeycomb change (1-5 slides), 6 had fibroblast foci (1-7 slides), and 3 had both
    –     RB in 19 (18 smokers), including 4 (current smokers) with DIP-like changes
    –     conventional (22) and high resolution (1) CT: nonspecific scarring in 5, emphysema in 6, no
          diffuse abnormalities (including patients with UIP, asbestosis and LCH)
    –     PFTs in 8 SRIF patients: obstruction in 6, normal in 2, and reduced DLco in 4
    –     follow-up in SRIF patients: one with dyspnea at 17 months post-op that cleared at 20 months

•       Conclusion
        SRIF resembles what Yousem previously described as fibrosis in RB
        (http://tinyurl.com/yousemRBILD) and may be a distinct lesion that overlaps RBILD/DIP (is DIP
        now dead?) and air space enlargement with fibrosis (http://tinyurl.com/KawabataAEF); distinction
        from UIP when combined with honeycomb change and fibroblast foci challenging at best!
PulmPathRev, April 2010 – Schmidt and Myers                                               2



Shigemitsu H et al. “Chronic interstitial pneumonitis in end-stage sarcoidosis” Eur Resp J 35:
695-97
• Purpose: To report the histologic findings in end-stage sarcoidosis patients who have undergone
   lung transplantation

•   Methods: Reviewed material from all sarcoidosis patients who underwent lung transplantation at
    USC.

           o Patients only included if initial biopsy reports used to diagnose sarcoidosis “contained
             descriptions compatible” with a diagnosis of sarcoidosis or if patients met ATS/ERS
             criteria for sarcoidosis.
           o All slides from explanted lungs and mediastinal/hilar lymph nodes reviewed by two
             pathologists, who graded average granuloma burden and interstitial fibrosis
           o Did not review original diagnostic material




•   Results:
           o Seven patients identified (5 women, 2 men)
           o 3/7 had “fibrotic granulomatous lung disease” without interstitial pneumonia
                     All of these patients had granulomas
           o 4/7 had moderate to severe interstitial pneumonia
                     Two of these patients had no granulomas anywhere; one had many granulomas
                     in lymph nodes but none in the lung
                     These two patients also had histologic findings of UIP, including fibroblast foci
           o Patients without interstitial pneumonia had longer time to transplant (mean 23.3 years)
             than those with interstitial pneumonia (4.8 years)

•   Conclusion:
          o A subset of patients with presumed end-stage sarcoidosis have a significant amount of
              interstitial fibrosis, including a pattern histologically indistinguishable from UIP. This
              could mean:
                       The development of interstitial fibrosis is a component of late-stage sarcoidosis
                       These patients had both UIP and sarcoidosis
                       These patients had UIP and not sarcoidosis
PulmPathRev, April 2010 – Schmidt and Myers                                               3




Sverzellati N et al. “Biopsy-proven idiopathic pulmonary fibrosis: spectrum of nondiagnostic
thin-section CT diagnoses” Radiology 254: 957-964
• Purpose: To characterize the spectrum of high-resolution CT scan diagnoses in patients with UIP
    on wedge lung biopsy.

•   Methods: Study group composed of consecutive patients with a clinical-radiographic-pathologic
    diagnosis of IPF (n=55) and compared to two control groups—one with patients diagnosed with
    IPF based on clinical-radiographic data (n=20) and one with patients with various other
    chronic/fibrotic interstitial lung diseases (n=48)
           o Lung biopsies reviewed by two pathologists
           o CT scans reviewed by three radiologists blinded to both clinical findings and to the
               purpose of the study
                        Listed their differential diagnoses (did NOT have to choose from a list) and
                        assign a likelihood to this diagnosis
           o Observations were weighted individually and between individuals
                        Given a combined probability of IPF based on the confidence of this diagnosis
                        from the three individual observers

•   Results: Of the 55 patients with biopsy-proven UIP:
           o CT interpreted as high-probability of IPF in 20 (36%), 13 (23%), and 9 (16%) of cases
           o When evaluated as individuals, of cases interpreted as low-probability of IPF:
                      Most frequent first choice diagnosis was NSIP (71%, 55%, and 61%)
                      Other first choice diagnoses included chronic HSP, sarcoidosis, and organizing
                      pneumonia
                      IPF not given as a differential diagnosis at all in 75%, 74%, and 68% of cases
           o When combined, 34 cases (62%) were called low-probability of IPF by all three
              observers
                      Other first choice diagnoses included NSIP (n=18; high probability in 16),
                      chronic HSP (n=4; all high probability), sarcoidosis (n=3; all high probability),
                      organizing pneumonia (n=1; high probability)
                      High probability of IPF in 15 (27%) and intermediate probability in 6 (11%)
           o “Fair” (k=0.39) interobserver agreement within study population
           o All patients, even those not diagnosed as IPF on CT, behaved like IPF
           o The paper did not discuss the observations from the two control groups

•   Conclusions: A high-resolution CT scan not read out as IPF does not effectively rule out the
    diagnosis of IPF
           o IPF can mimic NSIP, chronic HSP, sarcoidosis, and organizing pneumonia on HRCT
               scans
           o Patients with the histologic findings typical of UIP and atypical imaging findings
               behave in the same fashion as patients with UIP and typical imaging findings
PulmPathRev, April 2010 – Schmidt and Myers                                                 4




Liote H et al. “Rituximab-induced lung disease: a systematic literature review” Eur Resp J 35:
681-87
• Purpose: Develop a comprehensive profile of clinical, radiological, and pathological features of
   rituximab lung toxicity.

•   Methods
    – systematic literature review (PubMed: English & French, 1997 – September 2008)
    – data collection included, 1) patient characteristics, 2) treatment modalities, 3) time to onset
      (interval between last infusion and symptoms), 4) tempo of onset, 5) respiratory and extra-
      respiratory manifestations (including radiology and pathology), 6) therapy, 7) impact of
      subsequent treatment ± rituximab

•   Results
    – 52 candidate cases → 7 excluded → 45 study cases
    – mean age 65 (43-80) years; men>women (2:1)
    – rate of occurrence = 8.4% (Korea) – 11% (Netherlands)
    – underlying diseases: DLBCL (30), low grade B-cell lymphoma (10), CLL (2), ITP (2), RA (1)
    – rituximab + combination chemotherapy (37), rituximab alone (7), rituximab + mtx (1)

                                                                          Time to Onset
                                                              Early         Delayed            Late
                                         Tempo of Onset      (day 1)      (days 7-21)       (> day 30)
                                         Hyperacute (hrs)       5              1
                                         Acute/subacute
                                                                               36
                                             (days)
                                        Chronic (wks-mos)                                         3
                                                                           OP only (5)
                                           Lung Biopsy        DAD      OP + NSIP/UIP (3?)
                                                                                                OP (3)
                                            Findings           (1)          DAD (2)
                                                                         hemorrhage (2)



                                               DOD              2              6                  0




•   Conclusion
    – Rituximab can cause lung disease that may take several forms, including an early/hyperacute
      form characterized by ARDS and DAD
    – Most patients have an acute/subacute onset after the third to fifth cycles that may be
      accompanied by a range of histologic changes including primarily OP ± an underlying chronic
      interstitial pneumonia
    – Add rituximab to the list of potential causes of OP, a finding common in patient who develop
      late onset disease
PulmPathRev, April 2010 – Schmidt and Myers                                             5




Klebe S et al. “Sarcomatoid mesothelioma: a clinical-pathologic correlation of 326 cases” Mod
Pathol 23: 470-79
• Purpose: To review a large series of sarcomatoid mesothelioma patients from the consultation
   experience of a single individual (Victor Roggli).

•   Methods: retrospective observational case based series
    – 326 (of 2000) mesothelioma cases received as medico-legal consults over a 25 year period
    – subclassified as conventional, conventional with desmoplastic (>10%, <50% of sampled
      tumor) features, desmoplastic (≥ 50% of sampled tumor), osteo-/chondrosarcomatous, or
      lymphohistiocytoid
    – IHC performed using a broad range and highly variable panel of immunostains
    – lung tissue analyzed for mineral fiber content in 61 and compared to database of non-
      sarcomatous and a non-asbestos exposed reference population (no details regarding these
      comparison groups in Methods)

•   Results
                      median age (range)                       70 yrs (41 – 94 years)
                      men/women                                        312/14
                      pleura/peritoneum                                319/7
                      histologic subtypes
                      – conventional                                143 (44%)
                      – conventional + desmoplastic features        110 (34%)
                      – desmoplastic                                70 (21%)
                      – osteo-/chondrosarcomatous                     8 (2%)
                      – lymphohistiocytoid                           2 (< 1%)
                      IHC staining
                       – keratin                                  261/280 (93%)
                       – vimentin                                 101/111 (91%)
                       – calretinin                                12/39 (31%)
                      pleural plaques                             144/182 (79%)
                      asbestosis (histological)                   34/127 (27%)
                      elevated asbestos content                    57/61 (93%)

    –   asbestos body counts showed a trend toward being higher in sarcomatoid mesotheiomas
        (1640/g wet lung tissue) compared to non-sarcomatoid mesotheliomas (348), and commercial
        amphiboles (i.e. amosite) counts were significantly higher (P = 0.03)
    –   survival at 2, 4, 6, 12 and 18 months was 70%, 50%, 30%, 10% and 5%, respectively

•   Conclusion
    Nothing new here in what is a retrospective biased experience heavily weighted toward medico-
    legal (= mostly legal) cases, but a handy reference next time you feel the need for a large N to
    support statements that sarcomatoid mesotheliomas are really bad tumors frequently associated
    with other evidence of occupational asbestos exposure!
PulmPathRev, April 2010 – Schmidt and Myers                                                           6

II. ARTICLES FOR NOTATION ONLY
Neoplastic diseases
Jesse S et al. “Fluorescence in situ hybridization testing algorithm improves lung cancer detection in bronchial
brushing specimens” Am J Respir Crit Care Med 181: 478-485
•   Purpose: To evaluate the performance of a testing algorithm that involves FISH for the diagnosis
    of lung cancer on cytology specimens

•   Methods: Patients underwent bronchoscopy for lesion suspicious for lung carcinoma. Brushing
    specimens were used to prepare two Thin-Preps—if cytology was positive, no additional testing
    performed; if cytology negative/atypical/suspicious, then FISH testing was performed with
    hypertetraploidy = positive FISH result. Gold standard considered pathologic confirmation of
    carcinoma (tbbx, TBNA, TTNA, or surgical resection)




•   Results: 55% of patients had cancer (n=189). Cytology positive in 14% (n=49)—sensitivity and
    specificity of 41% and 100% for central tumors and 20% and 100% for peripheral tumors. FISH
    positive in 26% (n=77)—detected an additional 18 central and 43 peripheral lesions BUT had
    false positive in 10 central and 6 peripheral lesions (no false positive cytology)

•   Conclusion: Reflex FISH testing on cytologically negative/atypical/suspicious bronchoscopic
    specimens can improve diagnostic yield but also has a higher false positive rate.

Schreiber D et al. “Survival outcomes with the use of surgery in limited-stage small cell lung cancer: Should its role
be re-evaluated?” Cancer 116 (5): 1350-57.
•   Purpose: To look at survival data in patients who underwent surgical resection of small cell lung
    cancer, for which radiation and systemic chemotherapy are currently the standard of care.

•   Methods: Identified patients through the SEER database and grouped patients into localized vs.
    regional disease; surgery vs. no surgery; and post-operative radiation therapy (PORT) vs. no
    PORT.
           o Study did NOT have access to chemotherapy data

•   Results: Overall surgery associated with mean survival of 28 months compared to 13 months with
    no sugery; patients with localized disease did even better. In N0 and N1 patients, there was no
    survival advantage for PORT; with N2 disease there was a survival benefit to PORT.
PulmPathRev, April 2010 – Schmidt and Myers                                                        7




•   Conclusion: Patients with small cell carcinoma do badly when they are resected—but they do
    worse when they aren’t resected.
           o Lack of chemotherapy data for a more complete comparison is unfortunate

Lin P-Y et al. “Tumor size matters differently in pulmonary adenocarcinoma and squamous cell carcinoma.” Lung
Cancer 67 (3): 296-300
•   Purpose: To evaluate whether the association between tumor size and nodal/distant metastases is
    different in adenocarcinoma and squamous cell carcinoma and to define a critical tumor size in
    predicting nodal/distant metastases

•   Methods: Reviewed 932 patients with primary non-small cell lung cancer with complete staging
    with imaging available and performed logistic regression was performed to identify the associated
    between tumor size and metastatic disease.

•   Results: With adenocarcinoma (72.6%; n=710), metastases increased at each size grouping and
    the percentage of metastases plateaued when size exceeded 2.5 cm. With squamous cell
    carcinomas (18.3%; n=171) the rate of metastasis was ~50% in all groups until 4.0 cm, after
    which the rate of metastases plateaued.

•   Conclusion: Adenocarcinoma and squamous cell carcinoma behave in biologically distinct
    fashions and have different associations in regard to tumor size and metastatic rates. Remains to
    be seen whether this may increase pressure on us to classify NSCLC more distinctly.

Wang T et al. “Five-year lung cancer survival: which advanced stage nonsmall cell lung cancer patients attain
long-term survival?” Cancer 116 (6) 1518-25.
•   Purpose: To try and identify pathologic and treatment variables that might predict for long-term
    survival in advanced-stage lung cancer patients.

•   Methods: Retrospective study which involved collecting data from the medical records of all
    patients diagnosed with advanced stage lung cancer (stages IIIA, IIIB, and IV) who had survived
    longer than 5 years.

•   Results: Only 6.6% of these patient survived 5 years and only 4.7% of advanced stage lung
    cancer patients ultimately survived the original tumor; 83% of these patients received aggressive
    multimodality therapy. Most survivors in the series came from one of several subgroups:
    resectable N2 disease, multiple lung tumors, T3N0, or single site distant metastasis. Median
    survival for patients with pleural disease (ie. malignant pleural effusion) was 5 months.

•   Conclusion: Despite advances in therapy, advanced stage lung cancer still has a bad prognosis
    with very poor long-term survival.
           o Although they had access to histologic type, they didn’t comment on any correlation
               between histology and outcomes.
PulmPathRev, April 2010 – Schmidt and Myers                                                       8

Nagano T et al. “Structural and biological properties of a papillary component generating a micropapillary
component in lung adenocarcinoma” Lung Cancer 67 (3): 282-89
•   Purpose: To explore relationship between papillary (PC) and micropapillary (MPC) subtypes of
    adenocarcinoma.

•   Methods
    – retrospective review of 445 consecutive resections of adca (2001-2003) from a single
      institution (Nat’l Cancer Center Hospital East, Chiba, Japan)
    – TMAs for IHC in a subset (74) of cases (intensity x percentage of + cells = staining score)
    – measured width of “papillae stalks” in PC

•   Results
    – 228/445 (60%) PC+ → 150/228 (66%) MPC+ (i.e. MPC seen only in PC)

    – PC MPC[+] = higher stage, ↑ LN mets, ↑ pleural
      invasion, and ↑ lymphovascular invasion compared to PC
      MPC[–] tumors
    – PC MPC[+] = narrower “stalks”, ↑ GLUT-1 staining (no
      differences in results of other IHC stains)

•   Conclusion
    Interest in papillary and micropapillary carcinoma continues
    to grow and with that growth I’m pretty sure I no longer
    know what “papillary” means, which may explain why my anecdotal experience is discordant
    with number of recent studies in which papillary carcinomas have become the most dominant
    subset of adcas. Have inserted a figure (2B) from current paper that argues PC MPC[+] have
    fundamental biologically differences that separates them from PC MPC[–], here illustrating
    method for measuring “stalks” in what appears to me to be a conventional acinar growth pattern.
    A dollar to the first person who can help me see either of these figures as “papillary” carcinomas
    (and remember, a bull headed bastard convinced against his will is a bull headed bastard still!).

Hollevoet K et al. “Diagnostic performance of soluble mesothelin and megakaryocyte potentiating factor in
mesothelioma” Am J Respir Crit Care Med 181: 620-625
•   Purpose: To compare diagnostic performance of two serum biomarkers of malignant pleural
    mesotheliomas (MPM): soluble mesothelin (SM), the current reference biomarker, and
    megakaryocyte potentiating factor (MPF), a promising newcomer that has not yet been validated.

•   Methods: Prospective analysis of consecutive patients recruited into 6 cohorts: 1) healthy controls
    without asbestos exposure (101), 2) healthy controls with documented asbestos exposure (89), 3)
    patients with benign asbestos-related disease (4), 4) patients with benign non-asbestos-related
    respiratory disease without pleural effusion (46), 5) patients with lung cancer (63), 6) patients with
    MPM (85).

•   Results
    – Both serum biomarkers showed similar characteristics and were equivalent in diagnostic
       performance (at 95% specificity, SM and MPF had sensitivities of 64% and 68%, respectively.
PulmPathRev, April 2010 – Schmidt and Myers                                                          9



•   Conclusion: Not really a pathology paper, at least not an anatomic pathology paper, but figured it
    was worth knowing that there is a serum biomarker for MPM.

Richards WG et al. “Proposed adjustments to pathologic staging of epithelial malignant pleural mesothelioma
based on analysis of 354 cases” Cancer 116 (6) 1510-17.
•   Purpose: To develop revised staging criteria that improve stratification of patients with
    epithelioid malignant pleural mesotheliomas (MPM) undergoing trimodality therapy that included
    extrapleural pneumonectomy.

•   Methods
    – retrospective review of medical records for BWH patients accumulated into the International
      Mesothelioma Program Patient Data Registry (all path data fields audited by 3 study
      pathologists)
    – T classification levels based on a complex model that combines prevalence of individual
      features with prognostic impact expressed as Hazard Ratios

•   Results
    – 354 patients with epithelial histology and complete T and N data from extrapleural
       pneumonectomy (median survival 18 months from date of surgery)
    – Reshuffling T categories and separating patients with N2 disease into two subsets (N2a and
       N2b) provided greater separation of
       patients into prognostic categories, not of
       which was good as illustrated in the
       attached figure (Figure 5).

•   Conclusion
    – A revised staging system as proposed will
      have some value at BWH for patients with
      epithelial histology undergoing trimodality
      therapy with curative intent, a highly
      selected group of patients! Completely
      unclear how this applies to much larger
      group of patients and therefore strikes me
      as much ado about almost nothing.

Itami H et al. “Pleural malignant mesothelioma with osteoclast-like giant cells” Pathology International 60 (3): 217-
221.
•   Purpose: To report unusual histologic variant of mesothelioma.

•   Results: Title says it all, although from photomicrographs truly doesn’t look all that distinctive to
    me!

•   Conclusion: I would rather scratch out my eyeballs, or perhaps spend the day with Rush
    Limbaugh, than read another fricking mesothelioma paper.
PulmPathRev, April 2010 – Schmidt and Myers                                                            10

Non-neoplastic diseases
Yi JE, Aubry M-C. “Pulmonary Pseudoneoplasms” Archives Pathol Lab Med 134(3): 417-26
•   Purpose: Review lesions that may be mistaken for neoplasms in preoperative imaging studies.

•   Methods: Nice review of literature and personal experience by two of the pulmonary pathology
    community’s best!

•   Results: Beautifully illustrated review of IMT (the one true neoplasm included because of
    historical link to category of “inflammatory pseudotumor”), organizing pneumonia, nodular
    lymphoid hyperplasia, apical cap, round atelectasis, sclerosing medastinitis and hyalinizing
    granuloma.

•   Conclusion: Nice reference for next time you’re speaking about any one of the entities covered!

Schneider F et al. “Asbestos fiber content of lungs with diffuse interstitial fibrosis: an analytical scanning electron
microscopic analysis of 249 cases.” Arch Pathol Lab Med 134(3): 457-61
•   Purpose: To expand on previous observations regarding reliability of current diagnostic criteria in
    patients with diffuse pulmonary fibrosis (DPF) without asbestos bodies (i.e. ≠ asbestosis) who
    purport asbestos exposure.

•   Methods: Retrospective observational case based study comparing 163 patients with asbestosis to
    86 patients with DPF and a reported history of asbestos exposure. All patients had fiber analysis.

•   Results
    – DPF = UIP (77%), NSIP (6%), DIP (4%), polymyositis (1%), and non-classifiable (12%)
                                  Asbestos Fiber Concentrations – Median (range)
                                   commercial amphiboles             noncommercial
                           coated & uncoated        uncoated           amphiboles              asbestos bodies
                                 170000              110000                <920                    23000
          asbestosis
                             (<520–540000)       (<660–7800000)      (<920–1220000)             (230-160000)
                                  <330                <490                 490                       16
             DPF
                              (<330-39000)         (<80-39000)        (<100-14000)                (0-7700)
    –   severity of fibrosis in asbestosis cases correlated with uncoated fiber burden for commercial
        amphiboles and asbestos body counts
    –   3 (of 86) DPF patients had commercial amphibole fiber burdens that overlapped with 95%
        prediction interval for asbestosis suggesting that they were examples of “occult asbesosis”

•   Conclusions: A history of asbestos exposure alone is insufficient to establish a diagnosis of
    asbestosis in patients with DPF. Furthermore, tissue asbestos analysis is not necessary in patients
    with classical features of UIP in whom no asbestos bodies are detected in surgical lung biopsy
    material by conventional light microscopy. Now THAT’S something worth knowing!

Roggli V et al. “Pathology of asbestosis—an update of the diagnostic criteria: report of the asbestosis committee of
the college of American pathologists and pulmonary pathology society.” Arch Pathol Lab Med 134 (3) 462-80
•   Purpose: To report current recommendations of an expert committee functioning under the
    auspices of both the CAP and the Pulmonary Pathology Society. This article forecast but not
    referenced in previously reviewed paper published in same issue of Archives, which is kind of
    weird given that Rogglie is senior/first author in both.
PulmPathRev, April 2010 – Schmidt and Myers                                                        11

•   Conclusion: THE current reference regarding pathological criteria for diagnosis of asbestosis,
    and in many respects a perfect companion to the paper by Schneider et al.

Mukhopadhyay S et al. “Pathologic findings in novel influenza A (H1N1) virus (“Swine flu”) infection” Am J Clin
Pathol 133: 380-387
•   Purpose: To describe the findings at autopsy of two patients who died of H1N1 influenza

•   Methods: Case series of two patients who underwent autopsy

•   Results: Case 1 (36-year-old obese man with hypertension) largely showed acute diffuse alveolar
    damage with some foci starting to organize and some intra-alveolar hemorrhage. Case 2 (46-year-
    old homeless woman with history of seizures, alcohol use, hepatitis C, stroke) showed severe
    acute bronchopneumonia with gram + cocci on tissue gram stain with a lesser extent of acute
    DAD. Bronchiolitis/tracheobronchitis was not present in either case.

•   Conclusion: Substantiating previous findings of DAD in association with H1N1 infection,
    sometimes with superimposed acute bronchopneumonia and intraalveolar hemorrhage.
          o Also did not report any cytopathologic change associated with influenza—did not
              perform immunohistochemistry
          o Some features classically associated with influenza (ie. bronchiolitis) are not always
              present

Jeon EJ et al. “Acute eosinophilic pneumonia associated with 2009 influenza A (H1N1)” Thorax 65: 268-70
•   Purpose: To report a previously unreported association with H1N1 influenza

•   Methods: Case report of a patient diagnosed with H1N1.

•   Results: Patient was a 20-year-old man without significant co-morbidities who presented with
    hypoxia and diffuse ground-glass opacities on both chest x-ray and CT scan. A BAL showed 39%
    eosinophils. All cultures were negative as was testing for allergies (total IgE, MAST allergen
    inhalant), parasitic infections, and HIV infection. He was subsequently diagnosed with both acute
    eosinophilic pneumonia as well as H1N1 infection.

•   Conclusion: Acute eosinophilic pneumonia is now among the numerous findings that have been
    associated with H1N1 infection and is something to be aware of in patients clinically suspected to
    have H1N1 infection.

Hage CA et al. “Diagnosis of histoplasmosis by antigen detection in BAL fluid” Chest 137: 623-28
•   Purpose: To evaluate the sensitivity/specificity of a quantitative Histoplasmosis antigen enzyme
    immunoassay (EIA) performed on BAL compared with direct examination and fungal culture

•   Methods: BAL speciments from patients suspected of having infection were analyzed. Gold
    standard = clinical manifestations of disease plus either histopathologic or culture evidence of
    organism

•   Results: 31 patients with histoplasma and 10 patients with blasto
           o Antigen detected by EIA in 29/31 histo, 8/10 blasto, and 5/60 with Aspergillus
               galactomannan; no positives in patients without infection
PulmPathRev, April 2010 – Schmidt and Myers                                                      12




                     Sensitivity 93.5%, specificity 97.8%
            o Cytology positive in 15/31 histo, 4/10 blasto
            o Culture positive in 15/31 histo, 6/10 blasto

•   Conclusion: EIA antigen detection of histoplasmosis is a sensitive, specific, and rapid (compared
    to 2-4 weeks with culture) method of fungus detection
            o Caveat of crossreactivity with some fungi with different treatment modalities (histo
               and blasto antigens are immunologically identical)

Leo F et al. “Structural lung damage after chemotherapy: fact or fiction?” Lung Cancer 67 (3): 306-10
•   Purpose: To assess whether or not pulmonary parenchymal damage due to chemotherapy may be
    evident in non-neoplastic lung tissue resected at the time of cancer operations

•   Methods: Restrospective study—10 patients undergoing pneumonectomy following at least 3
    cycles of preoperative platinum-based induction chemotherapy; 10 non-chemotherapy controls
    matched for age, sex, side of resection, and FEV. Two pathologists reviewed all non-tumor
    sections; if damage was present, characterized extent of changes as diffuse (>50%), focal (<50%)
    or normal (<10%)

•   Results: Severe diffuse parenchymal damage in 8 patients—7 chemo and 1 control
           o 7 in chemo group (70%): included BOOP, DAD, DIP, and UIP
                      2 pts with focal changes and 1 normal
           o 1 in control group (10%) with acute bronchopneumonia
                      8 pts with focal changes and 1 normal
           o Patients with diffuse changes were associated with both lower pre-op DLCO and worse
               outcomes postoperatively (4 of 8 with post-op respiratory failure)

•   Conclusion: Patients undergoing neoadjuvent chemotherapy have a high rate of histologic
    evidence of parenchymal damage but without a specific histologic pattern (BOOP was most
    common)
           o Still doesn’t explain if chemo caused these changes, only that they are more often seen
               in chemo patients

				
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