Case Studies

Gamal Rabie Agmy, MD, FCCP

Professor of chest Diseases, Assiut university

Case No. 1

• A 27-year-old man is referred to you for evaluation of an abnormal chest radiograph. About 5 months ago, he consulted a doctor because of excessive thirst. Evaluation resulted in the diagnosis of diabetes insipidus, which responded favorably to desmopressin administered nasally. Recently, he started to notice shortness of breath when climbing stairs, and a chest radiograph was obtained.

• Patient history reveals significant tobacco smoking, up to two packs daily, for at least 14 years. The patient noticed the shortness of breath for at least 2 years, and recently, he noted a point of tenderness over the chest wall, lateral to the posterior axillary line on the left.

• Oxygen saturation is 94% while breathing room air, and the rest of his vital signs were normal. Auscultation reveals only rare crackles without prolongation of the expiratory phase. There is a point of tenderness over the left sixth and seventh ribs in the posterior axillary line, and a chest CT scan is obtained.

The most likely diagnosis is:

• A. Metastatic tumor of unknown primary site.

• B. Sarcoidosis.

• C. Langerhans cell histiocytosis.

• D. Idiopathic pulmonary fibrosis.

• This patient exhibits most of the recognized features of pulmonary Langerhans cell histiocytosis (LCH), previously known as eosinophilic granuloma and histiocytosis X: pulmonary changes involving the middle and upper parts of the lungs with irregularly shaped cystic and nodular lesions of varying size; involvement of a flat bone (the rib); and diabetes insipidus in a young person who smokes (choice C is correct). The only frequently en countered complication that is not present in this patient is a history of spontaneous pneumothorax. The radiographic findings, especially when a CT scan shows cystic and nodular lesions.

• Cystic, nodular, and fibrotic lesions seen on CT scans are the most frequent findings, followed by the presence of bone lesions in up to 20% of patients, and diabetes insipidus in up to 15% of patients. Spontaneous pneumothorax occurs in 15% to 25% of patients, although not in this patient. Other manifestations contributing to morbidity and mortality include pulmonary hypertension and the development of a pulmonary neoplasm. The most important treatment for pulmonary LCH is cessation of smoking.

• Glucocorticoids and immunosuppressive agents have not been proven to be effective. Smoking cessation alone will not alleviate pain in the symptomatic rib lesions. Radiation therapy has been useful in controlling progression and reducing pain. Similarly, smoking cessation alone will not control diabetes insipidus; therefore, replacement therapy should continue.

• The bone lesion could be due to a metastatic cancer, but the chest radiograph does not show distinct nodules and is not consistent with metastatic cancer. Patients with sarcoidosis may have diabetes insipidus and may have extensive fibrosis late in the disease, but bone lesions are rare (choice B is incorrect). While the fibrotic lesions may be similar to those found in patients with idiopathic pulmonary fibrosis (IPF), bone lesions are not found in IPF and diabetes insipidus is not associated with IPF.

The most likely diagnosis is:

• A. Metastatic tumor of unknown primary site.

• B. Sarcoidosis.

• C. Langerhans cell histiocytosis.

• D. Idiopathic pulmonary fibrosis.

Lung Cysts

By

Gamal Rabie Agmy , MD , FCCP

Professor of Chest Diseases ,Assiut University

Lung Cysts

Differential Diagnosis

Pulmonary fibrosis (Honeycombing)

Lymphangliomyomatosis

Langerhans cell histiocytosis

Lymphocytic Interstitial Pneumonia (LIP)

Birt-Hogg-Dubé syndrome (BHDS)

Rough Reticular Fine Reticular

Traction

Bronchiectasis

and

Interface

sign

Honey

combing

UIP UIP or NSIP

Usual Interstitial Pneumonia

UIP

HRCT Findings

Reticular opacities, thickened intra- and

interlobular septa

Irregular interfaces

Honey combing and parenchymal distorsion

Ground glass opacities (never prominent)

Basal and subpleural predominance

Basal and subpleural

distribution

UIP

The Many ‘HRCT Faces’ of NSIP

Honeycombing not a

prominent feature

!!!!

Lymphangioleiomyomatosis

(LAM)

HRCT Morphology

Thin-walled cysts (2mm - 5cm)

Uniform in size / rarely confluent

Homogeneous distribution

Chylous pleural effusion

Lymphadenopathy

in young women

Lymphangioleiomyomatosis

(LAM)

Tuberous Sclerosis (young man)

Langerhans Cell Histiocytosis

HRCT Findings

Small peribronchiolar nodules (1-5mm)

Thin-walled cysts (< 1cm),

Bizarre and confluent

Ground glass opacities

Late signs: irreversible / parenchymal fibrosis Honey comb lung, septal thickening,

bronchiectasis

1 year later

Peribronchiolar Nodules Cavitating nodules and cysts

Langerhans Cell Histiocytosis

Langerhans Cell Histiocytosis

Langerhans Cell Histiozytosis

Key Features

Upper lobe predominance

Combination of cysts and noduli

Characteristic stages

Increased Lung volume

Sparing of costophrenic angle

S

M

O

K

I

N

G

Langerhans Cell Histiocytosis

Langerhans Cell Histiocytosis

Differential Diagnosis

Only small nodules Sarcoidosis, Silicosis

Only cysts idiopathic Fibrosis

LAM

Destructive emphysema

.......after cessation of smoking

Benign lymphoproliferative

disorder Diffuse interstitial infiltration of

mononuclear cells

Not limited to the air ways as

in follicular Bronchiolitis

LIP = Lymphocytic Interstitial

Pneumonia

Sjögren: LIP

LIP = Lymphocytic Interstitial

Pneumonia

Rarely idiopathic

In association with: Sjögren’s syndrome

Immune deficiency syndromes, AIDS

Primary biliary cirrhosis

Multicentric Castlemean’s disease

Sjoegren disease

Dry eye and dry mouth

Fibrosis, bronchitis and bronchiolitis

LIP

Overlap

Sarcoid, DM/PM, MXCT

SLE, RA (pleural effusion)

Up to 40 x increased risk for lymphoma (mediastinal

adenopathy) and

2 x times increased risk for neoplasma

Young woman Dry mouth Smoker

LAM LIP Histiocytosis

Wegener‘s disease

Rheumatoid Arthritis

History of recurrent pneumothorax, lung cysts, and skin

lesions (fibrofolliculomas) with normal lung function is

consistent with the diagnosis of Birt-Hogg-Dubé

syndrome

Birt-Hogg-Dubé syndrome

• BHDS is an autosomal dominantly inherited genodermatosis that predisposes a person to the development of cutaneous hamartomas (fi brofolliculomas), kidney neoplasms, lung cysts, and spontaneous pneumothorax.

• The BHD locus has been mapped to the short arm of chromosome 17(17p11.2). BHD is composed of 14 exons, and more than 40 unique mutations in BHD have been reported.

• Most BHD germline mutations are frameshift or nonsense mutations that are predicted to truncate

the BHD protein, folliculin.

Centrilobular Emphysema

Panlobular Emphysema

Mosaic pattern and its

differential

Where is the pathology ???????

in the areas with increased density meaning there is ground glass

in the areas with decreased density meaning there is air trapping

Pathology in black areas

Airtrapping: Airway

Disease

Bronchiolitis obliterans (constrictive bronchiolitis) idiopathic, connective tissue diseases, drug reaction,

after transplantation, after infection

Hypersensitivity pneumonitis granulomatous inflammation of bronchiolar wall

Sarcoidosis granulomatous inflammation of bronchiolar wall

Asthma / Bronchiectasis / Airway diseases

Airway Disease

what you see……

In inspiration sharply demarcated areas of seemingly increased

density (normal) and decreased density

demarcation by interlobular septa

In expiration ‘black’ areas remain in volume and density

‘white’ areas decrease in volume and increase in

density

INCREASE IN CONTRAST

DIFFERENCES

AIRTRAPPING

Bronchiolitis

obliterans

Early Sarcoidosis

Chronic EAA

Hypersensitivity pneumonitis

Extr. Allerg. Alveolitis (EAA) HRCT

Morphology

chronic: fibrosis

Intra- / interlobular septal thickening

Irregular interfaces

Traction bronchiectasis

acute - subacute

acinar (centrilobular) unsharp densities

ground glass (patchy - diffuse)

Pathology in white Areas

Alveolitis / Pneumonitis

Ground glass desquamative intertitial pneumoinia (DIP)

nonspecific interstitial pneumonia (NSIP)

organizing pneumonia

In expiration both areas (white and black) decrease in

volume and increase in density

DECREASE IN CONTRAST

DIFFERENCES

DI

P

Cellular

NSIP

Mosaic Perfusion

Chronic pulmonary embolism

LOOK FOR

Pulmonary hypertension

idiopathic, cardiac disease, pulmonary

disease

CTEPH =

Chronic thrombembolic

pulmonary hypertension

Case No. 2

• An 81-year-old man comes to an outside hospital complaining of abdominal pain. The patient has a CT scan of the abdomen showing bilateral hydronephrosis, small bowel obstruction, and a new bladder mass. The patient undergoes surgical removal of the bladder mass, reported to be transitional cell carcinoma, and is discharged several days later. The patient now comes to your ED complaining of no urine output for 3 days and abdominal distension without any other symptoms.

•

• The patient’s past medical history is significant for congestive heart failure. On physical examination, the patient appears comfortable. The examination is notable for normal vital signs, decreased breath sounds in the lower one half of his right hemithorax, nontender abdomen with hypoactive bowel sounds, and pitting edema to the knees bilaterally.

• Lab studies show: elevated brain-type natriuretic peptide (BNP) of 1,450 pg/mL (1,450 ng/L), BUN of 44 mg/dL (15.7 mmol/L), creatinine of 9.0 mg/dL (796 mol/L), WBC count of 7,000/L (7.0 × 109/L), hematocrit of 33% (0.33), and platelet count of 277 × 103/L (277 × 109/L). ABGs show a pH of 7.41, Pco2 of 39 mm Hg, and Pao2 of 72 mm Hg. His echocardiogram shows a left ventricular EF of 10% and global hypokinesis.

• A CT scan of the chest, abdomen, and pelvis is obtained. The reported CT findings include a right-sided pleural effusion, prominence of right retroperitoneal fluid collection, and bilateral prominence of the renal pelvises.

• Thoracentesis of the right pleural effusion reveals clear yellow fluid with a protein level of 1.1 g/dL (11.0 g/L) (serum: 5.2 g/dL, 52.0 g/L), lactate dehydrogenase (LDH) level of 75 U/L (1.25 kat/L) (serum: 224 U/L, 3.7 kat/L), glucose level of 93 mg/dL (5.2 mmol/L), pH of 7.20, and WBC count of 46/mm3 (0.046 × 109/L).

Which of the following is the best option to treat this patient’s pleural effusion?

• A. Diuresis.

• B. Broad-spectrum antibiotics.

• C. Bilateral nephrostomy tubes.

• D. Therapeutic thoracentesis.

• This patient has a right-sided, low pH transudative pleural effusion compatible with a urinothorax, further supported by evidence of bilateral obstructive uropathy seen on CT scan, and it is best treated by relief of the obstruction (choice C is correct). Urinothorax is noted as the only cause of low-pH transudative pleural effusion, as in this patient, although the pleural fluid pH may be normal.

• Urinothorax is the presence of urine within the pleural space most often due to bilateral obstructive uropathy or trauma. Thoracentesis provides significant clues, including the effusion being transudative with a low pH, as in this patient. The pleural fluid smelled like urine, as was noted in this patient but not reported in the case summary. Glucose values may be normal or reduced and the protein level is usually 1 g/dL (10 g/L). The LDH level may be high, misleading the clinician from the diagnosis. The pleural fluid to serum creatinine ratio is 1.0 (median value of 4.0), with this finding being sensitive but not specific. This patient’s pleural fluid creatinine level was 22 mg/dL (1,945 mol/L), with a pleural fluid to serum creatinine ratio of 2.4.

• The two most likely pathways for development are bilateral obstruction of the urinary tract caused by bilateral ureteral or distal obstruction, as in this patient, and trauma to the urinary tract (often iatrogenic and acute) that may be unilateral.

• Both cause extravasation of urine that moves retroperitoneally and ultimately into the pleural space.

• Although this patient likely has congestive heart failure as evidenced by an elevated BNP level and an ejection fraction of 10%, diuresis will not specifically treat the urinothorax.

• The patient has no evidence of infection, including being afebrile and having a normal WBC count; therefore, antibiotics are not warranted . The patient’s effusion is asymptomatic, and the primary treatment is relief of his obstructive uropathy; therefore, therapeutic thoracentesis is not indicated.

Which of the following is the best option to treat this patient’s pleural effusion?

• A. Diuresis.

• B. Broad-spectrum antibiotics.

• C. Bilateral nephrostomy tubes.

• D. Therapeutic thoracentesis.

Case No. 3

• A 47-year-old woman has had severe asthma for many years. She currently is receiving salmeterol/fluticasone, 500 g bid; albuterol, 1 to 2 inhalations prn; and additional beclomethasone.

• Despite this therapy, she has had two asthma exacerbations in the past year, requiring oral corticosteroids, and one hospitalization.

• She has documented allergy to house dust mites and cats, but environmental therapy in the past has not been particularly helpful.

• Her FEV1 was 64% of predicted. Her serum IgE level was 300 IU/mL (normal, 30 IU/mL). You contemplate initiating therapy with omalizumab.

Which of the following statements would be correct?

• A. An IgE level of 68 IU/mL would be predictive of an excellent response to therapy (normal, 30 IU/mL).

• B. ED visits will be reduced.

• C. The dosage administered is dependent only on body weight.

• D. Clinical response can be judged within 2 weeks.

• This patient has poorly controlled asthma despite the use of combination therapy even with additional inhaled corticosteroids. She has an elevated IgE level and, thus, would be an ideal candidate for a trial of omalizumab.

• In a randomized prospective trial of add-on omalizumab in 419 patients with inadequately controlled, severe, persistent allergic asthma despite optimized care, patients treated with omalizumab had a reduction in the rate of ED visits by 44% in addition to many other benefits.

• Pretreatment clinical characteristics poorly defi ne the patient who is likely to respond to omalizumab. The baseline serum IgE level has only a broad predictive value. Patients with levels below 75 IU/mL tend to have relative poor responses when examining ED visits, asthma quality-of-life questionnaires, and FEV1 as outcomes, although there may be a reasonably good response in severe exacerbation rates and physician global assessment.

• Clinical benefi ts with omalizumab are seen when serum-free IgE levels are 20.8 IU/mL (50 ng/mL) after the initiation of therapy. Th e ability of omalizumab to achieve these levels is dependent on dose, the patient’s weight, and baseline serum total IgE level.

• A dosing table has been designed to account for body weight and serum IgE level. A plateau of improvement in asthma symptoms and morning peak expiratory flow has been seen between 12 to 16 weeks after treatment onset. About 40% of patients will demonstrate a response within 4 weeks of initiating treatment, whereas more than 60% will have a response by 16 weeks (choice D is incorrect). Of the patients who responded by 16 weeks, less than two-thirds will have shown a response by 4 weeks, suggesting that a trial of therapy should continue for at least 4 months.

Which of the following statements would be correct?

• A. An IgE level of 68 IU/mL would be predictive of an excellent response to therapy (normal, 30 IU/mL).

• B. ED visits will be reduced.

• C. The dosage administered is dependent only on body weight.

• D. Clinical response can be judged within 2 weeks.

Case No. 4

• A 40-year-old woman comes for evaluation of progressive dyspnea on exertion. Her symptoms started insidiously 1 year ago and have progressed to the point that she can climb less then one fl ight of stairs or walk one city block at a quick pace. She denies nocturnal symptoms. She has a nonproductive cough but does not have any other symptoms.

• Her past history is remarkable only for hypothyroidism for which she takes thyroxine. She is a nonsmoker with no recent travel, traditional HIV risk factors, or infectious contacts.

• Her physical examination is remarkable only for slight tachypnea and an arterial oxygen saturation of 89% at rest. Saturation decreases to a low of 79% during a 6-min walk. A chest radiograph was reported as abnormal, which led to performing a CT scan (Fig 52-A). Bronchoscopy and bronchoalveolar lavage (BAL) fl uid analysis were unhelpful, so a

• video-assisted thoracoscopic biopsy was performed.

Which of the following statements about this condition is true? • A. A trial of prednisone therapy is warranted

initially.

• B. Granulocyte-macrophage colony-stimulating factor (GM-CSF) subcutaneous therapy works best in patients with a predisposing condition.

• C. Inhaled GM-CSF is the primary treatment modality.

• D. The patient should be offered whole lung lavage.

• The CT scan (see Fig 52-A) reveals a diff use, geographic, crazy paving pattern suggestive, but not diagnostic, of pulmonary alveolar proteinosis (PAP). The biopsy reveals diff use intra-alveolar filling by granular proteinaceous material in which there are sharply delineated round empty spaces, cholesterol clefts, and scattered foamy macrophages and intra-alveolar granular proteinaceous material, with adjacent area of intraalveolar foamy macrophages and interstitial chronic inflammation. Together, these findings are characteristic of PAP.

• The treatment of choice is whole lung lavage . Prednisone has no beneficial effect in PAP and would be contraindicated given the increased prevalence of disseminated, opportunistic infections in this disease.

• Anti-GM-CSF antibodies have been found in the serum and BAL fl uid in patients with idiopathic PAP, leading to the use of subcutaneous GM-CSF therapy of the disease. However, patients with PAP secondary to an underlying condition (eg, hematologic malignancies, immunoglobulin defi ciency, HIV infection) do not have these antibodies and, therefore, there is no role for GM-CSF therapy.

• Although there are reports of successful use of inhaled GM-CSF in PAP, response rates are generally lower than with whole lung lavage, and this would be considered salvage therapy should lavage not work.

Which of the following statements about this condition is true? • A. A trial of prednisone therapy is warranted

initially.

• B. Granulocyte-macrophage colony-stimulating factor (GM-CSF) subcutaneous therapy works best in patients with a predisposing condition.

• C. Inhaled GM-CSF is the primary treatment modality.

• D. The patient should be offered whole lung lavage.

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Case No. 5

• A 25-year-old African American woman is referred for increasing shortness of breath and cough. She notes dyspnea on exertion (one-block walk), increasing over the past 6 months. She does not have chest pain, hemoptysis, fever, or weight loss. She recalls a “lung collapse” last year that required placement of a “tube” to correct the problem.

• She also recalls, more recently, some “fluid around her lung” that was white in appearance. She had since been lost to follow-up. She has a 10 pack-year history of tobacco use and has been trying to quit. Physical examination is notable for stable vital signs and bilateral crackles on lung examination. There is no clubbing. Her chest radiograph reveals increased reticular opacities. Her CT scan is shown in Figures 58-A and 58-B. Results of laboratory studies are

• unremarkable.

The most likely underlying histopathologic finding in the lung is which of the following?

• A. Smooth muscle proliferation along the lymphatics, interstitium, and bronchovasculature.

• B. Alternating areas of normal lung, interstitial inflammation, fibroblastic foci, and honeycomb changes.

• C. Centrally scarred stellate nodules with a polymorphic infl ammatory infiltrate.

• D. Noncaseating granulomas in the interstitium and around the vessels and bronchi.

• This patient has findings consistent with the diagnosis of lymphangioleiomyomatosis (LAM). LAM is a rare disease

• (prevalence 1 to 2 per million) affecting premenopausal women with a mean age of 35 years. The disorder is

• characterized by proliferation of atypical smooth muscle in the bronchovasculature, lymphatics, and interstitium of the

• lung (choice A is correct), as well as in the abdomen and pelvis. Typically, these smooth-muscle cells stain positive with the monoclonal antibody HMB-45 (a melanoma-related tumor marker).

• Clinically, patients have symptoms of dyspnea, cough, chest pain, and hemoptysis. The physical examination may reveal decreased breath sounds, crackles, and sometimes ascites and/or abdominal masses. Spontaneous pneumothoraces and/or chylothoraces may also be found. Radiographically, LAM is characterized by cyst formation and chronic reticular opacities. Hyperinflation develops as the disease progresses. Pleural effusions and pneumothoraces may also be present. CT scanning can reveal diff use, homogenous cystic disease, with cysts ranging from a few millimeters to 1 cm in size (6-cm cysts have been reported); characteristically, nodularity is absent. Pulmonary function testing most commonly shows mixed obstructive and restrictive physiology with an elevated total lung capacity and residual volume and a reduced diff using capacity, but up to one-third of patients can have normal pulmonary function.

• Complications of LAM include recurrent pneumothoraces in 50% of patients, chylous effusions in approximately one-third of patients, chylous ascites, and renal angiomyolipomas in up to 50% of patients. These latter tumors can develop in the kidneys or in other solid organs (uterus, ovaries, liver, and spleen) and are composed of blood vessels, smooth muscle, and fat.

• Treatment for LAM has included hormonal manipulation with the use of antiestrogens, progesterones, and/or oophorectomy with variable results. Lung transplantation has been performed for LAM, although disease recurrence has been documented. Recently, sirolimus, acting via suppression of mammalian target of rapamycin (mTOR) signaling, has been studied with a primary endpoint of decreasing angiomyolipoma volume.

• An interesting secondary finding was an improvement in spirometry of 5% to 10% in FEV1 and FVC, which was only partially sustained after discontinuation of sirolimus. The prognosis with LAM is variable, but median survival is often reported to be 8 to 10 years. The cause of death is usually respiratory failure.

• Pathologic evidence of sarcoidosis is characterized by noncaseating granulomas in the interstitium and around vessels and bronchi. The chest CT reveals hilar and mediastinal lymphadenopathy, beading or irregular thickening of the bronchovascular bundles, nodules along bronchi, vessels, and subpleural regions, and occasionally, ground glass opacifi cation. Pneumothoraces and pleural effusions are uncommon (choice D is incorrect).

• Pathology of Langerhans cell histiocytosis (choice C) is characterized by the presence of Langerhans cells, eosinophils, lymphocytes, neutrophils, and alveolar macrophages predominantly in the interstitium and around bronchovascular structures, forming centrally scarred stellate nodules

The most likely underlying histopathologic finding in the lung is which of the following?

• A. Smooth muscle proliferation along the lymphatics, interstitium, and bronchovasculature.

• B. Alternating areas of normal lung, interstitial inflammation, fibroblastic foci, and honeycomb changes.

• C. Centrally scarred stellate nodules with a polymorphic infl ammatory infiltrate.

• D. Noncaseating granulomas in the interstitium and around the vessels and bronchi.

Case No. 6

• A 65 year-old retired auto mechanic had a chest radiograph during a preoperative assessment for a cholecystectomy.

Which of the following statements is correct concerning the likely underlying diagnosis?

• A. The patient is at an increased risk of developing interstitial lung disease.

• B. Biopsy of one of the lesions would likely reveal several ferruginous bodies.

• C. The underlying abnormality most commonly involves the visceral pleura.

• D. The lesions are at high risk of transformation to malignant mesothelioma.

• The patient’s chest radiograph reveals the classic changes associated with benign pleural plaques associated with asbestos exposure. Given that the patient has had enough exposure to asbestos, likely through brake work in his job as an auto mechanic, he is also at risk for developing asbestosis, which is lung fibrosis caused by asbestos dusts.

• Both pleural and interstitial lung disease are related to the magnitude and duration of exposure to asbestos. With the exception of benign asbestos effusion, which can occur within a few years of initial exposure, most

• manifestations tend to occur after 20 to 30 years of exposure. Pleural and interstitial diseases often coexist, with pleural changes reported in up to 80% of patients with asbestosis. In fact, classic pleural plaques allow for a relatively firm clinical diagnosis of asbestosis when interstitial changes are present.

• Pleural plaques are the most common manifestation of asbestos exposure. They are found in a higher proportion of male than female patients, and the incidence of pleural plaques increases with increasing age. Pleural plaques are discrete areas of fibrosis that typically arise from the parietal pleura. On rare occasion, they may arise from the visceral pleura, but this is not the typical pattern.

• The classic distribution of the plaques on chest radiograph is the posterolateral chest wall between the seventh and 10th ribs, the lateral chest wall between the sixth and ninth ribs, and the dome of the diaphragm (virtually pathognomonic for asbestos plaques). The apices and costophrenic angles are typically spared. CT scan findings will support this distribution and may also reveal paravertebral plaques not seen well on chest radiographs.

• Calcification, as seen in this patient, is reported in 10% to 15% of cases and becomes more prevalent with long-standing plaques. On gross inspection, plaques are white, shaggy growths originating from the inner surface of the rib. Histologic examination reveals a relatively acellular “basket-weave” pattern of collagen bundles. Asbestos fibers are often seen, but asbestos bodies are typically absent. An asbestos body is an asbestos fiber that has been coated in an iron-rich material; therefore, they also are called ferruginous bodies. Pleural plaques do not typically cause symptoms, and most data suggest no adverse impact on pulmonary function. The current preponderance of evidence suggests that they do not undergo malignant transformation.

• Other pleural diseases associated with asbestos exposure include benign pleural effusions, diffuse pleural thickening (which, in contrast, predominantly involves the visceral pleura and can cause significant ventilatory impairment), rounded atelectasis, and malignant mesothelioma. Patients exposed to asbestos are also at increased risk of developing bronchogenic carcinoma, particularly if they are current or past smokers, which has a synergistic effect on risk.

Which of the following statements is correct concerning the likely underlying diagnosis?

• A. The patient is at an increased risk of developing interstitial lung disease.

• B. Biopsy of one of the lesions would likely reveal several ferruginous bodies.

• C. The underlying abnormality most commonly involves the visceral pleura.

• D. The lesions are at high risk of transformation to malignant mesothelioma.