¯ditorial Approach to the solitary pulmonary nodule A solitary pulmonary nodule (SPN) is currently defined as a single pa- renchymal lung lesion which is 3 cm or less in diameter, and relatively spher- ical in contour. Some authorities consider that this definition does not ap- ply if there are major surrounding or associated abnormalities on a stan- dard chest radiograph. SPNs provide some of the more vexing clinical chal- lenges facing a pulmonary practitioner. These lesions are common, as ap- proximately 170,000 SPN are detected each year in the United States 1 . Approximately 1 in 500 standard chest radiographs in adults will show an SPN 2 (GL). Solitary pulmonary nodules are malignant, usually bronchogenic car- cinomas, in 20-40% of cases 3 . Early resection of a malignant nodule im- proves the otherwise dismal prognosis of bronchogenic carcinoma 2,3 . In several reports, the 5-year survival has been as high as 75-80% 4,5 . Resec- tion of a benign nodule however, rarely confers significant benefit to the patient, and carries its own likelihoods for mortality and morbidity. MANAGEMENT GOALS The goals are to resect all malignant SPNs promptly, and, at the same time, to avoid resection of benign nodules where possible. The criterion has always been, and still is, that an indeterminate nodule should be regarded as malignant unless proof of benignity can be obtained. Conse- quently, the most important practical question is how to differentiate benign from malignant (or probably) SPNs prior to surgery. TESTING FOR BENIGNITY Two criteria for benignity of SPNs were proposed in the 1950s: nod- ular calcification and retrospective stability 6 These are useful and still employed, although it is now clear that some modifications of this dic- tum are required 7,8 . Intranodular calcification may present a variety of appearances. Fea- tures indicative of benignity include central, diffuse, concentric rings or "popcorn" patterns. Patterns of eccentric calcification or multiple small L.T. Vaszar, G.A. Lillington Palo Alto Medical Foundation Key words: lung, nodule, diagnosis, lung cancer, screening Correspondence: Glen A. Lillington, M.D. Ombudsman Palo Alto Medical Foundation 795 El Camino Real Palo Alto, CA 94301
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Åditorial
Approach to the solitary pulmonary nodule
A solitary pulmonary nodule (SPN) is currently defined as a single pa-renchymal lung lesion which is 3 cm or less in diameter, and relatively spher-ical in contour. Some authorities consider that this definition does not ap-ply if there are major surrounding or associated abnormalities on a stan-dard chest radiograph. SPNs provide some of the more vexing clinical chal-lenges facing a pulmonary practitioner. These lesions are common, as ap-proximately 170,000 SPN are detected each year in the United States1.Approximately 1 in 500 standard chest radiographs in adults will show anSPN2 (GL).
Solitary pulmonary nodules are malignant, usually bronchogenic car-cinomas, in 20-40% of cases3. Early resection of a malignant nodule im-proves the otherwise dismal prognosis of bronchogenic carcinoma2,3. Inseveral reports, the 5-year survival has been as high as 75-80%4,5. Resec-tion of a benign nodule however, rarely confers significant benefit to thepatient, and carries its own likelihoods for mortality and morbidity.
MANAGEMENT GOALS
The goals are to resect all malignant SPNs promptly, and, at the sametime, to avoid resection of benign nodules where possible. The criterionhas always been, and still is, that an indeterminate nodule should beregarded as malignant unless proof of benignity can be obtained. Conse-quently, the most important practical question is how to differentiatebenign from malignant (or probably) SPNs prior to surgery.
TESTING FOR BENIGNITY
Two criteria for benignity of SPNs were proposed in the 1950s: nod-ular calcification and retrospective stability6 These are useful and stillemployed, although it is now clear that some modifications of this dic-tum are required7,8.
Intranodular calcification may present a variety of appearances. Fea-tures indicative of benignity include central, diffuse, concentric rings or"popcorn" patterns. Patterns of eccentric calcification or multiple small
concentric deposits can be benign or malignant (Fig-ure 1), and in such cases, transthoracic needle biopsyor even diagnostic thoracotomy may still be indicated.Absence of calcification favors malignancy, but doesnot prove it. Even in a nodule with central calcifica-tion, malignancy is occasionally present9. With any ap-parently benign calcification pattern, it is prudent tomonitor with serial x-rays or CT scans for severalmonths or a year to detect growth, which might suggestmalignancy.
Retrospective stability implies little or no growth ofthe nodule, and is ordinarily assessed by comparison ofany available prior chest x-rays with the current imag-es. Stability has traditionally been defined as no de-tectable increase in nodule size during the previous 24months or longer. This criterion is not always absolute,mainly because attempting to detect and monitorgrowth of small nodules using standard x-rays some-times provides misleading results. In such instances, asmall nodule may double or even triple in size beforethe increase in volume is recognized10. The accuracy ofdetecting growth is improved if the nodule is 1.0 cm orgreater in diameter.
Prior computed tomographic (CT) scans, if avail-able, are much more reliable in assessing retrospectivestability than standard chest x-rays, particularly if thenodule is small (less than 10 mm in diameter). Retro-
grade assessment of nodule growth by comparing CTimages with standard chest x-ray images may lead toserious errors10.
If the time interval between the first available andcurrent images is less than 2 years, it is may be appro-priate in many instances to continue the evaluation withCT scans at 3-6 month intervals.
BIOPSY TESTS
Transthoracic needle aspiration biopsy. This rela-tively simple and safe test can be very valuable, and isoften decisive. The test has a 80 to 95% sensitivity formalignancy, and a specificity of approximately 50%11.The biopsy needle is positioned under fluoroscopic orCT guidance.
If the biopsy fails to establish that the nodule is ma-lignant, there are two further possibilities. The biopsymaterial may provide convincing evidence for a specif-ic benign lung disease, in which case the nodule is usu-ally classified as "benign". If the biopsy material is notdefinitive for either malignant or benign disease, theclassification is "indeterminate". In the latter situation,it is often desirable to repeat the biopsy. On-site tech-nology for immediate sampling of the biopsy materialfacilitates repeat sampling in a single session and re-duces the likelihood of "indeterminate" results12,13.
In the case of solitary nodules, an endobronchialbiopsy through a bronchoscope has a relatively low sen-sitivity, unless the lesion is large in size and central inlocation. It is only employed occasionally in patientswith SPNs.
IMAGING TESTS
Computed Tomography (CT). Chest CT is not ableto definitively establish malignancy or benignity in mostsolitary nodules, but it will often provide informationthat is very helpful in estimating the likelihood of ma-lignancy. CT is invaluable in determining whether thelesion is intrapulmonary, and provides much more ac-curate measurements of nodular diameters13. It mayalso demonstrate hitherto unsuspected multiple lesionsin the lungs.
CT may prove or strongly suggest that the lesion is
Figure 1. Patterns of calcification in solitary pulmonary nod-ules. A, central; B, laminated; C, diffuse; D, popcorn; E, stip-pled, and F, eccentric. Patterns A through D are virtually al-ways indicative of benignity. Pattenrs E and F may occur inbenign or malignant nodules. (From Lillington GA: Systemicdiagnostic approach to pulmonary noduls, in AP Fishman [ed]:Pulmonary Disease and Disorders [ed 2]. New York, McGraw-Hill, 1988, p 1947. Used by permission).
19PNEUMON Number 1, Vol. 16, January - April 2003
benign if the nodule is a hamartoma, a vascular lesion,or has a benign calcification pattern not apparent inthe standard chest x-rays.
Features suggestive of malignancy include large sizeof the nodule, certain features of the nodule-lung in-terface (Figure 2), the absence of calcification, and de-monstrable proof of growth of the nodule with serial x-rays or CT scan studies. CT is superior to standard chestroentgenograms in all of these respects, and also pro-vides valuable information on the possible presence ofenlarged mediastinal nodes.
Magnetic Resonance Imaging (MRI) is not usefulfor the detection or identifying malignancy in solitary
nodules, but it can be helpful in detecting and assessinghilar/and mediastinal adenopathy.
Positron Emission Tomography (PET). The PETscan modality now plays a major role in the evaluationof solitary nodules14,15. The most accurate and helpfultechnique is a combined CT/PET scan, which is partic-ularly helpful for achieving precise localization of theabnormality. The overall sensitivity for tumors is 96.8%,but false negative results may occur with bronchoalve-olar tumors, and with malignant nodules less than 1 cmin diameter. As false positives may occur in active in-flammatory lesions, the specificity is only 77.8%14. Apositive result strongly suggests malignancy and sur-gery should be actively considered. A negative PET scanstrongly suggests benignity, but does not absolutely ruleout malignancy.
PET scans are also very helpful in detection of hi-lar, mediastinal and even distant metastases16.
CALCULATION OF THE PROBABILITY OF CANCER(PCA)
An estimate of the probability that the solitary nod-ule is a cancer is useful in the formulation of manage-ment strategies. The value of PCA can be calculated byan assessment of "predictor variables", which includeclinical data (age, smoking history, presence or absenceof previous malignancies) and radiographic character-istics (position of nodule in the lung, diameter of thenodule, edge characteristics, cavity wall thickness, andpresence or absence of calcifications). Bayesian analy-sis17,18 or logistic regression19 can be employed to pro-vide a quantitative estimation (PCA) that the SPN ismalignant.
Calculating the PCA of SPNs is simplified by on-line algorithms, which can be accessed from the Inter-net with the following URL: http://www.chestx-ray.com/SPN/SPNProb.html. Experienced observers are capa-ble of estimating PCA with considerable accuracy inmany cases by reviewing the predictor variables with-out formal calculations of probability.
MANAGEMENT STRATEGIES
In practice, most SPNs initially fall into the catego-
Figure 2. Characteristic appearances of nodule edges. Type I issharp and smooth and the probability of cancer based on thisis 20%. Type 2 is sharp but lobulated, and the probability thatthe nodule is malignant is about 45%. Type 3 shows irregularundulations, and one or two spiculations. The likelihood of ma-lignancy is 2:1 in this case. Type 4. There are multiple spicula-tions. This has been termed "corona radiata" or "corona mali-gna". The odds favoring malignancy are 14:1 in such cases. (Re-draw from Siegelman SS, Khouri NF, Fishman EK, et al: Sol-itary pulmonary nodules: CT assessment. Radiology 1986;160(8): 307-312, Used by permission).
ry of "indeterminate". This includes cases in which be-nign patterns of calcification are not present, and ret-rospective determination of stability is not possible ornot decisive.
There are five available strategies in these circum-stances. These are not mutually exclusive, and are of-ten employed sequentially. "Effectiveness" is measuredby 5-year survival after the initial detection of the SPN.Ignoring the presence of the nodule is not an appropri-ate strategy!
Thoracotomy. This is commonly chosen as the ini-tial (and definitive) strategy because it is both diagnos-tic and therapeutic. Decision analysis studies20 suggestthat if the PCA is relatively high (>60 %), prompt tho-racotomy is the most effective and cost-effective strat-egy. However, thoracotomy may be considered at vir-tually any PCA level if the patient and/or the physicianso choose. Surgical mortality is 1-4%. Compared withstandard (classic) thoracotomy, morbidity is lower withVideo Assisted Thoracoscopy (VAT). If other strate-gies are first employed, thoracotomy is necessarily de-layed to some degree, and there is concern that thepassage of time might allow a curable lesion to becomeincurable20.
Transthoracic needle biopsy. This may be employedat any calculated PCA level, and in the past has beenconsidered to be the most effective strategy over inter-mediate levels of PCA (10-60%). A positive biopsy fortumor indicates that prompt thoracotomy is required.If the biopsy proves a specific benign lesion, thoracot-omy is deferred, but it is prudent to follow the subse-quent course of the nodule by serial CT scans for atleast a year.
An indeterminate biopsy result is not proof of be-nignity or malignancy, and further action must be tak-en. In such cases, the further options may include arepeat needle aspiration biopsy, a PET scan, a "Watchand Wait" approach (see below) or a prompt thoracot-omy
"Wait and watch" strategy. This is a prospective de-termination of stability, determined by serial CT stud-ies after the detection of the SPN. It may be a reason-able choice20 if the PCA is very low <10%, but it isimportant that the patient understands the possible"hazard of delay"20,21. The initial CT followup should be
3-6 weeks after the detection of the nodule, and then at3 month intervals for at least two years, or even longer insome cases.
Growth is measured in terms of the "doubling time"- the time taken for the nodule to double its volume.An increase in diameter of 28% indicates a doubling ofvolume. Malignant nodules tend to have doubling timesbetween 80 and 140 days. Benign nodules usually donot grow in size, although slow growth of the nodulemay occur in some instances. Most authorities wouldprobably advise prompt thoracotomy if the calculateddoubling time is shown to be less than one year, butsome malignant nodules have considerably greater dou-bling times. If the lesion has shown any detectable in-crease in size, thoracotomy or VAT is often carried out.
Some students of SPN management consider thatWait and Watch is rarely indicated.
PET Scan strategy. This test has such high sensitiv-ities and specificities that its use is really a strategy, lim-ited only by the restricted availability of the equipmentrequired. Pet scans may be employed in conjunctionwith or following the initiation of other strategies. Arecent study has suggested that PET scan should bethe initial strategy in most cases22.
A positive test strongly suggests malignancy and inmost cases should mandate thoracotomy. If the resultsof PET scans and the PCA are discordant, needle aspi-ration biopsy may be advisable.
MANAGEMENT PATHWAYS
Spherical lung lesions greater than 3 centimeters indiameter are very frequently malignant, and should bebiopsied or resected without delay in most instances.The pathways employed in the assessment of solitarynodules are not very appropriate for these larger mass-es. Factors such as patient preference or the concur-rent presence of serious concurrent diseases must beconsidered. Needle biopsy or PET Scans may help inthe decision process under such circumstances.
Previous chest x-rays or chest CT scans should besought, and compared with the current studies. Thesemay provide a retrograde estimation of stability, regard-less of the size of the nodule or mass. Recognizablegrowth in the prior two years carries a high likelihood
21PNEUMON Number 1, Vol. 16, January - April 2003
that the nodule is malignant, and resection must be seri-ously considered. Comparison of current with previousstudies may be seriously misleading, particularly if thenodule is small or if previous studies were obtained withstandard x-rays rather than CTs ( Henschke).
Needle aspiration biopsy should be the initial strat-egy if the solitary or multiple pulmonary nodules arepresent in a subject with a prior history of an extrapul-monary neoplasm, or with other clinical features sug-gesting the possibility that the nodule is metastatic. Insome cases a VATS biopsy may be required.
The clinical value of PCA calculation lies in its usein suggesting the most effective management strategyor sequence of strategies. If the calculated PCA is 15-20% or less, the Wait and Watch strategy is reasonablealthough not imperative. Biopsy should still be consid-ered. If the PCA is 60% or greater, prompt thoracoto-my is usually advisable. These suggestions are not ab-solute, and it is clear that the wishes of the patient mustbe given major consideration.
In the intermediate range of probabilities (20 to60%), the use of needle biopsy has generally been fa-vored in most instances. If the biopsy is nondiagnostic,it may be repeated one or more times, and if the resultis still indeterminate, the further two choices includeimmediate thoracotomy, PET scanning, or Watch andWait in selected circumstances. If the biopsy indicatesa specific benign process, including benign tumor orgranulomatous disease, it is often prudent to carry outWatch and Wait, with repeat x-rays or CT scans everythree months for a year or so.
The use of PET scanning has recently been recom-mended as the initial strategy in many or most cases,particularly if the PCA is within the wide intermediatechange. An initial cost-effective study22 provides sup-port for this, although further studies are clearly desir-able.
Ideally, the patient should play an active role in thedecision process. This requires a thorough discussionof the pros and cons of the various strategies.
STAGING
Ìost malignant SPNs fall into the clinical categoryof T1 N0 M0, but it is still important to obtain a high
resolution CT scan of the chest to explore the status ofthe hilar and mediastinal nodes. Enlargement of thenodes does not, in itself, invariably prove nodal involve-ment with tumor. PET scans are particularly helpful inthis situation. Mediastinal node biopsy will sometimesbe required.
SCREENING FOR LUNG CANCER
The development of the helical single pass chest CTscan has spurred attempts to detect and resect lung can-cers as small as 2-3 mm in diameter. The supposition isthat early detection and prompt surgical resection willreduce the mortality from lung cancer. The efficacy ofCT lung screening however remains to be determinedby the several studies now in progress23.
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Non-occupational environmental factors and lung cancer
A. Papagiannis
Cigarette smoke is by far the major extrinsic (non-genetic) cause of lung cancer. A small number ofcases of this disease may be due to other environmental factors which act either independently orsynergistically with tobacco smoke. The effect of environmental carcinogens is most obvious inoccupational settings where the responsible substance may occur in relatively high concentrations.However, certain substances may cause carcinogenesis even after non-occupational exposure. Thedetailed study of environmental effects is fraught with methodological problems. However, it is clearthat factors such as radon, arsenic, asbestos, urban pollution, and to a lesser degree socioeconomicconditions and nutrition, may be implicated in a small number of lung cancer cases. The avoidance ofall these factors is not practical, and is not expected to have a significant impact on the incidence oflung cancer as long as the major carcinogen, tobacco, is not effectively controlled. Pneumon 2003,16(1):29-37.
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Frequency and outcome of childhood bronchial asthma in the town of Larissa
Krommydas G, Goulgoulianis KI, Molyvdas PA
The purpose of this study was to estimate the frequency of bronchial asthma in childhood in thetown of Larissa and to assess the possible effects of social status, environmental factors, the child�smedical and family history on the course of the disease. A brief asthma questionnaire was distributedand completed by 754 families with at least one child attending a public day nursery in Larissa. Ofthese, 120 were found to have a child with symptoms consistent with asthma in the past year. Childrenwere 4-8 years old and the questionnaire was completed by their parents. The International Study ofAsthma and Allergy in Childhood (ISAAC)-Phase I questionnaire with additional items referring tothe socio-economic status of the family, indoor environment factors and parental smoking habitswas used. A child with asthma was identified in seventy families. Two years later the course of thedisease was evaluated in 66 of those families, using a modified ISAAC questionnaire. The frequen-cy of bronchial asthma in the study population was 9.3%, with the frequency of asthma attacksdeclining with age. The majority of the children had mild asthma. Allergic rhinitis was found in31.4% and allergic dermatitis (eczema) in 14.2%. Parental smoking was not related to asthmaticattacks. Allergic rhinitis and conjunctivitis were strongly related to asthmatic attacks on reevaluationtwo years later. These results suggest an important role of atopic disease in the course of asthma andconfirm the reports of declining attack frequency with advancing age. Pneumon 2003, 16(1):38-48.
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15. Leung R, Wong G, Lau J et al. Increasing trend of asth-
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1. Burney P. Epidemiology of asthma. Allergy 1993; 48:17-218.
2. Myers TR. Pediatric asthma epidemiology: incidence,morbidity and mortality. Respir Care Clin N Am 2000;6:1-14.
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8. Zacharasiewicz A, Zidek T, Haidinger G, Waldhor T,Suess G, Vutuc C. Indoor factors suggestive of asthma
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ma and allergic disease in Hong Kong schoolchildren. JAllergy Clin Immunol 1996; 97:375.
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Prevalence of gastroesophageal reflux disease symptoms in bronchial asthma patients in Greece
A. Roussos, I. Gerogianni, I. Lagogianni, F. Tsimpoukas, N. Filippou, I. Eliopoulos
9th Department of Pulmonary Medicine, �SOTIRIA� Chest Diseases Hospital, Athens, Greece
A high prevalence of gastroesophageal reflux disease (GERD) symptoms in patients with bronchialasthma has been shown in several reports from North America and Europe. However, no data fromGreece are available. The aim of this study is to assess the prevalence of GERD symptoms in Greekasthmatics. A total of 92 asthmatics (50 males and 42 females, aged 42.9±14.2 years) referred to ouroutpatient clinic, and 85 age- and sex-matched healthy control subjects were asked to complete astructured questionnaire on the presence of GERD symptoms. The prevalence of heartburn andregurgitation was higher in asthmatics (81.5% and 57.6%, respectively) than in controls (32.9% and
17.6%, respectively, p<0.01). None of the medications routinely used in the treatment of asthma wasassociated with increased prevalence of GERD symptoms. Our results suggest that Greek asthmaticsreferred to a tertiary care center have a significantly higher prevalence of GERD symptoms comparedto controls. Additional studies in the general population of asthmatic patients are required to furtherclarify the relationship between asthma and GERD in Greece. Pneumon 2003, 16(1):59-66.
3. Perrin-Fayolle M, Bel A, Kofman J, Harf R, Montag-non B, Pacheco Y, Daubet J, Nesmoz J, Perpoint B.Asthma and gastroesophageal reflux. Results of a sur-vey of over 150 cases. Poumon Coeur 1980; 36:225-30
4. O� Connell S, Sontag SJ, Miller T. Asthmatics have ahigh prevalence of reflux symptoms regardless of the useof bronchodilators. Gastroenterology 1990; 98:A97.
5. Field SK, Underwood M, Brant R, Cowie R. Prevalenceof gastroesophageal reflux symptoms in asthma. Chest1996; 109:316-22
6. Harding SM, Sontag SJ. Asthma and Gastroesophagealreflux. Am J Gastroenterol 2000; 95(Suppl 1):23-32
7. Alexander JA, Hunt LW, Patel AM. Prevalence, Patho-physiology and treatment of patients with asthma andgastroesophageal reflux disease Mayo Clin Proc 2000;75:1055-1063
9. Locke GR, Talley NJ, Fett SL, Zinsmeister AR, MeltonLJ. Prevalence and clinical spectrum of gastroesophagealreflux: a population-based study in Olmsted Country,Minnesota. Gastroenterology 1997; 112:1448-1456.
10. Ìansfield LE, Stein MR. Gastroesophageal reflux andasthma: A possible reflex mechanism. Ann Allergy 1978;41:224-226.
11. Mansfield LE, Hameister HH, Spaulding HS, Smith NJ,Glab N. The role of the vagus nerve in airway narrowingcaused by intraesophageal hydrochloric acid provocativeand esophageal distention. Ann Allergy 1981; 47:431-434.
12. Spaulding HS, Mansfield LE, Stein MR, Sellner JC,Gremillion DE. Further investigation of the associationbetween gastroesophageal reflux and bronchoconstric-
way function and symptoms in asthmatic patients withmarked bronchial hyperreactivity. Chest 1989; 96:995-998.
14. Wright RA, Miller SA, Corsello BF. Acid-induced esoph-ago-bronchial-cardiac reflexes in humans. Gastroenter-ology 1990,99:71-73.
15. Schan CA, Harding SM, Haile JM, Bradley LA, RichterJE. Gastroesophageal reflux-induced bronchoconstric-tion: An intraesophageal acid infusion study using state-of-the-art technology. Chest 1994; 105:731-737.
16. Harding SM, Guzzo MR, Maples RV. Gastroesophagealreflux -induced bronchoconstriction: Vagolytic doses ofatropine diminish airway responses to esophageal acidinfusion. Am J Respir Crit Care Med 1996; 151:A589.
17. Lodi U, Harding SM, Coghlan HC, Guzzo MR, WalkerLH. Autonomic regulation in asthmatics with gastroe-sophageal reflux. Chest 1997; 111:65-70.
18. Field SK. A critical review of studies of effects of simu-lated or real gastroesophageal reflux on pulmonary func-tion in adult asthmatics. Chest 1999; 115:848-856.
19. Mittal RK, Baladan DH. The esophagogastric junction.N Engl J Med 1997; 336:924-932.
20. Vincent D, Cohen-Jonathan AM, Leport J, MerroucheM, Geronimi A, Pradalier A, Soule JC. Gastro-oesoph-ageal reflux prevalence and relationship with bronchialreactivity in asthma. Eur Respir J 1997; 10:2255-2259.
21. Tuchman DN, Boyle JT, Pack AI, Scwartz J, KokonosM, Spitzer AR, Cohen S. Comparison of airway respons-es following tracheal or esophageal acidification in thecat. Gastroenterology 1984; 87:872-881.
22. Herve P, Denjean A, Jian R, Simonneau G, Duroux P.Intraesophageal perfusion of acid increases the broncho-motor response to methacholine and to isocapnic hyper-ventilation in asthmatic subjects. Am Rev Respir Dis1986; 134:986-989.
23. Donnelly RJ, Berrisfold RG, Jack CI, Tran JA, EvansCC. Simultaneous tracheal and esophageal pH monitor-ing: investigating reflux-associated asthma. Ann Thorac
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Surg. 1993; 56:1029-1033.24. De Vaalt KR, Castell DO Current diagnosis and treat-
ment of gastroesophageal reflux disease. Mayo clinicProc. 1994; 69:867-876.
25. Sontag SJ, Connell S, Khandelwal S, Miller T, Nem-chausky B, Schnell TG, Serlovsky R. Most asthmaticshave gastroesophageal reflux with or without bronchod-ilator therapy. Gastroenterology 1990; 99:613-620.
26. Harding SM, Guzzo MR, Richter JE. The prevalence ofgastroesophageal reflux in asthma patients without re-flux symptoms. Am J Respir Crit Care Med 2000; 162:34-39.
Communicating hydrocephalus and severe hyponatremia in a patient with tuberculous meningitis
H. Sinani, F. Tsidemiadou, M. Michalia, K. Roukas, A. Koutsikou,G. Pantazis, F. Klouva-Molyvda
A case of miliary tuberculosis, tuberculous meningitis and severe hyponatremia, in a 19 year old manfrom Pakistan, is presented. The patient was admitted comatose to the ICU. A CT scan of the brainrevealed a communicating hydrocephalus and external ventricular drainage was performed.Hydrocephalus is a common complication of tuberculous meningitis, and may be even fatal if leftuntreated. External ventricular drainage has both therapeutic and predicting value for the benefit ofshunt surgery. Prompt ventriculoperitoneal shunting improves outcome, particularly in those patientswho present with minimal neurological deficit. Neurological deterioration occurring in a patient undertreatment for tuberculous meningitis may have various causes and always requires urgent radiologicalassessment. Pneumon 2003, 16(1):74-79.
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1. MC Raviglione, DE Snider, A Kochi. Global epidemi-ology of tuberculosis. Morbidity and mortality of a worldwide epidemic. JAMA 1995; 273:220-6
2. D Bouros, J Demoiliopoulos, P Panagou, N Yiatromano-lakis, M Moschos, A Paraskeyopoulos, D Demoiliopou-los, N Siafakas. Incidence of tuberculosis in Greek armedforces from 1965-1993. Respiration 1995; 62:336-340.
3. Ravindra Kumar Garg. Tuberculosis of the central ner-vous system. Postgrad. Med. J. 1999; 75:133-140.
4. PM Small, PC Hopewell, SP Singh et al. The epidemiol-ogy of tuberculosis in San Francisco: a population- basedstudy using conventional and molecular methods. N EnglJ Med 1994; 330:1703-9.
5. UK Misra, J Kalita, M Srivastava, et al. Prognosis of tu-berculous meningitis a multivariate analysis. J NeurolSci 1996; 137:57-61.
6. G Thwaites, TTH Chau, NTH Mai, F Drobniewski, KMcAdam, J Farrar. Tuberculous meningitis. J Neurol.Neurosurg. Psychiatry 2000; 68:289-299.
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9. JM Mathew, V Rajshenkhar, MJ Chandy. Shunt surgeryin poor grade patients with tuberculous meningitis and
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hydrocephalus: effects of response to external ventricu-lar drainage and other variables on long term outcome.J Neurol Neurosurg Psychiatry 1998; 65:115-118.
10. A Ross Hill, J Uribari, J Mann, T Berl. Altered watermetabolism in tuberculosis: role of Vasopressin. TheAmerican Journal of Medicine 1990; 88:357-364.
11. PK Narotam, M Kemp, R Buck, E Gouws, JR VanDellen, KD Bhoola. Hyponatremic Natriuretic syndromein tuberculous meningitis. The probable role of AtrialNatriuretic peptide. Neurosurgery 1994; 34(6):982-988.
12. P F Barnes. Rapid diagnostic tests for tuberculosis.Progress but no gold standard. Am J Respir Crit CareMed 1997; 155:1497-1498.
13. Joint Tuberculosis Committee of the British ThoracicSociety. Chemotherapy and management of tuberculo-sis in the United Kingdom : recommendations 1998.Thorax 1998; 53:536-48.
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Thoracoscopic excision of ectopic parathyroid adenoma
D. Garbis, K. Iliadis, A. Hatzinis, A. Stathoulopoulos, A. Kontaxis
Thoracic Surgery Department, Diagnostic & Therapeutic Center of Athens ́ ´HYGEIA´´
The vast majority of parathyroid adenomas are excised through a cervical incision. The ectopic ones,which are usually are localized in the mediastinum, are excised through sternotomy or thoracotomy.In recent years, it has been possible to resect this kind of adenomas with the use of video assistedthoracoscopic surgery (VATS), this technique offering the advantage of lower morbidity. We describea case of a patient with end stage renal failure and tertiary hyperparathyroidism with ectopic parathyroidadenoma localized on the aortic arch, between the origin of the left carotid artery and left subclavianartery. The adenoma was excised using VATS and the patient was discharged on the first postoperativeday following excision. CT scans, parathormone and Ca blood levels returned to normal. Pneumon2003, 16(1):80-85.
Key words: ectopic parathyroid adenoma, VATS
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a report of two cases and review of the literature. J AmColl Surg 1997; 185(5):481-5.
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anterior mediastinotomy. Mayo Clin Proc 1991; 66:1110-3.
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14. Forster R, Storck M, Schafer R, Honig E, Lang G, Lie-wald F. Thoracoscopy versus thoracotomy: a prospec-tive comparison of trauma and quality of life. Langen-becks Arch Surg 2002 Apr; 387(1):32-6.
Ìåôáóôáôéêü ðáñáãáããëßùìá ðíåýìïíïòóå óõíäõáóìü ìå in situ âñïã÷ïãåíÝò êáñêßíùìá
Pulmonary metastatic paraganglioma in association with in situ bronchogenic carcinoma
K. Katsoulis, G. Papachristos, Th. Zaramboukas, Th. Kontakiotis, A. Nalbantis
We present a case of pulmonary metastatic paraganglioma in association with in situ bronchogeniccarcinoma. The primary tumor was located in the retroperitoneum and was surgically excised six yearsago. The metastatic tumor was accidentally found on a chest x-ray and was initially considered as aprimary bronchogenic carcinoma. The patient underwent lobectomy during which a metastaticparaganglioma was diagnosed. Paragangliomas are tumors of the neuroendocrine system, usually locatedin the abdomen. Pulmonary paragangliomas are rarely found. They are considered functioning whenlarge amounts of catecholamines are excreted and they are surgically treated prognosis being satisfactory.Pneumon 2003, 16(1):86-90.
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8. Lack EE. Pathology of adrenal and extra-adrenalparaganglia. Major problems in pathology. Vol 29. WBSaunders, Philadelphia, 1994.
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10. Lee YN, Hori JM. Chemodectoma of the lung. J SurgOncol 1972;4:33-36.
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2. Lack EE. Tumors of the adrenal gland and extra-adre-nal paraganglia. In: Atlas of tumor pathology, 3rd series,fascile 19, Washington DC: Armed Forces Institute ofPathology, 1997.
3. Fries JG, Chamberlin JA. Extra-adrenal pheochromocy-toma: literature review and report of a cervical pheo-chromocytoma. Surgery 1968;63:268-279.
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Á case of bronchiolitis obliterans organizing pneumonia mimicking bronchogenic carcinoma
K. Potaris, P. Michos, J. Gakidis, E. Machera
A 48-year-old man was admitted with hemoptysis, malaise, fatigue and anorexia in the last twentydays. A centrally located, 3 cm soft tissue mass in the right lower lobe of the lung was discovered onradiologic evaluation. His clinical and laboratory evaluation was unrevealing. Bronchoscopy, bronchialcultures and brushing were all negative. He underwent right thoracotomy with the radiologic suspicionof lung cancer. The frozen section was implying malignancy and the patient underwent a right lowerlobectomy with mediastinal lymph node dissection. However, the routine histologic report showedbronchiolitis obliterans organizing pneumonia. Corticosteroids were not given and there is no clinicalor roentgenographic evidence of recurrence of the disease twelve months postoperatively. This interestingcase demonstrates that not only clinical or roentgenographic findings of bronchiolitis obliteransorganizing pneumonia but frozen section too, can be confused with those of lung cancer. Pneumon2003, 16(1):91-96.
5. Cordier JF, Loire R, Brune J. Idiopathic bronchiolitisobliterans organizing pneumonia. Definition of charac-teristic clinical profiles in a series of 16 patients. Chest
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2. Yang DG, Kim KD, Shin DH, Choe KO, Kim SK, andLee WY. Idiopathic bronchiolitis obliterans with orga-nizing pneumonia presenting with spontaneous hydrop-neumothorax and solitary pulmonary nodule. Respirol-ogy 1999; 4(3):267-270
3. Domingo JA, Perez-Calvo JI, Carretero JA, Ferrando J,