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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Neurofibromatosis type 1 &#40;NF1&#41; is an autosomal dominant genetic syndrome caused by mutations in the NF1 gene that encodes neurofibromin protein which acts as a tumor suppressor&#46; It has a wide range of clinical features&#44; it is characterized by cutaneous signs&#44; notably neurofibromas&#44; caf&#233;-au-lait macules&#44; iris hamartomas as well as axillary and inguinal freckling&#46; It affects one in every 3000 people&#44; 30&#8211;50&#37; of which are sporadic form cases&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Respiratory involvement may be result from diverse ailments such as pulmonary hypertension&#44; kyphoscoliosis&#44; bilateral diaphragmatic paralysis&#44; etc&#46;&#44; as well as sporadic cases of diffuse pulmonary disease associated with NF1 &#40;NF1-DLD&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> We present a patient with both concomitant diseases&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A 62-year-old woman with a past smoking history of 100<span class="elsevierStyleHsp" style=""></span>packs&#47;year without preceding pulmonary pathology but previously diagnosed with NF1 &#40;sporadic form&#41; in her youth&#46; She had been diagnosed a year earlier of an infiltrating ductal carcinoma in her right breast treated with sequential neoadjuvant therapy and subsequent mastectomy&#46; She was treated in Emergency Department because of fever and cough in the previous 4 days&#46; Physical examination showed bilateral wheezing without other relevant findings&#44; except for countless neurofibromas &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>A&#41;&#46; Leukocytosis with left shift and acute respiratory failure was observed&#46; Chest radiograph displayed thickening of peribroncovascular interstice with left basal predominance &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>B&#44; C&#41; and multiple and bilateral irregular thin-walled aerial cysts were seen in the high resolution computed tomography &#40;CT&#41;&#44; converging in upper zones mimicking emphysema &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>D&#44; E&#41;&#46; Her pulmonary function tests were&#58; FVC 1400<span class="elsevierStyleHsp" style=""></span>cc &#40;61&#46;7&#37;&#41;&#59; FEV1 890<span class="elsevierStyleHsp" style=""></span>cc &#40;47&#37;&#41;&#59; FEV1&#47;FVC 63&#46;4 &#40;77&#46;3&#41;&#59; DLCOsb 29&#46;2&#37;&#59; DLCO&#47;VA 39&#46;3&#37;&#46; Based on these findings&#44; diagnosis of NF1-DLD was established &#40;without any other organs involved&#41;&#46; Following oxygen&#44; bronchodilators&#44; antibiotics &#40;levofloxacin&#41; and corticosteroids treatment&#44; she presented a favorable outcome and was discharged from hospital after 4 days&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Three main Neurofibromatosis types have been described&#58; 1 &#40;NF1&#41;&#44; 2 &#40;NF2&#41; and schwannomatosis&#46; NF1 is the most frequent subgroup&#44; characteristics of which are described above&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> NF2 is a hereditary syndrome&#44; caused by mutations in NF2 gene that encodes merlin protein&#44; a tumor suppressor&#44; which occurs in 1 out of 25&#44;000 inhabitants&#44; without lungs being involved&#46; Schwannomatosis&#44; on the other hand&#44; is caused by mutations in SMARCB1 and LZTR<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> tumor suppressor genes and affects 0&#46;58 in 1&#44;000&#44;000 people&#46; Familial and sporadic cases have also been described&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">NF1-DLD was first described by Davies<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and has an estimated prevalence of 7&#8211;23&#37; of NF1 patients&#46; Respiratory symptoms are often weak and pulmonary function tests can show any pattern type&#44; including obstructive &#40;43&#37;&#41;&#44; restrictive &#40;37&#37;&#41; or mixed &#40;17&#37;&#41;&#46; Carbon monoxide diffusing capacity is usually affected at an early stage&#46; Common chest CT findings include upper lobe predominant cystic and thin-walled bullous disease &#40;25&#37;&#41;&#44; basilar reticular abnormalities &#40;25&#37;&#41; and diffuse ground-glass opacification which can be associated with minimal honeycombing &#40;37&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Pathogenesis of cyst and bullae formation is unknown and it not infrequent for these findings to be confused with emphysema&#44; especially in smokers&#46; Despite the fact that observed lung injuries in NF1- DLD could be attributed to patient smoking behavior&#44; as in the case of our patient&#44; their presence in non-smokers is more plausibly due to neurofibromatosis pathogenesis itself&#46; Pathological findings of the few cases of NF1-DLD patients who have undergone lung biopsy appear to support the hypothesis that cystic lesions are of NF1 origin rather than of smoking pathogenesis&#44;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> owing to the presence of lymphocytic inflammation in alveolar septa&#44; as happens in interstitial lymphoid pneumonia&#46; Some authors argue that it could be a fibrotic environment with activation of fibroblasts and collagen production&#46; It has also been suggested that NF1 may increase lungs sensitivity to cigarette smoking&#44; causing early development of emphysema-like changes in these patients&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Hitherto&#44; no specific treatment has been approved for patients with NF1&#46; Consequently&#44; early diagnosis and genetic counseling are of vital importance&#46; Current research is focused on identifying potential therapeutic targets for any of disease manifestations&#46; Neurofibromin contains gene sequences that are similar to tumor suppressor proteins&#44; which act as negative regulators of RAS pathway&#46; In NF1&#44; as neurofibromin gene mutations cause greater activity of this protooncogene &#40;RAF&#47;MEK and AKT&#47;MTOR signaling pathways&#41;&#44; with these patients experiencing increased cell replication&#59; this would be one of the therapeutic targets currently being evaluated&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Treatment for respiratory symptoms consists of giving up smoking and prescription of tiotropium bromide for symptomatic dyspnea relief in emphysematous patients&#46; Corticosteroids&#44; intended as anti-inflammatory&#44; have not succeeded in slowing the pace of the disease progression&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">In summary&#44; when dealing with a Von Recklinghausen&#39;s patient&#44; pulmonary involvement &#40;NF1-DLD&#41; should be discarded&#46; As respiratory symptoms may be negligible&#44; it is necessary to perform pulmonary function tests and chest CT to confirm and assess the type of injuries&#44; as well as the extent of the disease&#46; Smokers must give up smoking immediately&#59; this crucial to stop disease progression&#46; Bronchodilators may help relieve symptoms should bronchial obstruction be present&#46;</p><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Author&#39;s contributions</span><p id="par0045" class="elsevierStylePara elsevierViewall">AC&#44; NR-N and LV were responsible for the conception and design of the study&#44; and wrote and edited the manuscript&#46; AM-A&#44; SC and JA contributed to the drafting and revision of the manuscript&#46; All authors read and approved the final manuscript&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0100" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Funding</span><p id="par0095" class="elsevierStylePara elsevierViewall">This study was undertaken without funding&#46;</p></span></span>"
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Honeycombing&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">0&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Skin nodules&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">39&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Subcutaneous nodules&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">50&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Scoliosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">23&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">9&nbsp;\t\t\t\t\t\t\n
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Letter to the Editor
Neurofibromatosis type I with lung involvement in a cancer patient
A. Casala,
Corresponding author
ana.casal.mourino@sergas.es

Corresponding author.
, N. Rodríguez-Núñeza, A. Martínez-Alegríab, S. Candamioc, J. Álvarezc, L. Valdésa,d
a Pneumology Department, Hospital Clínico Universitario, Santiago de Compostela, Spain
b Radiology Department, Hospital Clínico Universitario, Santiago de Compostela, Spain
c Oncology Department, Hospital Clínico Universitario, Santiago de Compostela, Spain
d Interdisciplinary Pneumology Research Group, Santiago de Compostela Health Research Institutions (Instituto de Investigaciones Sanitarias de Santiago de Compostela/IDIS), Santiago de Compostela, Spain
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; Multiple cutaneous neurofibromas in a NF1 patient&#46; &#40;B&#44; C&#41; Chest X-ray in which thickening of the peribroncovascular interstice with left basal predominance is observed&#46; &#40;D&#44; E&#41; High resolution computed tomography &#40;axial plane and pulmonary window&#41; through upper lobes above and below carina showing multiple thin-walled irregular aerial cysts&#44; that tend to converge in upper areas&#44; with similar appearance to emphysema&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Neurofibromatosis type 1 &#40;NF1&#41; is an autosomal dominant genetic syndrome caused by mutations in the NF1 gene that encodes neurofibromin protein which acts as a tumor suppressor&#46; It has a wide range of clinical features&#44; it is characterized by cutaneous signs&#44; notably neurofibromas&#44; caf&#233;-au-lait macules&#44; iris hamartomas as well as axillary and inguinal freckling&#46; It affects one in every 3000 people&#44; 30&#8211;50&#37; of which are sporadic form cases&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Respiratory involvement may be result from diverse ailments such as pulmonary hypertension&#44; kyphoscoliosis&#44; bilateral diaphragmatic paralysis&#44; etc&#46;&#44; as well as sporadic cases of diffuse pulmonary disease associated with NF1 &#40;NF1-DLD&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> We present a patient with both concomitant diseases&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A 62-year-old woman with a past smoking history of 100<span class="elsevierStyleHsp" style=""></span>packs&#47;year without preceding pulmonary pathology but previously diagnosed with NF1 &#40;sporadic form&#41; in her youth&#46; She had been diagnosed a year earlier of an infiltrating ductal carcinoma in her right breast treated with sequential neoadjuvant therapy and subsequent mastectomy&#46; She was treated in Emergency Department because of fever and cough in the previous 4 days&#46; Physical examination showed bilateral wheezing without other relevant findings&#44; except for countless neurofibromas &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>A&#41;&#46; Leukocytosis with left shift and acute respiratory failure was observed&#46; Chest radiograph displayed thickening of peribroncovascular interstice with left basal predominance &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>B&#44; C&#41; and multiple and bilateral irregular thin-walled aerial cysts were seen in the high resolution computed tomography &#40;CT&#41;&#44; converging in upper zones mimicking emphysema &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>D&#44; E&#41;&#46; Her pulmonary function tests were&#58; FVC 1400<span class="elsevierStyleHsp" style=""></span>cc &#40;61&#46;7&#37;&#41;&#59; FEV1 890<span class="elsevierStyleHsp" style=""></span>cc &#40;47&#37;&#41;&#59; FEV1&#47;FVC 63&#46;4 &#40;77&#46;3&#41;&#59; DLCOsb 29&#46;2&#37;&#59; DLCO&#47;VA 39&#46;3&#37;&#46; Based on these findings&#44; diagnosis of NF1-DLD was established &#40;without any other organs involved&#41;&#46; Following oxygen&#44; bronchodilators&#44; antibiotics &#40;levofloxacin&#41; and corticosteroids treatment&#44; she presented a favorable outcome and was discharged from hospital after 4 days&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Three main Neurofibromatosis types have been described&#58; 1 &#40;NF1&#41;&#44; 2 &#40;NF2&#41; and schwannomatosis&#46; NF1 is the most frequent subgroup&#44; characteristics of which are described above&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> NF2 is a hereditary syndrome&#44; caused by mutations in NF2 gene that encodes merlin protein&#44; a tumor suppressor&#44; which occurs in 1 out of 25&#44;000 inhabitants&#44; without lungs being involved&#46; Schwannomatosis&#44; on the other hand&#44; is caused by mutations in SMARCB1 and LZTR<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> tumor suppressor genes and affects 0&#46;58 in 1&#44;000&#44;000 people&#46; Familial and sporadic cases have also been described&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">NF1-DLD was first described by Davies<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and has an estimated prevalence of 7&#8211;23&#37; of NF1 patients&#46; Respiratory symptoms are often weak and pulmonary function tests can show any pattern type&#44; including obstructive &#40;43&#37;&#41;&#44; restrictive &#40;37&#37;&#41; or mixed &#40;17&#37;&#41;&#46; Carbon monoxide diffusing capacity is usually affected at an early stage&#46; Common chest CT findings include upper lobe predominant cystic and thin-walled bullous disease &#40;25&#37;&#41;&#44; basilar reticular abnormalities &#40;25&#37;&#41; and diffuse ground-glass opacification which can be associated with minimal honeycombing &#40;37&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Pathogenesis of cyst and bullae formation is unknown and it not infrequent for these findings to be confused with emphysema&#44; especially in smokers&#46; Despite the fact that observed lung injuries in NF1- DLD could be attributed to patient smoking behavior&#44; as in the case of our patient&#44; their presence in non-smokers is more plausibly due to neurofibromatosis pathogenesis itself&#46; Pathological findings of the few cases of NF1-DLD patients who have undergone lung biopsy appear to support the hypothesis that cystic lesions are of NF1 origin rather than of smoking pathogenesis&#44;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> owing to the presence of lymphocytic inflammation in alveolar septa&#44; as happens in interstitial lymphoid pneumonia&#46; Some authors argue that it could be a fibrotic environment with activation of fibroblasts and collagen production&#46; It has also been suggested that NF1 may increase lungs sensitivity to cigarette smoking&#44; causing early development of emphysema-like changes in these patients&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Hitherto&#44; no specific treatment has been approved for patients with NF1&#46; Consequently&#44; early diagnosis and genetic counseling are of vital importance&#46; Current research is focused on identifying potential therapeutic targets for any of disease manifestations&#46; Neurofibromin contains gene sequences that are similar to tumor suppressor proteins&#44; which act as negative regulators of RAS pathway&#46; In NF1&#44; as neurofibromin gene mutations cause greater activity of this protooncogene &#40;RAF&#47;MEK and AKT&#47;MTOR signaling pathways&#41;&#44; with these patients experiencing increased cell replication&#59; this would be one of the therapeutic targets currently being evaluated&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Treatment for respiratory symptoms consists of giving up smoking and prescription of tiotropium bromide for symptomatic dyspnea relief in emphysematous patients&#46; Corticosteroids&#44; intended as anti-inflammatory&#44; have not succeeded in slowing the pace of the disease progression&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">In summary&#44; when dealing with a Von Recklinghausen&#39;s patient&#44; pulmonary involvement &#40;NF1-DLD&#41; should be discarded&#46; As respiratory symptoms may be negligible&#44; it is necessary to perform pulmonary function tests and chest CT to confirm and assess the type of injuries&#44; as well as the extent of the disease&#46; Smokers must give up smoking immediately&#59; this crucial to stop disease progression&#46; Bronchodilators may help relieve symptoms should bronchial obstruction be present&#46;</p><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Author&#39;s contributions</span><p id="par0045" class="elsevierStylePara elsevierViewall">AC&#44; NR-N and LV were responsible for the conception and design of the study&#44; and wrote and edited the manuscript&#46; AM-A&#44; SC and JA contributed to the drafting and revision of the manuscript&#46; All authors read and approved the final manuscript&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0100" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Funding</span><p id="par0095" class="elsevierStylePara elsevierViewall">This study was undertaken without funding&#46;</p></span></span>"
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                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">&#37;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Chest computed tomography&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">&#37;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Mottled&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">32&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Linear densities&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">61&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Reticular abnormality&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Nodular densities&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">13&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Bullae&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Bullae&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">73&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Emphysema&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Bullae in upper localization&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Honeycombing&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Subcutaneous nodules&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Scoliosis&nbsp;\t\t\t\t\t\t\n
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          "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Most common radiological findings &#40;X-ray and chest computed tomography&#41; in diffuse pulmonary disease associated with NF1&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;5</span></a></p>"
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                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "M&#46; Lammert"
                            1 => "J&#46;M&#46; Friedman"
                            2 => "L&#46; Kluwe"
                            3 => "V&#46;F&#46; Mautner"
                          ]
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                      ]
                    ]
                  ]
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                    0 => array:2 [
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                            1 => "E&#46;A&#46; Chiocca"
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Article information
ISSN: 25310437
Original language: English
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