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• W2129606243 abstract "A 29-year-old Asian woman complained of a left pleuritic chest pain and exertional dyspnea without cough for 7 days. She denied any fever and weight loss. The patient was a nonsmoker and had no underlying disease. Before admission, she was sufficiently healthy to undertake scuba diving. The patient's family history was noncontributory, and no genetic disorders were noted for the patient or her family members. She did not have a recent history of trauma and was not taking any medication, including herbal medication and oral contraceptives. Her last menstrual period had been 2 weeks before visiting the hospital. On physical examination, breath sounds were diminished at the left base without stony dullness to percussion. There was no palpable lymphadenopathy, and no skin lesions were observed. The results of laboratory tests, including CBC count and chemistry panel, were within normal range. Arterial blood gas on room air had the following values: pH, 7.42; Paco2, 31.4 mm Hg; Pao2, 87.3 mm Hg; and 97% saturation. Chest radiograph showed a left pneumothorax. Coarse reticular opacities and multiple cystic changes with ill-defined parenchymal opacification were also noted in both lower lung fields (Fig 1). Chest CT scan showed a pneumothorax in the left lung and innumerable small, thin-walled cysts scattered evenly over both lung fields. Ill-defined ground-glass attenuation was noted in the intervening parenchyma of both lower lobes (Figs 2A, 2C). Thoracic duct dilatation was suspected (Fig 2B). However, pleural effusion was not noted initially. Abdominal CT scan showed no abnormal manifestations, such as renal mass, ascites, or lymphadenopathy.Figure 2A, Axial chest CT scan with lung window settings demonstrates multiple small cysts with thin walls in both lungs, ill-defined ground-glass attenuation in intervening parenchyma of both lower lobes, and left-side pneumothorax. B, Thoracic duct dilatation is suspected behind the descending aorta (arrow). Pleural effusion is absent. C, Coronal reformatted image with lung window setting shows the parenchymal lesions with vertical distribution.View Large Image Figure ViewerDownload Hi-res image Download (PPT) To obtain a definite diagnosis of the lung lesion and treat the pneumothorax, a video-assisted thoracoscopic lung biopsy with insertion of chest tube was performed in the left lung. Two days after the surgical biopsy, the pleural fluid via chest tube drainage became milky and the volume of the fluid increased from 400 mL/d to 900 mL/d. The fluid revealed an exudative effusion, with a fluid lactate dehydrogenase level of 474 U/L, fluid protein level of 2.5 g/dL, serum protein level of 4.9 g/dL, and fluid triglyceride level of 302 mg/dL. The cell count showed a leukocyte count of 2,900/uL (2% neutrophils, 97% lymphocytes) without evidence of malignancy. The patient was treated with somatostatin and a fat-free diet, followed by octreotide and nil per os with total parenteral nutrition. One month after the surgical lung biopsy, the chest tube was removed. However, after the removal of the chest tube, left pleural effusion reaccumulated and ill-defined opacification in the right lung was seen in a subsequent chest radiograph (Fig 3A). At that time, she complained of dyspnea, and the laboratory test revealed a leukocyte count of 1,590/uL, absolute neutrophil counts of 770/uL, and high-sensitivity C-reactive protein level of 0.72 mg/dL (0.01–0.47 mg/dL). We treated her empirically with antibiotics and chest tube reinsertion. The right parenchymal lesions regressed as the left effusion decreased (Fig 3B). Cultures of blood, urine, and sputum were all negative for microorganisms. Microscopic examination of the lung specimens showed that bronchial vessels were prominent along the interstitium, and multiple cysts were surrounded by smooth muscle-like cells (Fig 4A). The smooth muscle-like cells tested positive for smooth muscle actin, desmin, human melanoma black-45, estrogen receptor, and progesterone receptor (Fig 4B). Diagnosis: Postoperative chylothorax and interstitial lymphatic edema in lymphangioleiomyomatosis Lymphangioleiomyomatosis (LAM) is a rare cystic lung disease with a female predominance, especially during the fertile phase of life. It is a kind of neoplastic disorder caused by proliferation and lymphangiogenesis of abnormal smooth muscle-like cells and can evolve not only in the lung and axial lymphatic system but also in any organ close to the lymphatic system.1Seyama K Kumasaka T Kurihara M Mitani K Sato T Lymphangioleiomyomatosis: a disease involving the lymphatic system.Lymphat Res Biol. 2010; 8: 21-31Crossref PubMed Scopus (49) Google Scholar, 2Taveira-DaSilva AM Steagall WK Moss J Lymphangiomyomatosis.Cancer Contr. 2006; 13: 276-285PubMed Google Scholar LAM phenotypes are either idiopathic (sporadic LAM) or associated with tuberous sclerosis complex (TSC-LAM). TSC is a genetic disorder characterized by hamartomatous skin lesions, seizure disorders, brain tumors, and mental retardation. LAM occurs in about 30% to 40% of patients with TSC.3Moss J Avila NA Barnes PM et al.Prevalence and clinical characteristics of lymphangioleiomyomatosis (LAM) in patients with tuberous sclerosis complex.Am J Respir Crit Care Med. 2001; 164: 669-671Crossref PubMed Scopus (258) Google Scholar, 4Costello LC Hartman TE Ryu JH High frequency of pulmonary lymphangioleiomyomatosis in women with tuberous sclerosis complex.Mayo Clin Proc. 2000; 75: 591-594Abstract Full Text Full Text PDF PubMed Scopus (246) Google Scholar The average age at the diagnosis of sporadic LAM is about 35 years,5Ryu JH Moss J Beck GJ NHLBI LAM Registry Group et al.The NHLBI lymphangioleiomyomatosis registry: characteristics of 230 patients at enrollment.Am J Respir Crit Care Med. 2006; 173: 105-111Crossref PubMed Scopus (359) Google Scholar, 6Taylor JR Ryu J Colby TV Raffin TA Lymphangioleiomyomatosis. Clinical course in 32 patients.N Engl J Med. 1990; 323: 1254-1260Crossref PubMed Scopus (433) Google Scholar, 7Chu SC Horiba K Usuki J et al.Comprehensive evaluation of 35 patients with lymphangioleiomyomatosis.Chest. 1999; 115: 1041-1052Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar and TSC-LAM presents at a younger age than sporadic LAM.5Ryu JH Moss J Beck GJ NHLBI LAM Registry Group et al.The NHLBI lymphangioleiomyomatosis registry: characteristics of 230 patients at enrollment.Am J Respir Crit Care Med. 2006; 173: 105-111Crossref PubMed Scopus (359) Google Scholar Recent research has revealed that mutations of the tuberous sclerosis genes, TSC1 or TSC2, lead to inappropriate cellular proliferation, migration, and invasion through constitutive activation in the Akt/mammalian target of rapamycin (mTOR) signaling pathway, which causes LAM and TSC.8Strizheva GD Carsillo T Kruger WD Sullivan EJ Ryu JH Henske EP The spectrum of mutations in TSC1 and TSC2 in women with tuberous sclerosis and lymphangiomyomatosis.Am J Respir Crit Care Med. 2001; 163: 253-258Crossref PubMed Scopus (116) Google Scholar, 9Kenerson H Folpe AL Takayama TK Yeung RS Activation of the mTOR pathway in sporadic angiomyolipomas and other perivascular epithelioid cell neoplasms.Hum Pathol. 2007; 38: 1361-1371Abstract Full Text Full Text PDF PubMed Scopus (194) Google Scholar The European Respiratory Society's 2010 international guidelines for LAM proposed that the diagnosis of LAM should be classified as definite, probable, and possible according to the clinical, radiologic, and pathologic criteria (Table 1).10Johnson SR Cordier JF Lazor R et al.Review Panel of the ERS LAM Task Force European Respiratory Society guidelines for the diagnosis and management of lymphangioleiomyomatosis.Eur Respir J. 2010; 35: 14-26Crossref PubMed Scopus (400) Google Scholar They proposed that LAM can be diagnosed definitely without a lung biopsy by characteristic high-resolution CT (HRCT) scan and one of the typical manifestations, such as renal angiomyolipoma (AML), chylous effusion, lymph node involvement, or TSC. In our case, although the patient presented characteristic radiologic findings, she did not have any compatible clinical features except the first pneumothorax and had been healthy enough to enjoy scuba diving before admission. Therefore, a surgical lung biopsy was performed for the pathologic confirmation and the control of the pneumothorax.Table 1European Respiratory Society Guidelines for LAMClassificationDiagnostic CriteriaDefiniteCharacteristicaMultiple (>10) thin-walled cysts with no other significant pulmonary involvement with the exception of multifocal micronodular lesion in TSC. or compatiblebOnly few (>2 and ≤10) cysts. lung HRCT scan and lung biopsy fitting the pathologic criteriacTwo lesions: cysts and a multifocal nodular proliferation of immature smooth muscle and perivascular epithelioid (LAM) cells. for LAM orCharacteristic lung HRCT scan and any of the following: Angiomyolipoma (kidney) Thoracic or abdominal chylous effusion Lymphangioleiomyoma or lymph node involved by LAM Definite or probable TSCProbableCharacteristic HRCT scan and compatible clinical history orCompatible HRCT scan and any of the following: Angiomyolipoma (kidney) Thoracic or abdominal chylous effusionPossibleCharacteristic or abdominal chylous effusionHRCT = high-resolution CT; LAM = lymphangioleiomyomatosis; TSC = tuberous sclerosis complex.a Multiple (>10) thin-walled cysts with no other significant pulmonary involvement with the exception of multifocal micronodular lesion in TSC.b Only few (>2 and ≤10) cysts.c Two lesions: cysts and a multifocal nodular proliferation of immature smooth muscle and perivascular epithelioid (LAM) cells. Open table in a new tab HRCT = high-resolution CT; LAM = lymphangioleiomyomatosis; TSC = tuberous sclerosis complex. Progressive dyspnea, recurrent pneumothorax, and chylous fluid retention are common respiratory signs in LAM. Chylothorax occurs in 0% to 14% of patients with LAM at presentation and in 22% to 39% of patients during the course of the disease.6Taylor JR Ryu J Colby TV Raffin TA Lymphangioleiomyomatosis. Clinical course in 32 patients.N Engl J Med. 1990; 323: 1254-1260Crossref PubMed Scopus (433) Google Scholar, 7Chu SC Horiba K Usuki J et al.Comprehensive evaluation of 35 patients with lymphangioleiomyomatosis.Chest. 1999; 115: 1041-1052Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar, 11Urban T Lazor R Lacronique J et al.Pulmonary lymphangioleiomyomatosis. A study of 69 patients. Groupe d'Etudes et de Recherche sur les Maladies “Orphelines” Pulmonaires (GERM“O”P).Medicine (Baltimore). 1999; 78: 321-337Crossref PubMed Scopus (306) Google Scholar It develops because of obstruction or disruption of the thoracic duct or its branches. An individualized approach is recommended for management of LAM-associated chylothorax, depending on its extent and the symptoms. Ryu et al12Ryu JH Doerr CH Fisher SD Olson EJ Sahn SA Chylothorax in lymphangioleiomyomatosis.Chest. 2003; 123: 623-627Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar showed that thoracentesis or observation was sufficient to control the effusion in eight patients with LAM and chylothorax. On the other hand, they also reported that surgical management, such as thoracic duct ligation and pleurectomy, was required for three intractable cases. We note, however, that these surgical interventions may cause bleeding or technical difficulties during lung transplantation, which is the final therapeutic option in LAM. Pulmonary function tests in LAM show variable patterns. Nationwide epidemiologic studies of LAM reported that a decreased diffusing capacity of the lung for carbon monoxide (Dlco) and obstructive physiology with reduced FEV1 were the most common findings.5Ryu JH Moss J Beck GJ NHLBI LAM Registry Group et al.The NHLBI lymphangioleiomyomatosis registry: characteristics of 230 patients at enrollment.Am J Respir Crit Care Med. 2006; 173: 105-111Crossref PubMed Scopus (359) Google Scholar, 13Hayashida M Seyama K Inoue Y Fujimoto K Kubo K Respiratory Failure Research Group of the Japanese Ministry of Health, Labor, and Welfare The epidemiology of lymphangioleiomyomatosis in Japan: a nationwide cross-sectional study of presenting features and prognostic factors.Respirology. 2007; 12: 523-530Crossref PubMed Scopus (87) Google Scholar, 14Park HY Nam HS Chung MP et al.A nationwide survey of lymphangioleiomyomatosis in Korea: recent increase in newly diagnosed patients.J Korean Med Sci. 2010; 25: 1182-1186Crossref PubMed Scopus (14) Google Scholar An elevated total lung capacity and low FEV1/FVC were considered poor prognostic factors in the initial evaluation. Serial measurements of FEV1, Dlco, and exercise performance on tests such as the 6-min walk test might be helpful for monitoring the disease progression.15Taveira-DaSilva AM Pacheco-Rodriguez G Moss J The natural history of lymphangioleiomyomatosis: markers of severity, rate of progression and prognosis.Lymphat Res Biol. 2010; 8: 9-19Crossref PubMed Scopus (77) Google Scholar Taveira-DaSilva et al16Taveira-DaSilva AM Steagall WK Rabel A et al.Reversible airflow obstruction in lymphangioleiomyomatosis.Chest. 2009; 136: 1596-1603Abstract Full Text Full Text PDF PubMed Scopus (42) Google Scholar found that a positive bronchodilator response was found in one-half of patients with LAM, who later showed a rapid decline in disease status. It is recommended that in patients with LAM, a pulmonary function test should be performed at the initial evaluation and at regular intervals during the follow-up to assess disease severity, progression, and responses to treatment.10Johnson SR Cordier JF Lazor R et al.Review Panel of the ERS LAM Task Force European Respiratory Society guidelines for the diagnosis and management of lymphangioleiomyomatosis.Eur Respir J. 2010; 35: 14-26Crossref PubMed Scopus (400) Google Scholar The patient performed a pulmonary function test after discharge, and the result showed that FEV1, FEV1/FVC, Dlco, and TLC were 51%, 53%, 31%, and 83%, respectively, with a positive bronchodilator response of 19%. Medical treatments for LAM include antiestrogen therapy, mTOR inhibitors, and inhaled bronchodilators if needed. Although progesterone is the most commonly used treatment, it should be reserved for patients who exhibit a rapid decline in lung function or symptoms, because of lack of evidence of its efficacy. Regarding sirolimus as an mTOR inhibitor, McCormack et al17McCormack FX Inoue Y Moss J National Institutes of Health Rare Lung Diseases Consortium; MILES Trial Group et al.Efficacy and safety of sirolimus in lymphangioleiomyomatosis.N Engl J Med. 2011; 364: 1595-1606Crossref PubMed Scopus (814) Google Scholar recently showed that in 89 patients with LAM with moderate lung impairment, sirolimus treatment of 12 months improved symptoms and stabilized lung functions, although the beneficial effect disappeared after discontinuation of the drug. Therefore, sirolimus may be useful for selected patients, depending on their risk-benefit ratio. Lung transplantation is recommended as a final option for end-stage pulmonary LAM. Recent reports indicate that the prognosis may be better with 10-year survival rates of 78% to 91% than that reported in early studies.6Taylor JR Ryu J Colby TV Raffin TA Lymphangioleiomyomatosis. Clinical course in 32 patients.N Engl J Med. 1990; 323: 1254-1260Crossref PubMed Scopus (433) Google Scholar, 11Urban T Lazor R Lacronique J et al.Pulmonary lymphangioleiomyomatosis. A study of 69 patients. Groupe d'Etudes et de Recherche sur les Maladies “Orphelines” Pulmonaires (GERM“O”P).Medicine (Baltimore). 1999; 78: 321-337Crossref PubMed Scopus (306) Google Scholar,13Hayashida M Seyama K Inoue Y Fujimoto K Kubo K Respiratory Failure Research Group of the Japanese Ministry of Health, Labor, and Welfare The epidemiology of lymphangioleiomyomatosis in Japan: a nationwide cross-sectional study of presenting features and prognostic factors.Respirology. 2007; 12: 523-530Crossref PubMed Scopus (87) Google Scholar, 14Park HY Nam HS Chung MP et al.A nationwide survey of lymphangioleiomyomatosis in Korea: recent increase in newly diagnosed patients.J Korean Med Sci. 2010; 25: 1182-1186Crossref PubMed Scopus (14) Google Scholar The characteristic features of HRCT scan in LAM are multiple (>10), well-defined cysts and no other significant pulmonary involvement, such as interstitial lung disease, except for multifocal micronodular pneumocyte hyperplasia in TSC.10Johnson SR Cordier JF Lazor R et al.Review Panel of the ERS LAM Task Force European Respiratory Society guidelines for the diagnosis and management of lymphangioleiomyomatosis.Eur Respir J. 2010; 35: 14-26Crossref PubMed Scopus (400) Google Scholar Because multiple cysts appear in lung in some other diseases, such as Langerhans histiocytosis X, pulmonary fibrosis, emphysema, pneumatocele, lymphocytic interstitial pneumonia, and Birt-Hogg-Dube syndrome, LAM should be differentiated according to the clinical findings and the specific radiologic pattern. In LAM, proliferation around the wall of the terminal bronchioles causes small airway obstruction, resulting in air trapping, emphysema, and pneumothorax.18Kirchner J Stein A Viel K et al.Pulmonary lymphangioleiomyomatosis: high-resolution CT findings.Eur Radiol. 1999; 9: 49-54Crossref PubMed Scopus (52) Google Scholar Proliferation of the smooth muscle cells surrounding the lymphatic vessels causes obstruction and thickening of interstitial tissue, resulting in pleural effusion and interstitial lymphatic edema. However, in some cases, these interstitial changes may be explained by additional factors, such as intercurrent relapsing infections. In the present case, we considered first that the ill-defined parenchymal opacification in the right lower lobe developed from combined nosocomial pneumonia, because the right lung lesion became noticeable during the long-term chylothorax, which might have caused malnutrition and subsequently infection. However, follow-up chest radiographs showed the right lung abnormality worsened gradually as the left chylothorax progressed. In addition, the radiologic finding of the right lung showed an improvement with a resolution of the left chylothorax through chest tube drainage. Therefore, we speculate that the right parenchymal opacification was lymphedema, an uncommon manifestation of LAM. The abdominal manifestations of LAM are renal AML, lymphangioleiomyoma, lymphadenopathy, and chylous ascites.19Pallisa E Sanz P Roman A Majó J Andreu J Cáceres J Lymphangioleiomyomatosis: pulmonary and abdominal findings with pathologic correlation.Radiographics. 2002; 22: S185-S198Crossref PubMed Scopus (110) Google Scholar Renal AML is the most frequent abdominal finding and occurs in 50% of patients with LAM. Avila et al20Avila NA Dwyer AJ Rabel A Moss J Sporadic lymphangioleiomyomatosis and tuberous sclerosis complex with lymphangioleiomyomatosis: comparison of CT features.Radiology. 2007; 242: 277-285Crossref PubMed Scopus (101) Google Scholar demonstrated that sporadic LAM is associated with more extensive lung involvement and a higher frequency of lymphangioleiomyoma, whereas renal and hepatic AML are more common in TSC-LAM. Cysts and multifocal nodular proliferation of immature smooth muscle and perivascular epithelioid cells (LAM cells) are two characteristic lesions of the disease.10Johnson SR Cordier JF Lazor R et al.Review Panel of the ERS LAM Task Force European Respiratory Society guidelines for the diagnosis and management of lymphangioleiomyomatosis.Eur Respir J. 2010; 35: 14-26Crossref PubMed Scopus (400) Google Scholar, 21Corrin B Liebow AA Friedman PJ Pulmonary lymphangiomyomatosis. A review.Am J Pathol. 1975; 79: 348-382PubMed Google Scholar In most cases, LAM can be confirmed using hematoxylin and eosin staining of the lesion tissue with compatible clinical and radiologic findings. Immunohistochemistry is useful for the diagnosis because LAM specimens are mostly positive for the smooth muscle markers α-actin, desmin, vimentin, and human melanoma black-45. In 50% of LAM cases, the tissue is positive for the estrogen and progesterone receptor.22Matsui K Takeda K Yu ZX et al.Downregulation of estrogen and progesterone receptors in the abnormal smooth muscle cells in pulmonary lymphangioleiomyomatosis following therapy. An immunohistochemical study.Am J Respir Crit Care Med. 2000; 161: 1002-1009Crossref PubMed Scopus (120) Google Scholar The patient presented with spontaneous pneumothorax and developed intractable chylous pleural effusion subsequent to a surgical lung biopsy. The chylothorax lasted for about 2 months, and it was managed successfully through long-term nil per os with somatostatin/octreotide and repeated pleurodesis. During the treatment of the chylous effusion, the ill-defined parenchymal opacification in the right lung became obvious, and the lesion waxed and waned, depending on the rate of left chylous fluid drainage. Finally, we concluded that the radiologic finding of the right lung was a manifestation of lymphatic edema. Clinicians should keep in mind that LAM is associated not only with multiple cysts, pneumothorax, and pleural effusion but also with pulmonary parenchymal opacification, which could be difficult to differentiate from more common infectious pneumonia in routine practice." @default.
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• W2129606243 title "A 29-Year-Old Woman With an Intractable Postoperative Pleural Effusion and Pulmonary Parenchymal Opacification" @default.
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