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Purpose@#Tropomyosin receptor kinase (TRK) inhibitors are approved for the treatment of neurotrophic receptor tyrosine kinase (NTRK) fusion-positive tumors. The detection of NTRK fusion using a validated method is required before therapeutic application. An interlaboratory comparison study of next-generation sequencing (NGS)–based NTRK gene fusion detection with validated clinical samples was conducted at six major hospitals in South Korea. @*Materials and Methods@#A total of 18 samples, including a positive standard reference and eight positive and nine negative clinical samples, were validated using the VENTANA pan-TRK (EPR17341) and TruSight Oncology 500 assays. These samples were then tested using four different NGS panels currently being used at the six participating institutions. @*Results@#NTRK fusions were not detected in any of the nine negative clinical samples, demonstrating 100% specificity in all six participating institutions. All assays showed 100% analytical sensitivity to identify the NTRK fusion status in formalin-fixed paraffin-embedded (FFPE) samples, although with variable clinical sensitivity. False-negative results were due to low tumor purity, poor RNA quality, and DNA-based sequencing panel. The RNA-based targeted NGS assay showed an overall high success rate of identifying NTRK fusion status in FFPE samples. @*Conclusion@#This study is the first to test the proficiency of NGS-based NTRK detection in South Korea with the largest participating institutions. RNA-based NGS assays to detect NTRK fusions can accurately characterize fusion transcripts if sufficient RNA of adequate quality is available. The comparative performance data will support the implementation of targeted NGS-based sequencing assays for NTRK fusion detection in routine diagnostics.
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Purpose@#There are clinical unmet needs in predicting therapeutic response and precise strategy for the patient with advanced biliary tract cancer (BTC). We aimed to identify genomic alterations predicting therapeutic response and resistance to gemcitabine and cisplatin (Gem/Cis)-based chemotherapy in advanced BTC. @*Materials and Methods@#Genomic analysis of advanced BTC multi-institutional cohorts was performed using targeted panel sequencing. Genomic alterations were analyzed integrating patients’ clinicopathologic data, including clinical outcomes of Gem/Cis-based therapy. Significance of genetic alterations was validated using clinical next-generation sequencing (NGS) cohorts from public repositories and drug sensitivity data from cancer cell lines. @*Results@#193 BTC patients from three cancer centers were analyzed. Most frequent genomic alterations were TP53 (55.5%), KRAS (22.8%), ARID1A (10.4%) alterations, and ERBB2 amplification (9.8%). Among 177 patients with BTC receiving Gem/Cis-based chemotherapy, ARID1A alteration was the only independent predictive molecular marker of primary resistance showing disease progression for 1st-line chemotherapy in the multivariate regression model (odds ratio, 3.12; p=0.046). In addition, ARID1A alteration was significantly correlated with inferior progression-free survival on Gem/Cis-based chemotherapy in the overall patient population (p=0.033) and in patients with extrahepatic cholangiocarcinoma (CCA) (p=0.041). External validation using public repository NGS revealed that ARID1A mutation was a significant predictor for poor survival in BTC patients. Investigation of multi-OMICs drug sensitivity data from cancer cell lines revealed that cisplatin-resistance was exclusively observed in ARID1A mutant bile duct cancer cells. @*Conclusion@#Integrative analysis with genomic alterations and clinical outcomes of the first-line Gem/Cis-based chemotherapy in advanced BTC revealed that patients with ARID1Aalterations showed a significant worse clinical outcome, especially in extrahepatic CCA. Well-designed prospective studies are mandatory to validate the predictive role of ARID1Amutation.
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Purpose@#Neuregulin 1 (NRG1) gene fusion is a potentially actionable oncogenic driver. The oncoprotein binds to ERBB3-ERBB2 heterodimers and activates downstream signaling, supporting a therapeutic approach for inhibiting ERBB3/ERBB2. However, the frequency and clinicopathological features of solid tumors harboring NRG1 fusions in Korean patients remain largely unknown. @*Materials and Methods@#We reviewed archival data from next-generation sequencing panel tests conducted at a single institution, specifically selecting patients with in-frame fusions that preserved the functional domain. The clinicopathological characteristics of patients harboring NRG1 fusions were retrospectively reviewed. @*Results@#Out of 8,148 patients, NRG1 fusions were identified in 22 patients (0.27%). The average age of the patients was 59 years (range, 32 to 78 years), and the male-to-female ratio was 1:1.2. The lung was the most frequently observed primary site (n=13), followed by the pancreaticobiliary tract (n=3), gastrointestinal tract (n=2, stomach and rectum each), ovary (n=2), breast (n=1), and soft tissue (n=1). Histologically, all tumors demonstrated adenocarcinoma histology, with the exception of one case of sarcoma. CD74 (n=8) and SLC3A2 (n=4) were the most frequently identified fusion partners. Dominant features included the presence of fewer than three co-occurring genetic alterations, a low tumor mutation burden, and low programmed death-ligand 1 expression. Various clinical responses were observed in patients with NRG1 fusions. @*Conclusion@#Despite the rarity of NRG1 fusions in Korean patients with solid tumors, identification through next-generation sequencing enables the possibility of new targeted therapies.
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Purpose@#Preclinical data indicate that response to radiotherapy (RT) depends on DNA damage repair. In this study, we investigated the role of mutations in genes related to DNA damage repair in treatment outcome after RT. @*Materials and Methods@#Patients with solid tumor who participated in next generation sequencing panel screening using biopsied tumor tissue between October 2013 and February 2019 were reviewed and 97 patients that received RT were included in this study. Best response to RT and the cumulative local recurrence rate (LRR) were compared according to absence or presence of missense, nonsense, and frameshift mutations in ATM and/or BRCA1/2. @*Results@#Of the 97 patients, five patients harbored mutation only in ATM, 22 in only BRCA1/2, and six in both ATM and BRCA1/2 (ATMmtBRCAmt). Propensity score matching was performed to select the control group without mutations (ATMwtBRCAwt, n=33). In total, 90 RT-treated target lesions were evaluated in 66 patients. Highest objective response rate of 80% was observed in ATMmtBRCAmt lesions (p=0.007), which was mostly durable. Furthermore, the cumulative 1-year LRR was the lowest in ATMmtBRCAmt lesions and the highest in ATMwtBRCAwt lesions (0% vs. 47.9%, p=0.008). RT-associated toxicities were observed in 10 treatments with no significant difference among the subgroups (p=0.680). @*Conclusion@#Tumors with ATM and BRCA1/2 mutations exhibited superior tumor response and local control after RT compared to tumors without these mutations. The results are hypothesis generating and suggest the need for integrating the tumor mutation profile of DNA repair genes during treatment planning.
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Background/Aims@#Intrahepatic cholangiocarcinoma (iCCA) with a ductal plate malformation (DPM) pattern is a recently recognized rare variant. The genomic profile of iCCA with DPM pattern needs to be elucidated. @*Methods@#Cases of iCCA with DPM pattern were retrospectively reviewed based on the medical records, pathology slides, and magnetic resonance imaging (MRI) reports collected between 2010 to 2019 at a single center. Massive parallel sequencing was performed for >500 cancerrelated genes. @*Results@#From a total of 175 iCCAs, five (2.9%) cases of iCCA with DPM pattern were identified. All cases were of the small duct type, and background liver revealed chronic B viral or alcoholic hepatitis. Three iCCAs with DPM pattern harbored MRI features favoring the diagnosis of hepatocellular carcinoma, whereas nonspecific imaging features were observed in two cases. All patients were alive without recurrence during an average follow-up period of 57 months. Sequencing data revealed 64 mutated genes in the five cases, among which FGFR2 and PTPRT were most frequently mutated (three cases each) including an FGFR2-TNC fusion in one case. Mutations in ARID1A and CDKN2A were found in two cases, and mutations in TP53, BAP1, ATM, NF1, and STK11 were observed in one case each. No IDH1, KRAS, or PBRM1 mutations were found. @*Conclusions@#iCCAs with DPM pattern have different clinico-radio-pathologic and genetic characteristics compared to conventional iCCAs. Moreover, FGFR2 and FGFR2 variants were identified. Altogether, these findings further suggest that iCCA with DPM pattern represents a specific subtype of small duct type iCCA.
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Molecular biomarker testing is the standard of care for non–small cell lung cancer (NSCLC) patients. In 2017, the Korean Cardiopulmonary Pathology Study Group and the Korean Molecular Pathology Study Group co-published a molecular testing guideline which contained almost all known genetic changes that aid in treatment decisions or predict prognosis in patients with NSCLC. Since then there have been significant changes in targeted therapies as well as molecular testing including newly approved targeted drugs and liquid biopsy. In order to reflect these changes, the Korean Cardiopulmonary Pathology Study Group developed a consensus statement on molecular biomarker testing. This consensus statement was crafted to provide guidance on what genes should be tested, as well as methodology, samples, patient selection, reporting and quality control.
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Molecular biomarker testing is the standard of care for non–small cell lung cancer (NSCLC) patients. In 2017, the Korean Cardiopulmonary Pathology Study Group and the Korean Molecular Pathology Study Group co-published a molecular testing guideline which contained almost all known genetic changes that aid in treatment decisions or predict prognosis in patients with NSCLC. Since then there have been significant changes in targeted therapies as well as molecular testing including newly approved targeted drugs and liquid biopsy. In order to reflect these changes, the Korean Cardiopulmonary Pathology Study Group developed a consensus statement on molecular biomarker testing. This consensus statement was crafted to provide guidance on what genes should be tested, as well as methodology, samples, patient selection, reporting and quality control.
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Purpose@#With changing fungal epidemiology and azole resistance in Aspergillus species, identifying fungal species and susceptibility patterns is crucial to the management of aspergillosis and mucormycosis. The objectives of this study were to evaluate performance of panfungal polymerase chain reaction (PCR) assays on formalin-fixed paraffin embedded (FFPE) samples in the identification of fungal species and in the detection of azole-resistance mutations in the Aspergillus fumigatus cyp51A gene at a South Korean hospital. @*Materials and Methods@#A total of 75 FFPE specimens with a histopathological diagnosis of aspergillosis or mucormycosis were identified during the 10-year study period (2006–2015). After deparaffinization and DNA extraction, panfungal PCR assays were conducted on FFPE samples for fungal species identification. The identified fungal species were compared with histopathological diagnosis. On samples identified as A. fumigatus, sequencing to identify frequent mutations in the cyp51A gene [tandem repeat 46 (TR46), L98H, and M220 alterations] that confer azole resistance was performed. @*Results@#Specific fungal DNA was identified in 31 (41.3%) FFPE samples, and of these, 16 samples of specific fungal DNA were in accord with a histopathological diagnosis of aspergillosis or mucormycosis; 15 samples had discordant histopathology and PCR results. No azole-mediating cyp51A gene mutation was noted among nine cases of aspergillosis. Moreover, no cyp51A mutations were identified among three cases with history of prior azole use. @*Conclusion@#Panfungal PCR assay with FFPE samples may provide additional information of use to fungal species identification. No azole-resistance mediating mutations in the A. fumigatus cyp51A gene were identified among FFPE samples during study period.
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Purpose@#Epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and ROSproto-oncogene 1 (ROS1) are ‘must-test’ biomarkers in the molecular diagnostics of advanced-stage lung cancer patients. Although single-gene assays are currently considered thegold standard for these genes, next-generation sequencing (NGS) tests are being introducedto clinical practices. We compared the results of current diagnostics and aimed to suggesttimely effective guidance for their clinical use. @*Materials and Methods@#Patients with lung cancer who received both conventional single-gene assays and subsequenttargeted NGS testing were enrolled, and the results of their tests were compared. @*Results@#A total of 241 patients were enrolled, and the EGFR real-time polymerase chain reaction,ALK fluorescence in situ hybridization (FISH), and ROS1 FISH assays exhibited 92.9%,99.6%, and 99.5% concordance with the NGS tests, respectively. The discordant cases weremostly false-negatives of the single-gene assays, probably due to technical limitation. Of158 cases previously designated as wild-type, EGFR, ALK, and ROS1 alterations were identifiedin 10.1%, 1.9%, and 1.3%, respectively, and other targetable alterations were identifiedin 36.1% of the cases. Of patients with additionally identified actionable alterations, 32.6%(31/95) received matched therapy with a clinical benefit of 48.4% (15/31). @*Conclusion@#Even though the conventional and NGS methods were concordant in the majority of cases,NGS testing still revealed a considerable number of additional EGFR, ALK, and ROS1 alterations,as well as other targetable alterations, in Korean advanced-stage lung cancer patients.Given the high frequency of EGFR and other targetable mutations identified in thepresent study, NGS testing is highly recommended in the diagnosis of Korean lung cancerpatients.
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Organizing pneumonia is characterized histologically by the formation of granulation-tissue plugs within the lumens of small airways. It was reported in association with various disorders including infection, drug reactions and collagen vascular diseases. However, there have been only a few reports on organizing pneumonia accompanied by systemic lupus erythematosus (SLE), especially in the pediatric population. Herein, we report a case of an adolescent with SLE who initially developed respiratory illnesses due to organizing pneumonia. A 14-year-old girl was referred to our clinic for protracted cough with fever, dyspnea, and hemoptysis. Her chest x-ray revealed predominant multifocal consolidations in bilateral lung fields with pleural effusion. Computed tomography scan showed patchy consolidations with surrounding ground-glass opacities and a crazy paving appearance with multiple centrilobular nodules. Laboratory tests exhibited pancytopenia, elevated blood urea nitrogen and creatinine, proteinuria, low serum levels of complements, and positivity for antinuclear antibody and anti-double-stranded DNA antibody, which were suggestive of SLE. Lung biopsy was performed to exclude the possibility of vasculitis and other mixed connective tissue diseases, which confirmed focal organizing pneumonia. Systemic steroid therapy, including high-dose methylprednisolone, was started. After the treatment, her respiratory symptoms and radiologic findings showed significant improvements. The patient has been followed up so far, and she has remined disease-free. This pediatric case of organizing pneumonia as the initial presentation of SLE alerts clinicians to consider thorough assessment of pulmonary manifestations of SLE in children.
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Liquid biopsy for detection of mutation from circulating tumor DNA is a new technology which is attractive in that it is non-invasive. Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) is an effective first line drug for advanced non-small cell lung cancer patients who harbor activating EGFR mutation. During the course of treatment, resistance against TKI arises which can be contributed to EGFR T790M mutation in about 50–60% of patients. Third generation TKI may overcome the resistance. In patients who cannot undergo tissue biopsy due to variable reasons, liquid biopsy is an excellent alternative for the detection of EGFR T790M mutation. However, this relatively novel method requires standardization and vigorous quality insurance. Thus, a standard set of guideline recommendations for liquid biopsy for EGFR mutation testing suitable for the Korean medical community is necessary. In this article, we propose a set of provisional guideline recommendations that was discussed and approved by the Cardiopulmonary Pathology Study Group of the Korean Society of Pathologists.
Subject(s)
Humans , Biopsy , Carcinoma, Non-Small-Cell Lung , DNA , Genes, erbB-1 , Insurance , Lung Neoplasms , Lung , Methods , Pathology , Protein-Tyrosine Kinases , ErbB ReceptorsABSTRACT
Next-generation sequencing (NGS) has recently emerged as an essential component of personalized cancer medicine due to its high throughput and low per-base cost. However, no sufficient guidelines for implementing NGS as a clinical molecular pathology test are established in Korea. To ensure clinical grade quality without inhibiting adoption of NGS, a taskforce team assembled by the Korean Society of Pathologists developed laboratory guidelines for NGS cancer panel testing procedures and requirements for clinical implementation of NGS. This consensus standard proposal consists of two parts: laboratory guidelines and requirements for clinical NGS laboratories. The laboratory guidelines part addressed several important issues across multistep NGS cancer panel tests including choice of gene panel and platform, sample handling, nucleic acid management, sample identity tracking, library preparation, sequencing, analysis and reporting. Requirements for clinical NGS tests were summarized in terms of documentation, validation, quality management, and other required written policies. Together with appropriate pathologist training and international laboratory standards, these laboratory standards would help molecular pathology laboratories to successfully implement NGS cancer panel tests in clinic. In this way, the oncology community would be able to help patients to benefit more from personalized cancer medicine.
Subject(s)
Humans , Consensus , High-Throughput Nucleotide Sequencing , Korea , Pathology, Molecular , Practice Guidelines as Topic , Quality ControlABSTRACT
Targeted therapies guided by molecular diagnostics have become a standard treatment of lung cancer. Epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) rearrangements are currently used as the best predictive biomarkers for EGFR tyrosine kinase inhibitors and ALK inhibitors, respectively. Besides EGFR and ALK, the list of druggable genetic alterations has been growing, including ROS1 rearrangements, RET rearrangements, and MET alterations. In this situation, pathologists should carefully manage clinical samples for molecular testing and should do their best to quickly and accurately identify patients who will benefit from precision therapeutics. Here, we grouped molecular biomarkers of lung cancers into three categories—mutations, gene rearrangements, and amplifications—and propose expanded guidelines on molecular testing of lung cancers.
Subject(s)
Humans , Biomarkers , Gene Rearrangement , Lung Neoplasms , Lung , Lymphoma , Pathology, Molecular , Phosphotransferases , Precision Medicine , Protein-Tyrosine Kinases , ErbB ReceptorsABSTRACT
Rearrangement of anaplastic lymphoma kinase (ALK) gene is the best predictor of response to crizotinib, an ALK tyrosine kinase inhibitor. However, the prevalence of the ALK fusion is low, so accurate patient identification is crucial for successful treatment using ALK inhibitors. Furthermore, most patients with lung cancer present with advanced-stage disease at the time of diagnosis, so it is important for pathologists to detect ALK-rearranged patients while effectively maximizing small biopsy or cytology specimens. In this review, we propose a guideline recommendation for ALK testing approved by the Cardiopulmonary Pathology Study Group of the Korean Society of Pathologists.
Subject(s)
Humans , Biopsy , Diagnosis , Gene Rearrangement , Lung Neoplasms , Lung , Lymphoma , Pathology , Phosphotransferases , Prevalence , Protein-Tyrosine KinasesABSTRACT
Transglutaminase 2 (TG2), a cross-linking enzyme, is involved in drug resistance and in the constitutive activation of nuclear factor kappa B (NF-kappaB). We investigated the association of non-small cell lung cancer (NSCLC) treatment efficacy with TG2 and NF-kappaB expression in 120 patients: 102 with adenocarcinoma and 18 with other histologic types. All patients underwent surgery; 88 received adjuvant chemotherapy, with 28 receiving platinum-based doublet chemotherapy as first-line treatment and 29 receiving epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) therapy. Patients' TG2 and NF-kappaB expression values were calculated semiquantitatively. The median TG2 value was 50 (range, 0-300) and the median NF-kappaB value was 20 (range, 0-240). Disease-free survival did not differ between the low- and high-TG2 groups. Among patients who received palliative platinum-based doublet chemotherapy, progression free survival (PFS) was longer in the low-TG2 group than in the high-TG2 group (11.0 vs. 7.0 months; P=0.330). Among those who received EGFR-TKI therapy, PFS was also longer in the low-TG2 group than in the high-TG 2 group (11.0 vs. 2.0 months; P=0.013). Similarly, in EGFR wild-type patients treated with EGFR-TKI, PFS was longer in patients with low TG2 expression (9.0 vs. 2.0 months; P=0.013). TG2 expression levels can predict PFS in patients with NSCLC treated with EGFR-TKI.
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Adenocarcinoma/drug therapy , Antineoplastic Agents/therapeutic use , Carcinoma, Non-Small-Cell Lung/drug therapy , Disease-Free Survival , GTP-Binding Proteins/biosynthesis , Lung Neoplasms/drug therapy , NF-kappa B/biosynthesis , Protein Kinase Inhibitors/therapeutic use , ErbB Receptors/antagonists & inhibitors , Transglutaminases/biosynthesis , Treatment OutcomeABSTRACT
BACKGROUND: Plasminogen activator inhibitor type 1 (PAI-1), an important regulator of plasminogen activator system which controls degradation of extracellular membrane and progression of tumor cells, and PAI-1 gene polymorphic variants have been known as the prognostic biomarkers of non-small cell lung cancer patients. Recently, experimental in vitro study revealed that transforming growth factor-beta1 initiated PAI-1 transcription through epithelial growth factor receptor (EGFR) signaling pathway. However, there is little clinical evidence on the association between PAI-1 A15T gene polymorphism and prognosis of Korean population with pulmonary adenocarcinoma and the influence of activating mutation of EGFR kinase domain. METHODS: We retrospectively reviewed the medical records of 171 patients who were diagnosed with pulmonary adenocarcinoma and undergone EGFR mutation analysis from 1995 through 2009. RESULTS: In all patients with pulmonary adenocarcinoma, there was no significant association between PAI-1 A15T polymorphic variants and prognosis for overall survival. However, further subgroup analysis showed that the group with AG/AA genotype had a shorter 3-year survival time than the group with GG genotype in patients with EGFR mutant-type pulmonary adenocarcinoma (mean survival time, 24.9 months vs. 32.5 months, respectively; p=0.015). In multivariate analysis of 3-year survival for patients with pulmonary adenocarcinoma harboring mutant-type EGFR, the AG/AA genotype carriers had poorer prognosis than the GG genotype carriers (hazard ratio, 7.729; 95% confidence interval, 1.414-42.250; p=0.018). CONCLUSION: According to our study of Korean population with pulmonary adenocarcinoma, AG/AA genotype of PAI-1 A15T would be a significant predictor of poor short-term survival in patients with pulmonary adenocarcinoma harboring mutant-type EGFR.
Subject(s)
Humans , Adenocarcinoma , Biomarkers , Carcinoma, Non-Small-Cell Lung , Genotype , Medical Records , Membranes , Multivariate Analysis , Phosphotransferases , Plasminogen Activator Inhibitor 1 , Plasminogen Activators , Plasminogen , Polymorphism, Single Nucleotide , Prognosis , ErbB Receptors , Retrospective StudiesABSTRACT
Mutations of the epidermal growth factor receptor (EGFR) are the strongest predictive factor for response to EGFR tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib. EGFR TKIs are approved in Korea as a first-line treatment for lung cancer patients with mutated EGFR. Rapid and accurate EGFR mutation testing is essential for patient selection and establishing targeted therapies with EGFR TKIs. Thus, a standard set of guideline recommendations for EGFR mutation testing suitable for the Korean medical community is necessary. In this article, we propose a set of guideline recommendations for EGFR mutation testing that was discussed and approved by the Cardiopulmonary Pathology Study Group of the Korean Society of Pathologists.
Subject(s)
Humans , Korea , Lung , Lung Neoplasms , Patient Selection , Protein-Tyrosine Kinases , Quinazolines , ErbB Receptors , Erlotinib HydrochlorideABSTRACT
We report a case of Caplan's Syndrome, which presented as multiple pulmonary nodules. A 58-year-old male was admitted to hospital due to multiple pulmonary nodules. In addition, the patient presented with multiple arthritis, and dyspnea on exertion. Rheumatoid arthritis had been diagnosed 35 years ago. The patient had worked as a stonemason for 20 years. Computed Tomography (CT) revealed numerous well-defined tiny nodules scattered in both lungs, which was suspicious of miliary tuberculosis or malignancy. The patient was started on antituberculous medications and referred to our hospital. First, a transbronchial lung biopsy was performed, which showed no evidence of granuloma. It was our opinion that the biopsy was insufficient, and a follow-up video-associated thoracoscopy was performed. The pathological report determined necrotizing granulomatous inflammation and silicosis on background. According to imaging studies, pathologic reports, and clinical symptoms, we concluded that the patient had Caplan's syndrome. We controlled his rheumatic medications, and instructed him to avoid exposure to hazardous dust.
Subject(s)
Humans , Male , Middle Aged , Arthritis , Arthritis, Rheumatoid , Biopsy , Caplan Syndrome , Dust , Dyspnea , Follow-Up Studies , Granuloma , Inflammation , Lung , Multiple Pulmonary Nodules , Silicosis , Thoracoscopy , Tuberculosis, MiliaryABSTRACT
We report a case of Mycobacterium intracellulare pulmonary infection presenting as a solitary pulmonary nodule (SPN). A 35-year-old male was admitted due to a SPN in the right upper lobe which was detected on the chest radiography being examed due to recurrent cough for 1 year. The computed tomography (CT) revealed a spiculated nodule containing air-bronchogram, which was suspicious of malignancy. We performed transbronchial biopsy and the pathology showed granulomatous inflammation with caseous necrosis. Under the presumptive diagnosis of pulmonary tuberculosis, we started anti-tuberculous medication including isoniazid, rifampin, ethambutol, and pyrazinamide. In one month, however, the sputum culture was positive for Mycobacterium intracellulare. The follow-up chest CT showed slight aggravation of the previous lesions. Under the final diagnosis of Mycobacterium intracellulare pulmonary infection presenting as a solitary pulmonary nodule, we changed the regimen to rifampin, ethambutol, and clarithromycin. The follow-up chest CT after the completion of treatment, revealed resolution of the previous lesions.
Subject(s)
Adult , Humans , Male , Biopsy , Clarithromycin , Cough , Ethambutol , Follow-Up Studies , Inflammation , Isoniazid , Lung , Lung Diseases , Mycobacterium avium Complex , Mycobacterium Infections, Nontuberculous , Necrosis , Pyrazinamide , Rifampin , Solitary Pulmonary Nodule , Sputum , Thorax , Tuberculosis , Tuberculosis, PulmonaryABSTRACT
We report a case of Mycobacterium intracellulare pulmonary infection presenting as a solitary pulmonary nodule (SPN). A 35-year-old male was admitted due to a SPN in the right upper lobe which was detected on the chest radiography being examed due to recurrent cough for 1 year. The computed tomography (CT) revealed a spiculated nodule containing air-bronchogram, which was suspicious of malignancy. We performed transbronchial biopsy and the pathology showed granulomatous inflammation with caseous necrosis. Under the presumptive diagnosis of pulmonary tuberculosis, we started anti-tuberculous medication including isoniazid, rifampin, ethambutol, and pyrazinamide. In one month, however, the sputum culture was positive for Mycobacterium intracellulare. The follow-up chest CT showed slight aggravation of the previous lesions. Under the final diagnosis of Mycobacterium intracellulare pulmonary infection presenting as a solitary pulmonary nodule, we changed the regimen to rifampin, ethambutol, and clarithromycin. The follow-up chest CT after the completion of treatment, revealed resolution of the previous lesions.