Subcarinal Adenopathy Research Articles

A RARE PRESENTATION OF SMALL CELL LUNG CARCINOMA METASTASIZING TO PHEOCHROMOCYTOMA

Abstract Introduction/Objective Tumor-to-tumor metastasis is a rare phenomenon in which primary tumor cells metastasize hematogenously into another unrelated tumor. We report an interesting case of a tumor-to-tumor metastasis of small cell lung carcinoma to pheochromocytoma of the adrenal gland. Methods/Case Report A 75-year-old female former cigarette smoker with a past medical history of hypertension presented with a two-day history of dyspnea and epigastric pain. Physical examination demonstrated elevated blood pressure only. A computerized axial tomography scan of the chest and abdomen showed an incidental 3.1 cm right adrenal mass and right hilar lymphadenopathy. Detailed biochemical workup showed elevated serum epinephrine, norepinephrine, and 24-hour urine metanephrine. Adrenalectomy showed a 5.8 cm tumor mass with solid lobulated yellow to pink-tan and focally hemorrhagic cut surfaces. Microscopic examination showed a neoplasm composed of two distinct components. The predominant component consisted of nests ("zellballen") of large polygonal cells with variable nuclear pleomorphism, abundant amphophilic to basophilic cytoplasm, and a delicate intervening fibrovascular stroma, without significant mitotic activity. The minor component was characterized by sheets and nests of "small blue cells" with round to ovoid nuclei, stippled nuclear chromatin pattern, scanty cytoplasm, patchy necrosis, and high mitotic activity (>20 mitoses per 10 HPF). Foci of small cell carcinoma deposits were also present in the lymphatic channels of pheochromocytoma. Immunohistochemical stains demonstrated cytoplasmic staining of predominant component tumor cells for synaptophysin, chromogranin, and the absence of staining for TTF-1, CK CAM 5.2, and Ki-67. However, minor component tumor cells demonstrated cytoplasmic staining for synaptophysin, membranous staining for CK CAM 5.2, and nuclear staining for TTF-1 and Ki-67(60%). A final diagnosis of composite pheochromocytoma (predominant) and small cell neuroendocrine carcinoma (minor) was rendered. The possibility of a” collision” tumor comprising primary small cell carcinoma of pulmonary origin metastatic to an adrenal pheochromocytoma in light of the patient's cigarette smoking history and the presence of right hilar lymphadenopathy was favored. The subsequent biopsy of the right subcarinal adenopathy showed small cell carcinoma. Results (if a Case Study enter NA) NA Conclusion To the best of our knowledge, this is the only case of metastasis to a pheochromocytoma from a small cell neuroendocrine lung carcinoma.

INDEPENDENT PERITONEAL CANCER, NEARLY MISSED AS A METASTASIS FROM LUNG CANCER

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Lung carcinoma is the leading cause of cancer-related mortality and nearly 50% of cases exhibit distal metastasis at the time of diagnosis. The most common sites of metastasis are brain, spine, nerve, adrenal gland, bone, liver, pleura, but rarely involves the peritoneum.[1] Peritoneal involvement in lung cancer is assumed to be due to metastasis from primary lung cancer. The occurrence of primary peritoneal adenocarcinoma and lung cancer together in one person is uncommon and difficult to distinguish from the metastatic spread. [2] CASE PRESENTATION: A 73-year-old female, smoker of 30 pack-year, presented with symptoms of abdominal bloating, distension, and loss of appetite. Computed tomography(CT) chest, abdomen, and pelvis showed moderate abdominal ascites consistent with peritoneal carcinomatosis, along with a 4.3 cm mass in the left lower lobe of the lung and 1.1 cm left-sided mediastinal lymph node. Paracentesis with ascitic fluid analysis was positive for adenocarcinoma. [Picture 1] She underwent endobronchial ultrasound with biopsy with immunohistochemistry staining which showed poorly differentiated squamous cell carcinoma [Picture 2]. Metastatic workup with a magnetic resonance imaging(MRI) of the brain was negative. Positron emission tomography-computed tomography scan showed a Fluorodeoxyglucose avid left lower lobe lung lesion with hilar and subcarinal adenopathy, consistent with primary lung malignancy. Pelvic ultrasound showed enlarged uterus secondary to multiple intramural fibroids. Labs showed Carcinoembryonic antigen level 1.2 and Alpha-fetoprotein 1.6. Oncology planned to start on carboplatin and paclitaxel along with pembrolizumab every 3 weeks for 4 cycles, followed by maintenance therapy with pembrolizumab every 3 weeks. She reported improvement in the abdominal bloating with the removal of 2-3 liter of peritoneal fluid weekly and symptomatic treatment. The patient continued to feel excessively tired and deteriorated within a few weeks. Unfortunately, the patient passed away before the start of the treatment. DISCUSSION: Peritoneal metastasis of primary lung carcinoma is very rare, only present in 2.7–16% of all lung cancer patients.[3] Advanced stage IV non-small cell lung cancer (NSCLC) and peritoneal adenocarcinoma can present in the same patient together, like in our case, which can be easily missed assuming it as metastatic cancer. Management of two separate cancers requires individualized treatment plans dissimilar to standard practices in the setting of a single tumor. A 1-year survival rate after cytotoxic chemotherapy is only 29% in patients with advanced NSCLC hence priority must be given to the treatment regimen that improves symptoms and prolongs survival. CONCLUSIONS: Therefore, one should always be suspicious and more effort should be made to improve the diagnostic approach and management to rule out any other underlying malignancy. Reference #1: McNeill PM, Wagman LD, Neifeld JP. Small bowel metastases from primary carcinoma of the lung. Cancer. 1987;59:1486–1489. Reference #2: MARÍA SERENO,1. Lung cancer and peritoneal carcinomatosis. Oncol Lett. 2013 Sep; 6(3): 705–708 Reference #3: Abrams HL, Spiro R, Goldstein N. Metastases in carcinoma; analysis of 1000 autopsied cases. Cancer. 1950;3:74–85. DISCLOSURES: No relevant relationships by Mary Grace Bethala, source=Web Response No relevant relationships by Apurwa Karki, source=Web Response No relevant relationships by Salman Khan, source=Web Response No relevant relationships by Shobha Mandal, source=Web Response

Post renal transplant pulmonary nocardiosis - A case report

Nocardiosis is a rare opportunistic infection caused by an aerobic actinomycete, producing either local or disseminated disease. It is a systemic infection that usually begins in the lungs and has high predilection for brain, skin and subcutaneous tissues. It commonly affects solid organ transplant recipients on immunosuppressive drugs. The incidence of nocardiosis in solid organ transplant recipients is about 0.6%. In India, nocardiosis was reported in 1.4% of renal transplant recipients. We report a case of pulmonary nocardiosis in a postrenal transplant recipient. Patient presented with features suggestive of pneumonia not responding to antibiotics. Initial sputum gram stain and AFB was negative. Chest radiograph showed right parahilar non-homogenous opacity, and CT chest revealed right parahilar, and subcarinal adenopathy. Bronchoscopy was done which showed purulent secretion from right 6th bronchial segment and AFB stain of broncho alveolar lavage fluid, showed weak acid fast filamentous bacteria, suggestive of nocardiosis. Patient was treated with antibiotics imipenem and co-trimoxazole. Patient responded well to treatment and pneumonia was resolved.

P50 A Case of a Patient Harboring an EGFR -T790M Mutation Positive in Squamous Cell Lung Cancer

Actually, the treatment of lung cancer who express driver mutations consist in block this target, the majority of this patients has an adenocarcinoma histology only few of them has the squamous type. We describe a case report of a 58-year-old female, non-smoker, with a persistent cough of 2 months of evolution. On May 2016, the CT scan reported lesion of 72x56mm in right segment 6, infiltration of hilum, pulmonary artery and mediastinal adenopathies. No extrathoracic disease. Biopsy: squamous cell carcinoma. Since the lesion was considered unresectable, she initiates concurrent ChT-RT (cisplatin / gemzar). After the 4th application, local progression was evidenced. Mutation studies, showed EGFRm Exon 19. She starts treatment with Afatinib (40mg / d) but, after 2 weeks, presented G3 gastrointestinal toxicity, so a dose-adjustment to 30mg / d was performed, G2 dermal toxicity also was reported. By December 2016, due to the response obtained, a medial and inferior lobectomy was performed. Pathological report (PR): middle lobe: pneumonitis. Lower lobe: squamous carcinoma. T: 3.5cm, G1, LVI (+), parenchymal margin (+). A PET / CT scan 4 weeks after the surgery, demonstrating right parahilar hypermetabolic lesion, pleural nodules and subcarinal adenopathy. The systemic treatment was restart in January 2017 with erlotinib 150mg /d. A PET / CT control 2 months later just showed slight metabolism in subcarinal adenopathy. She remains asymptomatic until October 2017, when presented aphasia and behavioral alterations. MRI: single left cortico-subcortical lesion of 2.2 x 2 cm with edema and subfalcial herniation. An hypo-fractionated radiotherapy scheme with corticoids was programmed but with minimal benefit. Six weeks after having completed RT (December 2017), greater neurological involvement is evidenced associated with weakness in lower limbs. MRI: lesion of 17.6 x17.3mm with contrast hyper-uptake and edema. CT thorax: no evidence of disease. Considering these findings and clinical deterioration a cerebral metastasectomy was performed. PR: squamous cell carcinoma. EGFRm deletion 19 (+) T790M (+). Due to the post-surgery clinical deterioration, the patient did not receive systemic treatment until March 2018, CT scan: multiple subcarinal adenopathies, contralateral pulmonary nodules and a 6mm nodule in the right lobe of the cerebellum. Patient is currently under treatment with osimertinib, with clinical neurological recovery and no respiratory symptoms. The use of TKI in SQCLC has a benefit in this patient, but the magnitude of this could be lower than adenocarcinoma according with a few series. However, this does not seem to be the case.

Predictive value of the early metabolic response in patients with advanced-stage non-small cell lung cancer

Fig. 1. Maximum intensity projection PET images. Axial fused PET/CT images. (A) Initial study. Increased uptake of F-FDG (SUVmax 7.6) in the nodule located in the anterior segment, upper lobe of the left lung (1). Radiotracer uptake in subcarinal adenopathy (SUVmax 9.1) related to tumor involvement (2). Heterogeneous metabolic activity in the left pleura, more intense in the middle posterior region (SUVmax 11.6) related to tumor implants (3). (B) Early response assessment (one month). Resolution of the initial metabolic activity in the nodule located in the left upper lobe of the lung (1), in the subcarinal adenopathy (2), and in the middle posterior pleural implant (3). An early complete metabolic response is observed.

Symptomatic hypercalcaemia in paediatric tuberculosis

To the Editors: A 13-yr-old Congolese female presented in early spring with a 6-month history of productive cough, progressive exertional dyspnoea and weight loss of 4.5 kg. 2 weeks prior to presentation she had developed high fevers and increasing lethargy. She had immigrated to the UK at the age of 2 yrs. She had not been overseas since and there was no history of contact with anyone with tuberculosis (TB). She had no past medical history and was fully immunised except for bacilli Calmette–Guerin. On examination she was cachectic and lethargic. There were no signs of clubbing, rickets or oedema. Her weight was 34 kg (less than third centile), height 148 cm (10th centile) and body mass index 15 kg·m−2 (less than first centile). She was tachycardic and tachypnoeic with oxygen saturations of 90% in air. There was dullness to percussion and widespread coarse crackles on auscultation throughout the left lung field and at the right apex. The chest radiograph showed extensive left lung and right upper lobe consolidation (fig. 1). Her C-reactive protein was 160 mg·L−1 and erythrocyte sedimentation rate was 90 mm·h−1. Her corrected calcium and phosphate were low, 1.96 mmol·L−1 (normal range 2.18–2.47 mmol·L−1) and 0.80 mmol·L−1 (0.75–1.50 mmol·L−1), respectively, with albumin and alkaline phosphatase levels of 23 g·L−1 (35–40 g·L−1) and 118 mmol·L−1 (30–200 mmol·L−1), respectively. Her Mantoux test was strongly positive (20 mm induration) and acid-fast bacilli were present in her sputum, which subsequently cultured Mycobacterium tuberculosis . In addition to consolidation, her chest computed tomography scan showed cavities within the distal bronchi, widespread tree-in-bud appearances throughout the left lower lobe and extensive mediastinal, paratracheal and subcarinal adenopathy. Standard quadruple anti-tuberculous therapy (isoniazid, rifampicin, ethambutol and pyrazinamide) was started. In view of her …

A Lung Cancer Responding to Hormonal Therapy

A 60-year-old woman presented with increasing dyspnoea and pain of several months duration. Radiology showed a 3 2.2-cm lung mass with mediastinal and subcarinal adenopathy and multiple vertebral metastases. A computed tomography-guided biopsy revealed a moderately differentiated adenocarcinoma. Immunohistochemistry showed positive staining for estrogen receptor (ER) (Figure 1a), thyroid transcription factor-1 (Figure 1b), and cytokeratin 7. The tumor was epidermal growth factor receptor (EGFR) positive as part of the entry criteria for a clinical trial. Staining was negative for progesterone receptor and cytokeratin 20, consistent with a lung primary. Her final diagnosis was of a T2N2M1 (stage IV) non-small cell lung cancer. Treatment was commenced with chemotherapy (cisplatin and vinorelbine) in combination with cetuximab and intravenous bisphosphonate therapy. Although she achieved a partial response that was maintained for 1 year, she progressed subsequently with her primary now measuring 4 3 cm (Figure 2a). Hormone replacement therapy, which she had commenced for menopausal symptoms, was stopped, and she was commenced on an aromatase inhibitor, exemestane. Within 3 weeks, her symptoms had improved, and repeat computed tomography scans 3 months later showed a decrease in the mass to 2.5 1.1 cm (Figure 2b), a partial response by Response Evaluation Criteria in Solid Tumors criteria, which was maintained for 6 months. Lung cancer is the leading cause of cancer death worldwide. The overall prevalence of smoking in any population has decreased in the past 20 years, but the relative decrease among women is much less. Women are more likely to be diagnosed with an adenocarcinoma than their male counterparts.1 Survival is better for women for all stages of lung cancer, even allowing for treatment differences.2 Genetic and molecular differences in lung cancers have been found between the sexes, includes differences in mutation rates of p53, EGFR, and k-RAS (Kirsten rat sarcoma) oncogene. The reasons for these differences in biologic behavior are not clear although it may be related to hormonal differences. Estrogens are implicated in the maturation, growth, and development of normal lung tissue. Hormone replacement therapy use is associated with a worse outcome in women with lung cancer, suggesting that estrogens may play a role in tumor progression.3 Two subtypes or ER have been described, ERand ER. ERreceptors are well characterized both in normal lung and malignant tumor samples, and immunohistochemistry positivity may be associated with an improved prognosis, particularly in males.4 Functional interactions between Departments of *Medical Oncology and †Histopathology, St James’s Hospital, Ireland. Disclosure: Ken J. O’Byrne has received Compensated Advisory Role, Honoraria, Research Funding, and other Remuneration with Pfizer, though not in relation to this case. Address for correspondence: Ian M. Collins, MB, MRCPI, HOPE Directorate, St James’s Hospital, Dublin 8, Ireland. E-mail: collins.ian@ gmail.com Copyright © 2010 by the International Association for the Study of Lung Cancer ISSN: 1556-0864/10/0505-0749 FIGURE 1. a, Estrogen receptor staining positive and (b) TTF-1 staining positive. TTF, transcription factor.

A 49-Year-Old Man With Concurrent Diagnoses of Lung Cancer, Sarcoidosis, and Multiple Regions of Adenopathy on Positron Emission Tomography

A 49-year-old, white man with a 100-pack-year smoking history presented with progressive scapular paresthesias and pain radiating down his right arm for 6 weeks. His medical history was significant for low-grade transitional cell bladder cancer status post transurethral bladder resection. He had multiple chemical exposures as a military aviator. He presented to another institution, where a CT chest scan demonstrated a 4.5 × 2.5-cm right apical lobulated and necrotic mass, bilateral hilar and subcarinal adenopathy, and tree-in-bud interstitial markings (Fig 1). He underwent fiberoptic bronchoscopy (FOB) with transbronchial biopsy (TBBx) of the right upper lobe (RUL) and transbronchial needle aspiration (TBNA) of a subcarinal lymph node. The TBBx demonstrated noncaseating granulomas, and subcarinal biopsy specimens showed lymphoid tissue without malignancy. He then presented to our institution for evaluation of increasing back and right arm pain. Physical examination was normal except for point tenderness over the suprascapular region of the right upper back with no palpable adenopathy.

Magnetic resonance findings in sarcoidosis of the thorax

Fifteen patients with sarcoidosis underwent thoracic MRI examinations. The T 2 signal intensity of lymphadenopathy varied, with no characteristic pattern noted. Three of four patients with bright lymph nodes on T 2 images had stage I sarcoidosis, but low intensity nodes were also seen in stage I patients. Coronal images were complementary to axial images and better depicted subcarinal adenopathy. MRI does not distinguish the lymphadenopathy of sarcoidosis from other entities, but is useful for defining the anatomic extent of disease and differentiating pulmonary artery enlargement from adenopathy.

The Correlation of Subcarinal Density Visualized on Plain Chest Roentgenograms with Computed Tomographic Scans

A prospective evaluation of 212 paired chest roentgenograms and computed tomographic (CT) scans was performed to determine the predictive value of detecting subcarinal adenopathy by finding increased subcarinal density on routine roentgenograms. Based on CT criteria for subcarinal lymphadenopathy, 37 true-positive and 124 true-negative cases of subcarinal adenopathy were found in 161 patients. Evaluation of density in the subcarinal area on the routine posteroanterior (PA) chest roentgenograms in these patients demonstrated a sensitivity of 72 percent and specificity of 96 percent for the detection of adenopathy when compared with established CT criteria. False-positive and false-negative appraisals of central mediastinal density on routine roentgenograms appear to be due to the super-imposition of other masses, bullae, or lack of appropriate roentgenographic contrast. The accuracy of predicting the presence or absence of subcarinal adenopathy from routine chest roentgenograms suggests that this observation is clinically useful and should be routinely evaluated.

Sagittal and coronal CT reconstruction for demonstration of subcarinal adenopathy.

Although standard sequential axial transverse images of the thorax obtained at 10 mm intervals are usually diagnostic for subcarinal lymph node enlargement, we have found reconstruction of the subcarinal area in both sagittal and coronal computed tomographic (CT) projections to provide a useful format for further defining important anatomic relationships. The normal CT anatomy of the subcarinal area is defined and contrasted with the appearance of adenopathy, esophageal cancer, and left atrial enlargement in various reconstructed formats. The clinical application of such imaging is useful in selected cases. Therefore, radiologists monitoring chest CT should perform appropriate reconstructions when indicated.