A 47-year-old-woman was admitted to our hospital complaining of thirst and dry cough after catching cold. Sjögren's syndrome (SjS) and systemic lupus erythematosus (SLE) were diagnosed. Chest X-P and CT findings suggested strongly that she had interstitial pneumonia. Thoracoscopic lung biopsy was therefore performed, and the biopsy specimens showed marked infiltration of small lymphocytes and of plasma cells into the alveolar walls and interlobular septa. Since the infiltrating cells were not atypical and gene analysis did not show mono-clonality, we made a diagnosis of lymphocytic interstitial pneumonia (LIP). Because the patient's symptoms appeared only after she caught cold, we suspected that virus infections were somewhat involved in the etiology of these diseases. The level of human herpesvirus-6 (HHV-6) antibody was high, and furthermore, HHV-6 was detected using the polymerase chain reaction from lung biopsy specimens. We suspected in this case that LIP, SjS, and SLE had appeared concomitantly after an active HHV-6 infection.
Xanthomatous pleuritis is a very rare type of chronic inflammation, with only 3 reports to date.1–3 However, the exact etiology of this disease is unknown. Herein, we present a case of xanthomatous pleuritis that might have been associated with pancreatic pleural effusion. CASE REPORT A 62-year-old male who regularly consumed alcohol (<20 g/day), was a nonsmoker, and had no medical history was referred to our hospital for exertional dyspnea. Laboratory examination revealed leukocytosis (11,200/μL); however, all other findings were normal (C-reactive protein, 0.62 mg/dL; serum amylase, 171 IU/L; serum lipase, 30 IU/L; tumor markers, negative; interferon-gamma release assay, negative). The chest radiograph showed left pleural effusion. Moreover, chest computed tomography (CT) revealed left pleural effusion. We performed thoracoscopy under local anesthesia for drainage and pathologic diagnosis as pleural effusion because of malignancy was considered. Pleural fluid examination revealed bloody exudative (protein, 5.0 g/dL; lactate dehydrogenase, 1264 IU/L; Rivalta reaction, positive; serum total protein, 6.9 g/dL; serum, lactate dehydrogenase 212 IU/L) and high level of amylase (13,355 IU/L). Thoracoscopy of the left thorax revealed diffuse yellow plaque-like deposits in the pleura (Fig. 1). Histology of the left pleural biopsy specimen showed inflammation and foamy cells (Fig. 2). There was no evidence of malignancies and infections, including Mycobacterium. Therefore, we considered the presence of pancreaticopleural fistula and performed further abdominal examinations. An enhanced CT and endoscopic retrograde cholangiopancreatography revealed pancreatic stones, main pancreatic duct dilatation, meandering pancreatic duct, and left pancreaticopleural fistula (Fig. 3). Distal pancreatectomy was performed after thoracic drainage with a chest tube to treat the pancreatic pleural fistula for prevention of pleural effusion recurrence and rule out pancreatic cancer. The surgically resected specimen of the pancreas showed chronic pancreatitis with pancreatic stones and no findings of malignancies. On the basis of these results, xanthomatous pleuritis with pancreaticopleural fistula because of chronic pancreatitis was finally diagnosed. The patient has had an uneventful course without recurrence for more than 4 years.FIGURE 1: A and B, Thoracoscopic image shows diffuse yellow plaque-like deposits in the pleura of the left thorax.FIGURE 2: Biopsy specimen of the pleura with yellow plaque-like deposit shows foamy cells (×400 magnification).FIGURE 3: Endoscopic retrograde cholangiopancreatography reveals meandering pancreatic duct and contrast outflow to the left thoracic cavity (red arrow).DISCUSSION To the best of our knowledge, this is the first report of xanthomatous pleuritis with pancreatic pleural effusion. Xanthomatous pleuritis is a very rare benign type of chronic inflammation, and only 3 cases have been reported in the literature.1–3 Although the exact etiology is uncertain, previous reports2–4 suggested that chronic inflammation, defective lipid transport, and hemorrhage might be the causes of xanthomatous inflammation. In the present case, chronic inflammation because of pancreaticopleural fistula might have caused xanthomatous pleuritis. Furthermore, aberrance of the lipid component of the pancreas might also be a cause of defective lipid transport. In addition, we present the thoracoscopic findings of xanthomatous pleuritis. Thoracoscopy showed diffuse yellow plaque-like deposits in the pleura. This finding was similar to that in a previous report by Bateman et al.3 Xanthoma comprises yellow plaque-like lesions characterized by the presence of lipid-containing histocytes and is commonly found in the gastrointestinal tract.5 The endoscopic finding of xanthoma in the gastrointestinal tract includes yellow spots,6,7 which is very similar to the finding in our case and a previous report.3 Hence, the yellow plaque-like deposits might be the characteristic finding in xanthomatous pleuritis. Physicians should consider the possibility of xanthomatous pleuritis when such thoracoscopy findings are observed. Furthermore, the thoracoscopy finding of xanthomatous pleuritis may indicate the possibility of the presence of pancreatic disease, even though pancreatic disease is not initially considered as a differential diagnosis when physicians examine patients with pleural effusion. Therefore, abdominal examinations, such as abdominal CT, ultrasound, or endoscopic retrograde cholangiopancreatography, should be performed when physicians confirm this thoracoscopy finding. Treatments for xanthomatous pleuritis are yet to be established, although steroids have been used in the previous cases.1,3 Since xanthomatous pleuritis was considered to be associated with pancreaticopleural fistula in the present case, we performed distal pancreatectomy, which led to a favorable outcome. It may be important to find out the underlying causes, such as pancreaticopleural fistula, when physicians diagnose xanthomatous pleuritis. In conclusion, the present case suggests that pancreatic pleural effusion might be a cause of xanthomatous pleuritis, and the thoracoscopic finding of yellow plaque-like deposits in pleura might be the characteristic finding of xanthomatous pleuritis.
A 69-year-old male non-smoker with a history of atopic asthma presented with symptoms suggestive of chronic obstructive pulmonary disease and this appeared to be corroborated by lung function testing and a chest radiograph. However, a chest CT showed no evidence of pulmonary emphysema and instead demonstrated free air along the bronchovascular sheaths indicative of pulmonary interstistial emphysema, possibly caused by repeated prior exacerbations of asthma. His lung function tests and symptoms improved within months of being treated for his airways disease but the CT findings were unchanged after 2 years.
The aim of the study was to elucidate the vasodilatory mechanism due to Cu 2+ by assessing nitric oxide (NO) production as determined by NOx (NO, NO 2 − , and NO 3 − ) that is released from human pulmonary arterial endothelial cell (HPAEC) monolayers using a NO chemiluminescence analyzer, and also to assess Ca 2+ movement using 45 Ca and fura 2 in HPAEC. Cu 2+ (10 −6 –10 −4 m ) significantly increased NO production in a dose‐dependent manner when extracellular Ca 2+ was present. 45 Ca influx into the adherent cells was dose‐dependently enhanced by Cu 2+ (10 −6 –10 −4 m ), but not by Mn 2+ , Zn 2+ or Fe 2+ . [Ca 2+ ] i , measured by monitoring the fluorescence changes of fura 2, was significantly elevated in the presence of Cu 2+ . The increase in [Ca 2+ ] i induced by Cu 2+ was inhibited by either diethyldithiocarbamate (DDC) or the depletion of extracellular Ca 2+ . The dihydropyridine receptor agonist, BayK8644, significantly attenuated the Cu 2+ ‐induced increase in [Ca 2+ ] i in a dose dependent manner and nitrendipine or nifedipine, the dihydropyridine receptor antagonists, dose‐dependently inhibited a Cu 2+ ‐induced increase in [Ca 2+ ] i . These results suggest that Cu 2+ activates eNOS through the mechanism of [Ca 2+ ] i elevation due to Ca 2+ influx into HPAEC and that the Cu 2+ ‐induced [Ca 2+ ] i elevation in HPAEC is likely due to activation of the dihydropyridine‐like receptors. British Journal of Pharmacology (1998) 125 , 1180–1187; doi: 10.1038/sj.bjp.0702197
Immune checkpoint inhibitors may cause specific immune-related reactions, such as pseudo-progression. In particular, malignant pleural effusion tends to worsen due to this phenomenon. However, the appropriate management in such cases is unclear.
Abstract Background Whether immunotherapy improves the efficacy or worsens adverse events of subsequent chemotherapy remains unclear. We performed a Phase 2 study to evaluate the efficacy and safety of nanoparticle albumin‐bound paclitaxel (nab‐paclitaxel) as a treatment for advanced non‐small cell lung cancer (NSCLC) after treatment with programmed cell death 1 or programmed death ligand 1 [PD‐(L)1] inhibitor failure. Methods Nab‐paclitaxel (100 mg/m 2 ) was administered on Days 1, 8, and 15 of a 28‐day cycle to patients with advanced NSCLC within 12 weeks after the failure of PD‐(L)1 inhibitor treatment. The primary endpoint was objective response rate (ORR) in all patients; the secondary endpoints were disease control rate (DCR), progression‐free survival (PFS), overall survival (OS), and safety. Results Thirty cases were registered, and 29 cases were included in the analysis. The ORR was 55.2% (95% confidence interval [CI]: 28.1%–79.6%) and the DCR was 86.2% (95% CI: 65.9%–97.0%). The median PFS was 5.6 months (95% CI: 4.4–6.7 months), and PFS rates at 1‐ and 2‐year timepoints were 34.5% and 13.3%, respectively. The median OS was 11.9 months (95% CI: 0.8–23.0 months). Good performance status and responder of previous PD‐(L)1 inhibitor therapy were independent predictors of PFS. Grade 3 or higher toxicities included leukopenia (27.6%), neutropenia (31.0%), peripheral sensory neuropathy (6.9%), increased alanine aminotransferase and aspartate aminotransferase levels (3.4%), and interstitial lung disease (3.4%). Conclusions Nab‐paclitaxel therapy improved ORR after PD‐(L)1 inhibitor treatment failure with a durable response of 13% and acceptable toxicities in patients with advanced NSCLC.
A 55-year-old man complained of acute onset of shoulder pain and dyspnea in the supine position. A diagnosis of bilateral diaphragmatic paralysis was made based on clinical inspection of his breathing pattern, radiographic appearance, and pulmonary function tests. He had had no traumatic or thoracic surgery or inflammatory episode. He did not suffer from diabetes, other central neural diseases, or any neoplastic disease. From the clinical feature and electromyographic findings, phrenic nerve involvement of brachial neuritis without any other muscle involvement was considered as a causative disease. When he received non-invasive intermittent positive-pressure ventilation by nasal mask in a supine position, his dyspnea was substantially attenuated and Carbon dioxide retention was lessened. After 1 year, his shoulder pain is still persisting and radiographic findings are not remarkably improved.
A survey on chemotherapy-induced nausea, vomiting and food intake was conducted on 126 outpatients receiving chemotherapy during a days from February 1 to February 12, 2010 in our hospital. Responses were obtained from 66 outpatients. In the acute phase, 11%of the patients developed nausea. In the late phase, 35%patients developed nausea. The development of nausea was significantly increased in the late phase, compared to the acute phase(p=0. 0008). Though nobody developed vomiting in the acute phase, 3% of the patients developed vomiting in the late phase. For food intake, in the acute phase, nobody showed areduced amount of diet, and 12% showednot eating. In the late phase, 26% of the patients showedreduced amount of food, and 8%not eating. Food intake was significantly decreased in the late phase, compared in acute phase(p=0. 0001). Currently, in our hospital, steroids and/or 5-HT3 antagonists are given for antiemetic therapy, but the effect is not enough. We should add other antiemetics, which act in the late phase.
