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A 47-year-old Chinese woman living in Japan was referred with a 2-month history of cough with hemoptysis. 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) showed increased FDG uptake into a pulmonary nodular lesion 25 mm in greatest dimension in the right upper lobe, and right hilar and mediastinal lymph nodes. Laboratory investigation did not reveal either eosinophilia or a marked elevation of serum IgE titer. A culture of bronchial lavage fluid was sterile and culture for mycobacteria was negative. Cytological examination results of transbronchial brushing samples were Class III. A partial resection of the right upper lobe was performed because of the possibility of primary lung cancer. Pathological examination of the nodular lesion showed helminthic eggs surrounded by dense inflammatory infiltrates, which mainly consisted of lymphocytes and eosinophils. Based on the findings of a serological study for helminth, the morphological characteristics of the eggs and the patient's history of eating raw crab, the patient was given a diagnosis of Paragonimus westermani, which can mimic primary lung cancer.

A 74-year-old man who received seasonal influenza vaccination at a clinic developed fever and cough the following morning. He was referred to our hospital on the 5th day after vaccination because of bilateral pulmonary infiltration shadows on a chest X-ray film. Despite the administration of sulbactam/ampicillin and roxithromycin after admission, his symptoms did not improve. His bronchoalveolar lavage fluid (BALF) obtained by bronchoscopy on the 8th hospital day revealed a CD4/CD8 ratio of 6.8, 109 x 10(4)/ml, and 39% and 16% increases in lymphocyte fractions and eosinophil levels, respectively. Transbronchial lung biopsy showed organizing pneumonia. A drug-induced lymphocyte stimulation test (DLST) for seasonal influenza vaccine with BALF showed 210% of seasonal influenza (S.I). These results indicate that this vaccine caused pneumonitis with a hypersensitive reaction, according to drug-induced lung injury criteria.

Objective: Since more solid malignancies are observed in transplant recipients treated with cyclosporine (CsA) than in healthy persons. We sought to describe the incidence of malignancy in patients treated with CsA for fibrosing interstitial pneumonia., Methods: We prospectively reviewed 43 patients who received CsA and prednisolone for fibrosing interstitial pneumonia over 180 days at our hospital between April 2004 and October 2008. The duration of CsA treatment was 632 +/- 364 days., Results: Malignancy developed in 6 (14.0%) patients. Time to diagnosis after medical intervention ranged from 394 days to 1325 days (mean, 783 days). Non-small cell lung cancer was diagnosed in 4 cases. These were discovered by routine computed tomography in all cases. Hepatocellular carcinoma and gastric cancer were each diagnosed in 1 case, respectively. Incidence of malignancy tended to be higher in patients who had been treated with CsA for 567 days or more than in those who had been treated for less than 567 days, but this was not statistically significant., Conclusion: Our results highlight the need for close follow-up for patients who receive CsA for over 2 years. This could lead to cancer detection at an early stage.

The clinical course of idiopathic pulmonary fibrosis (IPF) is chronic, but some patients with IPF have phases of accelerated deterioration superimposed on the chronic course of their illness, which is referred to as acute exacerbation (Aex) of IPF. To evaluate the clinical feature of Aex of IPF, we analyzed clinical findings of the 112 patients with IPF admitted to our hospital from 1994 to 2004. Of the 112 patients 56 with IPF died during the observation period due to Aex (42.9%), lung cancer (21.4%), chronic respiratory failure (14.3%), and lower respiratory infections (8.9%). Aex of IPF was seen 28 of 112 patients with IPF (25.0%) and 24 patients (85.7%) died with Aex. The median survival time (MST) after the onset of Aex was 0.9 months. The 5-yr survival rate of all patients with IPF was 38.3% and the MST was 3.1 yrs after diagnosis. On the other hand, the 5-yr survival rate and MST was 10.7% and 0.6 yrs in patients with Aex of IPF. We treated the patients with Aex with methylprednisolone pulse therapy in combination with cyclophosphamide or cyclosporine A, which did not significantly improve the outcome of Aex. In conclusion, there is little evidence that currently accepted treatments are effective in Aex of IPF, and further studies are needed to clarify the pathogenesis and contribute to the prevention of Aex.

A 28-year-old man was admitted for further examination after overinflation of the right lung was observed on a screening chest radiograph. The chest radiograph on admission showed increased radiolucency of the left lung and overinflation of the right lung, associated with a shift of the mediastinum toward the midline on expiration. High-resolution CT on expiration showed air trapping in the left lung and in part of the right lower lobe. Pulmonary perfusion scintigraphy showed a markedly decreased perfusion in these areas. Pulmonary angiography revealed small left pulmonary arteries with diminished peripheral vascular branches. Bronchoscopy showed no abnormality of either bronchus. Swyer-James syndrome was diagnosed on the basis of these findings. Although bronchial damage due to the lower respiratory tract infection during childhood is considered a very important factor in the pathogenesis of this syndrome, many patients have no history of airway infection, as in this case. This is a rare case of Swyer-James syndrome presenting with marked overinflation of the unaffected lung in an asymptomatic adult. Progression of this compensative overinflation probably involved asymptomatic damage caused by the weakness of the affected lung.

A 67-year-old woman complaining of dyspnea was referred to our hospital because of an abnormal chest radiography shadow. Computed tomographic (CT) scans as well as magnetic resonance images (MRI) demonstrated a mid-mediastinal mass of 9 cm in diameter, surrounded by the superior vena cava (SVC), the ascending aorta, the azygos vein arch and the trachea at the subaortic level. The left main bronchus was stenotic, probably because of expansion of the tumor, which seemed to be the cause of the dyspnea. Routine examinations disclosed no metastatic or primary lesions elsewhere. The tumor was surgically resected. It measured 8 x 7 x 5 cm. The pathological diagnosis was benign vagus nerve Schwannoma, consisting of the histologies of both Antoni A and B types. We have reported this case because Schwannoma should be included in the differential diagnosis of mediastinal tumors even when it occurs in the middle of the mediastinum.

A 78-year-old man was referred to our department because of an abnormal shadow on the chest radiograph and liver dysfunction after lung resection for lung cancer. Following the operation, loxoprofen sodium was administered to control his chest pain. A chest radiograph on admission showed airspace consolidation in the right lower lung field. In addition, leukocytosis and elevation of CRP were observed. Although piperacillin sodium was given to him, airspace consolidation on a chest radiograph was increased. A bronchoalveolar lavage fluid study showed that total cell counts and proportion of lymphocytes were increased, and the CD4/CD8 ratio was 1.77. A transbronchial lung biopsy specimen revealed organizing pneumonia with Masson bodies. Furthermore, a lymphocyte stimulation test for loxoprofen sodium was positive. From the clinical course, laboratory data and pathologic findings, we considered this case to be loxoprofen sodium-induced BOOP. Withdrawal of loxoprofen sodium and treatment with corticosteroid resulted in marked improvement of the clinical findings. Although a rare occurrence, it is important to recognize that BOOP can be caused by loxoprofen sodium.

Purpose: Histamine has multiple biological functions and its immunomodulatory actions are not fully understood. In the current study, we investigated the effect of cimetidine, which is a histamine-2 receptor antagonist, on the progress of transplanted Lewis lung cancers using a mouse model., Methods: A piece of Lewis lung cancer weighing 15 mg was transplanted into the subcutaneous space on the back of each C 57 BL/6 mouse. Mice were randomized into a no-treatment control group (CO) or one of two treatment groups. In the treatment groups, 16 mg/kg/day (LD) or 160 mg/kg/day (HD) of cimetidine was orally administered from one week before the day of transplantation to the time of sacrifice. Subcutaneous tumors and lungs were excised on the 28th or 42nd postoperative day., Results: The mean vascular densities of the subcutaneous tumors on day 28 were 55.7 +/- 23.9/mm2 in CO, 88.0 +/- 16.3/mm2 in LD and 122.6 +/- 16.9/mm2 in HD (p < 0.05; CO vs. LD or HD, LD vs. HD). On day 42, mean weights of the subcutaneous tumors and the numbers of metastatic lung tumors were 6.0 +/- 2.1 g in CO, 7.9 +/- 1.2 g in LD and 10.0 +/- 1.9 g in HD (p < 0.05; CO vs. HD), and 7.5 +/- 6.0 in CO, 17.0 +/- 3.0 in LD and 19.8 +/- 7.4 in HD (p < 0.05; CO vs. HD), respectively., Conclusions: These results suggest that cimetidine dose-dependently enhances the angiogenesis, growth and metastasis of surgically transplanted Lewis lung cancer in a mouse model of this type.

We report a case of neurogenic pulmonary edema associated with epileptic seizure. A 36-year-old woman had had several episodes of fainting and postictal respiratory failure, and since July 1998 had been admitted to a nearby hospital three times. On October 12, 1999, she was again admitted to a nearby hospital with the same symptom, and was transferred from that hospital to ours for evaluation of the recurrent respiratory disorder. Low-grade fever, mild leukocytosis, hypoxemia and bilateral diffuse opacities were observed as previously on chest radiography, and improved within several days without any specific therapy. The negative C reactive protein level, normal cardiac function and faintly bloody bronchoalveolar lavage fluid were also observed. There was no evidence of aspiration pneumonia, infectious disease, or underlying heart or lung disease. Electroencephalography showed spikes in accord with the left temporal lobe, and the cause of the patient's fainting was thought to be temporal lobe epilepsy. After all other causes had been excluded, this case was diagnosed as neurogenic pulmonary edema associated with epileptic seizure. Only about 40 cases of the postictal pulmonary edema have been reported since 1908, and the pathophysiologic mechanism of this condition is still unknown. Neurogenic pulmonary edema associated with epileptic seizure is rare, but the importance of awareness of this condition needs to be emphasized because it is suspected to be the cause of unexpected sudden death in epileptics. We should consider the disease as important in the differential diagnosis of acute respiratory failure associated with epilepsy.

Cigarette smoking is the primary preventable cause of various diseases and death. Smoking has been causally related to lung cancer, other malignancies, atherosclerosis, coronary heart disease, and chronic obstructive pulmonary disease. There have been few studies, however, of whether the ordinary citizen in Japan understand the risks of serious diseases caused by smoking. Four hundred and thirty six people attended a seminar of respiratory diseases entitled "Cigarette smoking and lung cancer; prevention and treatment of asthma; senile care and prevention of pneumonia". After the seminar, unsigned questionnaires were filled out by 403 of those in attendance. Three hundred eighty nine (165 males and 224 females) respondents correctly answered the questionnaires, and these were analyzed in the study. Attendants comprised 243 who had never smoked (63%), 99 former smokers (25%), and 39 current smokers (10%). Three hundred forty seven attendants (89%) answered that smoking is harmful to the health, and 371 (95%) that it is causally related to lung cancer. In contrast, lower numbers of attendants answered that smoking is causally related to other diseases: pulmonary emphysema, 65% of the responses; chronic bronchitis, 68%; laryngeal cancer, 77%; myocardial infarction, 53%; and atherosclerosis, 49%. Of the 39 current smokers, 27 answered that they would stop smoking after the seminar. Although many people partly understand the risks of smoking, they do not have a clear knowledge of the risks of diseases besides lung cancer. Education about the risks of smoking and about smoking cessation is required.

A 16-year-old boy with acute respiratory distress syndrome (ARDS) due to near-drowning was admitted to our hospital. ARDS was treated with low-level nitric oxide (NO) inhalation (ranging from 4 ppm to 1 ppm) for 24 days. Oxygenation was improved and pulmonary hypertension was reduced after NO inhalation, but systemic blood pressure, heart rate, and cardiac output were not affected. PaO2 improved from 153 Torr to 354 Torr under identical ventilating conditions (F1O2 1.0), and mean pulmonary arterial pressure fell from 40 mm Hg to 27 mmHg. It has been reported that NO inhalation alleviates ventilation-flow mismatch and pulmonary hypertension. It is unclear, however, whether this therapy improves the prognosis for ARDS. In our patient, NO inhalation was effective in alleviating the oxygenation impairment and pulmonary hypertension associated with ARDS.

We performed thoracoscopic biopsies of small pulmonary nodules in 13 patients by placing hookwires adjacent to the target nodules under computed tomographic (CT) guidance. Biopsies were successfully performed in 10 of the 13 patients. Placement of individual hookwires for this purpose took from 20 to 50 minutes (30 minutes on average). Excisional biopsies of individual nodules required 20 to 60 minutes (37 minutes on average). Although pneumothorax developed in one patient, treatment was not considered necessary. This biopsy technique was unsuccessful in 3 cases, in 2 of which the hookwire became dislodged, and in 1 of which the target nodule was not contained in the resected specimen. These experiences seemed to underscore the importance of placing CT-guided hookwires more deeply into lung tissue near the target nodules. The technique appears to be useful for thoracoscopic biopsies of peripheral pulmonary nodules that otherwise would be difficult to identify by endoscopic probing forceps.

A 65-year-old man was admitted to our hospital because of mild dyspnea. A chest roentgenogram showed diffuse reticulonodular shadows in both lung fields. The concentration of CA19-9 in serum was high. Pancreatic cancer and other diseases were considered as causes, but no definitive diagnosis could be made. An open-lung biopsy was done, and examination of a specimen resulted in the diagnosis of idiopathic interstitial pneumonia (chronic type). Immunohistochemical staining with anti-CA19-9 antibody was positive. The lumens of microscopic honeycomb structures and fibrotic areas were covered with flattened and cuboidal metaplastic epithelial cells, which stained positively for anti-CA19-9 antibody.

To clarify role of alveolar macrophages in the pathogenesis of idiopathic interstitial pneumonia (IIP), we studied (1) the localization and expression of monocyte chemoattractant protein-1 (MCP-1) in IIP by immunohistochemistry and in situ hybridization. (2) the role of MCP-1 in macrophage recruitment to be lung, and (3) the clinical usefulness of measuring MCP-1. (1) In IIP, MCP-1 was observed in cuboidal and flattened metaplastic epithelial cells, alveolar macrophages, and vascular endothelial cells. In contrast, no epithelial cells from patients without IIP stained positive for MCP-1, although alveolar macrophages and vascular endothelial cells were labeled. MCP-1 production by epithelial cells in IIP may be caused by the metaplastic nature of the epithelial cells and may be a main cause of the irreversible progression of IIP. (2) MCP-1 levels in bronchoalveolar lavage fluid (BALF) were significantly higher in the IIP, the interstitial pneumonia due to collagen vascular disease (IP-CVD) and sarcoidosis groups than in normal controls. In the IIP group, the MCP-1 level was significantly higher than in any other patient groups. In all three groups of patients, the monocyte chemotactic activity in BALF correlated positively with the MCP-1 levels in BALF, and were neutralized by anti-MCP-1. (3) BALF MCP-1 levels were significantly higher than serum MCP-1 levels in the IIP group, and they were lower in the IP-CVD and non-specific interstitial pneumonia groups. Serum MCP-1 levels reflected the activity of interstitial lung diseases, especially during treatment with corticosteroids. These results indicate (1) that MCP-1 plays a significant role in the recruitment of monocytes into the lung in IIP, (2) that measuring MCP-1 levels both in BALF and in serum may help discriminate IIP from other types of interstitial lung diseases, and (3) that monitoring the serum MCP-1 level may be useful in estimating the activity of interstitial lung diseases.

A 57-year-old woman with congenital syphilis had a productive cough, fever, cholecystolithiasis, and paralytic ileus. She had a 30-year history of recurrent bronchitis accompanied by yellowish serous sputum. A chest radiograph showed bilateral infiltrates resulting from aspiration pneumonia, and a reduction in volume of the right middle and right lower lobes. After recovering from paralytic ileus, she still had fever and biliptysis. Bronchoscopy revealed bile filling the right basal bronchi. Emergency laparotomy and throacotomy revealed a gall stone, splenomegaly, marked atrophy of the right lobe of the liver, and adhesion between the right pleura and the diaphragm. A T-tube cholangiogram showed that the right hepatic duct communicated with the right basal bronchus. Despite ligation of the right hepatic duct, biliptysis continued. The patient died due to rapidly progressing hepatorenal failure. Syphilis gummosa due to congenital syphilis was suspected as a cause of the bronchobiliary fistula, but was not confirmed pathologically. The surgical specimen showed only nonspecific fibrosis with calcification. Bronchobiliary fistula is rare in Japan; we know of only 6 other reported cases.

A 73-year-old man was admitted to our hospital with pneumonia in the right S6 induced by Streptococcus milleri and with left pleural thickening. He had histories of diabetes mellitus for 30 years and pulmonary tuberculosis 35 years ago. The pneumonia resolved completely after administration of ceftazidime and clindamycin for 10 days, but the pleural thickening remained and computed tomography revealed that it was an encapsulated effusion without calcification. An aspirate was turbid yellow with a high concentration of lipids, and consisted of dominant crystals and scattered cells, 80% of which were yeasts and 20% of which were macrophages phagocytizing them. Only Candida parapsilosis developed in culture. The same silent pleural shadow was identified on chest X-ray films obtained over the previous 7 years. The persistent pleuritis was diagnosed as saprophytic infection with C. parapsilosis.

A 60-year-old man presented with sudden palpitations in September 1993, and was admitted to hospital with a diagnosis of atrial fibrillation and heart failure. The patient was suspected of having collagen disease, because of a positive test for antinuclear antibodies and a high sedimentation rate. He was referred to lou hospital. Chest radiographic findings were suggestive of cardiomegaly and cardiac murmurs were audible, which indicated the presence of heart disease. A chest Ct scan revealed a lesion surrounding the intramediastinal large vessels and the heart from the level of the confluence of the left brachiocephalic vein and the superior vena cava. Suspicion of a mediastinal tumor led the patient to be admitted to the respiratory department. Percutaneous needle biopsy with a Trucut needle revealed non-specific chronic inflammation. An abdominal CT scan showed that the lesion surrounding the descending aorta traversed the diaphragm, reached the renal pelvis along both renal arteries, and caused narrowing of the ureter and left hydronephrosis. Based on these findings, retroperitoneal fibrosis was diagnosed. Treatment with steroids caused the lesion to shrink.

A 19-year-old endotracheally intubated women was admitted to our hospital in severe status asthmaticus that was not relieved by inhalation of beta 2-agonists or by epinephrine, aminophylline, or corticosteroids. A chest radiography revealed pneumomediastinum and subcutaneous emphysema. Pressure-limited mechanical ventilation at a peak airway pressure of 20--30 cmH2O failed to ventilate the lungs, and caused a left pneumothorax and atelectasis. Extracorporeal lung assist (ECLA) was begun and enabled repeated suctioning through a fiberoptic bronchoscope for more than a minute with no serious complications. During ECLA aerosol therapy with a large dose of a beta 2-agonist (procatherol 0.15 mg) increased the tidal volume with no adverse effects. Atelectatic areas of the lungs re-expanded, pulmonary function improved, and ECLA was stopped 86 hours after it had been started. We suggest that, although it is highly invasive, ECLA can be useful in patients with status asthmaticus refractory to mechanical ventilation, and can allow endobronchial suctioning to be done safely.

Macrophages have specific functions related to the sites where they are found. Pulmonary alveolar macrophages (PAM) may play an important role the clearance of invading and degenerative substances from the alveolar spaces. To clarify the mechanisms of the clearance by macrophages, we studied the role of scavenger receptors (SR) and Fc receptors (FcR) of PAM. 1) SR: Expression and localization of SR in human PAM. Type I and II SRs were expressed in human PAM, and the two SRs were confirmed in the same cells by double staining method using polyclonal antibodies to the SRs. These SRs were localized on the cell membrane and the endosome in part. The expression of SR in PAM from normal nonsmokers, smokers and patients with pneumoconiosis was studied, but there were no differences among these groups. Kinetics of SR and acetylated low density lipoprotein (acLDL) in PAM. SR recognized acLDL, and SR and acLDL-Au conjugates were concentrated in a coated pit 2 min after incubation. The conjugates were then internalized in the endosome 5 min after incubation. A few acLDL-Au conjugates were present in the endosome near the nucleus, but most of them were found in the lysosome 10 min after incubation. SR was found in the Golgi apparatus 15 min after incubation. These results suggest that SR in PAM may play an important role in the removal of alveolar surfactant. 2) FcR: Effects of FcR mediated phagocytosis on O2-release and phagosome-lysosome fusion in the phagosome of PAM.(ABSTRACT TRUNCATED AT 250 WORDS)

It is sometimes difficult to clinically diagnose mycoplasma pneumonia at an early stage before the rise of titer of antibody to Mycoplasma pneumoniae. Mycoplasma pneumonia may be related with T-lymphocyte activity, and its inflammatory process is different from that of bacterial pneumonia. Adenosine deaminase (ADA) activity is a predominant T-lymphocyte enzyme, and its plasma activity is high in diseases in which cellular immunity is stimulated. In this study, we have investigated 31 cases with pneumonia (11 cases of mycoplasma pneumonia and 20 cases of bacterial pneumonia) within 10 days after onset to evaluate the usefulness of ADA measurement in the diagnosis of mycoplasma pneumonia. Serum ADA activity in the group of mycoplasma pneumonia was 32.1 +/- 12.0 U/l (63.9-18.8 U/l), that of non-mycoplasma pneumonia 12.5 +/- 3.3 (4.6-18.6) U/l, and that of normal control 14.0 +/- 3.4 (6.3-19.3) U/l. ADA activity of the group of mycoplasma pneumonia was significantly higher than those of non-mycoplasma pneumonia and normal control (p less than 0.001). This results suggest that serum ADA activity in patients with acute pneumonia may be useful for the early diagnosis of mycoplasma pneumonia.

A 44-year-old man was admitted with increasing dyspnea and butterfly shadow on his chest roentgenogram. Both the bronchoalveolar lavage and transbronchial lung biopsy (TBLB) led to a diagnosis of pulmonary alveolar proteinosis. CEA level in his bronchoalveolar lavage fluid (BALF) (216.8 ng/ml) was markedly elevated more than that in his serum (50.6 ng/ml). The localization of CEA on TBLB specimen stained by peroxidase-antiperoxidase technique using anti-CEA antibody was investigated and it was found that some alveolar epithelial cells and the material filling the alveoli were positively stained. Functions of alveolar macrophages in BALF were also studied, that is, adherence to glass, cell spreading, the nitroblue tetrazolium reduction, phagocytosis of immunobeads, and the activity of lysosomal enzymes, and found that all of those functions were lower than that of normal smokers. It was suggested that type II alveolar epithelial cells were those which produced and secreted CEA into the alveoli, as they do surfactant-like material in pulmonary alveolar proteinosis, and that the dysfunction of alveolar macrophages was secondary to the overingestion of the proteinaceous material in the alveoli.