[RESPIRATORY IMPEDANCE MEASURING BY MostGraph-01 IS AFFECTED BY OBESITY].

BACKGROUND: The forced oscillation technique (FOT) is a noninvasive method of measuring respiratory impedance, which includes respiratory system resistance (Rrs) and reactance (Xrs). The MostGraph-01 FOT device recently became clinically available in Japan, but standard impedance values for this device have not been determined in Japan. OBJECTIVE: To assess the correlation between spirometry parameters and respiratory impedance in obese (body mass index [BMI]>=25) and non-obese (BMI<25) subjects. METHODS: Clinical data were collected from 63 subjects without respiratory diseases who underwent spirometry and MostGraph-01 from January to October 2014. We investigated the correlation between spirometry parameters and respiratory impedance, and assessed the differing correlations among obese and non-obese subjects. RESULTS: The Rrs at 5 Hz (R5) was significantly correlated with vital capacity (VC), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV1). The Xrs at 5 Hz (X5), frequency of resonance (Fres), and low-frequency reactance area (ALX) were significantly correlated with the VC, FVC, and FEV1. Obese subjects showed a significantly lower X5 (median, -0.68 cmH2O/l/s vs. -0.35), higher Fres (median, 9.76 Hz vs. 7.46), and higher ALX (median, 2.65 cmH2O/l vs. 1.24) compared to non-obese subjects. Moreover, the VC, FVC, and FEV1 were more highly correlated with R5, X5, Fres, and ALX in nonobese subjects than in obese subjects. A p value of less than 0.05 was considered statistically significant. CONCLUSION: For MostGraph-01, it is suggested that obesity may influence Xrs rather than Rrs.

Changes in lung function and health status in patients with COPD treated with tiotropium or salmeterol plus fluticasone.

BACKGROUND AND OBJECTIVE: The effects of tiotropium, a long-acting anticholinergic drug, were compared with those of the combination of salmeterol, a long-acting beta(2)-agonist, and fluticasone, an inhaled corticosteroid, in patients with COPD. METHODS: A 4-month, randomized, open cross-over study of tiotropium, 18 microg once daily, versus salmeterol, 50 microg, plus fluticasone, 200 microg, twice daily, was conducted in patients with COPD. Efficacy was assessed by spirometry and responses to the St George's Respiratory Questionnaire (SGRQ). After 4 months, patients were asked to select their subsequent therapy and indicate the reasons for their selection. RESULTS: A total of 78 patients completed the study. There were no significant differences in the improvements in FEV(1) or SGRQ scores between the therapies. Similar numbers of patients selected tiotropium (42.3%) and salmeterol plus fluticasone (57.7%). However, those who preferred one of the therapies demonstrated greater improvements in SGRQ scores with that therapy. One subgroup of patients (30.8%) showed greater improvements in dyspnoea and FEV(1) in response to tiotropium, and the other subgroup of patients (35.9%) showed greater improvements in dyspnoea and FEV(1) in response to salmeterol plus fluticasone. Some patients (14.1%) selected salmeterol plus fluticasone because of positive effects on sputum expectoration. CONCLUSIONS: The study was unblinded and the results need to be interpreted with caution. However, tiotropium and salmeterol plus fluticasone had similar overall effects on pulmonary function and SGRQ scores in patients with COPD. Responses to the two therapies were heterogeneous, and the patients who showed greater improvements in FEV(1) or SGRQ scores with one of the therapies preferred it for their subsequent treatment.

[A case of small cell lung carcinoma complicated by Lambert-Eaton myasthenic syndrome].

A 54-year old man was admitted with general fatigue, muscle weakness and dyspnea on effort. Medical examinations led to a diagnosis of small cell lung carcinoma (SCLC) with Lambert-Eaton myasthenic syndrome (LEMS). Marked improvement of SCLC and symptoms of LEMS were recognized twice during chemoradiotherapy. On his third admission, he showed muscle weakness, dysaethesia, and neurodysfunction of the bladder and rectum. We initially considered these symptoms to be due to spinal metastasis because MRI findings showed multiple spinal metastases. However, electoromyogram and nerve conduction study demonstrated that his muscle weakness resulted from LEMS though dysethesia and neurodysfunction of bladder and rectum were caused by spinal metastasis. We believe that it is important to perform electomyogram and nerve conduction studies, not only radiographic findings, to detect the "hidden" symptoms of LEMS.

[Case of HLA-DR8 positive sarcoidosis following polymyositis and Sjögren's syndrome].

A 69-year-old woman had been found to have idiopathic interstitial pneumonia (fibrotic NSIP) in 1997. Proximal muscle weakness appeared in April 2005. Chest CT revealed hilar and mediastinal lymphadenopathy. Polymyositis and Sjögren's syndrome were subsequently diagnosed. We assumed that the interstitial pneumonia had preceded polymyositis and Sjögren's syndrome. A muscle biopsy and transbronchial needle aspiration biopsy demonstrated noncaseating epithelioid cell granulomas. A diagnosis of sarcoidosis complicated with polymyositis and Sjögren's syndrome was made from these findings. Moreover, her HLA genotype contained DR8. HLA-DR8 is considered to be associated with polymyositis, Sjögren's syndrome, and sarcoidosis in Japanese patients. This case suggests the possibility that there are common immunological and genetical pathogenetic mechanisms in autoimmune diseases and sarcoidosis.

[Case of acute interstitial pneumonia that responded to therapy but relapsed six months later].

A 66-year-old man was admitted because of general fatigue. A chest computed tomography showed bilateral alveolar consolidation and ground glass opacities. Although we treated him with broad-spectrum antibiotics, his symptoms and chest image findings did not improve. Thoracoscopic lung biopsy (rS2, S9) was performed. The specimens showed obstructive type intraluminar organization and interstitial inflammatory thickening. Membranous organization was seen in a limited area. The etiology of the illness could not be identified. We diagnosed acute interstitial pneumonia (AIP) because the specimens showed diffuse alveolar damage pattern (DAD/P) and because of unknown etiology. The symptoms and chest image findings were improved on treatment with corticosteroid and cyclophosphamide. However, he was readmitted because of dyspnea 6 months later after the thoracoscopic lung biopsy. Chest computed tomography showed bilateral diffuse ground glass opacities and reticular opacities in both lower lobes. We employed mechanical ventilation, antibiotics, sivelestat sodium hydrate and steroid pulse therapy, but he died without any response to treatment. The findings of autopsy revealed DAD/P accompanied by a new lesion mainly composed of membranous organization and hyaline membrane. We believe this case is valuable when considering the variety of responses to treatment of AIP and prognosis.

[A case of miliary tuberculosis showing acute respiratory failure during pregnancy].

A 36-year-old Philippine woman had had fever and general fatigue from September, 2006 (11th week of pregnancy). She was admitted with high fever, general fatigue and dyspnea on October 16, 2006 (13th week of pregnancy). A chest radiograph on admission showed bilateral miliary shadows and ground glass shadows. She already had severe hypoxia on admission. As acid-fast bacilli were positive in urine (Gaffky 8) and sputum (Gaffky 1), we diagnosed as miliary tuberculosis and pulmonary tuberculosis complicated with acute respiratory distress syndrome (ARDS). We treated her with antituberculosis chemotherapy, corticosteroid, sivelestat sodium hydrate, direct hemoperfusion using a polymyxin B immobilized column, and mechanical ventilation, but she died due to respiratory failure. We emphasize that in this case pregnancy has the risk of to causing disease progression of miliary tuberculosis and we should treat immediately and intensively for miliary tuberculosis complicated with ARDS.

[Case of allergic bronchopulmonary aspergillosis successfully treated with itraconazole].

A 58-year-old woman had a productive cough but not from bronchial asthma. A chest radiograph revealed infiltrative shadows in right middlelung field on September, 2004. Aspergillus fumigatus was detected in a sputum culture. She was treated with oral itraconazole. After the treatment, infiltrative shadows on her chest radiograph disappeared. On October 2005, her peripheral blood showed eosinophilla, a high serum level of total immunoglobulin E (IgE), and a chest radiograph revealed new infiltrative shadows in both lung fields. A chest computed tomography revealed multiple nodular shadows and central bronchiectasis. We detected a mucoid plug which showed a large number of eosinophils pathologically by bronchoscopy. Aspergillus niger was detected in a bronchial lavage fluid. We therefore made a diagnosis of allergic bronchopulmonary aspergillosis (ABPA). The decreases of peripheral blood eosinophils and a serum IgE level were recognized and multiple nodular shadows disappeared by reinstitution of itraconazole. However, a chest computed tomography revealed new infiltrative shadows. Therefore, we treated her with the concomitant administration of oral itraconazole and inhaled corticosteroid. All laboratory data and image findings were improved. It is critical to consider the both aspects of allergy and infection in the treatment for ABPA.

[Pneumocystis carinii pneumonia in a patient with hyper-IgE syndrome].

A 15-year-old girl with abnormal findings detected on a medical check-up chest x-ray film was admitted to our center. High-resolution computed tomography, performed upon hospitalization, demonstrated panlobular nodular darkening in left lung fields, and an expanding, blended, map-like darkening near the pleura. Since a Grocott stain-positive cyst was confirmed histopathologically by transbronchial lung biopsy, the patient was given a diagnosis of Pneumocystis carinii pneumonia. Drug therapy was initiated with sulfamethoxaxole trimethoprim (Baktar), and on the 58th day, chest CT confirmed that the darkening observed at admission had virtually disappeared. Underlying diseases, such as AIDS, malignant lymphoma and secondary immunodeficiency caused by immunosuppressive agents or adrenocorticosteroids, were excluded as the cause of P. carinii pneumonia based on clinical/laboratory findings. Under the suspicion of the possibility of primary immunodeficiency, various immunological competence tests were performed. However, no abnormal findings indicating cell-mediated immunity, humoral immunity, complement immune function, neutrophil phagocytic capacity, or bactericidal capacity were recognized. Since significant increase of serum IgE suggested hyper-IgE syndrome, IgE antibody specific to Staphylococcal enterotoxin A and B, and the exotoxins of Staphylococcus aureus were measured with positive results. Since all three diagnostic criteria for hyper-IgE syndrome (i.e., high serum IgE values, positive IgE antibody specific to Staphylococcal enterotoxin and recurrent infection) were fulfilled, hyper-IgE syndrome was diagnosed. This is a rare case of hyper-IgE syndrome as a result of P. carinii pneumonia.

[A case of Wegener's granulomatosis associated with the syndrome of inappropriate secretion of ADH].

A 68 year-old woman was admitted with fever, productive cough and sore throat. A chest radiograph and a chest computed tomography showed multiple nodules in both lungs. Thoracoscopic lung biopsy was performed. The specimens showed vasculitis and geographic basophilic necrosis with palisading histiocytes, giant cells, and neutrophils. Wegener's granulomatosis was diagnosed. On the 5th hospital day, the serum sodium level was 128 mEq/l. Since secretion of antidiuretic hormone had continued despite a low plasma osmolarity, we diagnosed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and initiated oral prednisolone and cyclophosphamide. As a result, the symptoms and image findings were improved, and serum sodium level became normal. This case was considered to be SIADH secondary to Wegener's granulomatosis.

[Clinical study of 90 cases of Mycoplasma pneumoniae pneumonia].

We investigated 90 patients with Mycoplasma pneumoniae (M. pneumoniae) pneumonia. Forty-four patients were men, 46 were women and the mean age was 43.1 years old. Twenty-nine patients were smokers and 28 had underlying diseases. As for diagnostic method, 16 were culture positive, 71 had a fourfold increase in antibody titer to M. pneumoniae, and 3 were both culture positive and had a fourfold increase in antibody titer. Regarding the degree of severity, 21 patients were classified as severe according to Japanese Respiratory Society diagnostic criteria, 11 patients were diagnosed as severe according to American Thoracic Society diagnostic criteria. Partial pressure of arterial oxygen (PaO2) of 18 patients were <60mmHg, 5 patients were under mechanical ventilation, and 3 patients died. Three of 16 patients treated with only beta-lactum antibiotics recovered. The 3 patients who died were M. pneumoniae culture-positive and two patients had polymicrobial infections. Severe pneumonia associated with Mycoplasma pneumoniae infection is not unusual. If a rapid diagnosis kit or culture method of M. pneumoniae pneumonia is not introduced, the pathogen might be unknown in cases of rapid death due to M. pneumoniae pneumonia. These data suggest that the mortality rate of M. pneumoniae pneumonia might be underestimated without these detection tests.

[Pulmonary tuberculosis with cerebellar lesion in a patient after anti-TNF-alpha (infliximab) treatment for rheumatoid arthritis].

We report a case of pulmonary tuberculosis in a 51-year-old Japanese woman, who received treatment with infliximab for active rheumatoid arthritis. She had cough and sputum after the second infusion of the drug, small nodular lesions of right lung field and left lower lobe on her chest CT and a small nodular lesion of right cerebellar lobe on her cranial MRI were identified. Mycobacterium tuberculosis was cultured from her sputum. Therefore, we diagnosed her illness as pulmonary tuberculosis with a cerebellar lesion. The patient was treated with anti-tuberculosis drugs and showed marked improvement in lesions of the lung and brain. We considered this case a tuberculosis reactivation after infliximab treatment because of the short interval between the administration of infliximab and the occurrence of tuberculosis, and the complication of extrapulmonary lesion that suggested brain tuberculoma.

[Community-acquired pneumonia with rhabdomyolysis].

We assessed the frequency and etiology of rhabdomyolysis in patients with community-acquired pneumonia. In 594 patients with community-acquired pneumonia whose serum CPK were measured, 25 patients (2.4%) were found to have rhabdomyolysis. Including 4 patients with mixed infections, the etiologies in 25 patients with community-acquired pneumonia with rhabdomyolysis were as follows: Legionella species, 11 patients (44%); Influenza virus, 6 (24%); Streptococcus pneumoniae, 4 (16%); Chlamydia psittaci, 3 (12%); Mycoplasma pneumoniae, 2 (8%); unknown 3 patients (12%). The rates of rhabdomyolysis for each etiologic category were as follows: Legionella species, 26.8% (11/41); Chlamydia psittaci, 21.4% (3/14); Influenza virus, 9.5% (6/63) ; Streptococcus pneumoniae, 4.7% (4/85);Mycoplasma pneumoniae, 3.1% (2/65). Renal dysfunction with a serum creatinine concentration greater than 1.5 mg/dl occurred in 6 patients (24%). Our experience illustrates that 5 pathogens can cause rhabdomyolysis in patients with community-acquired pneumonia. Legionella species are the most common organisms followed by Influenza virus, Streptococcus pneumoniae, Chlamydia psittaci, Mycoplasma pneumoniae.