[A suspected case of acute respiratory failure caused by ritodrine hydrochloride].

A 36-year-old woman was admitted to the obstetric department because of possible premature labor of twins at 35 weeks. She had been treated by ritodrine hydrochloride, a tocolytic agent, for 1 week, and delivered healthy twins by cesarean operation. After the operation, she suddenly complained of dyspnea with associated hypoxemia and was admitted to our hospital. She presented with hypoxemia and was given a diagnosis of pulmonary edema. She was given a diuretic with ventilator therapy, and improved rapidly. However, an echocardiogram showed continuing left ventricular systolic dysfunction after 3 months. From these results, this case was suspected to be pulmonary edema due to ritodrin after myocardial failure, including peripartum cardiomyopathy.

Low expression of T-cell co-stimulatory molecules in bone marrow-derived dendritic cells in a mouse model of chronic respiratory infection with Pseudomonas aeruginosa.

Pseudomonas (P.) aeruginosa frequently colonizes the respiratory tract of patients with chronic respiratory tract infections such as diffuse panbronchiolitis (DPB). The number of dendritic cells (DCs) that play a central role in immune functions as antigen-presenting cells is reportedly increased in the bronchiolar tissues of patients with DPB. However, the functions of DCs in chronic P. aeruginosa respiratory tract infection have not been defined. Here, we assessed the functions of DCs and the effect of macrolide antibiotics that are therapeutic agents for DPB, in a murine model of DPB caused by P. aeruginosa. Mice were intubated with either P. aeruginosa- or saline-precoated tubes for 80 days. Thereafter, the expression of T-cell co-stimulatory molecules (CD40, CD80, and CD86) and cytokine secretion (interleukin (IL)-10, IL-6, IL-12p40, and tumor necrosis factor (TNF)-alpha) on bone marrow-derived DCs stimulated by lipopolysaccharide were examined by flow cytometry and enzyme-linked immunosorbent assays. The expression of co-stimulatory molecules was significantly decreased in mice infected with P. aeruginosa compared to the saline-treated control mice, but production of these cytokines did not significantly differ between the two groups. Pretreatment with clarithromycin ex vivo decreased CD40 expression on DCs obtained from P. aeruginosa-infected mice and also decreased the production of IL-6, IL-12p40 and TNF-alpha by DCs. These findings suggest that chronic P. aeruginosa infection alters DC functions and that macrolides function as anti-inflammatory agents by modulating the functions of DCs in chronic P. aeruginosa infection.

[Case of acute exacerbation after video-assisted thoracoscopic surgery in a patient with chronic hypersensitivity pneumonitis].

A 65-year-old man had been admitted with exertional dyspnea 2 years previously. Reticular shadows in bilateral lower lung fields were detected on chest roentogenogram and observed the natural course. The clinical symptoms and radiological findings progressed one month later and then he was admitted to our hospital to be examined for diagnosis and treatment. Video-assisted thoracoscopic surgery (VATS) was performed and chronic hypersensitivity pneumonitis was diagnosed. At five days after the surgery, dyspnea and radiological findings deteriorated and we diagnosed acute exacerbation of chronic hypersensitivity pneumonitis. He was treated immediately with steroid pulse therapy, immunosuppressant and polymyxin B-immobilized fiber column-direct hemoperfusion, which relieved his clinical symptoms and radiological findings. Although this is a very rare case, we have to consider the possibility of acute exacerbation of chronic hypersensitivity pneumonitis after VATS, as we do in idiopathic pulmonary fibrosis.

[Case of nonspecific interstitial pneumonia associated with aortitis syndrome].

A 32-year-old woman was admitted to our hospital because of fever and back pain. Two months previously, she had been given a diagnosis of bacterial pneumonia based on the same symptoms and recovered after antibiotic treatment. Chest CT scans on admission showed a consolidation and thickened pleura in the right lower lobe. Bronchoalveolar lavage fluids showed an alveolar hemorrhage. Lung biopsy specimens showed thickened pulmonary arteries and fibrotic nonspecific interstitial pneumonia (NSIP). Three years later, she was admitted with fever and pain of the left arm and aortitis syndrome was diagnosed. In this case of NSIP pattern associated with aortitis syndrome we speculate that repeated pulmonary infarction and alveolar hemorrhages caused the NSIP pattern.