Barriers and Facilitators to the Implementation of an Electronic Patient-Reported Outcome System at Cancer Hospitals in Japan.

Background and objective Implementing electronic patient-reported outcomes (ePROs) in oncology practice has shown substantial clinical benefits. However, it can be challenging in routine practice, warranting strategies to adapt to different clinical contexts. In light of this, this study aimed to describe the implementation process of the ePRO system and elucidate the provider-level implementation barriers and facilitators to a novel ePRO system at cancer hospitals in Japan. Methods We implemented an ePRO system linked to electronic medical records at three cancer hospitals. Fifteen patients with solid cancers at the outpatient oncology unit were asked to regularly complete the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE™) questionnaire and European Organization for Research and Treatment Core Quality of Life questionnaire (EORTC QLQ C30) by using the smartphone app between October 2021 and June 2022. Thirteen healthcare professionals were interviewed to identify implementation barriers and facilitators to the ePRO system by using the Consolidated Framework for Implementation Research framework. Results The healthcare professionals identified a lack of clinical resources and a culture and system that emphasizes treatment over care as the main barriers; however, the accumulation of successful cases, the leadership of managers, and the growing needs of patients can serve as facilitators to the implementation. Conclusions Our experience implementing an ePRO system in a few Japanese oncology practices revealed comprehensive barriers and facilitators. Further efforts are warranted to develop more successful implementation strategies.

Effect of cigarette smoking on the development of murine chronic pigeon breeder's lung. The difference between a short-term and a long-term exposure.

Previous reports suggested that cigarette smoke had a protective effect of on the development of hypersensitivity pneumonitis (HP). However, smoking rate in chronic pigeon breeder's lung (PBL) seemed to be high in our clinical experiences. We developed a murine model of PBL by intranasal instillation with pigeon dropping extracts (PDE) for 4 weeks (short-term exposure) and 17 weeks (long-term exposure) to investigate the effect of cigarette smoke on disease processes. In this model, lung inflammation associated with the production of anti-PDE antibodies and antigen dependent lymphocyte proliferation was induced. Long-term exposure to PDE without cigarette smoking resulted in an increase in lung weight/body weight ratio, total cell number in bronchoalveolar lavage (BAL) fluid, and content of hydroxyproline in the lung compared to shortterm exposure. After a short-term exposure, cigarette smoke lessened the lymphocytosis in BAL fluid, and lymphocyte proliferation. On the other hand, after a long-term exposure cigarette smoke increased lung hydroxyproline. These results suggest that a short-term cigarette smoking attenuates lung inflammation, but a long-term cigarette smoking enhances lung inflammation with fibrosis.

TGF-beta and glutathione promote tissue repair in cigarette smoke induced injury.

We studied the effect of cigarette smoke extract (CSE) on a three-dimensional (3-D) co-culture model with epithelial cells and mesenchymal cells to clarify how epithelial cells protect lung tissue from cigarette smoke in-vivo. Two types of gels were prepared. The one was the co-culture of human fetal lung fibroblasts (HFL-I) embedded in type-I collagen gel, with alveolar epithelial cells (A549) cultured covering the top of the gel. The other was HFL-I cells alone. After 48 hours from CSE exposure, gel contraction, levels of fibronectin, transforming growth factor (TGF)-beta and GSH were assessed. CSE inhibited fibroblast-mediated gel contraction and this inhibition was lessened in co-culture associated with higher GSH concentration and TGF-beta1 level as compared to the level in HFL-I cells alone. CSE lowered fibronectin level to a lesser extent in co-culture as compared to the level in HFL-I cells alone. Exogenous TGF-beta1 restored the inhibition of gel contraction by CSE independent of GSH level. Cigarette smoke may interfere with 3-D co-culture gel contraction by diminishing GSH, fibronectin and TGF-beta1 action in the epithelial-mesenchymal interaction.

A clinical study of hypersensitivity pneumonitis presumably caused by feather duvets.

BACKGROUND: Bird fancier's lung (BFL) is a type of hypersensitivity pneumonitis induced by the inhalation of bird-related antigens. The BFL induced by feathers is difficult to diagnose because feathers are generally unrecognized as a causative antigen. OBJECTIVE: To determine the clinical features of BFL presumably induced by feather duvets (feather duvet lung) to provide clues for diagnosis. METHODS: We performed a retrospective review of the medical records of patients with feather duvet lung evaluated between April 1, 2000, and June 30, 2003, at the Tokyo Medical and Dental University Hospital in Japan. RESULTS: Seven patients with feather duvet lung were included in this study; 4 patients had acute disease and 3 had chronic BFL. Duration of contact with feather duvets was 1 month to 10 years. Serum KL-6 and surfactant protein D levels were elevated in all the patients. Specific antibodies against avian antigens were positive in acute BFL but negative in chronic BFL. Antigen-induced lymphocyte proliferation in peripheral blood or bronchoalveolar lavage cells was positive in all the patients. The diagnosis was confirmed by an environmental or inhalation provocation test. CONCLUSIONS: Feather duvets can induce acute and chronic BFL. Physicians should be aware of feather duvets as a cause of BFL because feather duvets are becoming more prevalent.

Chronic bird fancier's lung presenting with acute exacerbation due to use of a feather duvet.

A 67-year-old man was admitted due to fever and exertional dyspnea. He used to raise budgerigars and hill mynahs from 1980 to 1988. He was diagnosed as having chronic bird fancier's lung (BFL) based on a positive peripheral lymphocyte proliferation to pigeon serum in 1994. His disease was stable until 2000. Three months before admission he became a daily user of a feather duvet. A chest CT showed newly-developed peribronchial ground-glass opacities and preexisting honeycombing. Inhalation provocation test was positive. Administration of steroids improved his condition. He has been well after refraining from the use of the feather duvet.

[The rate of airflow limitation among the elderly undergoing spirometry in a university hospital].

The aim of this study was to examine the rate of airflow limitation among the elderly undergoing spirometry prior to surgical operation, and to evaluate whether or not spirometry is useful for the early detection of COPD. A total of 3,086 patients (1,717 men and 1,369 women) ranging in age from 40 to 93 underwent screening spirometry from January to December 2003 in Tokyo Medical and Dental University Hospital. Among the total population, 2,135 patients (1,188 men and 947 women) were ordered to undergo the spirometry prior to surgical operation, airflow limitation (FEV1/FVC < 70%) was observed in 19.5% (n=417) of the cases and was considerably more frequent in men than in women(27.0%[n=321] vs. 10.1%[n=96]). The rate of FEV1/FVC < 70% in those 2,135 patients increased with age: 6.2%, 9.9%, 19.2%, 32.5% and 34.1% of patients in their 40s, 50s, 60s, 70s, 80s and over, respectively. Among the patients with airflow limitation, 35% of the cases revealed FEV1 > or = 80% predicted; 50%, 50 < or = FEV1 < 80% predicted; 14%, 30 < or = FEV1 < 50% predicted; 1%, FEV1 < 30% predicted. Patients with mild to moderate airflow limitation rarely consulted the pulmonary medicine department. The prevalence of airflow limitation was more frequent among in- and out-patients than in the random sample population. Spirometry prior to surgical operation is useful for the early detection of COPD and these data could be an important source for medical staff seeking a definitive diagnosis of patients revealing airflow limitation.

[Pneumoconiosis diagnosed in a dentist].

A 74-year-old man was admitted to our hospital because of exertional dyspnea in January 2003. He had first noticed slight exertional dypnea in 1997, which had since gradually progressed. He has been a dentist since the age of 23. Chest radiography demonstrated bilateral reticular shadows, infiltrates, and thickened pleural adhesion, which had progressed for one year and five months. Chest CT scans disclosed irregular peribronchial opacities, centrilobular nodules, and interlobular septal lines. Bronchoalveolar lavage fluid showed an increase in total cells and lymphocytosis with an increased CD 4/CD 8 ratio. Transbronchial lung biopsy demonstrated fibrosis around bronchioles, involving adjacent alveolar structures and scattered birefringent particles under polarized light. Energy-dispersive X-ray analysis (EDXA) of the small particles around the bronchioles using electron microscopy showed high peaks for silicon (Si) and aluminium (Al). Pneumoconiosis, possibly induced by some of the mechanical and technical procedures of dentistry, was diagnosed.

[Chronic summer-type hypersensitivity pneumonitis presenting with acute exacerbation].

A 77-year-old man was admitted to our hospital. He had first noticed a cough, sputum production, and low-grade fever during the summer of 1988. He was diagnosed as having summer-type hypersensitivity pneumonitis (HP) in 1989 on the basis of positive findings of anti-Trichosporon antibodies in the serum and bronchoalveolar lavage (BAL) fluid and and in environmental provocation tests. Thereafter, he presented with re-exacerbation of his disease in summer every year. In 1995, he retired from his work at a moldy hotel and moved to another house to avoid the causative antigen completely. There was no recurrence for the following 5 years. He suffered from cough, sputum production, and dyspnea 4 months after returning to his previous moldy house in October, 2000. A chest CT scan showed peribronchial and subpleural honeycombing, ground glass opacities, and traction bronchiectasis. BAL demonstrated that the lymphocyte count had changed from 78.9% to 42.9% and the CD4/CD8 ratio from 0.39 to 4.07 in 12 years. Antigen avoidance and steroid therapy have improved his condition. However, he stayed repeatedly in his moldy house, and finally died from acute exacerbation in March, 2002. Postmortem examination demonstrated diffuse alveolar damage (DAD) superimposed on honeycombing in the lungs.

[A case of acute bird fancier's lung caused by feather duvet].

A 57-year-old woman was admitted to our hospital because of cough and low-grade fever for 2 months and shortness of breath for 2 weeks. She had raised two budgerigars for the last 15 years and had been using a feather duvet for one year. A chest radiograph showed diffuse ground-glass opacities in both lung fields, and a chest CT scan showed centrilobular micronodules and ground-glass opacities. Bronchoalveolar lavage (BAL) revealed a marked increase in lymphocytes, and a transbronchial lung biopsy (TBLB) specimen showed alveolitis due to the infiltration of mononuclear cells. Since she had specific antibodies against pigeon and budgerigar dropping extracts and her peripheral blood lymphocytes proliferated on addition of pigeon serum, she was diagnosed as having bird fancier's lung (BFL). She was treated with steroids, which brought about a marked improvement. After she visited her husband who had been hospitalized where a feather duvet was provided for each patient, both subjective and objective findings deteriorated. This deterioration was preventable when she wore a protective mask for micro-dust while visiting her husband. The feather duvets seemed to induce acute BFL in this case, though raising budgerigars may well be related to her sensitization with bird-related antigens.

The effect of seratrodast on eosinophil cationic protein and symptoms in asthmatics.

Thromboxane A2 (TXA2), an arachidonate derivative, is a potent bronchoconstrictor; therefore, blocking TXA2 should attenuate airway narrowing. Seratrodast, a TXA2 receptor antagonist, is expected to be a potent antiasthmatic. It was reported that seratrodast reduced bronchial hyperresponsiveness. However, it is controversial whether it reduces airway inflammation. We studied some additional effects of oral seratrodast to inhaled corticosteroids on 10 adult asthmatics in an open-label, crossover design study. Eosinophil cationic protein (ECP) levels in serum and sputum, peak expiratory flow rate (PEF), clinical symptoms, and airway responsiveness were evaluated. Clinical symptom scores were improved by administration of seratrodast (p < 0.05). The addition of seratrodast to asthmatic patients significantly improved mean PEF (p < 0.05). In addition, withdrawal of seratrodast resulted in deterioration of PEF. Airway hyperresponsiveness to acetylcholine measured by Astograph was improved by administration of seratrodast (p < 0.01), and returned to the level of "run-in period" after withdrawal. Administration of seratrodast decreased the concentration of ECP in sputum significantly (p < 0.05), and sputum ECP significantly increased again after withdrawal of (p < 0.05). These results suggest that seratrodast improves clinical symptoms andairway hyperresponsiveness by reducing airway inflammation. Seratrodast may be useful as an anti-inflammatory agent and beneficial when added to inhaled corticosteroids in the treatment of bronchial asthma.

Effect of cigarette smoke on fibroblast-mediated gel contraction is dependent on cell density.

Cigarette smoke exposure has been associated with a variety of diseases, including emphysema. The current study evaluated the interaction of cell density and cigarette smoke extract (CSE) on fibroblast contraction of collagen gels. Protein levels of transforming growth factor (TGF)-beta1, fibronectin, PGE(2), and TGF-beta1 mRNA were quantified. Although both 5 and 10% CSE inhibited contraction by low-density fibroblasts (1 x 10(5) cell/ml), only 5% CSE augmented contraction in higher-density cultures (3-5 x 10(5) cells/ml). CSE also inhibited fibronectin and TGF-beta1 production in low-density cultures but stimulated fibronectin production in high-density cultures. Active TGF-beta1 was readily detectable only in higher-density cultures and was markedly augmented by 5% CSE. In contrast, although TGF-beta1 mRNA expression was inhibited in high-density cultures by 10% CSE, expression was increased in the presence of 5% CSE. These results suggest that CSE-induced inhibition of low-density fibroblast contraction is due to inhibition of fibronectin production, whereas CSE's stimulatory effect on high-density cells is the result of increased release of TGF-beta1. These effects may help explain the varied pathologies associated with exposure to cigarette smoke.

Evaluation of subclinical respiratory tract inflammation in heavy smokers who switch to a cigarette-like nicotine delivery device that primarily heats tobacco.

Cigarette smoking remains a major public health problem. For smokers who cannot or do not wish to quit, few options exist to reduce health risks. A cigarette-like nicotine delivery device that heats rather than burns tobacco might deliver nicotine with fewer toxins. The current study was designed to determine whether asymptomatic heavy smokers who did not wish to quit had improvement in lower respiratory tract inflammation after switching to Eclipse, a cigarette-like nicotine delivery device that primarily heats rather than burns tobacco. Twelve smokers of at least 40 cigarettes daily, asymptomatic and in good health, underwent paired bronchoscopies, bronchoalveolar lavages and endobronchial biopsies before and after 2 months of using Eclipse. Eight normal non-smoking individuals were evaluated on one occasion for comparison. Inflammation was assessed by direct inspection and by cytological parameters. Goblet cell metaplasia was assessed histologically. Compared to non-smokers, smokers had increased visible inflammation, increased recovery of inflammatory cells and increased percentage of goblet cells. There were significant reductions in all these parameters following a switch to Eclipse use, although the improvement did not reach the normal range. No significant differences were observed in peripheral blood measures. Nicotine levels were generally maintained, and exhaled carbon monoxide (CO) levels trended strongly upward. One individual experienced a transient twofold increase in CO and concurrently experienced transient headaches. Eclipse use may be a strategy to reduce the health risks for heavy smokers unwilling or unable to quit.