Favipiravir is an oral broad-spectrum inhibitor of viral RNA-dependent RNA polymerase that is approved for treatment of influenza in Japan. We conducted a prospective, randomized, open-label, multicenter trial of favipiravir for the treatment of COVID-19 at 25 hospitals across Japan. Eligible patients were adolescents and adults admitted with COVID-19 who were asymptomatic or mildly ill and had an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1. Patients were randomly assigned at a 1:1 ratio to early or late favipiravir therapy (the same regimen starting on day 6 instead of day 1). The primary endpoint was viral clearance by day 6. The secondary endpoint was change in viral load by day 6. Exploratory endpoints included time to defervescence and resolution of symptoms. Eighty-nine patients were enrolled, of whom 69 were virologically evaluable. Viral clearance occurred within 6 days in 66.7% and 56.1% of the early and late treatment groups (adjusted hazard ratio [aHR], 1.42; 95% confidence interval [95% CI], 0.76–2.62). Of 30 patients who had a fever (≥37.5°C) on day 1, time to defervescence was 2.1 days and 3.2 days in the early and late treatment groups (aHR, 1.88; 95%CI, 0.81–4.35). During therapy, 84.1% developed transient hyperuricemia. Favipiravir did not significantly improve viral clearance as measured by RT-PCR by day 6 but was associated with numerical reduction in time to defervescence. Neither disease progression nor death occurred to any of the patients in either treatment group during the 28-day participation (Japan Registry of Clinical Trials jRCTs041190120).

CT densitometry showed a distinct lobar distribution of emphysema. Pulmonary function is significantly different between predominantly upper- and lower-lobe emphysema groups.

The aim of this study was to determine the relationship between the radiological pattern of Mycoplasma pneumoniae and the level of cell-mediated immunity of the host.Computed tomographic (CT) scans of the chest and the results of the purified protein derivative (PPD) test were studied during the acute stage of infection in 54 patients with M. pneumoniae pneumonia. The CT findings were used to divide the patients into two groups: one group had a predominance of nodular opacities with a centrilobular distribution (Group N; n=29); and the other showed a predominance of an airspace consolidation (Group C; n=25).Forty out of 54 subjects had negative tuberculin skin tests (<10 mm induration). The positive rate of PPD reaction was higher in Group N (13 out of 29) compared to Group C (1 out of 25) (p=0.0005); whilst pleural effusion appeared more frequently in Group C (10 out of 25) than in Group N (3 out of 29) (p=0.023). There was no significant difference between Groups N and C in white blood cell and lymphocyte counts, level of antibodies to M. pneumoniae in sera, and severity of the disease.These findings suggest that the characteristics of the host cell-mediated immunity might influence the pattern of pulmonary lesions in M. pneumoniae infection. Eur Respir J., 1996, 9, 669-672. The cell-mediated immunity (CMI) of the host plays an important role in the development of Mycoplasma pneumoniae pneumonia (MP) [1,2]. MIZUTANI et al. [3] reported that the delayed hypersensitivity skin reactions to M. pneumoniae antigen appeared to correlate with severity of pneumonia in human MP. FOY et al. [4] reported that MP infection in patients with immunodeficiency syndrome had a lack of radiological chest findings. PUTMAN et al. [5] reported a bilateral reticulonodular pattern when MP was associated with sarcoidosis. These manifestations suggest that pulmonary infiltrates of MP might be a result of the immunological reaction of the host.The purified protein derivative (PPD) reaction is used to confirm past infection by Mycobacterium tuberculosis, and to determine the CMI of the host. In Japan, most individuals have CMI to PPD due to the nearly universal bacille Calmette-Guérin (BCG) vaccination in childhood. Transient tuberculin anergy has been observed (57-61%) [6,7] during the early stage of MP. TSUNEKAWA et al. [7] reported that blastogenic lymphocyte response to PPD and PPD-induced gamma-interferon (IFN-γ) production were significantly reduced in tuberculin-negative patients with MP. However, the relationship between the pattern of pulmonary lesions and host CMI level in MP has not been evaluated.The findings of chest radiography of MP are varied; CLYDE [8] noted four frequent patterns suggesting MP: bronchopneumonia; nodular infiltration; plate-like atelectasis; and hilar adenopathy. Bronchopneumonia of MP is accompanied by thickening of bronchi, streaks of interstitial infiltration, and small areas of subsegmental atelectasis. The changes are produced by the presence of peribronchial inflammatory cell infiltrati...

A 53-year-old womanwasadmitted to our hospital complaining of cough, low grade fever, chest pain and sicca symptoms. A chest radiograph showed an abnormal shadow and chest computed tomography revealed a tumor in left S6. She was diagnosed as Sjogren's syndrome by sialography and histological findings of labial biopsy. The surgically resected tumor specimen showed proliferation of lymphoid cells with lymphoepithelial lesions, which were positive for CD20 and kappa light chain. Kappa light chainpositive amyloid was found within the tumor. The tumor showed rearranged kappa light chain genes. The diagnosis was pulmonary mucosa associated lymphoid tissue lymphoma with amyloid production. (Internal Medicine 41 : 309-311, 2002)

C Ch hr ro on ni ic c e eo os si in no op ph hi il li ic c p pn ne eu um mo on ni ia a p pr ro og gr re es ss si in ng g t to o l lu un ng g f fi ib br ro os si is s ABSTRACT: A 65 year old Japanese man was hospitalized with fever. Opacities distributed mainly in the subpleural regions were found on chest computed tomographic scan (CT), and these promptly cleared with corticosteroid therapy.Four years later, he presented with severe eosinophilia. Both chest X-ray and high resolution CT scan showed ground-glass opacities and honeycombing, suggesting lung fibrosis. A lung biopsy demonstrated intra-alveolar eosinophil infiltration, interstitial thickening with eosinophil infiltration, and a widely-distributed desquamative interstitial pneumonia-like reaction. With corticosteroid therapy, the ground-glass opacities decreased with a corresponding clinical improvement, although lung honeycombing and blood eosinophilia remained.In this case, circulating intercellular adhesion molecule-1 and circulating and bronchoalveolar lavage fluid eosinophil granule proteins were felt to be more effective markers for evaluating disease activity than the blood eosinophil number.

SUMMARY ICAM‐1 plays an important role in inflammatory diseases. To assess level of soluble ICAM‐1 in the circulation and inflamed lesions, we measured levels of soluble ICAM‐1 in the circulation and bronchial veolar lavage fluid (BALF) of patients with idiopathic pulmonary fibrosis (IPF) and with pulmonary sarcoidosis (PS) and of healthy volunteers (HV), and we also analysed ICAM‐I expression of BALF cells in some patients and HV. IPF patients had significantly higher levels of circulating ICAM‐1 than HV, while PS patients did not. By contrast, significantly increased levels of BALF soluble ICAM‐1 were found in PS patients compared with those of HV, but not in IPF patients. There were no significant differences in the proportions of ICAM‐1+ BALF lymphocytes in IPF patients, PS patients and HV. whereas significantly increased proportions of ICAM‐1 pulmonary alveolar macrophages were found in PS patients compared with those of HV, but not in IPF patients. There was a significant positive correlation of BALF soluble ICAM‐1 levels to BALF lymphocyte proportions in PS patients. Although the source of BALF soluble ICAM‐1 is unclear. BALF soluble ICAM‐1 appears to reflect the grade of local activity of sarcoidosis. An interesting discrepancy between soluble ICAM‐1 levels in the circulation and BALF was found in IPF patients, and this might be an important clue to an understanding of this disorder.

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