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BackgroundIt is critical for clinicians seeing outpatients with coronavirus disease 2019 (COVID-19) to identify those who will require oxygen therapy after the hospital visit. Although studies on biomarkers predicting mortality or ventilator requirement in hospitalized patients with COVID-19 have been conducted, research on biomarkers predicting the need for oxygen therapy in outpatients is sparse.MethodsPatients with COVID-19 who visited Asahikawa City Hospital on an outpatient basis were included in the study. In total, 287 new outpatients visited between April 2021 and September 2021, and 142 underwent blood testing. All blood tests were performed before any treatments for COVID-19 were started. Demographic information, laboratory data, and clinical treatment information were extracted from the electronic medical records. Risk factors associated with oxygen therapy were explored.ResultsIn total, 40 of 142 patients who underwent blood testing required oxygen therapy within 7 days after blood samples were taken, and all other patients recovered without oxygen therapy. C-reactive protein (CRP) and lactate dehydrogenase (LDH) levels were significantly higher in patients who required oxygen therapy, and their cutoffs were 36 mg/L (sensitivity, 0.802; specificity, 0.725) and 267 U/L (sensitivity, 0.713; specificity, 0.750), respectively. Multivariate logistic regression identified age, body mass index, CRP ≥ 36 mg/L, and LDH ≥ 267 U/L as significant risk factors for oxygen therapy requirement. This study suggests that elevated CRP and LDH levels are independent risk factors for oxygen therapy in outpatients with COVID-19. Further confirmatory studies are needed.

BackgroundRecent data from clinical trial suggest that antibody cocktail therapy, a combination of the monoclonal antibodies casirivimab and imdevimab, has been shown to rapidly reduce the viral load and markedly decrease the risk of hospitalization or death among high-risk patients with coronavirus disease 2019 (Covid-19). However, it remains unclear how effective in a real-life clinical setting the therapy is.MethodsWe retrospectively analyzed mild to moderate Covid-19 patients with one or more high-risk factors for severe disease who consecutively underwent the antibody cocktail therapy of the disease in our institute in June 2021 through early September 2021, compared to those with high-risk factors who were isolated in non-medical facilities consecutively during the same period, thereby being not given the antibody cocktail therapy there. The key outcome was the percentage of patients with Covid-19-related deterioration which needed additional medical interventions, such as oxygen support or other antiviral therapies.ResultsData from 55 patients with initially receiving antibody cocktail therapy and 53 patients with isolation into non-medical facilities are analyzed. 22 (41.5 %) of 53 patients with isolation facilities were finally hospitalized to receive medical interventions. On the other hand, 13 (23.6 %) of 55 patients with antibody cocktail therapy in our hospital subsequently underwent further medical interventions because of the progression. In multivariate analysis with variables of age, BMI, and high-risk factors, the antibody cocktail therapy significantly reduced 70 % in the need for further medical interventions compared to the initial isolation in the non-medical facilities (odds ratio=0.30, 95%CI [0.10-0.87], p=0.027). Furthermore, patients with 96% or above of SPO2 were significantly more favorable for the therapy than those with 95% or below of SPO2.ConclusionThe treatment of antibody cocktail was closely linked to reduction in the need for further medical interventions. The result indicates that the antibody cocktail therapy is associated with reducing the strain on hospitals, which is related to the improvement of medical management for public health care in Covid-19 pandemic era.

Background Recent data from clinical trial suggest that antibody cocktail therapy, a combination of the monoclonal antibodies casirivimab and imdevimab, has been shown to rapidly reduce the viral load and markedly decrease the risk of hospitalization or death among high-risk patients with coronavirus disease 2019 (Covid-19). However, it remains unclear how effective in a real-life clinical setting the therapy is. Methods We retrospectively analyzed mild to moderate Covid-19 patients with one or more high-risk factors for severe disease who consecutively underwent the antibody cocktail therapy of the disease in our institute in June 2021 through early September 2021, compared to those with high-risk factors who were isolated in non-medical facilities consecutively during the same period, thereby being not given the antibody cocktail therapy there. The key outcome was the percentage of patients with Covid-19-related deterioration which needed additional medical interventions, such as oxygen support or other antiviral therapies. Results Data from 55 patients with initially receiving antibody cocktail therapy and 53 patients with isolation into non-medical facilities are analyzed. 22 (41.5 %) of 53 patients with isolation facilities were finally hospitalized to receive medical interventions. On the other hand, 13 (23.6 %) of 55 patients with antibody cocktail therapy in our hospital subsequently underwent further medical interventions because of the progression. In multivariate analysis with variables of age, BMI, and high-risk factors, the antibody cocktail therapy significantly reduced 70 % in the need for further medical interventions compared to the initial isolation in the non-medical facilities (odds ratio=0.30, 95%CI [0.10-0.87], p=0.027). Furthermore, patients with 96% or above of SPO2 were significantly more favorable for the therapy than those with 95% or below of SPO2. Conclusion The treatment of antibody cocktail was closely linked to reduction in the need for further medical interventions. The result indicates that the antibody cocktail therapy is associated with reducing the strain on hospitals, which is related to the improvement of medical management for public health care in Covid-19 pandemic era.

The patient was referred to us for suspected Bechet’s disease and was finally diagnosed with osteitis and skin lesions caused by secondary syphilis. The syphilitic osteitis was confirmed by PCR using a biopsy of the spinal lesion.

The 2-step method is an algorithm to detect toxigenic

The patient was referred to us for suspected Bechet's disease and was finally diagnosed with osteitis and skin lesions caused by secondary syphilis. The syphilitic osteitis was confirmed by PCR using a biopsy of the spinal lesion.

Summary Background Secreted phosphoprotein 1 (SPP1) is a cytokine with pleiotrophic immunological activities, including activation of macrophage chemotaxis and T-helper type 1 (Th1) immune responses. SPP1 gene polymorphisms have been shown to be associated with several immune inflammatory diseases including multiple sclerosis (MS), which is characterized by fewer allergic symptoms and lower numbers of allergen sensitizations. Objective The present study examined whether SPP1 gene polymorphisms are associated with total serum IgE levels, atopy and asthma in a Japanese population. Methods This case–control association analysis examined 611 subjects, including 268 subjects with asthma. We genotyped three promoter and two exon polymorphisms at SPP1: −1687A/G; −381T/C; −94 deletion/G; 5891C/T; and 7052T/C. Results Association analyses of SPP1 polymorphisms showed that homozygosities for the 5891T allele (P=0.009) and 7052C allele (P=0.001) were significantly associated with increased levels of total IgE in non-asthmatic subjects. However, these variants were not associated with asthma and atopy. Interestingly, individuals carrying the 5891C allele, which is more prevalent in patients with MS in Japanese populations, displayed significantly lower levels of total serum IgE. Individuals homozygous for the 7052C allele, which is associated with development of systemic lupus erythematosus, displayed significantly higher total serum IgE levels. Conclusion These findings suggest that genetic polymorphisms in SPP1 may play a role in controlling basal levels of total serum IgE, independent of atopy.

Retinoic acid (RA) is known to accelerate wound healing and induce cell differentiation. All- trans RA (ATRA) exerts its effect by binding retinoic acid receptors, which are members of the nuclear receptor family. We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-κB. We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. ATRA and its stereodimer 9- cis retinoic acid (9- cis RA) inhibited IL-4-induced release of eotaxin at 10-6M by 78.0 and 52.0%, respectively ( P < 0.05). ATRA and 9- cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10-6M by 52.3 and 53.5%, respectively ( P < 0.05). In contrast, neither ATRA nor 9- cis RA had any effects on TNF-α-induced eotaxin production. In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Interestingly, ATRA had no effects on IL-4-induced tyrosine phosphorylation, nuclear translocation, or DNA binding activity of STAT6. Activating protein-1 was not involved in ATRA-mediated transrepression of eotaxin with IL-4 stimulation. The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. These findings raise the possibility that RA may reduce eosinophilic airway inflammation, one of the prominent pathological features of allergic diseases such as bronchial asthma.

The CC chemokine regulated upon activation, normal T-cell expressed and secreted (RANTES) attracts eosinophils, basophils, and T cells during inflammation and immune response, indicating a possible role for this chemokine in asthma. Both the -403A and -28G alleles of the RANTES promoter region exhibit significantly enhanced promoter activity in reporter constructs in vitro. We therefore investigated the genetic influence of these alleles on the development of asthma using case-control analysis in a Japanese population (298 patients with asthma and 311 control subjects). Given the evidence for heterogeneity of asthma according to age at onset, we divided patients with asthma into three subgroups: 117 late-onset patients with asthma (onset at more than 40 years of age), 83 middle-onset patients with asthma (onset at 20 to 40 years of age), and 98 early-onset patients with asthma (onset at less than 20 years of age). The -28G allele was significantly associated with late-onset asthma (odds ratio = 2.033; 95% confidence interval, 1.379–2.998; corrected p < 0.0025) but was not associated with the other two asthma subgroups. The -403A allele was not associated with any of the asthma subgroups. Further evidence of the importance of the -28G allele was a significant increase in the production of RANTES in vitro in individuals who carried this allele. Our findings suggest that, among Japanese, the -28G allele of the RANTES promoter region confers susceptibility to late-onset asthma.

A 33-year-old woman used waterproofing spray and subsequently developed cough, sputum and chest pain about 8 hours later accompanied by dyspnea, fever and general fatigue. She was admitted to our hospital 4 days after the symptoms appeared. A chest CT scan on the first visit revealed diffuse mild centrilobular nodular opacities and ground-glass opacities in both lung fields. Hemosiderin-laden macrophages accounted for 11% of the histiocytes found in her bronchoalveolar lavage fluid, which also contained blood. Based on these findings, the patient was given a diagnosis of diffuse alveolar hemorrhage. This is the first report in Japan of diffuse alveolar hemorrhage occurring after the use of a waterproofing spray.