Positive antiphospholipid antibodies and pulmonary embolism in a patient with adalimumab-induced lupus.

It is known that administration of tumor necrotic factor (TNF) inhibitors induces lupus. The case of a Crohn's disease patient who had been treated with adalimumab (ADA) and showed positive anti-DNA and antiphospholipid antibodies and developed pulmonary embolism is presented. Fortunately, early diagnosis and intervention helped her survive. Although ADA was withdrawn, the Crohn's disease did not recur, and the autoantibodies became negative without any steroid therapy. It is important to recognise that administration of TNF inhibitors may be associated with antiphospholipid syndrome. It is necessary to perform therapeutic interventions such as TNF inhibitor withdrawal and prompt anticoagulant therapy when such pathology is suspected.

Predicting in-hospital death in pneumonic COPD exacerbation via BAP-65, CURB-65 and machine learning.

INTRODUCTION: There is no established clinical prediction model for in-hospital death among patients with pneumonic COPD exacerbation. We aimed to externally validate BAP-65 and CURB-65 and to develop a new model based on the eXtreme Gradient Boosting (XGBoost) algorithm. METHODS: This multicentre cohort study included patients aged ≥40 years with pneumonic COPD exacerbation. The input data were age, sex, activities of daily living, mental status, systolic and diastolic blood pressure, respiratory rate, heart rate, peripheral blood eosinophil count and blood urea nitrogen. The primary outcome was in-hospital death. BAP-65 and CURB-65 underwent external validation using the area under the receiver operating characteristic curve (AUROC) in the whole dataset. We used XGBoost to develop a new prediction model. We compared the AUROCs of XGBoost with that of BAP-65 and CURB-65 in the test dataset using bootstrap sampling. RESULTS: We included 1190 patients with pneumonic COPD exacerbation. The in-hospital mortality was 7% (88 out of 1190). In the external validation of BAP-65 and CURB-65, the AUROCs (95% confidence interval) of BAP-65 and CURB-65 were 0.69 (0.66-0.72) and 0.69 (0.66-0.72), respectively. XGBoost showed an AUROC of 0.71 (0.62-0.81) in the test dataset. There was no significant difference in the AUROCs of XGBoost versus BAP-65 (absolute difference 0.054; 95% CI -0.057-0.16) or versus CURB-65 (absolute difference 0.0021; 95% CI -0.091-0.088). CONCLUSION: BAP-65, CURB-65 and XGBoost showed low predictive performance for in-hospital death in pneumonic COPD exacerbation. Further large-scale studies including more variables are warranted.

The prognostic factors of in-hospital death among patients with pneumonic COPD acute exacerbation.

BACKGROUND: Pneumonic acute exacerbation of chronic obstructive pulmonary disease (COPD-AE) is associated with worse outcomes compared with non-pneumonic COPD-AE. We aimed to explore prognostic factors among patients with pneumonic COPD-AE. METHODS: This multicentered retrospective cohort study was conducted across five hospitals in Japan. Hospitalized patients ≥40 years of age with pneumonic COPD-AE who were administered systemic corticosteroids during hospitalization were included. Patients with other causes of respiratory failure, daily systemic steroid users, and patients who were not treated with systemic steroids were excluded. Based on existing clinical prediction models, the following potential prognostic factors were selected in advance: age, blood eosinophil count, blood urea nitrogen, respiratory rate, diastolic blood pressure, and altered mental status. Multivariate logistic regression was conducted to determine the association between potential prognostic factors and in-hospital death. RESULTS: After excluding 897 patients based on the exclusion criteria, 669 patients with pneumonic COPD-AE who were administered systemic corticosteroids were included. The in-hospital mortality rate was 5.1%. Altered mental status was associated with mortality (odds ratio, 4.47; 95% confidence intervals, 2.00 to 10.00), and eosinophilia was associated with a lower risk of mortality (odds ratio, 0.19; 95% confidence intervals: 0.06 to 0.56). CONCLUSIONS: Altered mental status may be a prognostic factor for in-hospital death among patients with pneumonic COPD-AE who were administered systemic corticosteroids. Moreover, eosinophilia may be a prognostic factor for lower in-hospital mortality rate among these patients.

Effectiveness of empirical anti-pseudomonal antibiotics for recurrent COPD exacerbation: a multicenter retrospective cohort study.

Although frequent chronic obstructive pulmonary disease (COPD) exacerbation has been associated with the isolation of Pseudomonas aeruginosa (PA) in sputum cultures, it remains unknown whether the empirical use of anti-pseudomonal antibiotics can improve outcomes in patients with frequent COPD exacerbations. This multicenter retrospective cohort study evaluated whether the empirical use of anti-pseudomonal antibiotics improves the length of the hospital stay in patients with recurrent COPD exacerbation (≥ 2 admissions from April 1, 2008 to July 31, 2020). For statistical analysis, a log-linked Gamma model was used. Parameters were estimated using a generalized estimating equation model with an exchangeable correlation structure accounting for repeated observations from a single patient. Covariates included age, body mass index, home oxygen therapy use, respiratory rate, heart rate, oxygen use on admission, mental status, systemic steroid use, activities of daily living, and the number of recurrences. Hospital-specific effects were specified as fixed effects. In total, 344 patients and 965 observations of recurrent COPD exacerbations were selected. Anti-pseudomonal antibiotics were used in 173 patients (18%). The estimated change in the length of the hospital stay between anti-pseudomonal and non-anti-pseudomonal antibiotics groups was 0.039 days [95% confidence interval; - 0.083, 0.162]. Anti-pseudomonal antibiotics could not shorten the length of the hospital stay.

Low-dose oestrogen-progestin associated pulmonary infarction mimicking pneumonia and pleurisy.

A 28-year-old woman with a history of treatment with a low-dose oestrogen-progestin (LEP) formulation presented to our hospital due to right chest pain. She had just been discharged from another hospital for pneumonia and pleurisy which had improved with antibiotics. Contrast-enhanced computed tomography (CT) revealed bilateral pulmonary emboli corresponding to the peripheral consolidations. The pulmonary emboli indicated that the peripheral consolidation was due to pulmonary infarction (PI). No aetiological factors were identified except for the history of LEP therapy. Although the typical CT images of PI are consolidations in the peripheral area, these finding are non-specific for PI. This case of PI was misdiagnosed as infection because of response to antibiotics and similar CT findings. Therefore, careful evaluation of the patient history and clinical findings are imperative for accurate diagnosis. Venous thromboembolism can occur frequently around 3 months after the start of LEP treatment.

Granulomatous-lymphocytic Interstitial Lung Disease Associated with Good's Syndrome That Responded to Immunoglobulin Therapy.

Good's syndrome is associated with thymoma and acquired immunodeficiency. A 54-year-old man visited our hospital with a complaint of cough. Chest imaging revealed diffuse nodular shadows and anterior mediastinal mass. Hypogammaglobulinemia and a decreased B lymphocyte count were found by a laboratory evaluation. The lung nodules markedly regressed after immunoglobulin therapy. The mediastinal mass and remaining nodule were surgically resected and diagnosed as a type AB thymoma and a necrotizing epithelioid granuloma with T lymphocyte-dominant alveolitis, respectively. The overall appearances of these lesions were mostly in line with the spectrum of granulomatous-lymphocytic interstitial lung disease associated with Good's syndrome.

Aerobic oxidation of thiols to disulfides catalyzed by trichlorooxyvanadium.

Thiols were converted into disulfide by the aerobic oxidation catalyzed by trichlorooxyvanadium in the presence of molecular sieves 3A.