BackgroundIn the ongoing COVID-19 pandemic, the susceptibility of patients with rheumatic diseases to COVID-19 remains unclear. We aimed to investigate susceptibility to COVID-19 in patients with autoimmune rheumatic diseases during the ongoing COVID-19 pandemic. MethodsWe did a multicentre retrospective study of patients with autoimmune rheumatic diseases in Hubei province, the epicentre of the COVID-19 outbreak in China. Patients with rheumatic diseases were contacted through an automated telephone-based survey to investigate their susceptibility to COVID-19. Data about COVID-19 exposure or diagnosis were collected. Families with a documented history of COVID-19 exposure, as defined by having at least one family member diagnosed with COVID-19, were followed up by medical professionals to obtain detailed information, including sex, age, smoking history, past medical history, use of medications, and information related to COVID-19. FindingsBetween March 20 and March 30, 2020, 6228 patients with autoimmune rheumatic diseases were included in the study. The overall rate of COVID-19 in patients with an autoimmune rheumatic disease in our study population was 0•43% (27 of 6228 patients). We identified 42 families in which COVID-19 was diagnosed between Dec 20, 2019, and March 20, 2020, in either patients with a rheumatic disease or in a family member residing at the same physical address during the outbreak. Within these 42 families, COVID-19 was diagnosed in 27 (63%) of 43 patients with a rheumatic disease and in 28 (34%) of 83 of their family members with no rheumatic disease (adjusted odds ratio [OR] 2•68 [95% CI 1•14-6•27]; p=0•023). Patients with rheumatic disease who were taking hydroxychloroquine had a lower risk of COVID-19 infection than patients taking other disease-modifying anti-rheumatic drugs (OR 0•09 [95% CI 0•01-0•94]; p=0•044). Additionally, the risk of COVID-19 was increased with age (adjusted OR 1•04 [95% CI 1•01-1•06]; p=0•0081).Interpretation Patients with autoimmune rheumatic disease might be more susceptible to COVID-19 infection than the general population.

Regulatory CD19 + CD24 hi CD27 + B cells were proved to be numerically decreased and functionally impaired in the peripheral blood (PB) from rheumatoid arthritis (RA), with the potential of converting into osteoclast-priming cells. However, the distribution and function of CD19 + CD24 hi CD27 + B cells in RA synovial fluid (SF) were unclear. In this study, we investigated whether RA SF CD19 + CD24 hi CD27 + B cells were increased and associated with bone destruction. We found that the proportion of RA SF CD19 + CD24 hi CD27 + B cells was increased significantly, and was positively correlated with swollen joint counts, tender joint counts and disease activity. CXCL12, CXCL13, CCL19 contributed to the recruitment of CD19 + CD24 hi CD27 + B cells in RA SF. Notably, CD19 + CD24 hi CD27 + B cells in the Sf from RA expressed significantly more RANKL compared to OA and that in the PB from RA. Critically, RA CD19 + CD24 hi CD27 + B cells promoted osteoclast (OC) differentiation in vitro, and the number of OCs was higher in cultures with RA SF CD19 + CD24 hi CD27 + B cells than in those derived from RA PB. Collectively, these findings revealed the accumulation of CD19 + CD24 hi CD27 + B cells in SF and their likely contribution to joint destruction in RA. Modulating the status of CD19 + CD24 hi CD27 + B cells might provide novel therapeutic strategies for RA. Rheumatoid arthritis (RA) is a common chronic autoimmune disease characterized by synovitis in multiple joints and progressive bone destruction 1. Mounting evidence indicates that the imbalance between bone loss and bone formation attributes to bone damage in RA 2. Bone-resorbing osteoclasts (OCs) are the cells responsible for bone erosion in RA patients 3. Receptor activator of NF-κB ligand (RANKL) and its receptor, RANK, are key positive extracellular regulators of osteoclast formation and activation 4,5. Early studies of RANKL production in RA indicated that synovial fibroblasts and activated T cells produce excess RANKL and may contribute to osteoclastic bone resorption 6-8. However, recent increasing researches have demonstrated that B cells play an important role in facilitating bone erosion in RA by both promoting OC differentiation and by suppressing osteoblast (OB) development 9-13. Scientists found that synovial B cells are a major source of RANKL and Fc-receptor like 4 (FcRL4) positive B cells are defined a pro-inflammatory, RANKLproducing B cells in RA 9,10. Thereafter, switched-memory B cells have been reported in RA peripheral blood and synovial tissue, where they are thought to express high level of RANKL and promoted osteoclastogenesis 11,12. Moreover, B cells have been proved to inhibit bone formation in RA by secreting multiple OB inhibitors 13 , furtherly indicating the tight relationship between B lymphocytes and bone homeostasis. As reported, CD19 + CD24 hi CD27 + B cells were identified as IL-10 producing B cell subsets in human, which also termed as regulatory B10 cells 14. Several studies have shown that these B10 cells were numerically decrea...

Objective: To analyze the characteristics of chest high resolution computed tomography (CT) images of coronavirus disease 2019 (COVID-19). Methods: This is a retrospective study analyzing the clinical records and chest high-resolution CT images of 46 consecutive patients who were diagnosed with COVID-19 by nucleic acid tests and treated at our hospitals between January 2020 and February 2020. Results: Abnormalities in the CT images were found in 44 patients (95.6%). The lesions were unilateral in eight patients (17.4%), bilateral in 36 patients (78.3%), single in seven patients (15.9%), and multiple in 37 patients (84.1%). The morphology of the lesions was scattered opacity in 10 patients (21.7%), patchy opacity in 38 patients (82.6%), fibrotic cord in 17 patients (37.0%), and wedge-shaped opacity in two patients (4.3%). The lesions can be classified as ground-glass opacity in eight patients (17.4%), consolidation in one patient (2.2%), and ground-glass opacity plus consolidation in 28 patients (60.9%). Conclusion: Most COVID-19 patients showed abnormalities in chest CT images and the most common findings were ground-glass opacity plus consolidation. Abbreviations:COVID-19: coronavirus disease 2019, CT: computed tomography,SARS-CoV-2: severe acute respiratory syndrome coronavirus 2, RNA: ribonucleic acid. doi: https://doi.org/10.12669/pjms.37.3.3504 How to cite this:Lu Y, Zhou J, Mo Y, Song S, Wei X, Ding K. Characteristics of Chest high resolution computed tomography images of COVID-19: A retrospective study of 46 patients. Pak J Med Sci. 2021;37(3):---------. doi: https://doi.org/10.12669/pjms.37.3.3504 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background This study describes an AIDS patient with central nervous systems tuberculosis, and cytomegalovirus infection who experienced immune reconstitution inflammatory syndromes associated to cytomegalovirus encephalitis and pulmonary tuberculosis while receiving antiretroviral therapy. Case presentation A 59-year-old male with fever of unknown origin with dizziness, fatigue, loss of appetite, fear of cold, occasional babbling during fever, and paroxysmal cough as the main symptoms three days was referred to our hospital Cerebrospinal fluid examination showed a cytomegaloviral load of 3.4×103 copies/ml and a positive mycobacterium tuberculosis recombination test. Cerebrospinal fluid gene X-pert MTB/RIF test showed mycobacterium tuberculosis infection without rifampicin resistance. Anti-tuberculosis treatment and anti-cytomegalovirus therapy were administered, and clinical and laboratory abnormalities were improved. The patient's CD4+ T lymphocyte count was 70 cells/μl, and antiretroviral therapy was started 24 days after the start of anti-tuberculosis treatment. Clinical symptoms reappeared on day 33 after antiretroviral therapy treatment. Relapsing - immune reconstitution inflammatory syndrome was considered as the most likely diagnosis. After the addition of a small amount of dexamethasone to continue anti-tuberculosis and anti-cytomegalovirus therapy, the patient's symptoms disappeared and imaging was reduced in scope. There was no recurrence of clinical symptoms at 2 years of outpatient follow-up. Conclusion It is important to take aware of the emergence of multiple infections and the associated immune reconstitution inflammatory syndrome in AIDS. Once the immune reconstitution inflammatory syndrome manifests, a proper diagnosis and continual of treatment are imperative to the patient's recovery.