The clinical characteristics and risk factors for severe COVID-19 in patients with COVID-19 and tuberculosis coinfection

Abstract

BackgroundUnder the wave of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) variant Omicron epidemic, the number of infectious cases has increased dramatically in Jilin Province, China since March 2022.The clinical features and severity of SARS-CoV-2 Omicron variant infection in tuberculosis (TB) patients are not yet clear.MethodsData were obtained from 153 patients with the Omicron variant and TB coinfection and 153 non-TB COVID-19 patients who had been hospitalized at Changchun Infectious Disease Hospital from March to June 2022.ResultsAmong these coinfection patients, 17 patients showed COVID-19-related pneumonia on chest imaging and 11 were diagnosed with severe COVID-19. The median duration of SARS-CoV-2 clearance was 13 days. The negative conversion time was associated with age, COVID-19-related pneumonia and antibody IgG. A higher white blood cell count, a lower lymphocyte percentage, a higher CRP level, and a higher D-dimer level were found in the severe group. Age and increased PCT were individual risk factors for the severity of COVID-19. Compared with the non-TB patients, the coinfection patients had higher severity of COVID-19 and the elder coinfection patients had a longer negative conversion time.ConclusionThis study found an association between age, pneumonia, antibody IgG and RNA negative conversion time in COVID-19 and TB coinfection patients, and age and increased PCT were risk factors for the severity of COVID-19.

Systematic review and meta-analysis of Tuberculosis and COVID-19 Co-infection: Prevalence, fatality, and treatment considerations

“…These findings emphasize the importance of tailored management approaches that address the complex interactions between TB and COVID-19. Consistent findings across multiple studies indicate that individuals with TB-COVID co-infection face a higher risk of hospital admission, longer time-to-recovery, and shorter time-to-death compared to individuals with single COVID-19 infection [ 21 , 23 – 25 ]. These observations underscore the unique challenges posed by the coexistence of TB and COVID-19 and emphasize the necessity for tailored management strategies that effectively address both diseases.…”

“…Additionally, Wang discussed the usage of Paxlovid, an antiviral therapeutic for COVID-19 treatment, and emphasized its contraindication in patients receiving rifampicin, one of the first-line agents for TB treatment, due to drug interactions as Paxlovid is a strong cytochrome P450 3A4 inhibitor. Consequently, Paxlovid was not deemed suitable for treating patients with active TB-COVID co-infection undergoing ATT [ 21 ].…”

“…Wang emphasized that despite the milder nature of infections with the Omicron variant compared to earlier variants, patients with TB-COVID co-infection do not exhibit the mild disease course observed in the general population [ 21 ]. Notably, the majority of patients in Wang’s study, 142 out of 153 co-infected individuals, were classified as nonsevere, with 10 being asymptomatic [ 21 ]. This may be attributed to lung parenchyma damage resulting from pulmonary remodeling due to persistent cavitation, fibrosis, or bronchiectasis, which is present in approximately 50% of cured TB patients and may increase susceptibility to COVID-19 and mortality rates [ 25 ].…”

COVID-19 Infection in Patients With Chronic Lymphocytic Leukemia Receiving Acalabrutinib in the Phase 3B ASSURE Study

“…Hypertension is well recognized as a risk factor for severe COVID-19. [12][13][14] The outcome of COVID-19 infection while using different antihypertensive medications is less clear, although some data may support a benefit. 15 It is possible that in the setting of a clinical trial, pre-existing hypertension may be better monitored and controlled than in realworld settings; however, assessing compliance with hypertensive medication was beyond the scope of the current trial, and other unknown factors may be influencing the results observed here.…”

Suppressive myeloid cells in SARS-CoV-2 and Mycobacterium tuberculosis co-infection

“…Both current active TB disease (defined as culture, molecular test, or other Mtb test positive, with symptoms or imaging changes that justify the initiation of full TB treatment) and previous TB, increase the risk of in-hospital mortality from coronavirus disease-2019 (COVID-19), and the case fatality rate for coinfection is higher than for COVID-19 alone ( 5 , 6 ). The lymphopaenia which characterizes COVID-19 is exaggerated in coinfection, and markers of inflammation such as D-dimer and ferritin are increased over and above the COVID-19 levels ( 7 , 8 ). Transcriptomics and RNAseq data from whole blood, peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage fluid (BALF) of patients with COVID-19, and those with TB across the clinical spectrum, has shown that there is similarity in the immunopathogenesis of the two diseases through commonly enriched genes in 12-gene disease-exacerbation hot spots ( 9 ).…”