HealthDay News — Intravenous antibiotics do not achieve greater sustained eradication of Pseudomonas aeruginosa in patients with cystic fibrosis compared with oral therapy, according to a study published in the October issue of The Lancet Respiratory Medicine.

Simon C. Langton Hewer, M.D., from the University of Bristol in the United Kingdom, and colleagues compared the effectiveness and safety of 14 days of intravenous ceftazidime and tobramycin (137 patients) versus 12 weeks of oral ciprofloxacin (149 patients) among randomly assigned patients seen at cystic fibrosis centers and with an isolate of P. aeruginosa. Both treatments were combined with 12 weeks of inhaled colistimethate sodium.

The researchers found that 44 percent of 125 participants in the intravenous group and 52 percent of 130 participants in the oral group achieved the primary outcome. Participants assigned to the intravenous group were less likely to achieve eradication of P. aeruginosa at three months and remain free of infection to 15 months, although the difference between the groups was not significant (relative risk, 0.84; 95 percent confidence interval, 0.65 to 1.09; P = 0.18). There were 11 serious adverse events reported, which occurred in 8 percent of patients in each group.

“Admission for intravenous therapy in the context of early P. aeruginosa infection (and without the presence of a significant pulmonary exacerbation), in adults and children with cystic fibrosis, should not be recommended,” the authors write.

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Two authors disclosed financial ties to the pharmaceutical industry.

Abstract/Full Text

Patients with rheumatic diseases from African and South-East Asian regions vs American and European regions reported greater difficulty in obtaining antimalarial drugs during the coronavirus disease 2019 (COVID-19) pandemic and had worse mental and physical outcomes, according to survey results presented at the American College of Rheumatology (ACR) Convergence 2020, held virtually between November 5 to 9, 2020. Results also indicated that antimalarial drugs for rheumatic disease treatment did not have a protective effect against COVID-19 infection or hospitalizations as a result of COVID-19.

To assess the effect of antimalarial drug shortages during the COVID-19 pandemic in patients with rheumatic diseases, the COVID-19 Global Rheumatology Alliance Patient Experience Survey was distributed online to patients or parents of pediatric patients who anonymously entered relevant data, including rheumatic disease diagnosis, medications, COVID-19 status, and disease outcomes. The primary outcome measure was the effect of drug shortages on patient disease activity, mental health, and physical health.

Of 9393 survey respondents (mean age, 46.1±12.8 years; 90.0% women), 6334 (67.4%) were White and 1576 (16.8%) were Latin American. A majority of patients (70.9%) were also receiving conventional synthetic disease-modifying antirheumatic drugs (csDMARDs).

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Among 3872 respondents receiving antimalarial drugs, 230 (6.2%) discontinued treatment due to drug shortages at their pharmacy. Compared with 6.8% of patients in the Americas and 2.1% in European regions, 21.4% in South-East Asia and 26.7% in African regions were affected by the inadequate supply of antimalarial drugs.

Overall, there were similar rates of COVID-19 infection among patients who received antimalarial drugs vs those who did not (6.7% vs 4.7%, respectively). Of 519 patients who were diagnosed with COVID-19, 68 (13.1%) indicated that their antimalarial medications were prescribed for the treatment of COVID-19 infection.

Patients who were unable vs able to obtain their antimalarial medications experienced higher levels of rheumatic disease activity (5.1 vs 4.3; t(244)=4.44; P <.001), poorer mental health (5.8 vs 6.3; t(252)=3.82; P <.001), and poorer physical health (5.6 vs 6.4; t(254)=5.97; P <.001).

Patients in certain regions, particularly Africa and South-East Asia, were found to be more affected by antimalarial drug shortages, a reminder of the “unintended harmful consequence of repurposing antimalarials without adequate evidence or benefit,” emphasizing “the importance of maintaining scientific rigor even in the context of a pandemic,” the study authors concluded.

Disclosures: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

In addition to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated lymphopenia, changes in frequency and activation of granulocyte subsets may be predictive of clinical worsening during coronavirus disease 2019 (COVID-19), according to study results published in the The Journal of Infectious Diseases.

A sudden deterioration 7 to 10 days after the onset of symptoms in 10% to 20% of patients is the hallmark of COVID-19 and can lead to an increased risk for acute respiratory distress syndrome, intensive care unit (ICU) admission, and death. Previous studies have explored the immune response in patients with COVID-19 and suggested that SARS-CoV-2 may induce unique patterns of immune dysregulation. However, no systemic approach of SARS-CoV-2-induced immune dysregulation at the phenotypic level has been performed to date.

In the current observational, prospective, multicenter study, researchers aimed to identify previously unreported immune markers able to categorize patients with COVID-19 from healthy control participants and to predict mild and severe disease.

In total, 26 patients with confirmed COVID-19 were included in the study (mild/moderate, 7 patients; severe, 19 patients) along with 25 healthy control participants. All participants received immunophenotyping of whole blood leukocytes via a multiparametric flow cytometry approach on hospital or ICU admission. Unsupervised analysis and mapping of leukocyte surface markers were performed to identify clinically relevant associations. The primary objective was to identify immunophenotypic patterns that were most accurately associated with COVID-19 diagnosis and severity.

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There were notable demographic differences between the mild and severe COVID-19 groups. When compared with the mild group, the severe group had an elevated body mass index (29 vs 24 kg/m2; P =.005), more frequent cases of hypertension (15 [79%] vs 2 [29%]; P =.03), increased levels of C-reactive protein (150 vs 17 mg/L; P =.0003), and significantly higher severity scores, including the World Health Organization (WHO) progression score (P <.0001) and the Sepsis-related Organ Failure Assessment (SOFA) score (P =.005).

Results suggested that phenotypic markers of circulating granulocytes could be used as strong discriminators between severity stages and individuals infected and uninfected with COVID-19. Unsupervised mapping of leukocyte surface markers identified a distinct granulocytic COVID-19 signature. Compared with control participants, patients with COVID-19 showed downregulation of eosinophil and basophil CRTH2, increased counts of CD15+CD16+ neutrophils, and a decreased expression of granulocytic CD11b. Furthermore, COVID-19 severity was associated with a more profound imbalance of granulocyte subsets and functional markers of the disease. The frequency of CD15+ granulocytes and CD15+CD16+ neutrophils were significantly increased (P =.002) and eosinophil CRTH2 expression significantly decreased in the severe vs mild group.

 Compared to mild COVID-19, severe COVID-19 disease was associated with the emergence of unique markers, including significantly increased expression of PDL1 checkpoint inhibitor in basophils and eosinophils. Both WHO and SOFA scores positively correlated (R2=0.567) with innate immune checkpoints like PDL1 expression and negatively correlated with neutrophil CD11b and eosinophil CRTH2 expression.

Study limitations included variable timing of blood sampling between the mild and severe COVID-19 groups and the small population size, which may preclude definitive conclusions; however, results in this study were homogenous in each subgroup and were consistent with published literature.

Researchers concluded, “Taken together, our data show an early and deep impairment of the immune response, and question the use of drugs that could alleviate the immune response in patients [with] COVID-19, especially in the most severe forms requiring intensive care unit admission.”

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.


Vitte J, Diallo AB, Boumaza A, et al. A granulocytic signature identifies COVID-19 and its severity. Published online September 17, 2020. J Infect Dis. doi:10.1993/infdis/jiaa591/5907982


Sirotich E, Kennedy K, Surangiwala S, et al. Antimalarial drug shortages during the COVID-19 pandemic: results from the global rheumatology alliance patient experience survey. Presented at: ACR Convergence 2020; November 5-9, 2020. Abstract 0007.

This article originally appeared on Rheumatology Advisor