Background Convalescent plasma is frequently administered to patients with Covid-19 and has been reported, largely on the basis of observational data, to improve clinical outcomes. Minimal data are available from adequately powered randomized, controlled trials. Methods We randomly assigned hospitalized adult patients with severe Covid-19 pneumonia in a 2:1 ratio to receive convalescent plasma or placebo. The primary outcome was the patient’s clinical status 30 days after the intervention, as measured on a six-point ordinal scale ranging from total recovery to death. Results A total of 228 patients were assigned to receive convalescent plasma and 105 to receive placebo. The median time from the onset of symptoms to enrollment in the trial was 8 days (interquartile range, 5 to 10), and hypoxemia was the most frequent severity criterion for enrollment. The infused convalescent plasma had a median titer of 1:3200 of total SARS-CoV-2 antibodies (interquartile range, 1:800 to 1:3200]. No patients were lost to follow-up. At day 30 day, no significant difference was noted between the convalescent plasma group and the placebo group in the distribution of clinical outcomes according to the ordinal scale (odds ratio, 0.83 (95% confidence interval [CI], 0.52 to 1.35; P=0.46). Overall mortality was 10.96% in the convalescent plasma group and 11.43% in the placebo group, for a risk difference of −0.46 percentage points (95% CI, −7.8 to 6.8). Total SARS-CoV-2 antibody titers tended to be higher in the convalescent plasma group at day 2 after the intervention. Adverse events and serious adverse events were similar in the two groups. Conclusions No significant differences were observed in clinical status or overall mortality between patients treated with convalescent plasma and those who received placebo. (PlasmAr ClinicalTrials.gov number, NCT04383535 .)

Introduction: Factor XIII (FXIII) deficiency may cause bleeding under certain clinical circumstances. Therapeutic plasma exchange (TPE) may lead to a transient deficiency. Objectives: To describe the clinical evolution of patients with acquired FXIII deficiency secondary to TPE. Methods: We respectively studied a cohort of consecutive patients from 2014 to 2019 who were treated with TPE with FXIII levels <50%. The FXIII was measured after the start of the TPE course, on days between the TPE sessions, due to suspected acquired deficiency. All TPE were performed using continuous flow cell separator. In all cases, the initial replacement fluid applied was albumin. Apheresis procedures were held at 24to 48 hours intervals. Results: Eighteen patients were included, 13 of them were recipients of kidney transplants. The main TPE prescription was humoral rejection. Median FXIII at diagnosis (measured on days between sessions of the TPE course) was 19%(IQR17-25). The median of apheresis procedures before measurement of FXIII was 3(IQR2-4). Among the total cohort, 10 patients suffered hemorrhages. None of the patients without history of kidney transplants had bleeding (n = 5), however, 10/13 with kidney transplants did. Five kidney transplant patients received therapy with FXIII concentrate because of lifethreatening bleeding. In all cases, the bleeding stopped within the first 24 hours. All patients had their FXIII levels measured again after finishing the TPE course, with normal results. Conclusions: TPE is an under-diagnosed cause of acquired FXIII deficiency since routine coagulation tests remain unaltered. It might cause major bleeding, particularly in patients with a recent history of surgery like kidney transplants.

BACKGROUND Etoricoxib is a selective inhibitor of cyclooxygenase 2 used mainly to treat osteoarticular pain. Here, we report the case of a patient who developed acute kidney failure and immune hemolytic anemia after the use of etoricoxib. STUDY DESIGN AND METHODS An 83‐year‐old female patient developed immune hemolytic anemia and acute kidney failure after treatment with etoricoxib for articular pain. Given the acute kidney failure, she required five hemodialysis sessions. She was discharged after 17 days. The case of immune hemolytic anemia and kidney failure was fully resolved. RESULTS The direct antiglobulin test was not only positive for IgG but also for C3b and C3d, showing a very intense reactivity (++++). The eluate's reactivity was weaker (++) and showed no defined specificity. The investigation of unexpected antibodies in the serum of the patient showed a reactivity pattern similar to the eluate's: weak reactivity without specificity. The serum of the patient was compared to urine and plasma samples of two groups of volunteers. The indirect antiglobulin test showed only a very strong reactivity with the urine samples of the volunteers who had received etoricoxib. DISCUSSION Considering that positive eluate is not the typical serologic profile of drug‐induced immune hemolytic anemia, developing in‐house techniques to show the causal link between them may be of interest to guide the treatment and avoid the empirical use of drugs. CONCLUSION Etoricoxib must be considered as a possible cause of acute kidney failure in cases of immune hemolytic anemia.

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