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Introduction: Extracorporeal photopheresis (ECP) is a procedure used to influence T-cell activity in patients suffering from immune-mediated cellular damage secondary to activated lymphocytes. Although well-tolerated, iron deficiency anemia (IDA) has been described. The goal herein is to describe IDA in patients who received extracorporeal photopheresis (ECP) treatment using UVAR (Therakos Inc) and CELLEX (Therakos Inc) instruments. Design and Methods: Patients treated with ECP from 2015 to 2019 were retrospectively analyzed. IDA was defined by a decrease in hemoglobin following treatment with concomitant decrease in mean cell volume, mean corpuscular hemoglobin concentration, increased RBC distribution width, and/or iron studies compatible with IDA. Results: During the four-year study period, thirty-four patients received ECP. Thirteen (38%) underwent treatment with the previous UVAR device while 21 (62%) received treatment on the newer CELLEX instrument. Nineteen (56%) of the cohort developed clinical and laboratory evidence of IDA with an average of 3.2 g/dL decrease in hemoglobin. Patients who developed IDA treated on the CELLEX instrument experienced a significantly greater drop in hemoglobin (P = .04) than those treated on the UVAR. Examining the CELLEX-treated patients, those who received the procedure at greater frequency experienced significantly greater drops in hemoglobin (P = .03). Conclusions: IDA is a risk of chronic ECP therapy and is likely secondary to retained blood components in the instrument. The temporal relationship between anemia and ECP treatment has a direct correlation with the treatment schedule. Patients undergoing ECP treatment should be closely monitored for the development of IDA.

Objectives Patients with coronavirus disease 2019 (COVID-19) have thromboembolic complications. Assessment of coagulation and other markers could be useful to understand their coagulopathy. Methods We performed a retrospective study of inflammatory and coagulation parameters, including prothrombin fragment 1.2 (PF1.2), thrombin-antithrombin complexes (TATs), fibrin monomers, and D-dimer, in hospitalized patients with COVID-19. We compared the markers in patients with thrombosis, admission to the intensive care unit (ICU), and poor outcome. Results Of the 81 patients, 9 (11%) experienced an acute thrombotic event (4 with pulmonary embolism, 3 with venous thrombosis, and 2 with stroke). PF1.2 was elevated in 32 (39%) patients, TATs in 54 (67%), fibrin monomers in 49 (60%), and D-dimer in 76 (94%). Statistically significant elevation in PF1.2 and TATs was seen in patients admitted to the ICU, while D-dimer and fibrin monomers were significantly elevated in patients with poor outcomes. The presence of multiple abnormal coagulation parameters was associated with ICU admission. Other parameters with statistically significant results included abnormal WBC counts and elevated C-reactive protein, which were associated with ICU admission and poor outcomes. Conclusions Our data demonstrate that abnormalities of biomarkers of hemostasis activation and inflammatory markers are associated with poor outcomes in patients with COVID-19.

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Kidney injury is a well-known sequelae of infectious endocarditis. Various types of kidney injury can be seen, including endocarditis-associated glomerulonephritis, and may affect nearly half of the patients with infectious endocarditis. Lactobacillus species are an infrequently documented cause of endocarditis. We present a case of Lactobacillus endocarditis-associated glomerulonephritis in a patient with a complex medical history including Lactobacillus infection of an artificial heart valve. To our knowledge, this is the first reported case of development of endocarditis-associated glomerulonephritis secondary to Lactobacillus species organisms. Furthermore, the patient’s renal biopsy revealed several frequently overlooked concomitant findings including anti-coagulant nephropathy and renal amyloidosis.