Long-term observation of antibody titers against SARS-CoV-2 following vaccination.

Objectives: We aimed to understand how SARS-CoV-2 antibody titer decrease following SARS-CoV-2 mRNA vaccination and to estimate the timing of booster vaccination. Study design: Six hundred sixty-two healthcare workers were administered with total of three doses of SARS-CoV-2 mRNA vaccine during the same short period. Of them, three volunteers were enrolled to measure anti-receptor binding domain (RBD) antibody titers (IgG) monthly following the second and the third doses. Methods: Serum anti-RBD antibody titers were measured monthly and the decay curve of the antibody was analyzed. We estimate the timing of the third and fourth vaccine based on the observed antibody titer decrease and the period of breakthrough infections in the vaccine recipients. Results: Anti-RBD antibody decreased exponentially following the 2nd dose. Between 108 and 117 days following the second dose, breakthrough infection of SARS-CoV-2 occurred in 11 out of the 662 vaccine recipients. Based on the decrease in anti-RBD antibody and the timing of the breakthrough infections, we estimate that the optimal timing of a third dose would be at earliest 108 days after the second dose, when anti-RBD antibody titers are less than 338 BAU/mL. The anti-RBD antibody titers were sustained relatively higher for 161 days following the third dose (416 days following the second dose). Conclusions: We estimate that the optimal timing of a third dose would be at earliest 108 days after the second dose, or anti-RBD antibody titers are less than 338 BAU/mL. We suggest that a fourth dose should be administered later than 161 days following the third dose.

[Heparin-induced thrombocytopenia with pseudo-pulmonary embolism in a patient who was newly introduced to hemodialysis treatment].

Pseudo-pulmonary embolism (PPE) superimposed on heparin-induced thrombocytopenia (HIT) is an important complication in patients undergoing hemodialysis (HD) treatment. We report the clinical profile of an HD patient with acute respiratory distress induced by PPE and HIT. A 67-year-old man with diabetic nephropathy and end-stage renal failure developed congestive heart failure. He was admitted to Kitasato University Hospital. He was introduced to HD treatment using low-molecular-weight heparin as an anticoagulant for an HD session on day 1 of admission. On day 11 after admission, he suddenly developed respiratory distress and hypoxia at 30 min after the start of the fifth HD session. The HD session was immediately discontinued, and oxygen inhalation improved his complaints and hypoxia. The platelet count decreased from 220 x 10(9)/L at the start of the HD session to 80 x 10(9)/L at the end of the HD session. We suspected HIT when blood clotting occurred in his hemodialyzer and blood circuit for HD during the HD session on day 12. Chest X-ray, electrocardiogram, echocardiography, and pulmonary microcirculation scintigraphy were normal. Serum analysis was positive for heparin-platelet factor 4 (PF4) antibody. We then diagnosed him with PPE superimposed on HIT. After the anticoagulant agent for HD was changed from low-molecular-weight heparin to nafamostat mesilate, his clinical symptoms and thrombocytopenia disappeared. PPE superimposed on HIT appeared approximately 7-10 days after the initial use of heparin for the HD session. PPE also led to acute respiratory distress, blood coagulation in the hemodialyzer and blood circuit for HD, as well as thrombocytopenia with less than a 50% decrease in platelet counts. The prognosis of PEE and HIT is good after discontinuing the use of heparin.