Letter to the Editor
Relapse of thrombotic thrombocytopenic purpura after COVID-19 vaccineWe report a case of a 48-year-old white female patient with a history of relapsing thrombotic thrombocytopenic purpura (TTP). The patient has been known to our department since 2015 when she was diagnosed for the first time with TTP with a high antibody titer (99 U/mL) against ADAMTS13 (A Disintegrin And MeTalloproteinase with a Thrombo-Spondin type 1 motif, member 13) and very low ADAMTS13 activity (Fluorescent Resonance Energy Transfer [FRET] assay: <3 %, normal range 45-138 %). She was treated with ten plasma-exchange (PEX) procedures and corticosteroids and obtained a complete remission. Her first relapse, in February 2019, presented as ecchymoses and severe thrombocytopenia; she was successfully treated again with seven PEX procedures and steroids. Afterwards, the patient was well and periodic blood cell counts (every 6 months, last check performed in October 2020) were normal. On March 12, 2021 the patient was referred to the emergency room of the city hospital of Mantua for a new onset of ecchymoses on both arms and forearms without any other symptoms or signs. The complete blood count demonstrated mild normocytic anemia (hemoglobin 11.5 g/dL, normal range 12.3-14.5 g/dL), moderate thrombocypenia (platelet count 94 × 10 9 /L, normal range 150− 400 × 10 9 /L), a coagulation profile and renal function within the normal range, and moderately increased lactate dehydrogenase (LDH, 637 UI/L, normal range 150-450 UI/L). On a peripheral blood smear, there were about 10 % schistocytes. ADAMTS13 activity was markedly reduced (FRET assay: <3 %) with a high titer of anti-ADAMTS13 antibodies (88 U/mL). Six days before the TTP relapse (March 6, 2021), the patient had received the second dose of the anti-COVID-19 vaccine produced by Pfizer-BioNTech (the first dose had been administered on February 11, 2021). At hospital admission the molecular search of SARS-COV-2 on nasopharyngeal swab was negative while anti-SARS-COV-2 IgG antibodies were 105 UA/mL (chemiluminescent immunoassay DiaSorin, positive >15 UA/mL). The patient was promptly treated with seven PEX procedures and steroids, with a rapid and excellent response (normalization of platelet count and LDH after the third PEX). This is the first case reported in literature of a TTP relapse following anti-COVID-19 vaccination. Other cases of vaccine-related thrombotic microangiopathies have been described, possibly related to the immune dysregulation and/or complement activation triggered by vaccination, particularly against influenza [1][2][3][4]. Further studies are needed to verify the possible association between microangiopathic thrombotic disorders with an autoimmune pathogenesis and the administration of vaccines against COVID-19.
ContributionC.S. and A.A.
Graft-versus-host disease (GvHD) causes severe mucositis, impairs feeding and favors infection. The objective of this study was to identify the impact of GvHD in the oral cavity. We reviewed all consecutive patients who developed oral GvHD after HSCT. The study period was over 14 years. 53 patients were identified. M/F = 1.4; median age was 48.6 years; the median follow-up was for up to 3 years and 6 months. Conditioning regimens included several drugs (e.g., busulfan, cyclophosphamide and fludarabine). In 11 cases, radiotherapy (RT) was also used. Patients treated with RT were more likely to have tooth decay requiring fillings (p = 0.029), to need canal root interventions (p = 0.005) and to have tartar requiring oral hygiene interventions (p = 0.011). Patients with a lymphoma diagnosis were more likely to develop perioral scleroderma and chronic oral GvHD (cGvHD) (p = 0.045). Oral acute GvHD (aGvHD) was seen in 26 patients (49.1%). 21 (39.6%) patients developed cGvHD. GvHD of the tongue was seen in 21 (40%) patients. Oral mucositis was seen in only 5 patients (9.4%). Conditioning regimens with RT are more likely to induce oral aGvHD. The tongue is often affected by GvHD.
sAPRIL is a novel indicator of shorter TTFT in B-CLL and a predictor of progression especially in patients otherwise considered at low risk according to validated prognostic factors.
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