BACKGROUND Thrombotic microangiopathy, characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage by microvascular thrombosis, has a high mortality rate; therefore, early diagnosis and treatment are important. Thrombotic thrombocytopenic purpura is caused by a deficiency of a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13 (ADAMTS13), and results in thrombotic microangiopathy. Influenza virus causes thrombotic thrombocytopenic purpura by inducing immunoglobulin G autoantibodies against ADAMTS13. We report a rare case of thrombotic thrombocytopenic purpura caused by influenza A without anti-ADAMTS13 antibody that was treated by plasma exchange. CASE REPORT A 57-year-old woman was admitted to our hospital because of hypoxemia. We diagnosed pneumonia and disseminated intravascular coagulation. Despite treatment, she developed thrombocytopenia, and we diagnosed thrombotic microangiopathy and started plasma exchange. With a PLASMIC score of 6 points and neuropsychiatric symptoms, we strongly suspected thrombotic thrombocytopenic purpura and started rituximab. However, ADAMTS13 activity by FRETS-VWF73 assay was 65%, and anti-ADAMTS13 antibody was negative. After 4 plasma exchanges and 2 rounds of rituximab, platelet numbers and lactate dehydrogenase and creatinine concentrations normalized on the 16th day of hospitalization. Subsequently, influenza A (H1N1) was identified in a nasopharyngeal swab collected on admission. Plasma enzyme-linked immunosorbent assay testing for chromogenic ADAMTS13 activity showed a significant decrease (<0.5%). Therefore, we diagnosed thrombotic thrombocytopenic purpura caused by influenza A without anti-ADAMTS13 antibody. CONCLUSIONS We present a rare case of thrombotic thrombocytopenic purpura without anti-ADAMTS13 antibody caused by influenza A virus successfully treated by plasma exchange. Influenza A may reduce ADAMTS13 activity without inducing autoantibodies.
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http://dx.doi.org/10.12659/AJCR.932251 | DOI Listing |
Medicine (Baltimore)
January 2025
Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macau, China.
Rationale: Thrombotic microangiopathies (TMA) caused by malignant hypertension is an acute and critical disease among rare diseases. Although renal biopsy pathology is a golden indicator for diagnosing kidney disease, it cannot distinguish between primary and secondary TMA and requires a comprehensive diagnosis in conjunction with other laboratory tests and medical history.
Patient Concerns: A 33-year-old young man was hospitalized due to unexplained kidney failure.
HCA Healthc J Med
December 2024
Neurology and Neurophysiology Center, Vienna, Austria.
Description This letter to the editor addresses limitations to holding COVID vaccines responsible for the diagnosis of thrombotic thrombocytopenic purpura and discusses the potential differential diagnoses that must be considered.
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January 2025
Division of Hematology and Medical Oncology, Oregon Health & Science University, Portland, Oregon, USA.
Hematologic complications are common in pregnancy and can significantly impact both maternal and fetal health. Recognizing and treating these complications can be challenging due to the limited evidence available to guide clinical consultants. Iron deficiency anemia is the most prevalent hematologic issue in pregnancy and often occurs due to increased maternal blood volume and the nutritional demands of the growing fetus.
View Article and Find Full Text PDFTransfus Apher Sci
December 2024
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Department of Laboratory Medicine, St. Michael's Hospital, Toronto, ON, Canada; Division of Hematology, St. Michael's Hospital, Toronto, ON, Canada. Electronic address:
Blood Adv
January 2025
KU Leuven Campus Kulak Kortrijk, Kortrijk, Belgium.
Allosteric regulation of ADAMTS13 (A Disintegrin And Metalloproteinase with ThromboSpondin type-1 motif, member 13) activity involves an interaction between its Spacer (S) and CUB1-2 domains to keep the enzyme in a closed, latent conformation. Monoclonal antibodies (mAb) uncouple the S-CUB interaction to open the ADAMTS13 conformation and thereby disrupt the global enzyme latency. The molecular mechanism behind this mAb-induced allostery remains poorly understood.
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