Search results for "Thrombotic microangiopathy"

showing 10 items of 17 documents

Genetic justification of severe COVID-19 using a rigorous algorithm

2021

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (…

0301 basic medicineMaleThrombomodulinSeverity of Illness Index0302 clinical medicineRisk FactorsImmunology and AllergyMedicineComplement ActivationRigorous algorithmmedicine.diagnostic_testHigh-Throughput Nucleotide SequencingComplement C3EculizumabEculizumabMiddle AgedHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsFactor HComplement Factor HFemaleAlgorithmsmedicine.drugmedicine.medical_specialtyThrombotic microangiopathyCritical CareImmunologyComplementADAMTS13 Protein03 medical and health sciencesInternal medicineFull Length ArticleSeverity of illnessGenetic predispositionGenetic susceptibilityHumansGenetic Predisposition to DiseaseGenetic TestingRisk factorGenetic testingAgedbusiness.industryThrombotic MicroangiopathiesCOVID-19medicine.diseaseComplement system030104 developmental biologySARS-CoV2business030215 immunologyClinical Immunology (Orlando, Fla.)
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Coronavirus Disease 2019–Associated Coagulopathy

2021

Patients with the severe form of coronavirus disease 2019 (COVID-19) have been frequently found to suffer from both arterial and venous thrombotic events due to the perpetuation of a hypercoagulable state. This phenomenon, termed COVID-19-associated coagulopathy (CC), is now considered a major component of the pathophysiology of this novel infectious disease, leading to widespread thrombosis. While at first, the vascular insults may be limited to the pulmonary microvasculature, as the disease progresses, systemic involvement occurs, culminating in distant organ thrombosis and multi-organ dysfunction syndrome. In this review article, we discuss recent insights into the pathophysiologic mecha…

ARDSPAI-1 Plasminogen Activator Inhibitor 1VTE venous thromboembolismDiseaseReview030204 cardiovascular system & hematologyCoronavirus Disease 20190302 clinical medicineCoagulopathy030212 general & internal medicineDIC disseminated intravascular coagulationDisseminated intravascular coagulationCOVID-19 Coronavirus disease 2019DVT deep vein thrombosisGeneral MedicineBlood Coagulation DisordersThrombosisICU intensive care unitTMA thrombotic microangiopathyDisease ProgressionCoronavirus Disease 2019 COVID-19 CoagulopathyVWF von Willebrand factormedicine.medical_specialtyThrombotic microangiopathyACE2 angiotensin-converting enzyme 2SARS-CoV-2 severe acute respiratory syndrome coronavirus 203 medical and health sciencesmedicineCoagulopathyHumansIntensive care medicineLY30 lysis at 30 minutesARDS acute respiratory distress syndromeHemostasisNO nitric oxideCoagulationbusiness.industrySARS-CoV-2COVID-19Thrombosismedicine.diseasetPA tissue plasminogen activatorReview articleIL interleukinCoronavirusVascular DisorderPE pulmonary embolismTF tissue factorbusinessCC COVID-associated coagulopathyMayo Clinic Proceedings
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Redefining outcomes in immune TTP: an international working group consensus report

2021

Abstract Immune-mediated thrombotic thrombocytopenic purpura (iTTP) is a potentially fatal thrombotic microangiopathy caused by autoantibody-mediated severe deficiency of ADAMTS13. Standardized definitions of response, exacerbation, remission, and relapse were initially proposed in 2003 and modified by the International Working Group for TTP in 2017. These definitions, which have been widely used in clinical practice and research, are based primarily on the platelet count and are benchmarked against the timing of discontinuation of therapeutic plasma exchange (TPE). They do not incorporate ADAMTS13 activity or the temporizing effects on the platelet count of caplacizumab, a novel anti–von W…

Adult0301 basic medicinemedicine.medical_specialtyConsensusThrombotic microangiopathyExacerbation[SDV]Life Sciences [q-bio]ImmunologyThrombotic thrombocytopenic purpuraMEDLINEADAMTS13 Protein030204 cardiovascular system & hematologyBiochemistry03 medical and health sciences0302 clinical medicineFibrinolytic AgentsRecurrencehemic and lymphatic diseasesvon Willebrand FactorHumansMedicineClinical significanceIntensive care medicinePlasma ExchangePurpura Thrombotic ThrombocytopenicPlatelet Countbusiness.industryDisease ManagementCell BiologyHematologySingle-Domain Antibodiesmedicine.diseaseADAMTS133. Good healthDiscontinuationTreatment Outcome030104 developmental biologyFemaleCaplacizumabbusinessBlood
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Protein�A immunoadsorption therapy for refractory, mitomycin�C?associated thrombotic microangiopathy

2007

BACKGROUND: Mitomycin C–associated thrombotic microangiopathy (TMA) has a poor prognosis with limited therapeutic options. Most patients die within 4 months of diagnosis due to pulmonary or renal failure. Here, a patient resistant to total plasma exchange (TPE) and immunosuppressive therapy with glucocorticoids, rituximab, vincristine, and splenectomy who was successfully treated with protein A immunoadsorption is described. CASE REPORT: A 29-year-old woman developed a TMA after chemotherapy with mitomycin C. She presented with thrombocytopenia, pulmonary edema, hemolytic anemia with presence of schistocytes, and renal failure. Immediate TPE (>120 times) and immunosuppressive therapy with g…

AdultHemolytic anemiamedicine.medical_specialtyThrombotic microangiopathyMitomycinmedicine.medical_treatmentImmunologySplenectomyGastroenterologyInternal medicinemedicineHumansImmunology and AllergyStaphylococcal Protein AImmunoadsorptionImmunosorbent TechniquesSalvage TherapyChemotherapyPurpura Thrombotic Thrombocytopenicbusiness.industryImmunosuppressionHematologymedicine.diseaseSurgerySchistocyteTreatment OutcomeHemolytic-Uremic SyndromeFemaleRituximabbusinessmedicine.drugTransfusion
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Renal disease associated with myeloproliferative neoplasms and myelodysplastic syndrome/myeloproliferative neoplasms

2020

Aims Renal changes in patients with myeloproliferative neoplasms (MPNs) or myelodysplastic syndrome (MDS)/MPNs have been addressed by few, respectively no, reports. The aim of this study was to focus on a systematic evaluation of renal biopsies in patients with MPNs or MDS/MPNs. Methods and results The cohort comprised 29 patients (23 men) aged 67 ± 11 years (mean ± standard deviation), diagnosed with chronic myeloid leukaemia (n = 5), polycythaemia vera (n = 9), primary myelofibrosis (n = 5), essential thrombocythaemia (n = 2), or chronic myelomonocytic leukaemia (n = 4), as well as MPNs or MDS/MPNs not otherwise specified (n = 4). Patients manifested with proteinuria (93%), partially in t…

AdultMale0301 basic medicinemedicine.medical_specialtyPolycythaemiaHistologyThrombotic microangiopathy610 MedizinRenal functionMesangial hypercellularityGastroenterologyPathology and Forensic MedicineNephropathyCohort Studies03 medical and health sciencesGlomerulonephritis0302 clinical medicineRisk FactorsNeoplasmshemic and lymphatic diseasesInternal medicine610 Medical sciencesmedicineHumansddc:610MyelofibrosisAgedAged 80 and overMyeloproliferative DisordersProteinuriaThrombotic Microangiopathiesbusiness.industryGlomerulonephritisGeneral MedicineMiddle Agedmedicine.diseaseMyelodysplastic-Myeloproliferative Diseases030104 developmental biologyMyelodysplastic Syndromes030220 oncology & carcinogenesisFemaleKidney Diseasesmedicine.symptombusiness
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Endotheliotropic (hemolytic) nephroangiopathy and its various manifestation forms (thrombotic microangiopathy, primary malignant nephrosclerosis, hem…

1980

In hemolytic-uremic syndrome (HUS) various lesion types in the kidneys are observed in childhood. These are designated as the “glomerular type=G type” (essentially identical with thrombotic microangiopathy), as “arterial type=A type” (essentially identical with primary malignant nephrosclerosis (PMN)) or as “mixed type=G/A type”. With reference to characteristic cases, the most important morphological findings are described. In adults, in whom other diagnostic terms are used besides HUS, the same nephropathological types are observed. In the two phases of life, there occurs in addition renal cortical necrosis in subtotal nephroangiothrombosis. The G type and A type also have a different cli…

Hemolytic anemiaMalePathologymedicine.medical_specialtyAnemia HemolyticThrombotic microangiopathyHypertension RenalAdolescentKidney GlomerulusKidneyRenal cortical necrosisInternal medicineDrug DiscoverymedicineHumansChildGenetics (clinical)KidneyNephrosclerosisMalignant nephrosclerosisChemistryInfantGeneral Medicinemedicine.diseaseMolecular medicineHemolysismedicine.anatomical_structureBlood pressureEndocrinologyChild PreschoolHemolytic-Uremic SyndromeMolecular MedicineFemaleKidney Cortex NecrosisKidney DiseasesKlinische Wochenschrift
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Sistemic calciphylaxis and thrombotic microangiopathy in a kidney transplant patient: Two mixing fatal syndromes?

2012

Abstract Abnormalities in calcium and phosphorus metabolism are common and metabolic bone diseases develop often in patients with chronic renal failure (CRF). Effective clinical management includes measures to control phosphorus retention and prevent hyperphosphataemia, to maintain serum calcium concentrations within the normal range and to prevent excess parathyroid hormone (PTH) secretion by the judicious use of vitamin D sterols. Certain of these interventions, however, appear to increase the risk of soft tissue and vascular calcification in patients with End Stage Renal Disease (ESRD), so current therapeutic approaches are thus being re-evaluated in an effort to limit these risks. Patie…

Parathyroidectomymedicine.medical_specialtyPathologyCalciplhylaxisThrombotic microangiopathymedicine.medical_treatmentHemolitic Huremic SyndromeSettore MED/08 - Anatomia PatologicaGastroenterologyPhosphorus metabolismEnd stage renal diseaseInternal medicineSettore MED/35 - Malattie Cutanee E VenereemedicineHumansKidney transplantationSettore MED/14 - NefrologiaCalciphylaxisThrombotic Microangiopathiesbusiness.industryCalciphylaxisEnd Stage Renal Disease; Hemolitic Huremic Syndrome; CalciplhylaxisGeneral MedicineModels Theoreticalmedicine.diseaseKidney TransplantationSettore MED/18 - Chirurgia GeneraleSecondary hyperparathyroidismEnd Stage Renal DiseasebusinessCalcificationMedical Hypotheses
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Pathological Findings in COVID-19 as a Tool to Define SARS-CoV-2 Pathogenesis. A Systematic Review

2021

Introduction: The World Health Organization declared the COVID-19 pandemic in March 2020. COVID-19 still represents a worldwide health emergency, which causesa severe disease that has led to the death of many patients. The pathophysiological mechanism of SARS-CoV-2 determining the tissue damage is not clear and autopsycan be auseful tool to improve the knowledge of this infection and, thus, it can help achieve a timely diagnosis and develop an appropriate therapy. This is an overview of the main post-mortem findings reporting data on the infection effects on several organs.Methods: A systematic literature search was conducted in the PubMed database searching for articles from 1 January to A…

Pathologymedicine.medical_specialtypathological findingThrombotic microangiopathyimmuno-thrombotic microangiopathyAutopsyDisease030204 cardiovascular system & hematologyPathogenesis03 medical and health sciencesautopsy0302 clinical medicinesystematic reviewhyperinflammatory statemedicinepathological findingsPharmacology (medical)Diffuse alveolar damagePathologicalPharmacologyLungSARS-CoV-2business.industrylcsh:RM1-950MicroangiopathyCOVID-19medicine.diseasediffuse alveolar damagelcsh:Therapeutics. Pharmacologymedicine.anatomical_structure030220 oncology & carcinogenesisSystematic ReviewbusinessFrontiers in Pharmacology
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A critical evaluation of caplacizumab for the treatment of acquired thrombotic thrombocytopenic purpura

2020

Introduction: Acquired thrombotic thrombocytopenic purpura (aTTP) is a thrombotic microangiopathy caused by inhibitory autoantibodies against ADAMTS13 protein. Until recently, the combination of plasma exchange (PEX) and immunosuppression has been the standard front-line treatment in this disorder. However, aTTP-related mortality, refractoriness, and relapse are still a matter of concern. Areas covered: The better understanding of the pathophysiological mechanisms of aTTP has allowed substantial improvements in the diagnosis and treatment of this disease. Recently, the novel anti-VWF nanobody caplacizumab has been approved for acute episodes of aTTP. Caplacizumab is capable to block the adh…

Thrombotic microangiopathyExacerbationvirusesmedicine.medical_treatmentADAMTS13 ProteinDiseaseBioinformaticsAutoantigens03 medical and health sciencesPlatelet Adhesiveness0302 clinical medicineFibrinolytic AgentsProtein DomainsCrotalid Venomsvon Willebrand FactormedicineHumansImmunologic FactorsMulticenter Studies as TopicLectins C-TypeMolecular Targeted TherapyDrug ApprovalClinical Trials as TopicAcquired Thrombotic Thrombocytopenic PurpuraPlasma ExchangePurpura Thrombotic Thrombocytopenicbusiness.industryStandard treatmentfungiImmunosuppressionDrugs InvestigationalHematologyAptamers NucleotideSingle-Domain Antibodiesbiochemical phenomena metabolism and nutritionmedicine.diseaseCombined Modality TherapyRecombinant ProteinsADAMTS13AcetylcysteineTreatment Outcome030220 oncology & carcinogenesisDrug Therapy CombinationCaplacizumabbusinessImmunosuppressive Agents030215 immunologyExpert Review of Hematology
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COVID-19 as a Potential Trigger for Immune Thrombotic Thrombocytopenic Purpura and Reason for an Unusual Treatment: A Case Report

2021

AbstractImmune thrombotic thrombocytopenic purpura (iTTP) is a rare autoimmune disorder characterized by severely reduced activity of the von Willebrand factor (VWF)-cleaving protease ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) due to autoantibodies. This leads to the development of pathogenic multimers of VWF, causing a thrombotic microangiopathy with decreased number of platelets, hemolysis, and life-threatening tissue ischemia of mostly brain, heart, and kidneys. Standard treatment of iTTP involves daily plasma exchange to remove ultra large multimers of VWF, inhibitors, substituting ADAMTS13, and the accompaniment of an immunosuppressive …

Thrombotic microangiopathybiologybusiness.industryThrombotic thrombocytopenic purpuraAutoantibodyHematology030204 cardiovascular system & hematologymedicine.diseaseADAMTS1303 medical and health sciences0302 clinical medicineVon Willebrand factorhemic and lymphatic diseases030220 oncology & carcinogenesisImmunologybiology.proteinmedicineRituximabPlateletCaplacizumabbusinessmedicine.drugHämostaseologie
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