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1.
BMC Pregnancy Childbirth ; 22(1): 142, 2022 Feb 21.
Article in English | MEDLINE | ID: covidwho-1706234

ABSTRACT

BACKGROUND: Thrombotic microangiopathy has been invoked as one of the most important mechanisms of damage in COVID-19 patients. Protease ADAMTS13 is a marker of microangiopathy responsible for controlling von Willebrand multimers size. Von Willebrand factor/ADAMTS13 ratio has been found impaired in COVID-19 patients outside pregnancy. METHODS: We prospectively investigated 90 pregnant women admitted to two tertiary academic hospitals in Italy with a laboratory-confirmed diagnosis of SARS-CoV-2 infection. Demographic, clinical information and routine laboratory data were collected at the hospital admission and until discharge. We investigated whether vonWillebrand /ADAMTS13 axis imbalance is a predictor of adverse outcomes. Logistic regression analysis, which controlled for potential confounders, was performed to evaluate the association between laboratory parameters and clinical outcomes. RESULTS: Most women (55.6%) were parae, with median gestational age at admission of 39 weeks. At hospital admission, 63.3% were asymptomatic for COVID-19 and 24.4% showed more than one sign or symptom of infection. Nulliparae with group O showed Willebrand / ADA MTS-13 ratios significantly lower than non-O, whereas in multiparae this difference was not observed. Logistic regression showed that ratio von Willebrand to ADAMTS13 was significantly and independently associated with preterm delivery (OR 1.9, 95%CI 1.1-3.5). CONCLUSION: This study shows an imbalance of vonWillebrand /ADAMTS13 axis in pregnant women with COVID-19, leading to a significantly higher and independent risk of preterm delivery. Monitoring these biomarkers might support decision making process to manage and follow-up pregnancies in this setting.


Subject(s)
ADAMTS13 Protein/blood , COVID-19/blood , Pregnancy Complications/blood , Premature Birth/blood , von Willebrand Factor/metabolism , Academic Medical Centers , Adolescent , Adult , Biomarkers/blood , COVID-19/complications , Female , Humans , Italy/epidemiology , Middle Aged , Pregnancy , SARS-CoV-2 , Tertiary Care Centers , Thrombotic Microangiopathies/etiology , Young Adult
2.
Int J Infect Dis ; 117: 322-325, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1693386

ABSTRACT

We report a case of a Japanese man with severe rhabdomyolysis and multiple thrombosis of arterioles after the first dose of mRNA-1273 vaccine. He developed rapidly progressive rhabdomyolysis and infarctions of multiple organs. Antiplatelet factor 4 antibody test was negative. Despite the intensive supportive care, including aggressive fluid administration, hemodialysis, administration of anticoagulants, high-dose steroid, and eculizumab, the patient ultimately died of multiple organ failure. Autopsy revealed multiple thrombosis in the arterioles and organ necrosis. Low serum complements and C3 deposition in the renal glomeruli detected by immunofluorescence suggested a possible immune-mediated mechanism. To our knowledge, this is the first case report of rhabdomyolysis and multiple thrombosis of the arterioles as an adverse event following COVID-19 vaccination.


Subject(s)
COVID-19 , Rhabdomyolysis , Thrombotic Microangiopathies , COVID-19 Vaccines/adverse effects , Humans , Male , Rhabdomyolysis/etiology , Thrombotic Microangiopathies/etiology
3.
MEDICC Rev ; 24(1): 32-35, 2022 Jan 31.
Article in English | MEDLINE | ID: covidwho-1579165

ABSTRACT

INTRODUCTION: During the pandemic caused by the SARS-CoV-2 virus, some patients who develop severe forms of COVID-19 present thrombotic microangiopathy in the course of the disease's clinical progression. METHODS: Data came from direct patient observation and clinical records. We performed a kidney biopsy and used optical microscopy and immunofluorescence techniques. RESULTS: We present the case of a 78-year-old male patient, mestizo, overweight with a history of high blood pressure, ischemic cardiopathy and chronic obstructive pulmonary disease who was first admitted to the hospital due to respiratory symptoms and diarrhea related to COVID-19, from which he recovered. He was subsequently readmitted with symptoms of acute renal dysfunction accompanied by mild anemia and thrombocytopenia; at the same time, he resulted negative for COVID-19 via a real-time polymerase chain reaction test. A kidney biopsy revealed thrombi in glomerular capillaries, acute tubular necrosis, thickening of extraglomerular blood vessel walls, and C3 deposits in the glomerular tufts. CONCLUSIONS: We describe a case of thrombotic microangiopathy with kidney biopsy in a patient recovering from COVID-19. Acute renal dysfunction is a form of thrombotic microangiopathy that has been observed in patients recovering from COVID-19.


Subject(s)
COVID-19 , Thrombotic Microangiopathies , Aged , Cuba , Humans , Kidney , Male , SARS-CoV-2 , Thrombotic Microangiopathies/diagnosis , Thrombotic Microangiopathies/etiology
4.
Br J Haematol ; 196(4): 902-922, 2022 02.
Article in English | MEDLINE | ID: covidwho-1566272

ABSTRACT

In 145 previously healthy non-critically ill young adults, coronavirus disease 2019 (COVID-19)-related symptoms, risk factors for thrombosis, coagulation and inflammatory parameters were compared, with 29 patients reporting unusual thrombotic events (UTEs) and 116 not having thrombotic events. The inflammatory indices, coagulation and prothrombotic platelet phenotype (PTPP) were significantly higher in patients with UTEs versus those without. Patients with UTEs were categorised according to detection of thrombophilic genes (TGs), coagulation and inflammatory markers to the non-TG and TG subcohort. A total of 38 UTEs were identified, which included splanchnic vein thrombosis (SVT; 11), stroke (six), cerebral vein thrombosis (five), thrombotic microangiopathy (four), limb ischaemia and inferior vena cava thrombosis (three each), ST-segment elevation myocardial infarction (two), superior vena cava thrombosis (two), upper limb deep venous thrombosis and retinal vein thrombosis, one each. We found a 55% prevalence of TGs mainly heterozygous coagulation factor II, thrombin (FII)-G20210A, Janus kinase 2 (JAK2)-V617F, protein-S, and antithrombin III deficiency with a high (76·9%) prevalence of venous UTEs, multiple vessels thrombosis, and recurrence rate among the TG versus non-TG subcohort. The presence of JAK2-V617F, and FII-G20210A mutations was linked with SVT. Thrombosis in the non-TG subcohort was associated with more haemorrhagic problems, thrombosis progression and a significantly higher level of inflammatory markers, PTPP, mean platelet volume, von Willebrand factor, and factor VIII, which remained high for up to 6 months, as well as elevated D-dimer. Acquired and inherited thrombophilia with endotheliopathy appeared to be a relevant mechanism to explain the occurrence of UTEs that are not correlated to COVID-19 severity.


Subject(s)
COVID-19/complications , Thrombophilia/diagnosis , Thrombosis/diagnosis , Blood Platelets/pathology , COVID-19/diagnosis , Factor VIII/analysis , Female , Humans , Longitudinal Studies , Male , Prospective Studies , Thrombophilia/etiology , Thrombosis/etiology , Thrombotic Microangiopathies/diagnosis , Thrombotic Microangiopathies/etiology , Young Adult , von Willebrand Factor/analysis
5.
Nephron ; 146(2): 197-202, 2022.
Article in English | MEDLINE | ID: covidwho-1528608

ABSTRACT

SARS-CoV-2 causes thrombotic microangiopathy (TMA) through the activation of an alternative and lectin complement pathway. TMA is one of the main reasons for acute kidney injury development in patients with COVID-19. In this study, we present 3 TMA cases with severe kidney injury triggered by SARS-CoV-2. In the absence of other TMA causes, we diagnosed the atypical hemolytic uremic syndrome, triggered by SARS-CoV-2 due to abnormal complement activation. Because of both coagulation factors activation, and the high level of D-dimer in patients with COVID-19, it is crucial to differentiate disseminated intravascular coagulation from TMA. The use of anticomplement therapies such as eculizumab should be considered in refractory cases of progressive COVID-19. Controlled clinical trials are required before a definitive statement can be made.


Subject(s)
COVID-19/complications , Thrombotic Microangiopathies/etiology , Adult , Aged , Antibodies, Monoclonal, Humanized/therapeutic use , COVID-19/virology , Complement Inactivating Agents/therapeutic use , Female , Humans , Male , Middle Aged , SARS-CoV-2/isolation & purification , Thrombotic Microangiopathies/drug therapy
8.
Br J Haematol ; 193(1): 43-51, 2021 04.
Article in English | MEDLINE | ID: covidwho-1066629
11.
J Thromb Thrombolysis ; 52(2): 468-470, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1002138

ABSTRACT

Acquired thrombotic thrombocytopenic purpura (TTP) is an autoimmune disease that can be triggered by different events, including viral infections. It presents as thrombotic microangiopathy and can lead to severe complications that often require management in the intensive care unit (ICU). We report a patient who presented with acquired TTP following COVID-19 infection. A 44-year-old woman presented to the emergency department with severe anemia, acute kidney injury and respiratory failure due to COVID-19. Clinical and laboratory findings were suggestive for thrombotic microangiopathy. On day 8 laboratory tests confirmed the diagnosis of acquired TTP. The patient needed 14 plasma exchanges, treatment with steroids, rituximab and caplacizumab and 18 days of mechanical ventilation. She completely recovered and was discharged home on day 51. Acquired TTP can be triggered by different events leading to immune stimulation. COVID-19 has been associated with different inflammatory and auto-immune diseases. Considering the temporal sequence and the lack of other possible causes, we suggest that COVID-19 infection could have been the triggering factor in the development of TTP. Since other similar cases have already been described, possible association between COVID and TTP deserves further investigation.


Subject(s)
COVID-19 , Plasma Exchange/methods , Purpura, Thrombotic Thrombocytopenic , Respiration, Artificial/methods , Respiratory Insufficiency , Rituximab/administration & dosage , Single-Domain Antibodies/administration & dosage , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Adult , COVID-19/complications , COVID-19/immunology , COVID-19/physiopathology , COVID-19/therapy , Female , Fibrinolytic Agents/administration & dosage , Humans , Immunologic Factors/administration & dosage , Male , Purpura, Thrombotic Thrombocytopenic/blood , Purpura, Thrombotic Thrombocytopenic/etiology , Purpura, Thrombotic Thrombocytopenic/physiopathology , Purpura, Thrombotic Thrombocytopenic/therapy , Respiratory Insufficiency/diagnosis , Respiratory Insufficiency/etiology , Respiratory Insufficiency/therapy , SARS-CoV-2/isolation & purification , SARS-CoV-2/pathogenicity , Thrombotic Microangiopathies/diagnosis , Thrombotic Microangiopathies/etiology , Treatment Outcome
12.
Int J Lab Hematol ; 43 Suppl 1: 129-136, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-998961

ABSTRACT

INTRODUCTION: Severe COVID-19 is often compounded by a prothrombotic state that is associated with poor outcomes. In this investigation, we aimed to evaluate ADAMTS13 activity, von Willebrand factor level (VWF:Ag), and the corresponding ADAMTS13 activity/VWF:Ag ratio, in patients with COVID-19 and for associations with disease progression and acute kidney injury (AKI). METHODS: Patients presenting to the emergency department (ED) with COVID-19 were enrolled in this prospective, observational study. ADAMTS13 activity and VWF:Ag were measured at index ED visit. The primary endpoint was severe AKI defined by KDIGO stage 2 + 3 criteria, while the secondary endpoint was peak 30-day COVID-19 severity. RESULTS: A total of 52 adult COVID-19 patients were enrolled. Overall, we observed that 23.1% of the cohort had a relative deficiency in ADAMTS13 activity, while 80.8% had elevated VWF:Ag. The ADAMTS13 activity/VWF:Ag ratio was significantly lower in patients with severe AKI (P = .002) and those who developed the severe form of COVID-19 (P = .020). The ADAMTS13 activity/VWF:Ag ratio was negatively correlated with age (P < .001) and LDH (P < .001), while positively correlated with hemoglobin (P = .041). After controlling for confounders, a one-unit increase in ADAMTS13/VWF:Ag ratio was associated with 20% decreased odds of severe AKI. CONCLUSION: A low ADAMTS13 activity:VWF:Ag ratio at ED presentation is associated with progression to severe COVID-19 disease and severe AKI, with a pattern suggestive of a secondary microangiopathy. Further interventional studies should be conducted to assess the restoration of ADAMTS13:VWF:Ag ratio in hospitalized patients with COVID-19.


Subject(s)
ADAMTS13 Protein/blood , Acute Kidney Injury/blood , COVID-19/blood , SARS-CoV-2 , Thrombotic Microangiopathies/etiology , von Willebrand Factor/analysis , ADAMTS13 Protein/deficiency , Acute Kidney Injury/etiology , Adult , Aged , COVID-19/complications , Comorbidity , Female , Humans , Male , Middle Aged , Prognosis , Prospective Studies , Severity of Illness Index , Thrombophilia/etiology
13.
Transplant Proc ; 53(4): 1211-1214, 2021 May.
Article in English | MEDLINE | ID: covidwho-989338

ABSTRACT

Coronavirus disease 2019 (COVID-19) is associated with high morbidity and mortality worldwide in both the general population and kidney transplant recipients. Acute kidney injury is a known complication of COVID-19 and appears to most commonly manifest as acute tubular injury on renal biopsy. Coagulopathy associated with COVID-19 is a known but poorly understood complication that has been reported to cause thrombotic microangiopathy on rare occasions in native kidneys of patients with COVID-19. Here, we report the first case of biopsy-proven thrombotic microangiopathy in a kidney transplant recipient with COVID-19 who developed acute pancreatitis and clinical features of microangiopathic hemolytic anemia. The patient recovered with supportive care alone.


Subject(s)
COVID-19/diagnosis , Kidney Transplantation/adverse effects , Pancreatitis/etiology , Thrombotic Microangiopathies/etiology , COVID-19/complications , COVID-19/virology , Creatinine/blood , Female , Humans , Kidney/pathology , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/therapy , Middle Aged , Pancreatitis/diagnosis , Platelet Count , SARS-CoV-2/isolation & purification , Tacrolimus/blood , Tacrolimus/therapeutic use , Thrombotic Microangiopathies/diagnosis , Transplantation, Homologous/adverse effects
14.
Nat Rev Cardiol ; 18(3): 194-209, 2021 03.
Article in English | MEDLINE | ID: covidwho-936141

ABSTRACT

The core pathology of coronavirus disease 2019 (COVID-19) is infection of airway cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that results in excessive inflammation and respiratory disease, with cytokine storm and acute respiratory distress syndrome implicated in the most severe cases. Thrombotic complications are a major cause of morbidity and mortality in patients with COVID-19. Patients with pre-existing cardiovascular disease and/or traditional cardiovascular risk factors, including obesity, diabetes mellitus, hypertension and advanced age, are at the highest risk of death from COVID-19. In this Review, we summarize new lines of evidence that point to both platelet and endothelial dysfunction as essential components of COVID-19 pathology and describe the mechanisms that might account for the contribution of cardiovascular risk factors to the most severe outcomes in COVID-19. We highlight the distinct contributions of coagulopathy, thrombocytopathy and endotheliopathy to the pathogenesis of COVID-19 and discuss potential therapeutic strategies in the management of patients with COVD-19. Harnessing the expertise of the biomedical and clinical communities is imperative to expand the available therapeutics beyond anticoagulants and to target both thrombocytopathy and endotheliopathy. Only with such collaborative efforts can we better prepare for further waves and for future coronavirus-related pandemics.


Subject(s)
Blood Coagulation Disorders/blood , Blood Platelet Disorders/blood , COVID-19/blood , Endothelium, Vascular/physiopathology , Inflammation/blood , Thrombosis/blood , Administration, Inhalation , Anticoagulants/therapeutic use , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/physiopathology , Blood Platelet Disorders/drug therapy , Blood Platelet Disorders/etiology , Blood Platelet Disorders/physiopathology , COVID-19/complications , COVID-19/drug therapy , COVID-19/physiopathology , Endothelium-Dependent Relaxing Factors/therapeutic use , Epoprostenol/therapeutic use , Heart Disease Risk Factors , Humans , Iloprost/therapeutic use , Inflammation/etiology , Inflammation/physiopathology , Nitric Oxide/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/blood , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/physiopathology , Thrombosis/etiology , Thrombosis/immunology , Thrombotic Microangiopathies/blood , Thrombotic Microangiopathies/drug therapy , Thrombotic Microangiopathies/etiology , Thrombotic Microangiopathies/physiopathology , Vascular Diseases/blood , Vascular Diseases/drug therapy , Vascular Diseases/etiology , Vascular Diseases/physiopathology , Vasodilator Agents/therapeutic use , Venous Thromboembolism/blood , Venous Thromboembolism/drug therapy , Venous Thromboembolism/etiology , Venous Thromboembolism/physiopathology
16.
Radiographics ; 40(6): 1574-1599, 2020 10.
Article in English | MEDLINE | ID: covidwho-810605

ABSTRACT

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) results in coronavirus disease 2019 (COVID-19), which was declared an official pandemic by the World Health Organization on March 11, 2020. The infection has been reported in most countries around the world. As of August 2020, there have been over 21 million cases of COVID-19 reported worldwide, with over 800 000 COVID-19-associated deaths. It has become apparent that although COVID-19 predominantly affects the respiratory system, many other organ systems can also be involved. Imaging plays an essential role in the diagnosis of all manifestations of the disease, as well as its related complications, and proper utilization and interpretation of imaging examinations is crucial. With the growing global COVID-19 outbreak, a comprehensive understanding of the diagnostic imaging hallmarks, imaging features, multisystemic involvement, and evolution of imaging findings is essential for effective patient management and treatment. To date, only a few articles have been published that comprehensively describe the multisystemic imaging manifestations of COVID-19. The authors provide an inclusive system-by-system image-based review of this life-threatening and rapidly spreading infection. In part 1 of this article, the authors discuss general aspects of the disease, with an emphasis on virology, the pathophysiology of the virus, and clinical presentation of the disease. The key imaging features of the varied pathologic manifestations of this infection that involve the pulmonary and peripheral and central vascular systems are also described. Part 2 will focus on key imaging features of COVID-19 that involve the cardiac, neurologic, abdominal, dermatologic and ocular, and musculoskeletal systems, as well as pediatric and pregnancy-related manifestations of the virus. Vascular complications pertinent to each system will be also be discussed in part 2. Online supplemental material is available for this article. ©RSNA, 2020.


Subject(s)
Betacoronavirus/physiology , Coronavirus Infections/diagnostic imaging , Lung/diagnostic imaging , Pandemics , Pneumonia, Viral/diagnostic imaging , Thromboembolism/diagnostic imaging , Thrombosis/diagnostic imaging , Angiography/methods , Angiotensin-Converting Enzyme 2 , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Coronavirus Infections/virology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Disease Progression , Fibrin Fibrinogen Degradation Products/analysis , Humans , Inflammation , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Pneumonia, Viral/virology , Pulmonary Artery/diagnostic imaging , Receptors, Virus/physiology , Respiratory Distress Syndrome/diagnostic imaging , Respiratory Distress Syndrome/etiology , SARS-CoV-2 , Symptom Assessment , Thromboembolism/blood , Thromboembolism/etiology , Thrombosis/blood , Thrombosis/etiology , Thrombotic Microangiopathies/diagnostic imaging , Thrombotic Microangiopathies/etiology , Tomography, X-Ray Computed/methods , Ultrasonography/methods
20.
Clin Appl Thromb Hemost ; 26: 1076029620938149, 2020.
Article in English | MEDLINE | ID: covidwho-651515

ABSTRACT

The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.


Subject(s)
Anticoagulants/therapeutic use , Betacoronavirus , Coronavirus Infections/complications , Pandemics , Pneumonia, Viral/complications , Thrombophilia/etiology , Thrombosis/prevention & control , Angiotensin II/metabolism , Arterial Occlusive Diseases/blood , Arterial Occlusive Diseases/epidemiology , Arterial Occlusive Diseases/etiology , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/epidemiology , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/etiology , Disease Outbreaks , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/prevention & control , Fibrin Fibrinogen Degradation Products/analysis , Fibrinolytic Agents/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Humans , Incidence , Inflammation , Pneumonia, Viral/blood , Pneumonia, Viral/epidemiology , Prognosis , Pulmonary Embolism/etiology , Pulmonary Embolism/prevention & control , Risk , SARS-CoV-2 , Sepsis/blood , Sepsis/complications , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/epidemiology , Thrombophilia/blood , Thrombophilia/drug therapy , Thrombosis/blood , Thrombosis/epidemiology , Thrombosis/etiology , Thrombotic Microangiopathies/etiology , Thrombotic Microangiopathies/prevention & control , Tissue Plasminogen Activator/therapeutic use
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