The role of infectious diseases in the catastrophic antiphospholipid syndrome

Garcı́a-Carrasco, Mario; Mendoza‐Pinto, Claudia; Macias-Díaz, Salvador; Lara, Fernando Vazquez de; Etchegaray‐Morales, Ivet; Romero, José Luis Gálvez; Méndez‐Martínez, Socorro; Cervera, Ricard

doi:10.1016/j.autrev.2015.07.009

Cited by 33 publications

(26 citation statements)

References 30 publications

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“…Inflammation induces increased coagulation by two different effects: by activating the cascade coagulation system and by downregulating the anti-coagulant mechanisms [29]. The endothelial cell and platelet activation occurring in CAPS is a key contributor to the genesis of a "thrombotic storm" [30] and in this setting, it is remarkable the role of infections as triggers of the disease [31]. It is of note that three Chinese COVID-19 patients admitted to ICU and presenting thrombotic events tested positive for anticardiolipin IgA antibodies as well as anti-β2 glycoprotein I IgA and IgG antibodies [32].…”

Section: Clinical Laboratory and Autoptic Similarities: Covid-19 Vsmentioning

confidence: 99%

COVID-19 gone bad: A new character in the spectrum of the hyperferritinemic syndrome?

Colafrancesco

Alessandri

Conti

et al. 2020

Autoimmunity Reviews

260

232

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The severe form of COVID-19 share several clinical and laboratory features with four entities gathered under the term "hyperferritinemic syndromes" and including macrophage activation syndrome (MAS), adult-onset Still's disease (AOSD), catastrophic anti-phospholipid syndrome (CAPS) and septic shock. COVID-19 systemic inflammatory reaction and "hyperferritinemic syndromes" are all characterized by high serum ferritin and a lifethreatening hyper-inflammation sustained by a cytokines storm which eventually leads to multi-organ failure. In this review, we analyze the possible epidemiological and molecular mechanisms responsible for hyper-inflammation in patients with severe COVID-19 and we underline the similarities between this condition and "hyperferritinemic syndromes" which would allow considering severe COVID-19 as a fifth member of this spectrum of inflammatory conditions.

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Section: Clinical Laboratory and Autoptic Similarities: Covid-19 Vsmentioning

confidence: 99%

COVID-19 gone bad: A new character in the spectrum of the hyperferritinemic syndrome?

Colafrancesco

Alessandri

Conti

et al. 2020

Autoimmunity Reviews

260

232

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“…The immunopathogenetic mechanisms that are subsequently activated entail a network of multiple proinflammatory factors including the Toll-like receptor 4 (TLR-4), which triggers a cytokine storm, followed by endothelial alterations that induce a procoagulant state ( 30 ).…”

Section: Can the Thromboembolic Diathesis During Some Cases Of Covmentioning

confidence: 99%

Entangling COVID-19 associated thrombosis into a secondary antiphospholipid antibody syndrome: Diagnostic and therapeutic perspectives (Review)

et al. 2020

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel β coronavirus that is the etiological agent of the pandemic coronavirus disease 2019 (COVID-19) that at the time of writing (June 16, 2020) has infected almost 6 million people with some 450,000 deaths. These numbers are still rising daily. Most (some 80%) cases of COVID-19 infection are asymptomatic, a substantial number of cases (15%) require hospitalization and an additional fraction of patients (5%) need recovery in intensive care units. Mortality for COVID-19 infection appears to occur globally between 0.1 and 0.5% of infected patients although the frequency of lethality is significantly augmented in the elderly and in patients with other comorbidities. The development of acute respiratory distress syndrome and episodes of thromboembolism that may lead to disseminated intravascular coagulation (DIC) represent the primary causes of lethality during COVID-19 infection. Increasing evidence suggests that thrombotic diathesis is due to multiple derangements of the coagulation system including marked elevation of D-dimer that correlate negatively with survival. We propose here that the thromboembolic events and eventually the development of DIC provoked by SARS-CoV-2 infection may represent a secondary anti-phospholipid antibody syndrome (APS). We will apply both Baconian inductivism and Cartesian deductivism to prove that secondary APS is likely responsible for coagulopathy during the course of COVID-19 infection. Diagnostic and therapeutic implications of this are also discussed.

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“…A systemic inflammatory syndrome characterized by fever, tachycardia, tachypnea, and leukocytosis commonly coexists and is associated with the extensive ischemic tissue damage [105,106]. Triggering factors identified in most patients include infections, surgery, obstetric complications, drugs or discontinuation of anticoagulants, and others [107,108]. The clinical manifestations are related to the specifics of organ involvement and include severe hypertension, acute renal failure, proteinuria, and hematuria (kidneys); ARDS, pulmonary embolism, and DAH (lungs); hypertensive and/or ischemic encephalopathy and stroke (central nervous system); coronary artery thrombosis and valve lesions (heart), and livedo reticularis, acrocyanosis, purpura, and others (skin) [109,110].…”

Section: Pulmonary Thromboembolism and Capsmentioning

confidence: 99%

Acute Respiratory Events in Connective Tissue Disorders

Papiris¹,

Manali²,

Kolilekas³

et al. 2016

Respiration

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Subacute-acute, hyperacute, or even catastrophic and fulminant respiratory events occur in almost all classic connective tissue disorders (CTDs); they may share systemic life-threatening manifestations, may precipitously lead to respiratory failure requiring ventilatory support as well as a combination of specific therapeutic measures, and in most affected patients constitute the devastating end-of-life event. In CTDs, acute respiratory events may be related to any respiratory compartment including the airways, lung parenchyma, alveolar capillaries, lung vessels, pleura, and ventilatory muscles. Acute respiratory events may also precipitate disease-specific extrapulmonary organ involvement such as aspiration pneumonia and lead to digestive tract involvement and heart-related respiratory events. Finally, antirheumatic drug-related acute respiratory toxicity as well as lung infections related to the rheumatic disease and/or to immunosuppression complete the spectrum of acute respiratory events. Overall, in CTDs the lungs significantly contribute to morbidity and mortality, since they constitute a common site of disease involvement; a major site of infections related to the ‘mater' disease; a major site of drug-related toxicity, and a common site of treatment-related infectious complications. The extreme spectrum of the abovementioned events, as well as the ‘vicious' coexistence of most of the aforementioned manifestations, requires skills, specific diagnostic and therapeutic means, and most of all a multidisciplinary approach of adequately prepared and expert scientists. Avoiding lung disease might represent a major concern for future advancements in the treatment of autoimmune disorders.

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The role of infectious diseases in the catastrophic antiphospholipid syndrome

Cited by 33 publications

References 30 publications

COVID-19 gone bad: A new character in the spectrum of the hyperferritinemic syndrome?

COVID-19 gone bad: A new character in the spectrum of the hyperferritinemic syndrome?

Entangling COVID-19 associated thrombosis into a secondary antiphospholipid antibody syndrome: Diagnostic and therapeutic perspectives (Review)

Acute Respiratory Events in Connective Tissue Disorders

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