Severe immune thrombocytopenic purpura in critical COVID-19: a case report

Lévesque, Valérie; Milaire, Émilie; Corsilli, Daniel; Rioux-Massé, Benjamin; Carrier, François Martin

doi:10.21203/rs.3.rs-32479/v1

Cited by 3 publications

(5 citation statements)

References 8 publications

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“…Furthermore, our case reiterates the finding that thrombocytopaenia can occur at a late presentation following the onset of COVID-19—in our case, occurring on day 10. 5 20 The patient’s platelet count in December 2019 was 152×10 9 /L and therefore he did not have thrombocytopaenia before admission. Platelet autoantibodies were not requested as evidence suggests they do not seem to direct treatment.…”

Section: Discussionmentioning

confidence: 96%

Severe thrombocytopaenia secondary to COVID-19

et al. 2020

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The SARS-CoV-2 infection has caused a pandemic with a case rate of over 290 000 lab-confirmed cases and over 40 000 deaths in the UK. There is little evidence to inform the optimal management of a patient presenting with new or relapsed acute idiopathic thrombocytopaenic purpura with concurrent SARS-CoV-2 infection. We present a case of severe thrombocytopaenia complicated by subdural haematoma and rectal bleed associated with COVID-19. A 67-year-old man, admitted with a non-productive cough and confusion, was found to be positive for COVID-19. Ten days after admission, his platelets decreased from 146×109/L to 2×109/L. His platelets did not increase despite receiving frequent platelet transfusions. He was non-responsive to corticosteroids and intravenous immunoglobulins. Romiplostim and eltrombopag were given and after 9 weeks of treatment, his platelet count normalised. He was deemed medically fit with outpatient follow-up in a haematology clinic.

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Section: Discussionmentioning

confidence: 96%

Severe thrombocytopaenia secondary to COVID-19

et al. 2020

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“…Regarding AIC cases reported after or concomitant to COVID-19 infection/pneumonia (Table 4), the most represented is ITP, with 23 patients (mostly case reports) that developed COVID-19-associated acute/severe thrombocytopenia. This cytopenia was not present before infection and was different from the frequently observed mild thrombocytopenia accompanying COVID-19 (14,(27)(28)(29)(30)(31)(32)(33). All cases resolved with steroids and/or IvIg with the exception of one patient who died for intraventricular hemorrhage and pulmonary embolism/pneumonia (27).…”

Section: Literature Reviewmentioning

confidence: 71%

Are Patients With Autoimmune Cytopenias at Higher Risk of COVID-19 Pneumonia? The Experience of a Reference Center in Northern Italy and Review of the Literature

2021

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During COVID-19 pandemic the care of onco-hematologic and autoimmune patients has raised the question whether they are at higher risk of infection and/or worse outcome. Here, we describe the clinical course of COVID-19 pneumonia in patients with autoimmune cytopenias (AIC) regularly followed at a reference center in Northern Italy. The study period started from COVID-19 outbreak (February 22, 2020) until the time of writing. Moreover, we provide a review of the literature, showing that most cases reported so far are AIC developed during or secondary to COVID-19 infection. At variance, data about AIC pre-existing to COVID infection are scanty. The 4 patients here described (2 autoimmune hemolytic anemias, AIHA, 1 Evans syndrome, and 1 immune thrombocytopenia) with COVID-19 pneumonia belong to a large cohort of 500 AIC patients, making this study nearly population-based. The observed frequency (4/501; 0.7%) is only slightly superior to that of the general population admitted to hospital/intensive care unit (0.28/0.03%, respectively) in Lombardy in the same period of observation. All cases occurred between March 21 and 25, whilst no more AIC were recorded later on. Although different in intensity of care needed, all patients recovered from COVID-19 pneumonia, with apparently no detrimental effect of previous/current immunomodulatory treatments. AIHA relapse occurred in two patients, but promptly responded to therapy. With limitations due to sample size, these results suggest a favorable outcome and a lower-than-expected incidence of COVID-19 pneumonia in patients with previously diagnosed AIC, and allow speculating that immunomodulatory drugs used for AIC may play a beneficial rather than a harmful effect on COVID-19 infection.

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“…Although the COVID-19-associated thrombocytopenia is usually mild, very severe hemorrhage has been reported in a small number of patients. 2,[12][13][14] Based on a study by Sabin et al on SARS-CoV-2induced ITP, no association was found between hemorrhage severity and COVID-19 severity. In another study, Sue Pavord et al found a sharp drop in platelets in the patients with end-stage COVID-19 due to multiple organ failure.…”

Section: Introductionmentioning

confidence: 99%

“…1 Because the exact etiology of ITP is unclear, the diagnosis should be made by differentiating it from other types of thrombocytopenia, such as thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, microangiopathic hemolytic anemia, and heparin-induced thrombocytepenia. 2,3 The etiology of ITP is unknown, but it appears to be due to genetic and acquired factors. 1,4 The ITP is a common acquired bleeding disorder, with a higher prevalence among children than adults.…”

Section: Introductionmentioning

confidence: 99%

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Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

Bahadoram

Saeedi-Boroujeni

Mahmoudian-Sani

2022

Med. Jadert. (Online)

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Millions of people around the world were, or are still involved with COVID-19 due to infection with SARS-CoV-2. In addition to hallmark symptoms, thrombotic problems, lymphopenia, and thrombocytopenia have also been reported in COVID-19 patients, of which ITP is the most common and occurs in more than one-third of COVID-19 patients. Hyperinflammation, cytokine storms, and generally immune dysregulation in a percentage of patients develop the main consequences of diseases such as ALI, ARDS and multiple organ failure. Some of the important events in the immunopathogenesis of this disease are disruption of T-cell effector differentiation and the destructive role of Th17 lymphocytes, neutrophil function and inflammatory macrophages. NLRP3-inflammasome hyperactivity causes serious dysfunction of innate immune cells and, consequently, T lymphocytes in many inflammatory disorders, most notably in the COVID-19. A closer look at the immunopathogenesis of ITP and COVID-19 brings us to common ground. The purpose of this study was to review and summarize the findings of various studies on the immunopathogenesis of ITP and its possible causes in COVID-19. Finally, enhanced differentiation of Th17 and Th1, the cell death called as pyroptosis, hyperinflammation and dysfunction of inflammatory neutrophils and macrophages, and NLRP3- inflammasome hyperactivity are important factors in the development of thrombocytopenia in patients with COVID-19. Further studies are needed to better understand immunopathogenesis and effective treatments for ITP, especially in inflammatory disorders

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Severe immune thrombocytopenic purpura in critical COVID-19: a case report

Cited by 3 publications

References 8 publications

Severe thrombocytopaenia secondary to COVID-19

Severe thrombocytopaenia secondary to COVID-19

Are Patients With Autoimmune Cytopenias at Higher Risk of COVID-19 Pneumonia? The Experience of a Reference Center in Northern Italy and Review of the Literature

Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

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