Recognising Immune Thrombocytopenic Purpura Emerging in the Setting of COVID-19 Illness

April 1, 2024

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Immune thrombocytopenic purpura (ITP) represents an important hematologic manifestation which can complicate COVID-19 illness through complex immunologic mechanisms that remain incompletely understood. Also termed idiopathic thrombocytopenic purpura, ITP features autoantibody attack of platelets leading to isolated low platelet counts (thrombocytopenia) and bleeding risk.

This article provides physicians and researchers an up-to-date overview on COVID-19-linked ITP including proposed pathophysiology, diagnostic approach, treatment considerations and implications for prognosis based on rapidly accumulating case reports and literature over the course of the pandemic.

Heightened awareness of this phenomenon allows appropriate detection and management of ITP arising in patients suffering acute SARS-CoV-2 infection. Further research may clarify the intricate interplay between COVID-induced hyperinflammation and subsequent autoimmunity inflicting platelet destruction in affected individuals.

Background on Immune Thrombocytopenic Purpura (ITP)

ITP represents the most common cause of isolated thrombocytopenia in otherwise healthy adults. An autoimmune disorder, autoantibodies recognising platelet surface proteins trigger their premature clearance from circulation, outpacing bone marrow production. This manifests clinically as mucocutaneous bleeding, easy bruising and fatigue correlating with falling platelet counts on bloodwork.

Standard first line ITP therapy revolves around steroids, intravenous immunoglobulin (IVIG) or splenectomy to attenuate autoantibody activity and boost platelet levels. Second line options target more selective immune modulation in severe, refractory or relapsing ITP.


COVID-19 Infection as a Trigger for ITP Onset

Analysis of numerous COVID-19 patient case reports reveals ITP onset following SARS-CoV-2 infection, either presenting simultaneously with acute viral illness or becoming apparent during subsequent recovery.

Post-infectious autoimmunity represents a recognised phenomenon with prior viruses also linked to ITP development in genetically prone individuals. However, the scale of global COVID-19 spread has allowed this association to become prominently apparent and concerning from a public health perspective.

Proposed explanations for the COVID-infection–ITP link include:

  • Direct platelet ACE2 receptor damage by the virus
  • Formation of platelet antibodies triggered by virus-platelet protein complexes
  • Loss of immune self-tolerance from the profound hyperinflammation COVID-19 incites

However, significant knowledge gaps persist regarding the precise interplay between this novel coronavirus and secondary autoimmune thrombocytopenia which future studies must address through longitudinal observation.

Presentation of COVID-Associated ITP

Thrombocytopenia is common among acutely ill COVID-19 patients given the recognized prothrombotic state this viral illness can induce. However, ITP represents an important subset of those developing isolated platelet depletion without other cell line suppression or coagulation abnormalities.

Besides merely low platelet counts, more extensive or severe bleeding patterns seem prevalent in COVID-ITP cases versus conventional ITP patients. Gingival bleeding, retinal hemorrhages, cerebral bleeds and heavy vaginal bleeding during menstruation appear overrepresented in emerging case data.

Despite overt bleeding, some patients with COVID-19-associated ITP also developed thromboembolic complications like stroke or venous thromboembolism. This further supports the notion of complex dysregulation of hemostatic pathways inflicted by SARS-CoV-2 which warrants further research.

Diagnostic Approach to COVID-Linked ITP

Distinguishing COVID-related ITP from other causes of low platelets can prove challenging amid the multisystem organ dysfunction the infection itself may trigger. Key principles aiding diagnosis include:

  • Timing relative to acute infection – ruling out early sepsis-induced thrombocytopenia
  • Normal white cells and hemoglobin – isolating platelet destruction
  • Checking for platelet autoantibodies
  • Examining blood smear morphology

Overall, COVID-associated ITP represents a primarily clinical diagnosis after exclusion of other thrombocytopenic disorders or secondary ITP drivers. Monitoring through recovery and following platelet trends proves informative regarding likely ITP persistence versus transient depletion during peak infection.

Treatment Approach to COVID-Linked ITP

General treatment guidelines for symptomatic ITP patients remain applicable to COVID-positive cases or those with onset following SARS-CoV-2 infection. However, recognizing potential for enhanced severity mandates vigilant monitoring and lower thresholds for aggressive intervention.

First-line management options for COVID-associated ITP include:

  • High dose steroids: dexamethasone, prednisone
  • Intravenous immunoglobulin (IVIG)
  • Intravenous anti-D immunoglobulin
  • Thrombopoietin receptor agonists like eltrombopag or romiplostim to stimulate platelet production

Refractory cases justify rapid escalation to second-line immunosuppressant agents after weighing risks of additive infection vulnerability in the COVID-19 era.


Prognosis and Implications of COVID-Linked ITP

ITP onset or exacerbation during acute COVID-19 illness appears to trigger severe, even life-threatening hemorrhage in a subset of patients based on early case observations. This may indicate the combination of SARS-CoV-2 induced inflammation and subsequent autoantibody generation can lead to profound platelet destruction and bleeding diathesis.

Among survivors of the initial infection, longitudinal follow up found most patients achieving partial or complete ITP remission by 6 months. However, around a third manifested persistent thrombocytopenia requiring ongoing immunomodulation at one year follow up in available data.

Overall, clinicians must recognise COVID-19 as a clear trigger for profound ITP with the potential for resistance to first and second line therapies. This represents an ongoing area of hematologic research which frontline providers and researchers must collaboratively investigate further in coming years.

Frequently Asked Questions Regarding COVID-19 and ITP

Below are responses to common queries when encountering COVID-19 patients developing acute thrombocytopenia concerning for underlying ITP:

What proportion of COVID-19 patients manifest ITP?

Estimates based on early case series suggest 1-5% of hospitalized COVID-19 cases demonstrate subsequent ITP onset. However, severe or fatal ITP complications appear very rare at the population level. Those suffering the most severe COVID pneumonia may face higher risk.

Does prior vaccination against COVID raise ITP risk too?

Yes, isolated reports also document apparent ITP arising post COVID-19 vaccination – both mRNA platforms and adenovirus vectors. The timing and lack of other explanations supports a causal link. However, vaccine-induced ITP still appears remarkably infrequent considering vast global deployment.

How quickly can ITP present after COVID illness resolves?

Available data indicates most cases of COVID-associated ITP are apparent during acute viral infection. However, delays between COVID recovery and subsequent platelet depletion between 1 week to 6 months were observed in minority of patients.

Can recurrent ITP bouts happen after COVID recovers?

Yes, COVID infection may reactivate prior quiescent ITP or instigate initial episode with high risk of follow up recurrences. Periodic screening bloodwork is reasonable for those recovering from COVID and any prior ITP history. New onset bleeding symptoms should prompt lab testing.

What is the role of testing for platelet antibodies to confirm ITP after COVID?

Checking for elevated platelet directed antibodies can help substantiate ITP as the cause of low platelets versus other COVID-related effects. However, negative serology does not rule out ITP, and positive tests can take time to manifest. Clinical judgement supersedes antibody presence or absence early on.

In summary, key takeaways regarding immune thrombocytopenic purpura associated with COVID-19 illness include:

  • Recognizing COVID infection as a trigger for acute, severe ITP through inflammation-autoimmunity pathways
  • ITP represents an isolated thrombocytopenia amid other COVID hematologic effects
  • Standard ITP treatments apply but often require aggressive dosing and vigilance
  • Prognosis relatively fair but COVID-ITP may demonstrate atypical resistance to therapy
  • Further research on pathophysiology and long-term outcomes remains urgently needed

Overall, elucidating the connection between SARS-CoV-2 infection and secondary immune destruction of platelets constitutes an ongoing international research priority for scientisits and clinical hematologists alike. Collaborative efforts focused on this phenomenon will guide prevention and allow optimal management strategies for affected patients.


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