Anticardiolipin antibodies and COVID‐19—A case report from America

To the Editor,

The novel coronavirus pandemic has represented a continuous challenge to the world's medical community since first reported in December 2019 until the present day. The atmosphere of uncertainty surrounding coronavirus disease 2019 (COVID‐19) has prompted an unprecedented effort to produce scientific literature to understand its physiopathology. In such a way, and even when the evidence is still limited, dysregulation in the coagulation has been recognized as a possible critical pathway of the disease, and theories with notable acceptance have been formulated. Among the recently published articles, there are those showing benefit from anticoagulation, some identified an elevated D‐dimer as a poor prognosis predictor, and some described thromboembolic events in patients with COVID‐19. We present a case of pulmonary embolism (PE) and detected anticardiolipin antibodies (aCL) in a patient with severe COVID‐19 pneumonia.

An 82‐year‐old‐male, with a history of hypertension and benign prostatic hyperplasia, walked in the emergency department complaining of 1‐week flu‐like symptoms and worsening shortness of breath. He appeared distressed, desaturating, and tachypneic. Initial workup was significant for mild leukocytosis with lymphopenia, increased lactate dehydrogenase, procalcitonin and C‐reactive protein, and highly elevated D‐dimer (39.863 µg/mL), as shown in Table 1. The chest X‐ray revealed dense and mixed alveolar and interstitial infiltrates compatible with pneumonia. COVID‐reverse transcription polymerase chain reaction was sent, the patient was admitted for COVID‐19 pneumonia with hypoxemic respiratory failure, and was started on hydroxychloroquine, azithromycin, and ceftriaxone, alongside ascorbic acid, zinc, and placed on oxygen. Due to abnormal D‐dimer, PE was suspected, and computed tomography‐angiogram of chest performed, confirming the bilateral infiltrates and minimal scattered bilateral PE, as marked in Figure 1. The above findings prompted the addition of full‐dose‐enoxaparin to the therapy. Upon the fourth day of hospitalization, the patient continued to deteriorate even with therapeutic anticoagulation and was transferred to the intensive care unit (ICU), where he was started on vasopressors and got intubated. Bedside echocardiography demonstrated right ventricle strain, worsening PE was suspected, warranting thrombolysis. Subsequent testing came up positive for antiphospholipid antibodies, but negative for lupus anticoagulant. Patient status transiently improved to the point of extubation trial, which the patient eventually failed, yet he refused to be reintubated. In the following days, the clinical course aggravated, and the patient expired on day 17 of hospitalization.

Table 1.

Laboratory findings

White cell count (×103/mcL)	11.11
Neutrophil ABS (×103/mcL)	9.83
Lymphocyte ABS (×103/mcL)	0.49
Hemoglobin, g/dL	12.4
Platelets count (×103/mcL)	256
Alanine transaminase, U/L	26
Aspartate transaminase, U/L	34
Creatinine, mg/dL	0.7
Procalcitonin, ng/mL	0.950
Lactate dehydrogenase, U/L	406
C‐reactive protein, mg/dL	20.46
D‐dimer, µg/mL
Admission	39.863
Day 3	2.435
Day 5	2.903
Day 11	0.880
Day 13	0.605
Ferritin, ng/mL	1064
Anticardiolipin antibodies	Positive
IgA (APL)	33.1
IgM (MPL)	16.7
IgG (GPL)	24.1

Abbreviations: APL, IgA phospholipid unit; GPL, IgG phospholipid unit; IgA, immunoglobulin A; IgG, immunoglobulin G; IgM, immunoglobulin M; MPL, IgM phospholipid unit.

Figure 1.

CT angiography of lungs. Note multiple small thrombus in the right middle lobe (panel A, white arrow heads) and right upper lobe (panel B, white arrow heads). CT, computed tomography

This paper aims to describe what seems to be the first case reported in the United States of synchronic presentation of PE in a COVID‐19 pneumonia patient who tested positive for aCL, rather than to demonstrate correlation among them. However, since the outbreak, several papers have been published depicting thromboembolic events in the settings of COVID‐19, that is, Zhang et al ¹ characterized seven cases in a single‐center, admitted for hypoxia, and who tested positive for the virus and subsequently developed acroischemia in the absence of administered vasopressor or overt sepsis. Furthermore, a recently accepted manuscript ² found that 25% within a cohort of patients with severe COVID‐19 pneumonia, developed venous thromboembolism. Similarly, Zhang et al ³ reported three cases of COVID‐19 with hypoxic respiratory failure admitted to ICU with newly diagnosed multiple cerebral infarctions (one case with additional lower limb ischemia), who tested positive for aCLs. Although it is well known that severe infections can lead to procoagulant states, such as sepsis‐induced coagulopathy or disseminated intravascular coagulation, and viral processes to the transient expression of aCLs, it remains unclear whether the novel coronavirus has a particular effect on the coagulation homeostasis or a direct role on aCLs production, premise that lead us to an even more fraught question of when is the appropriate time to start anticoagulation in a patient with COVID‐19? Should we standardize its use among these patients? Or should we opt for a case‐based approach? Looking at the present situation, the latter seems more judicious. Early recognition of thromboembolic events and a prompt intervention will be crucial for the prognosis.

We profoundly encourage the healthcare providers in the frontlines to keep tracking and reporting COVID‐19 cases, we may be able to recognize patterns in the middle of the current cloudiness.

CONFLICT OF INTERESTS

The authors declare that there are no conflict of interests.

AUTHOR CONTRIBUTIONS

All the authors contributed to the design and implementation of the report, to the analysis of the information, and the writing of the manuscript.