Successful Treatment of a 39-Year-Old COVID-19 Patient with Respiratory Failure by Selective C-Reactive Protein Apheresis

Jan Torzewski, Oliver Zimmermann, Stefan Kayser, Franz Heigl, Florian Wagner, Ahmed Sheriff, Christian Schumann, Jan Torzewski, Oliver Zimmermann, Stefan Kayser, Franz Heigl, Florian Wagner, Ahmed Sheriff, Christian Schumann

Abstract

BACKGROUND High C-reactive protein (CRP) plasma levels in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are associated with poor prognosis. CRP, by activating the classical complement pathway and interacting with macrophages via Fc gamma receptors, can cause pulmonary inflammation with subsequent fibrosis. Recently, we have reported first-in-man CRP apheresis in a "high-risk" COVID-19 patient. Treatment was unfortunately clinically unsuccessful. Here, we report on successful CRP apheresis treatment in a "lower-risk" COVID-19 patient with respiratory failure. CASE REPORT A 39-year-old male patient suffering from fatigue, dyspnea, and fever for 4 days was referred to us. The patient had to be intubated. Polymerase chain reaction (PCR) analysis of a throat smear revealed SARS-CoV-2 infection. Mutation analysis revealed the VOC B. 1.1.7 variant. CRP levels were 79.2 mg/L and increased to 161.63 mg/L. Procalcitonin (PCT) levels were continuously normal (<0.5 ng/ml). Antibiotic therapy was started to avoid bacterial superinfection. CRP apheresis was performed once via central venous access. CRP levels declined from a maximum of 161.63 mg/L to 32.58 mg/L. No apheresis-associated adverse effects were observed. Subsequently, CRP plasma levels declined day by day and normalized on day 5. The patient was extubated on day 5 and discharged from the Intensive Care Unit (ICU) on day 6. A second low CRP peak (maximum 22.41 mg/L) on day 7 remained clinically inapparent. The patient was discharged in good clinical condition with a CRP level of 6.94 mg/L on day 8. CONCLUSIONS SARS-CoV-2 infection can induce an uncontrolled CRP-mediated autoimmune response of ancient immunity. In this patient, the autoimmune response was potently and successfully suppressed by early selective CRP apheresis.

Conflict of interest statement

Conflict of interest: Ahmed Sheriff is founder and shareholder of Pentracor GmbH. Stefan Kayser is an employee of Pentracor GmbH

Conflicts of Interest

Ahmed Sheriff is founder and shareholder of Pentracor GmbH. Stefan Kayser is an employee of Pentracor GmbH.

Figures

Figure 1.
Figure 1.
Supine chest X-ray immediately after intubation and computed tomography (axial/coronal) on admission (A, B) showing typical bilateral infiltrates and beginning of fibrosing alveolitis (black arrows).
Figure 2.
Figure 2.
(A) CRP levels (reference range 0.00–5.00 mg/L) during the course of the patient’s hospital stay. CRP levels were elevated on admission (79.2 mg/L) and sharply increased on day 2 (maximum 161.63 mg/L). Due to CRP apheresis (light red columns) via central venous access, CRP levels markedly dropped and further declined later on. A second low CRP peak (22.41 mg/L) on day 7 remained clinically inapparent. (B) PCT levels (reference range <0.5 ng/mL) remained normal during the hospital stay.
Figure 3.
Figure 3.
(A) CRP apheresis (light red column) and course of CK/CK-MB and LDH plasma levels. Only CK slightly increased, likely due to positioning of the patient (muscular CK). In contrast, CK-MB levels remained normal. (B) CRP apheresis (light red column), bilirubine, international normalized ratio (INR), and creatinine levels. Normal values for each parameter.
Figure 4.
Figure 4.
(A) CRP apheresis (light red column) and course of Horovitz quotient [16]. Horovitz quotient changed from severe (PaO2/FIO2 ≤100 mmHg) to moderate (PaO2/FIO2 ≤200 mmHg) after intubation and ventral positioning, then worsened during CRP apheresis due to dorsal positioning. After CRP apheresis, however, Horovitz quotient, independent from dorsal or ventral positioning, significantly improved until extubation and hospital discharge. (B) CRP apheresis (light red column) and course of lactate (reference range 0.5–1.6 mmol/L). Lactate remained normal during the hospital stay.

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Source: PubMed

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