# Compound Heterozygous Protein C Deficiency Presenting With Splenic Infarction After COVID-19: A Case Report

**Authors:** Saki Imai, Soichiro Ishimaru, Masayuki Hirai, Makito Tanaka, Tetsushi Yoshikawa

PMC · DOI: 10.7759/cureus.101852 · Cureus · 2026-01-19

## TL;DR

A 17-year-old with a rare protein C deficiency developed severe blood clots and a splenic infarction after recovering from COVID-19, highlighting the need for close monitoring in such patients.

## Contribution

This case report highlights the risk of thrombosis in protein C deficiency patients during and after COVID-19, even after initial recovery.

## Key findings

- A patient with compound heterozygous protein C deficiency developed VTE and splenic infarction after COVID-19.
- Thrombotic events occurred despite anticoagulant therapy and initial clinical improvement.
- The case underscores the need for individualized anticoagulation strategies in such patients during and after infection.

## Abstract

Congenital protein C deficiency is a rare autosomal recessive disorder that predisposes patients to severe thrombosis due to markedly reduced protein C activity. Although primarily associated with venous events, an increased risk of arterial thrombosis is also recognized, particularly in severe cases. We report the case of a 17-year-old male patient with compound heterozygous protein C deficiency who developed venous thromboembolism (VTE) after coronavirus disease 2019 (COVID-19) and subsequently experienced splenic infarction despite anticoagulant therapy. Diagnosed shortly after birth following neonatal purpura fulminans, he had been maintained on long-term warfarin therapy. The patient presented with fever and cough and was diagnosed with COVID-19 by antigen testing. Soon after symptom onset, he developed right thigh pain with rapidly expanding ecchymosis, leading to a diagnosis of recurrent VTE. Intravenous heparin and fresh frozen plasma (FFP) were initiated. Although his symptoms and coagulation markers improved by day 10, he developed sudden abdominal pain on day 11, and a contrast-enhanced CT scan revealed a partial splenic infarction. Anticoagulation was intensified, and he subsequently recovered without sequelae. COVID-19 can precipitate both venous and arterial thrombosis through endothelial injury and inflammation. This case illustrates that thrombotic events may occur even after apparent clinical and biochemical improvement, emphasizing the need for careful monitoring and individualized anticoagulation strategies in patients with protein C deficiency during and after COVID-19.

## Linked entities

- **Chemicals:** warfarin (PubChem CID 54678486)
- **Diseases:** protein C deficiency (MONDO:0019145), venous thromboembolism (MONDO:0005399), splenic infarction (MONDO:0006978), coronavirus disease 2019 (MONDO:0100096), purpura fulminans (MONDO:0000809)

## Full-text entities

- **Genes:** SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, TAT (tyrosine aminotransferase) [NCBI Gene 6898], CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, PROC (protein C, inactivator of coagulation factors Va and VIIIa) [NCBI Gene 5624] {aka APC, PC, PROC1, THPH3, THPH4}
- **Diseases:** congenital coagulation disorders (MESH:D025861), Abdominal pain (MESH:D015746), cough (MESH:D003371), endothelial injury (MESH:D057772), venous and arterial thrombosis (MESH:D020246), Ecchymosis (MESH:D004438), infection (MESH:D007239), coagulation (MESH:D001778), Splenic Infarction (MESH:D013159), rupture (MESH:D012421), COVID-19 (MESH:D000086382), endothelial dysfunction (MESH:D014652), VTE (MESH:D054556), hematologic and thrombotic diseases (MESH:D006402), thigh pain (MESH:D010146), arterial thrombosis (MESH:D002341), inflammation (MESH:D007249), trauma (MESH:D014947), thrombosis (MESH:D013927), post-COVID (MESH:D000094024), autosomal recessive disorder (MESH:D030342), purpura fulminans (MESH:D055665), hematologic malignancies (MESH:D019337), fever (MESH:D005334), hypercoagulability (MESH:D019851), congenital thrombophilia (MESH:C540694), tenderness (MESH:D063806), purpura (MESH:D011693), embolic disease (MESH:D004617), infarction (MESH:D007238), Congenital protein C deficiency (MESH:D020151)
- **Chemicals:** bilirubin (MESH:D001663), Cr (MESH:D002857), Anact C (-), glucose (MESH:D005947), creatinine (MESH:D003404), warfarin (MESH:D014859), Heparin (MESH:D006493), GLU (MESH:D018698), urea nitrogen (MESH:C530477)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** c.1268delG, c.631C>T

## Full text

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## Figures

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## References

12 references — full list in the complete paper: https://tomesphere.com/paper/PMC12915839/full.md

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Source: https://tomesphere.com/paper/PMC12915839