Case Report
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Respirol. Aug 8, 2021; 11(1): 12-17
Published online Aug 8, 2021. doi: 10.5320/wjr.v11.i1.12
Like father, like son: Pulmonary thromboembolism due to inflammatory or hereditary condition? Two case reports
Pedro Hannun, Walter Hannun, Hugo Hyung Yoo, Lucilene Resende
Pedro Hannun, Hugo Hyung Yoo, Lucilene Resende, Department of Internal Medicine, Botucatu Medical School, São Paulo State University - UNESP, São Paulo 18618-687, Brazil
Walter Hannun, Department of Institutional Relations, Santa Catarina Hospital, São Paulo 01310-000, Brazil
Author contributions: All authors were responsible for the study conception and design; Hannun P wrote the manuscript; all authors contributed to the manuscript revision and final version approval.
Informed consent statement: Informed written consent for publication of this report and use of any accompanying images was obtained from both patients.
Conflict-of-interest statement: The authors report no conflict of interest.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Pedro Hannun, MHSc, Department of Internal Medicine, Botucatu Medical School, São Paulo State University - UNESP, Prof. Mário Rubens Guimarães Montenegro Avenue, s/n, São Paulo 18618-687, Brazil. pgch2003@gmail.com
Received: March 7, 2021
Peer-review started: March 7, 2021
First decision: May 6, 2021
Revised: May 17, 2021
Accepted: July 14, 2021
Article in press: July 14, 2021
Published online: August 8, 2021
Processing time: 149 Days and 14.6 Hours
Abstract
BACKGROUND

Venous thromboembolism, which includes deep venous thrombosis and pulmonary embolism, is a well-known causal disorder with high morbidity and mortality rates. Inherited or acquired conditions affecting components of coagulation and fibrinolysis systems have been linked to venous thromboembolism pathogenesis as they may lead to a pro-inflammatory state in human bodies. Toxoplasmosis is a zoonosis that potentially leads to acute systemic cachectic-inflammatory effects in experimental animal models but is not yet proven in humans. It is known that venous thrombosis can occur during acute inflammatory/infectious diseases, although it is not well established with regard to toxoplasmosis alone.

CASE SUMMARY

A 70-year-old Caucasian man and his 32-year-old son developed general malaise, chills, fever, and myalgia, having established a diagnosis of toxoplasmosis. Twenty days later, they presented dry cough leading to further investigations that revealed an incidental deep venous thrombosis plus pulmonary embolism in them both. Thrombophilia screening showed both patients had a factor V Leiden mutation heterozygosis. Father and son completely recovered without any sequalae after anticoagulant treatment. They have not presented symptom recurrence of either medical disorder during 1 year of follow-up.

CONCLUSION

Toxoplasmosis may enhance the risk of venous thromboembolism in patients showing factor V Leiden mutation heterozygosis.

Keywords: Factor V Leiden mutation; Thrombophilia; Venous thromboembolism; Deep venous thrombosis; Toxoplasmosis; Inflammation; Case report

Core Tip: This paper describes two closely related patients simultaneously infected by Toxoplasma gondii who concurrently presented their first venous thromboembolism episode. Further investigation revealed a factor V Leiden mutation in them both. The association between these two morbid conditions suggests that systemic infection/ inflammation may enhance the risk of venous thromboembolism in people carrying this kind of pro-thrombophilia mutation. As far as we know, this is the first report of that association. We believe that this paper provides an insight into this important issue bringing potential help for clinical decision-making processes by doctors around the world.