Case Report: Co‐Occurrence of Lung Adenocarcinoma and Congenital Dysfibrinogenemia—Diagnostic and Perioperative Management Challenges

TL;DR

A 67-year-old woman with lung cancer and a rare blood clotting disorder required special treatment to manage bleeding risks during surgery.

Contribution

Highlights the importance of genetic testing and tailored fibrinogen therapy in managing coagulation disorders during oncologic surgery.

Findings

Fibrinogen concentrate was more effective than plasma-derived products in normalizing fibrinogen levels pre-surgery.

Genetic testing confirmed a CD diagnosis and identified thrombotic risk via the FGA c.103C>T mutation.

Individualized thromboprophylaxis is essential to balance bleeding and clotting risks in CD patients undergoing surgery.

Abstract

Congenital dysfibrinogenemia (CD), a rare autosomal dominant coagulation disorder, poses significant perioperative challenges in oncologic surgery due to hypofibrinogenemia and variable bleeding‐thrombosis risks.

A 67‐year‐old woman presented with a 2.9 × 1.4 cm spiculated mass in the right middle lobe (RML) and persistent hypofibrinogenemia (0.56–0.58 g/L). Despite conventional fresh frozen plasma and cryoprecipitate transfusions, fibrinogen levels remained critically low. Preoperative optimization with human fibrinogen concentrates (total 4.0 g) normalized levels to 1.76 g/L within 24 h, enabling video‐assisted thoracoscopic (VATS) RML lobectomy with systematic lymphadenectomy (pT1cN0M0, Stage IA3). Postoperatively, fibrinogen gradually declined to 0.68 g/L at 1‐month follow‐up, necessitating extended surveillance. Genetic testing identified a heterozygous FGA c.103C>T (Arg35Cys) mutation, confirming CD diagnosis and thrombotic risk.

This case establishes three paradigms: (1) Mandatory comprehensive coagulation profiling in pulmonary resection candidates to identify CD; (2) superiority of fibrinogen concentrate over plasma‐derived products for rapid, sustained hemostasis in CD; (3) individualized thromboprophylaxis balancing hemorrhagic‐thrombotic risks through genetic risk stratification.

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