# 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.

## Key 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.