Pregnancy is characterized by progressive hemostatic adaptation: increased fibrinogen synthesis, enhanced thrombin generation, and reduced fibrinolytic potential together prepare the maternal circulation for delivery-related blood loss. A fall in fibrinogen during pregnancy or the immediate postpartum period therefore does not carry the same meaning as an equivalent value outside of pregnancy. It may instead represent loss of a pregnancy-specific hemostatic reserve. Fibrinogen concentration is consistently associated with the severity of postpartum hemorrhage, but randomized trials have not shown that empirical replacement in all women with early postpartum hemorrhage improves clinical outcomes. This narrative review summarizes current evidence on pregnancy-associated fibrinogen deficiency and dysfunction, with emphasis on pathophysiology, trial findings, fibrinogen thresholds, replacement strategies, congenital fibrinogen disorders, and research gaps. Current data support using fibrinogen as both a severity marker and a selective treatment target, interpreted according to gestational age, bleeding phenotype, placental involvement, and resource setting. Direct evidence generated in low-resource settings is limited; no randomized trial of fibrinogen measurement or replacement has been conducted in such a setting.

According to Globocan, in 2022, the highest incidence of hepatocellular carcinoma (HCC) was observed in Asia, which accounted for 75% of the global burden of liver cancer 1. In the Republic of Kazakhstan in 2022, the incidence of liver cancer was 5.1 per 100,000 population, with a mortality rate of 2.9, respectively. For the period 2014-2022, HCC had the lowest five-year survival rate among all malignant neoplasms in Kazakhstan2,3. The treatment of HCC across various stages involves a range of clinical strategies4. Sorafenib is currently the primary drug in the treatment of HCC 4,5 and doxorubicin is used in transarterial hepatic artery chemoembolization (TACE)8. However, their use results in cardiotoxicity leading to cancer therapeutics-related cardiac dysfunction (CTRCD)9. CRTCD manifests as cardiovascular disease symptoms in patients with HCC, reflecting irreversible structural changes in the myocardium10. BJMS, Vol. 24 No. 04 October’25 Page : 1189-1196