Acquired hemophilia A (AHA) is a rare bleeding disorder characterized by spontaneous bleeding in individuals with no previous personal or family history of bleeding, caused by the development of autoantibodies against coagulation Factor VIII (FVIII). These autoantibodies may be associated with drugs, autoimmune disorders, malignancies, and pregnancy. Pregnancy-associated AHA (PA-AHA) is a very rare condition, accounting for approximately 1%-5% of all AHA cases. Emicizumab, a bispecific FVIII-mimetic monoclonal antibody, was originally approved for Congenital Hemophilia A (with or without FVIII inhibitors) and has since gained widespread recognition and clinical utility in the management of AHA as well. We report a case of PA-AHA that was successfully managed with emicizumab. A 46-year-old woman was admitted with vaginal bleeding and extensive ecchymoses. The patient's obstetric history was notable for a twin gestation achieved through in vitro fertilization (IVF) using donor oocytes. The patient reported recurrent ecchymoses and menorrhagia beginning in the postpartum period. Laboratory examination revealed severe anemia with normal platelet counts and prothrombin time (PT), but a markedly prolonged activated partial thromboplastin time (aPTT) of 94.5 s. Immunological and virology testing, as well as cancer biomarkers, were negative. Initially, the patient received bypassing hemostatic therapy with recombinant activated Factor VII (rFVIIa), along with intensive immunosuppressive therapy (IST) consisting of corticosteroids, rituximab, and cyclophosphamide, in accordance with current international recommendations. However, no clinical response was observed. Treatment with emicizumab was subsequently initiated according to the proposed dosing schedule. Within 2 days, all bleeding manifestations resolved rapidly. Notably, FVIII activity, measured using a chromogenic assay, remained markedly reduced. After 566 days of follow-up, FVIII activity spontaneously normalized, allowing discontinuation of emicizumab. No further bleeding episodes were observed. Although emicizumab is increasingly incorporated into the management of AHA, clinical experience in PA-AHA remains limited. The present case adds to the existing literature by supporting the safety and efficacy of emicizumab in PA-AHA, highlighting its role as an effective hemostatic bridge to remission in complex clinical settings.

Several biosimilars of the low-molecular-weight heparin enoxaparin are available on the market, but no studies have compared the effects of branded versus biosimilar enoxaparin on coagulation assays. The aim of this study was to compare the in vitro anticoagulant effects of the branded enoxaparin (Clexane) and three biosimilar versions (Critinox, Inhixa, and Qnox) on a panel of coagulation assays. A platelet-poor plasma pool was spiked with five concentrations of four different enoxaparins (range 0.2-2.0 IU/mL). These were measured using the chromogenic anti-Xa assay and chromogenic anti-IIa assay. The following coagulation assays were performed in duplicates for each enoxaparin preparation: prothrombin time (PT), activated partial thromboplastin time (aPTT), PT-derived fibrinogen, Clauss fibrinogen, thrombin time (TT), dilute Russell's viper venom time (dRVVT) screen and confirm, one-stage factors VII, VIII, and IX, and chromogenic assays for factors VIII and IX. Positive correlations were observed between increasing concentrations of the different enoxaparins and PT, aPTT, TT, and dRVVT screen and confirm. Negative correlations were observed with all one-stage factor assays and chromogenic FVIII. No consistent correlation was observed for the fibrinogen assays and chromogenic FIX. All enoxaparin preparations had an estimated mean anti-Xa:anti-IIa activity ratio between 3.12:1 and 3.92:1. There were no statistically significant differences between the four preparations of enoxaparin. This study showed that branded and biosimilar versions of enoxaparin exhibited very similar in vitro anticoagulant effects across the coagulation assay panel tested.

Laparoscopic embryo transfer in pigs has been explored as a minimally invasive alternative to conventional laparotomic methods, which often lead to surgical risks such as adhesions, prolonged recovery, and postoperative complications. This study is the first to report the generation of genetically modified pigs via embryo transfer using a laparoscopic approach. Gene-edited embryos were prepared by delivering the CRISPR/Cas9 system via electroporation to target the Coagulation Factor VIII, WDR45, and IL2RG genes and then transferred into the oviducts of five recipient gilts using a laparoscopic technique. Embryos putatively carrying modifications in the Coagulation Factor VIII and WDR45 genes were each transferred into a single recipient gilt, and both recipients became pregnant. In contrast, embryos putatively carrying a modification in the IL2RG gene were transferred into three recipient gilts, of which two became pregnant. In total, four recipient gilts were carried to full term, resulting in the birth of 9 live piglets. Genotyping confirmed that all of the offspring carried the genetic modifications, demonstrating this method may have potential for producing genetically modified pigs. The successful production of live gene-edited offspring demonstrates the feasibility of laparoscopic embryo transfer for genetically modified embryos. Although further research, including a large number of recipient pigs, as well as direct comparisons with conventional laparotomy, is needed to evaluate embryo survival, implantation efficiency, and animal welfare, laparoscopic embryo transfer represents a feasible approach for generating genetically modified pigs.

Livedoid vasculopathy (LV) is a rare, chronic vascular disorder marked by painful, recurrent ulcerations that primarily affect the lower extremities. It is frequently associated with hypercoagulable states, although its pathophysiology remains incompletely understood. We present the case of a 25-year-old woman with a longstanding history of LV, elevated factor VIII, increased lipoprotein(a), recurrent kidney stones, and iron deficiency anemia who presented with worsening lower-extremity ulcerations. An extensive workup excluded other hypercoagulable and connective-tissue conditions, leaving elevated factor VIII and lipoprotein(a) as the most likely contributors to her disease. Although her symptoms initially resolved with treatment, they recurred over time, and management was further complicated by her desire for future pregnancy, which precluded the use of several standard anticoagulant therapies. Her regimen was ultimately centered on pentoxifylline and low-dose aspirin to control symptoms while minimizing risk to a future pregnancy. This case illustrates the importance of individualized treatment planning in LV, particularly when hypercoagulable risk factors intersect with reproductive goals.

Proximal avulsion of the rectus femoris tendon is an uncommon injury in athletes and is rarely associated with direct trauma and extensive hematoma. We describe a 25-year-old competitive taekwondo athlete who developed acute hip flexor weakness and thigh swelling after a direct anterior thigh kick. Bedside musculoskeletal ultrasound demonstrated disruption of rectus femoris architecture with intramuscular hematoma, and magnetic resonance imaging confirmed complete avulsion of both proximal heads of the rectus femoris with tendon retraction and a large associated hematoma. The patient had sustained a recent prior quadriceps injury with hematoma. Recurrent hematoma development warranted hematologic testing, which revealed an isolated Factor VIII deficiency. Given his high functional demands, he underwent open surgical repair. This case highlights the importance of early imaging and consideration of operative management in high-level athletes presenting with trauma-related rectus femoris avulsion. It also highlights the importance of hematologic workups in athletes presenting with unexplained recurrent hematomas to effectively risk-stratify surgery and return to sport.

Acquired haemophilia A (AHA) is a rare autoimmune bleeding disorder resulting from the development of inhibitory autoantibodies against factor VIII (FVIII). Malignancy is a recognised association, although colorectal cancer remains an uncommon underlying cause. We report a 68-year-old woman with sigmoid adenocarcinoma who developed severe postoperative haemoperitoneum associated with progressive activated partial thromboplastin time prolongation, an initial FVIII activity of 52 IU/dL that subsequently declined to 2 IU/dL, and development of an FVIII inhibitor measuring 9.7 BU. The case highlights diagnostic challenges associated with AHA, particularly the risk of delayed diagnosis and the complexities of balancing immunosuppressive intensity alongside haemostatic therapy. We then present a review of current literature to guide management for this rare condition and emerging therapies.