His blood chemistry was unremarkable. identify the conditions that are associated with nonbovine thrombin AFVD. We assume that AFVD should be kept in mind for patients who present with multiple haemorrhages. strong class=”kwd-title” Keywords: acquired factor V deficiency, corticosteroids, factor V inhibitors, haemorrhage, urinary tract infection Introduction Coagulation factor V is a coagulation protein that is synthesized by the liver and possibly by megakaryocytes. Factor V is present in the blood plasma as a single-chain polypeptide (80%) and in platelet Ibrutinib Racemate -granules (20%). Factor V participates in procoagulantion because it is a cofactor of the prothrombinase complex. Factor V also plays an important role in the anticoagulant pathway because it plays a pivotal role in haemostasis: its inactivated form participates in the inactivation of factor VIII via activated protein C (APC). Thus, factor V plays an essential role in both procoagulant and anticoagulant pathways. Factor V functional disorders can cause haemorrhagic or thrombotic events. Acquired factor V deficiency (AFVD) is a rare haemostatic disorder that is generally because of the development of antibodies against factor V. AFVD was first reported in 1955 [1,2], and there are approximately 200 case reports or case series describing this disorder in the current literature. The majority of cases of AFVD have occurred in the presence of associated risk factors that include bovine thrombin exposure during surgical procedures, antibiotic administration (especially antibiotics of the lactam group), cancers, and autoimmune disorders. The clinical manifestations of AFVD are variable and range from asymptomatic laboratory anomalies to fatal haemorrhagic or thromboembolic events. Here, we report a Chinese case of AFVD that presented with haematuria followed by multiple haemorrhages that resulted from an extremely low level of factor V inhibitor and was potentially secondary to a urinary tract infection. Case report Our patient was a 64-year-old man who was admitted to our hospital with a 15-day history of haematuria and a 6-day history of nose and tonsil bleeding. The DLL1 patient was previously evaluated in another hospital, and levofloxacin was prescribed with a diagnosis of cystitis. The coagulation profile revealed both a prolonged prothrombin time (PT) of 113.80?s (11C14.5?s) and an activated partial thromboplastin time (APTT) of more than 180?s (28C45?s). Haemostatic drugs were prescribed for his bleeding. However, these drugs did not correct his PT or APTT, and he subsequently developed nose and tonsil bleeding. His past medical history included prostatic hyperplasia for 10 years and a surgery after a car accident in 2011. However, he had no history of significant coagulation disorders with prior surgical procedures or other family bleeding history. He had no documented history of medicines. Upon physical examination, slight tenderness was present on epigastric palpation and kidney region percussion. Upon laboratory examination, his haemoglobin level was 105?g/l (115C150?g/l), his red blood cell count was 3.28??109/l (3.8C5.1??109/l), his white blood cell count was 7.9??109/l (3.5C9.5??109/l), his platelet count was 162??109/l (125C350??109/l), and his fibrinogen was 3.98?g/l (2C4?g/l). The blood chemistry revealed no liver dysfunction (Table ?(Table1).1). The coagulation profile revealed both a prolonged PT of 51.70?s (11C14.5?s) and an APTT of more than 180?s (28C45?s; Table ?Table2).2). His factor V activity was markedly reduced (2% of normal; Table ?Table3).3). The levels of factors VII/VIII and factor IX were within the reference ranges. His blood chemistry was unremarkable. The overall results indicated the presence of antibodies against factor V and suggested a diagnosis of AFVD. A standard Bethesda assay confirmed the presence of factor V inhibitor with a low level of 1.9?BU. The patient received an infusion of fresh frozen plasma (FFP) with a partial correction of his coagulation parameters (Table ?(Table2).2). Subsequently, the factor V inhibitor was undetectable. However, the FFP exhibited no obvious effect Ibrutinib Racemate on restoring the plasma factor V activity (Table ?(Table3).3). The patient was discharged because his bleeding stopped. Table 1 Laboratory findings thead Blood chemistry /thead ALT17 (9C50?IU/l)K3.78 (3.50C5.30?mmol/l)AST15 (15C40?IU/l)Cl103 (99C110?mmol/l)GGT31 (10C60?IU/l)AKP90 (45C125?IU/l)SerologyLDH270 (120C230?IU/l)HBsAgCTP73.2 (6.0C85.0?g/l)HBsAbCALB45.2 (40.0C55.0?g/l)HBeAgCTBIL5.3 (5.0C21.0?mol/l)HBeAbCDBIL2.1 (0.0C6.0?mol/l)HBcAb-IgGCIBIL3.2 (2.0C15.0?mol/l)HCV AbCBUN5.68 (2.30C7.80 mmol/l)HCV AgCCr65 (262C115?mol/l)PreS1-AgCNa142 (137C147 mmol/l)TP-AbC Open in a separate window AKP, alkaline phosphatase; ALB, albumin; ALT, alanine aminotransferase; AST, aspartate transaminase; BUN, blood urea nitrogen; CYP4F2, cytochrome P450 4F2; CYP4V2, cytochrome P450 4V2; DBIL, direct bilirubin; GGT, -glutamyl transpeptidase; HBsAg, hepatitis B surface antigen; HBsAb, antibody to hepatitis B surface antigen; HBeAg, hepatitis B e-antigen; HBeAb, antibody to hepatitis B e-antigen; HBcAb, antibody to hepatitis B core antigen; HCV Ab, antibody to hepatitis C virus; HCV Ag, hepatitis C antigen; IBIL, indirect bilirubin; JAK2, Janus kinase 2; KLKB1, kallikrein B1; LDH, lactic dehydrogenase; PreS1-Ag, PreS1 antigen; SERPINC 1, serpin C1; TBIL, total bilirubin; TP, total protein; TP-Ab, treponema pallidum antibody; C, negative. Table 2 Prothrombin time and activated partial thromboplastin time results after the first and Ibrutinib Racemate second admissions Open in a separate window Table 3 Factor V activity.