Background: Factor X (FX) deficiency is a rare autosomal recessive inherited bleeding disorder, with an estimated prevalence of approximately 1 in 1,000,000 individuals. According to the most recent data published by the World Federation of Hemophilia, no cases of FX deficiency have been reported in Cambodia to date. Case Report: A 14-year- and 7-month-old Cambodian boy presented with recurrent gum bleeding. His medical history was notable for multiple hematomas, joint ankylosis, and blue sclera. He was born to second-degree consanguineous parents, with no known family history of bleeding disorders. Laboratory evaluation revealed prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT) and severely reduced FX activity (< 1%), consistent with a diagnosis of severe congenital FX deficiency. Bleeding was successfully managed with fresh frozen plasma, initially administered at 15 mL/kg, followed by maintenance doses of 5 mL/kg twice daily. Conclusion: FX deficiency, though rare, should be considered in the differential diagnosis of pediatric patients presenting with recurrent gingival or mucocutaneous bleeding in conjunction with prolonged PT and APTT. This consideration is particularly important in resource-limited settings such as Cambodia, especially in children born to consanguineous parents and after more common coagulopathies have been excluded. In low-resource settings, where FX concentrates are often unavailable or unaffordable, fresh frozen plasma remains the primary treatment option.

Duloxetine, a widely used antidepressant, has not been adequately studied for its long-term adverse effects. This study aims to characterize the long-term safety of duloxetine in the real world. FAERS data from Q1 2004 to Q3 2024 were retrieved, covering adverse event (AEs) reports related to duloxetine. The data were analyzed using algorithms such as ROR, PRR, BCPNN, and MGPS. A total of 4876 AEs were collected, involving 52,205 patients. The top three System Organ Classes (SOCs) were psychiatric disorders, nervous system disorders, and general disorders and administration site conditions. The top three preferred terms based on signal strength were dysphoria (n = 2316, ROR 211.37, PRR 209.43, IC 6.73, EBGM 105.95), telangiectasia congenital (n = 5, ROR 96.55, PRR 96.55, IC 6.06, EBGM 66.69), and affect lability (n = 2520, ROR 85.2, PRR 84.35, IC 5.92, EBGM 60.66). In addition to the AEs already mentioned in the drug label, our study identified unexpected AEs related to congenital, familial and genetic disorders, such as telangiectasia congenital, factor X deficiency, and hemoglobinopathy, emphasizing the safety risks of duloxetine exposure during pregnancy. Furthermore, we observed rare adverse reaction signals, such as phagophobia, lymphocytic oesophagitis, coma blister, and junctional ectopic tachycardia. Notably, female patients reported more cases of drug withdrawal syndrome and opsoclonus myoclonus, while male patients more frequently reported sleep sex, sensory disturbance, semenuria, paedophilia, affect lability, and activation syndrome. Duloxetine may pose an undiscovered risk of AEs related to congenital, familial and genetic disorders. Our findings provide healthcare professionals with evidence to weigh the risks and benefits of duloxetine treatment, particularly for patients of different genders. Further prospective studies are needed to explore rare and unexpected AEs.

In patients with severe congenital factor X deficiency, spontaneous intracranial hemorrhage (ICH) is particularly frequent in early childhood. We describe a case of fetal death at 26 weeks due to massive ICH. Gene panel analysis of postmortem samples revealed homozygosity for a pathologic F10 gene variant (c.1210T>C, p.Cys404Arg), which impedes correct folding of the catalytic serine protease domain and, therefore, causes a significant reduction in FX levels. The parents, not consanguineous but of the same ethnic community, were found to be heterozygous for this variant and did not have any personal or family history of abnormal bleeding. To the best of our knowledge, this is the first reported case of severe FX deficiency resulting in ICH diagnosed through postmortem genetic analysis. It illustrates the importance of exploring the etiology of fetal or neonatal ICH, which may impact future pregnancies, and the treatment of a potential coagulopathy in the child.

Factor X deficiency is one of the rarest coagulation disorders representing 10% of all rare bleeding diseases with a frequency of 1:1,000,000. A 39-year-old male patient with no previous medical conditions was admitted to the hospital with a left carpal ganglion for surgical excision. Routine preoperative laboratory examination revealed a high international normalized ratio of 5.4 IU (0.8-1.1) and a prothrombin time of 72.2 s (10.9-13.6), with an isolated factor X level of less than 5%. Genetic testing for congenital factor X deficiency identified a homozygous mutation c.271 > A (p.Glu91). Vitamin K supplementation did not improve his international normalized ratio or increase factor X levels; hence, surgery was delayed. The patient was re-hospitalized to remove a wisdom tooth, during which fresh frozen plasma was administered. An allergic reaction complicated this procedure in the form of a rash on the body. As a result, the tooth was removed without active bleeding. This report presents a unique factor X deficiency case with limited treatment options to improve factor X levels after failed vitamin K administration and an allergic reaction to fresh frozen plasma. A physician's observation and ongoing follow-up were the only reasonable approaches in treating the patient with mild to moderate factor X deficiency due to lack of prothrombin complex concentrates or factor X replacement at the center at the time.