Summary: Purpose: Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts due to the destruction of platelets by autoantibodies. The presence of hepatitis B core antibodies (anti-HBc) is a marker of previous or occult hepatitis B virus (HBV) infection, which may influence the clinical course and treatment outcomes in ITP patients. Methods: This retrospective study investigated the impact of anti-HBc positivity on the clinical outcomes and response to treatment in ITP patients. A total of 116 patients with ITP were divided into 2 groups: those who were anti-HBc positive (n = 31) and those who were anti-HBc negative (n = 85). Clinical data, including platelet counts at diagnosis and during follow-up, response to corticosteroid treatment and remission rates were analyzed. Results: The results indicated that anti-HBc positive patients had significantly lower platelet counts at diagnosis (p = 0.009) and a longer hospital stay (p = 0.042). Additionally, these patients demonstrated lower complete response rates to initial corticosteroid treatment at 1 month (p = 0.001) and 6 months (p = 0.021) compared to anti-HBc negative patients; however, there were no significant differences in overall response or durable response rates between the groups at 12 months. The risk of relapse was higher in anti-HBc positive patients (p = 0.041). Conclusion: These findings suggest that anti-HBc positivity may be associated with a more severe disease course and reduced treatment efficacy in ITP, highlighting the importance of assessing hepatitis B serological markers when managing ITP patients.

Aims: Hereditary thrombophilias are genetic conditions that increase thromboembolic risk, with heightened thrombotic potential during pregnancy due to the associated hypercoagulable state. These conditions are recognized as significant risk factors for recurrent pregnancy loss (RPL), defined as the loss of two or more consecutive pregnancies before the 20th gestational week, affecting approximately 1-2% of women of reproductive age. RPL is multifactorial, influenced by genetic, environmental, and hormonal factors, with advanced maternal age and previous pregnancy loss being prominent risk factors. While the role of hereditary thrombophilias in adverse pregnancy outcomes remains controversial, studies have reported inconsistent findings regarding their association with RPL. Methods: This retrospective cohort study included 736 women with a history of RPL and aimed to investigate the relationship between genetic thrombophilia variants and recurrent pregnancy loss, focusing on their impact on miscarriage risk. Genetic testing using PCR panels identified common mutations such as Factor V Leiden, MTHFR, PAI-1, and prothrombin G20210A. Results: Statistical analyses revealed no significant associations between these variants and RPL. Conclusion: The findings suggest that, despite the prevalence of certain mutations, their contribution to miscarriage risk may be limited, underscoring the importance of selective genetic testing. This study highlights the need to optimize genetic screening practices to avoid unnecessary testing and reduce healthcare costs, supporting a more targeted approach in managing patients with RPL.

We report a rare case of coexistence of chronic lymphocytic leukaemia (CLL) and polycythemia vera (PV) in a patient initially diagnosed and treated for CLL. A 61-year-old man presented with fatigue and night sweats, with laboratory tests showing elevated haemoglobin, hematocrit (HCT), leukocyte count and splenomegaly. Peripheral blood smear revealed lymphocytosis with basket cells, and flow cytometry confirmed CLL (RAI stage II). FISH analysis was negative for del13q, del11q, trisomy 12, del 17p and del6q. Chemotherapy was started because of B symptoms. Persistent splenomegaly and elevated HCT at follow-up prompted further evaluation, which revealed a JAK2 V617F mutation and an erythropoietin (EPO) level <1 mIU/mL, confirming PV. The patient achieved remission for CLL, but required hydroxyurea and acetylsalicylic acid for PV. The coexistence of CLL and PV is rare and the underlying mechanisms are not well understood, although a common clonal haematopoietic stem cell origin or germline mutations are possible explanations. Although chemotherapeutic agents are known to induce PV, the elevated HCT at the time of CLL diagnosis suggests a pre-existing relationship between the two diseases. Therefore, elevated HCT in CLL patients should prompt consideration of PV.