Fingolimod has been used for about ten years to treat multiple recurrent sclerosis. It has been reported that Fingolimod causes an elevation in liver enzymes. In this case report, the clinical and laboratory parameters im-proved after discontinuation of the drug. However, there is no publication in the literature regarding acute liver failure and liver transplantation fol-lowing Fingolimod treatment. In this article, we presented a 33 – year – old female patient who developed acute liver failure and underwent liver transplantation after Fingolimod treatment for recurrent multiple sclerosis.

Congenital hemophilia B is a rare X-linked recessive bleeding disorder caused by factor IX deficiency. Acquired hemophilia A is a rare, acquired bleeding disorder that presents with new-onset bleeding, especially in older adults, due to the development of auto-antibodies against factor VIII (FVIII). This case report presents the medical management of a patient with congenital hemophilia B and acquired hemophilia A. We highlight the limitations of maintaining factor levels with factor replacement therapy alone, particularly in hemophilia patients who have developed factor inhibitors. In addition, we draw attention to the need for dose escalation, the cost, and the need for immune-tolerance induction therapy. This case illustrates that when the current diagnosis does not explain the full clinical picture and laboratory data are inadequate, it is important to continue to seek alternative diagnoses and cost-effective treatment.

Introduction: Leishmaniasis is a zoonosis caused by Leishmania spp. parasites through the bite of infected female sandflies and has three main forms: visceral (VL), cutaneous (CL) and mucocutaneous (MCL). VL is endemic in many countries around the world. It is on the World Health Organisation's (WHO) list of neglected diseases and is difficult to diagnose due to its non-specific clinical manifestations. VL is characterised by fever, hepatosplenomegaly and bone marrow suppression. The diagnosis is made by the presence of amastigotes in tissue or blood samples or serological and DNA-based techniques. Case: Our patient was a 30-year-old male did not have any immunodeficiency. He was characterised by persistent fever, pancytopenia, hepatosplenomegaly and multiple millimetric hypoechoic solid nodules in the spleen. The diagnosis of VL was confirmed using all three parasitological, serological and molecular methods. Cure was achieved by treatment with liposomal amphotericin B (L-AmB). Discussion: VL should be considered in the differential diagnosis of patients with fever of unknown cause, pancytopenia and hepatosplenomegaly. The presence of solid nodular lesions in the spleen may also shed light in favour of VL