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Possible Liposomal Amphotericin B-Triggered Intracerebral Hemorrhage in Kala-Azar with Hemophagocytic
Shiv Narayan Sahu1, Avneet Kumar Gupta1, Prasan Kumar Panda1
1Department of Internal Medicine (ID Division), and of 2 Pathology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India.
Abstract:
Introduction: Liposomal amphotericin B is the treatment of choice for visceral leishmaniasis (VL), but its potential adverse effects, including hematologic and neurologic complications, remain a subject of concern. Hemophagocytic lymphohistiocytosis (HLH) is a rare but severe hyperinflammatory syndrome that can occur in VL, and the development of intracerebral hemorrhage (ICH) during treatment adds a critical dimension to patient management. While ICH is an uncommon complication, its possible association with liposomal amphotericin B warrants further exploration.
Case Study: This report discusses a middle-aged man who presented with a 4-month history of recurrent fever. He also reported progressive breathlessness, a sensation of heaviness in the left abdomen, and pedal edema over the past 4 weeks. Additionally, he experienced black discoloration of urine and stool for 2 weeks. Physical examination revealed massive splenomegaly, melena, hematuria, and pancytopenia. Bone marrow aspiration confirmed hemophagocytosis, and the recombinant kinesin antigen-39 (rk39) test for VL was positive. An H-score of 234 indicated a 98-99% probability of HLH. The patient was initiated on treatment with a single dose of liposomal amphotericin B. However, on the fourth day of therapy, he developed a sudden onset of headache followed by altered sensorium. Neuroimaging revealed ICH with surrounding edema and intraventricular extension, causing a significant mass effect. Given the temporal association with treatment initiation, liposomal amphotericin B-induced ICH was considered a potential etiology. He was managed conservatively with three units of single-donor platelets and showed gradual neurological improvement without further invasive intervention. He was eventually discharged in a hemodynamically stable condition.
Conclusion: This case describes the potential risk of ICH as an adverse or trigger effect of liposomal amphotericin B in the setting of VL and HLH. Clinicians should remain vigilant for neurological complications during treatment, emphasizing the importance of close monitoring and individualized therapeutic decisions to optimize patient outcomes.
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