Possible Liposomal Amphotericin B-Triggered Intracerebral Hemorrhage in Kala-Azar with Hemophagocytic Lymphohistiocytosis: A Case Study

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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Publication Details

Journal
Current Drug Safety
Published
2025-10-15
DOI
https://doi.org/10.2174/0115748863398954250926095224
Citations
1
Primary Topic
Research on Leishmaniasis Studies
Type
article
Field-Weighted Citation Impact
1.88
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article

Possible Liposomal Amphotericin B-Triggered Intracerebral Hemorrhage in Kala-Azar with Hemophagocytic Lymphohistiocytosis: A Case Study

Prasan Kumar Panda, Avneet Kumar Gupta, Sudhansu Sekhar Sahu, Shalini Singh
1 citations
Current Drug Safety
Research on Leishmaniasis Studies
1.88
article

Possible Liposomal Amphotericin B-Triggered Intracerebral Hemorrhage in Kala-Azar with Hemophagocytic Lymphohistiocytosis: A Case Study

Prasan Kumar Panda, Avneet Kumar Gupta, Sudhansu Sekhar Sahu, Shalini Singh
article en
1 citations

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.

Current Drug SafetyVol. 20
All India Institute of Medical Sciences Rishikesh (IN)
Openalex Percentile: Top 11%
Research on Leishmaniasis Studies
1.88
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