ArticleCureus2025
Hemophagocytic Lymphohistiocytosis in HIV/AIDS: Who Fired the First Shot, the Virus or Its Companions?
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemophagocytic lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome caused by uncontrolled activation of T-lymphocytes and macrophages. It is classified as either familial (genetic) or acquired. Among acquired forms, infections are a common trigger, with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) and associated opportunistic infections frequently considered in the differential diagnosis. We report the case of a 20-year-old Hispanic male who presented with nausea and vomiting and was found to have bi-cytopenia, high ferritin level, mild splenomegaly, decreased natural killer (NK) cells, and bone marrow findings consistent with HLH. He was also diagnosed with HIV/AIDS, which was considered the underlying trigger for HLH, and was initiated on dexamethasone per HLH-2004 protocol. The patient was started on intravenous amphotericin B for disseminated histoplasmosis, along with trimethoprim-sulfamethoxazole (TMP-SMX) for Pneumocystis jirovecii pneumonia prophylaxis. Due to worsening mental status, increased amphotericin B and TMP-SMX dose for presumed central nervous system (CNS) histoplasmosis and toxoplasmosis, respectively. Brain magnetic resonance imaging (MRI) revealed multiple ring-enhancing lesions, and cerebrospinal fluid (CSF) was positive for Toxoplasma gondii. Amphotericin B was subsequently de-escalated, while TMP-SMX was continued at therapeutic dosing. The patient was co-managed in a multidisciplinary approach involving infectious disease, hematology, and neurology specialists. We conclude that early diagnosis of HLH is critical to prevent disease progression and improve patient outcomes. Identifying and treating the underlying trigger remains the cornerstone of effective management. The use of timely diagnostic tools and a multidisciplinary approach is essential to avoid delays in recognizing HLH and initiating appropriate therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.