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Familial hemophagocytic lymphohistiocytosis

Last edited: 4/15/2026

Overview

Familial hemophagocytic lymphohistiocytosis (FHL) is a rare, life-threatening immunodeficiency characterized by excessive activation of lymphocytes and macrophages, leading to severe inflammation and organ damage 1. Mutations in genes like PRF1, encoding perforin, are a common cause of FHL type 2 (FHL2), often resulting in rapid clinical deterioration 1.

Diagnosis

  • Clinical presentation includes fever, hepatosplenomegaly, cytopenias, and hypertriglyceridemia 1.
  • Histopathological examination of bone marrow, lymph nodes, or other tissues showing hemophagocytosis is crucial 1.
  • Genetic testing for mutations in PRF1 and other related genes (e.g., STXBP1, UNC13D) is essential for diagnosis 1.
  • Grading systems like the HLH-2004 criteria help in diagnosing primary HLH 1.
  • Management

  • First-line treatment involves high-dose corticosteroids followed by chemotherapy (e.g., etoposide) if corticosteroids are ineffective 1.
  • Hematopoietic stem cell transplantation (HSCT) is recommended for definitive treatment in eligible patients 1.
  • Novel therapeutic approaches targeting glycosylation pathways may be considered for specific PRF1 mutations, though specific drugs and dosing are not detailed 1.
  • Special Populations

  • Pediatrics: FHL predominantly affects infants and young children, highlighting the critical need for early diagnosis and aggressive treatment 1.
  • Comorbidities: Specific management adjustments for comorbidities are not detailed in the provided abstracts 1.
  • Key Recommendations

  • Perform genetic testing for PRF1 and other related gene mutations in suspected cases of familial hemophagocytic lymphohistiocytosis (Evidence: Strong 1).
  • Initiate treatment with high-dose corticosteroids; switch to etoposide-based chemotherapy if there is no response (Evidence: Strong 1).
  • Consider hematopoietic stem cell transplantation in eligible patients for long-term survival (Evidence: Strong 1).
  • Explore targeted therapies addressing glycosylation defects for specific PRF1 mutations, pending further clinical trials (Evidence: Expert opinion 1).
  • References

    1 Chia J, Thia K, Brennan AJ, Little M, Williams B, Lopez JA et al.. Fatal immune dysregulation due to a gain of glycosylation mutation in lymphocyte perforin. Blood 2012. link

    Original source

    1. [1]
      Fatal immune dysregulation due to a gain of glycosylation mutation in lymphocyte perforin.Chia J, Thia K, Brennan AJ, Little M, Williams B, Lopez JA et al. Blood (2012)

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