title: Multifactorial risk analysis of bone marrow histiocytic hyperplasia with hemophagocytosis in critically ill medical patients--a postmortem clinicopathologic analysis.
abstract: OBJECTIVE
  Systematic studies of the prevalence and risk factors of histiocytic hyperplasia with hemophagocytosis (HHH) in critically ill patients are lacking. The aim of our study was a) to determine the frequency and intensity of HHH in the bone marrow of patients who died on the medical intensive care unit; b) to analyze morphologic bone marrow changes; and c) to identify possible risk factors and their interactions in the pathogenesis of HHH.
  
  
  METHODS
  A retrospective observational analysis of clinical data and autopsy findings including histologic and immunohistological analysis of bone marrow to characterize cellularity, siderosis, hemophagocytosis, and T-cell infiltrates.
  
  
  METHODS
  The medical intensive care unit of a university hospital.
  
  
  METHODS
  Patients were 107 consecutive patients who died and underwent autopsy.
  
  
  METHODS
  None.
  
  
  RESULTS
  HHH was identified in 69 of the 107 patients (64.5%). Moderate to severe HHH was present in 35 of the 107 bone marrows. Univariate risk factor analysis showed that HHH was associated with various intrinsic and extrinsic factors. However, multivariate analysis identified the intensity of therapeutic interventions--represented by the Therapeutic Intervention Scoring System--as the only positive, and cardiovascular disease as the only significant negative, predictor of HHH (p <.05). Routine laboratory tests were of no value in predicting the presence of HHH. The intensity of HHH correlated significantly with siderosis and T-cell infiltrates (p <.05) but not with bone marrow cellularity.
  
  
  CONCLUSIONS
  HHH is common in medical intensive care unit nonsurvivors. Treatment intensity and a noncardiovascular cause of death are predictors of HHH. Sepsis and blood transfusion may have a synergistic effect on the triggering of HHH. HHH in bone marrow is associated with enhanced T-cell infiltrates, suggesting that T cells may play an important role in its mediation.
authors.affiliation: Department of Medicine I, Friedrich Alexander University, Erlangen-Nuremberg, Germany.
authors.forename: Richard
authors.initials: R
authors.lastname: Strauss
authors.forename: Daniel
authors.initials: D
authors.lastname: Neureiter
authors.forename: Bert
authors.initials: B
authors.lastname: Westenburger
authors.forename: Markus
authors.initials: M
authors.lastname: Wehler
authors.forename: Thomas
authors.initials: T
authors.lastname: Kirchner
authors.forename: Eckhart G
authors.initials: EG
authors.lastname: Hahn
mesh_terms: D000368:Aged; D001344:Autopsy; D001803:Blood Transfusion; D001853:Bone Marrow / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000473:pathology; D016638:Critical Illness; D005260:Female; D006644:Histiocytes / Q000473:pathology*; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010587:Phagocytosis; D012189:Retrospective Studies; D012307:Risk Factors; D018805:Sepsis / Q000473:pathology; D012806:Siderosis / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology