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Multiorgan involvement and circulating IgG1 predict hypocomplementaemia in IgG4-related disease.

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Hypocomplementaemia, common in IgG4-related disease (IgG4-RD), is linked to disease extent, particularly lymph node and lung involvement. IgG1 levels, not IgG4, correlate with this complement deficiency, suggesting complement activation in IgG4-RD.

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Area of Science:

  • Immunology
  • Rheumatology
  • Pathophysiology

Background:

  • Hypocomplementaemia is frequently observed in patients diagnosed with IgG4-related disease (IgG4-RD).
  • Understanding the clinical features and underlying mechanisms associated with hypocomplementaemia in IgG4-RD is crucial for disease management.

Purpose of the Study:

  • To identify specific IgG4-related disease (IgG4-RD) features associated with hypocomplementaemia.
  • To explore the mechanisms of complement activation in the context of IgG4-RD.

Main Methods:

  • A single-centre cross-sectional study was conducted involving 279 patients meeting IgG4-RD classification criteria.
  • Unadjusted and multivariable-adjusted logistic regression analyses were employed to identify factors linked to hypocomplementaemia.

Main Results:

  • Hypocomplementaemia was present in 32% of patients.
  • Initially, involvement of multiple organs, lymph nodes, lungs, pancreas, liver, and kidneys showed associations with hypocomplementaemia.
  • After adjustment, lymph node and lung involvement remained significantly associated, while renal involvement was attenuated. Fibrotic manifestations and lacrimal gland involvement showed inverse associations.
  • Hypocomplementaemia correlated with higher concentrations of all IgG subclasses and IgE. Crucially, only IgG1, not IgG4, independently correlated with hypocomplementaemia after adjustment.

Conclusions:

  • Hypocomplementaemia in IgG4-RD is associated with the overall extent of the disease and is not exclusive to renal involvement.
  • The study highlights a significant independent correlation between IgG1 levels and hypocomplementaemia in IgG4-RD, challenging the role of IgG4.
  • These findings suggest that complement activation plays a role in the pathophysiology of IgG4-related disease.