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The following is a summary of “Longitudinal assessment of immunoglobulin response and disease progression in critically ill patients with community acquired pneumonia,” published in the December 2024 issue of Critical Care by Rademaker et al. 

Low endogenous immunoglobulin (Ig) levels are common in sepsis, but the impact on outcomes and the benefit of Ig replacement therapy (IgRT) remain uncertain despite the critical role in fighting encapsulated pathogens. 

Researchers conducted a retrospective study to examine the relationship between serial Ig levels and disease progression in patients with critical illness with community-acquired pneumonia (sCAP) caused by encapsulated or other pathogens. 

They analyzed data of patients suffering from critical illness with CAP and a PaO₂ /FiO₂ ratio < 200, with or without septic shock, using an existing biorepository where microbiological causes were adjudicated protocolized. Generalized linear mixed models assessed associations between IgG and IgM levels (measured on admission days 1, 3, and 7) and disease progression (Sequential Organ Failure Assessment (SOFA) 88score on days 2, 4, and 8) for all-cause sCAP and cases involving Streptococcus (S.) pneumoniae or Haemophilus (H.) influenzae 

The results showed among 255 eligible patients with CAP, 82 (32%) cases were caused by S. pneumoniae or H. influenzae. Low IgG levels (< 7.0 g/L) were observed in 151 patients (59%), low IgM levels (< 0.4 g/L) in 77 patients (30%), and both were low in 56 patients (22%). A lower IgG level was linked to a slightly higher SOFA score at admission (β = −0.07 per 1 g/L IgG, P = 0.029), but IgG decline over time was not associated with an increase in SOFA score (β = −0.04, P = 0.564). IgM levels showed no significant association with SOFA score changes, regardless of the presence or absence of S. pneumoniae or H. influenzae. 

Investigators concluded the patients with critical illness with CAP, IgG and IgM dynamics in the 1st week of ICU stay were not associated with clinically relevant changes in disease course, regardless of the causative pathogen. 

Source: ccforum.biomedcentral.com/articles/10.1186/s13054-024-05197-3