Inflammatory Markers in Pediatric Bacterial Sepsisvs. SARS-CoV-2 Infection: A Retrospective Study

Interpreting Rheumatology Laboratory Tests

Background: Acute respiratory distress syndrome (ARDS) is ultimately an inflammatory state. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are inflammatory markers. The aim of this study was to evaluate the value of the ESR, CRP and APACHE II score as prognostic factors for patient with ARDS. Methods: We retrospectively analyzed the medical records of 87 ARDS patients. The predictors (APACHE II score, ESR and CRP) and outcomes (mortality and length of the total hospital stay, the ICU stay and mechanical ventilator care) were obtained from the patients' records. The patients were grouped according to survival as the Survivor and Non survivor groups. We compared the APACHE II score, the ESR and the CRP level between the survivor group and the nonsurvivor group. We evaluated the correlation between the predictors and the outcomes. The initial ESR, CRP level and APACHE II score were checked at the time of ICU admission and the second ESR and CRP level were checked days after ICU admission. Results: Thirty-eight (43.7%) patients remained alive and 49 (56.3%) patients died. The APACHE II score was significantly lower for the survivor group than that for the non survivor group ( vs , respectively, p=0.006). The initial ESR and CRP level were not different between the survivor and non-survivor groups (ESR vs , respectively, p=0.93, CRP vs , respectively, p=0.68). The decrement of the CRP level for the survivor group was greater than that for the non survivor group ( vs , respectively, p=0.003). Correlation analysis revealed the initial ESR was positively correlated with the length of the total hospital stay and the ICU stay (correlation coefficient of the total hospital days: R=0.43, p=0.001, correlation coefficient of the ICU stay: R=0.39, p=0.014). Conclusion: The initial APACHE II score can predict the mortality of ARDS patients, and the degree of the early CRP change can be a predictor of mortality for ARDS patients. The initial ESR has positive correlation with the ARDS patients' duration of the total hospital stay and the ICU stay.

Cardiology Patient Page. C-reactive protein: a simple test to help predict risk of heart attack and stroke.

Obesity is commonly linked with a pro-inflammatory condition, marked by elevated levels of inflammatory biomarkers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Sleeve gastrectomy, a widely utilized bariatric procedure, aims to achieve substantial weight loss and enhance metabolic function. This study aims to examine the impact of body mass index (BMI) reduction following sleeve gastrectomy on the levels of inflammatory markers CRP and ESR in obese individuals. A prospective observational study was carried out on patients with obesity who underwent sleeve gastrectomy between 2020 and 2022 at Luqman Hakim Medical Education Center. CRP and ESR levels were recorded preoperatively and then at 6- and 12-month post-surgery. Simple regression analysis was employed to evaluate the correlation between BMI reduction and changes in CRP and ESR levels over time. A significant reduction in BMI, CRP, and ESR levels was observed at both 6- and 12-month post-surgery. However, regression analysis indicated that BMI reduction did not significantly predict changes in ESR (B = 0.209, p = 0.262) or CRP (B = 0.274, p = 0.079) at the 6-month and 12-month follow-ups (CRP: B = 0.123, p = 0.138; ESR: B = 0.122, p = 0.453). While sleeve gastrectomy significantly reduces BMI and inflammatory markers such as CRP and ESR in patients with obesity, the direct association between BMI reduction and these markers was not statistically significant. Further studies are warranted to elucidate the underlying mechanisms and identify other potential predictors of inflammatory marker reduction post-surgery.

Inflammatory markers such as the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels have always been a part of the diagnostic criteria for periprosthetic joint infection (PJI), but they perform poorly anticipating the outcome of reimplantation. D-dimer has been reported in a small series as a potential marker to measure infection control after single-stage revisions to treat PJI. Nonetheless, its use to confirm infection control and decide the proper timing of reimplantation remains uncertain. (1) What is the best diagnostic threshold and accuracy values for plasma D-dimer levels compared with other inflammatory markers (ESR and CRP) or what varying combinations of these tests are associated with persistent infection after reimplantation? (2) Do D-dimer values above this threshold, ESR, CRP, and varying test combinations at the time of reimplantation indicate an increased risk of subsequent persistent infection after reimplantation? We retrospectively studied the electronic medical records of all 53 patients who had two-stage revisions for PJI and who underwent plasma D-dimer testing before reimplantation at one of two academic institutions from November 22, 2017 to December 5, 2020. During that period, all patients undergoing two-stage revisions also had a D-dimer test drawn. The minimum follow-up duration was 1 year. We are reporting at this early interval (rather than the more typical 2-year time point) because of the poorer-than-expected performance of this diagnostic test. Of these 53 patients, 17% (9) were lost to follow-up before 1 year and could not be analyzed; the remaining 44 patients (17 hips and 27 knees) were studied here. The mean follow-up was 503 ± 135 days. Absence or persistence of infection after reimplantation were defined according to the Delphi criteria. The conditions included in these criteria were: (1) control of infection, as characterized by a healed wound without fistula, drainage, or pain; (2) no subsequent surgical intervention owing to infection after reimplantation; and (3) no occurrence of PJI-related mortality. The absence of any of the aforementioned conditions until the final follow-up examination was deemed a persistent infection after reimplantation. Baseline patient characteristics were not different between patients with persistent infection (n = 10) and those with absence of it after reimplantation (n = 34) as per the Delphi criteria. Baseline patient characteristics evaluated were age, gender, self-reported race (white/Black/other) or ethnicity (nonHispanic/Hispanic), BMI, American Society of Anesthesiologists (ASA) status, smoking status(smoker/nonsmoker), and joint type (hip/knee). The optimal D-dimer threshold to differentiate between persistence of infection or not after reimplantation was calculated using the Youden index. A receiver operating characteristic curve analysis was performed to test the accuracy of D-dimer, ESR, CRP, and their combinations to establish associations, if any, with persistent infection after reimplantation. A Kaplan-Meier survival analysis (free of infection after reimplantation) with a log-rank test was performed to investigate if D-dimer, ESR, and CRP were associated with absence of infection after reimplantation. Survival or being free of infection after reimplantation was determined as per Delphi criteria. Alpha was set at p < 0.05. In the receiver operating characteristic curve analysis, with an area under the curve of 0.62, D-dimer showed low accuracy and did not anticipate persistent infection after reimplantation. The optimal D-dimer threshold differentiating between persistence of infection or not after reimplantation was 3070 ng/mL. When using this threshold, D-dimer demonstrated a sensitivity of 90% (95% CI 55.5% to 99.7%) and negative predictive value of 94% (95% CI 70.7% to 99.1%), but low specificity (47% [95% CI 29.8% to 64.9%]) and positive predictive value (33% [95% CI 25.5% to 42.2%]). Although D-dimer showed the highest sensitivity, the combination of D-dimer with ESR and CRP showed the highest specificity (91% [95% CI 75.6% to 98%]) defining the persistence of infection after reimplantation. Based on plasma D-dimer levels, with the numbers available, there was no difference in survival free from infection after reimplantation (Kaplan-Meier survivorship free from infection at minimum 1 year in patients with D-dimer below 3070 ng/mL versus survivorship free from infection with D-dimer above 3070 ng/mL: 749 days [95% CI 665 to 833 days] versus 615 days [95% CI 471 to 759 days]; p = 0.052). Likewise, there were no associations between high ESR and CRP levels and persistent infection after reimplantation, but the number of events was very small, and insufficient power is a concern with this analysis. In this preliminary series, with the numbers available, D-dimer alone had poor accuracy and was not associated with survival free from infection after reimplantation in patients who underwent two-stage exchange arthroplasty. D-dimer alone might be used to establish that PJI is unlikely, and the combination of D-dimer, ESR, and CRP should be considered to confirm PJI diagnosis in the setting of reimplantation.Level of Evidence Level IV, diagnostic study.

Giant Cell Arteritis: Read the Fine Print!

C-reactive protein (CRP) and cardiovascular disease is a very hot topic at present. Excitement and interest have spilled over dramatically from the scientific literature into the media and popular press leading to much speculative comment. However, rigorously controlled and reproducible studies are now laying the basis for a more realistic consensus. The article in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology from Carmen van den Berg’s laboratory makes a notable contribution to this process. 1 See page 1225 Shortly after its discovery in 1929 as “the acute phase protein,” increased production of CRP was recognized as a characteristic feature of the response to acute myocardial infarction, and until the 1960’s detection of CRP was widely used for routine monitoring of acute rheumatic fever. In 1961 Irving Kushner, in one of the first applications of the then new technique of immunofluorescence, demonstrated the deposition of rabbit CRP in experimental myocardial infarction lesions. The association between CRP and cardiovascular disease thus has a very long history. In 1979 Kushner reported the kinetics of the acute phase CRP response to human acute myocardial infarction, and soon afterward we first investigated critically the behavior of CRP in clinical coronary artery disease and myocardial infarction.2 We observed that persistently elevated circulating CRP concentrations after an infarct were associated with a poor prognosis, although at that time we were focusing mainly on CRP as a sensitive nonspecific marker of all the various complications of coronary occlusion and their treatment. The current phase of interest in CRP and cardiovascular disease started in the early 1990’s with observations of increased CRP concentrations in some patients with “active coronary syndromes” and some individuals with acute myocardial infarction tested very soon after onset of pain, before the acute phase response to infarction could have started. These findings were consistent with the growing recognition at that time of the importance of inflammation in atherogenesis and the inflammatory nature of unstable atherosclerotic lesions. At the same time the large European prospective study (ECAT) of coagulation factors as possible prognostic markers in outpatients with stable and unstable angina unexpectedly revealed that the baseline value of CRP, which had only been included as a control for the acute phase behavior of some clotting proteins, significantly predicted future coronary events.3 The assay used was insufficiently sensitive to detect CRP in many of the samples in the ECAT study, and we therefore developed the first automated high-sensitivity method to re-assay their 3000 samples. Separately we also used this method to study, in collaboration with the Maseri group, carefully characterized patients with severe unstable angina who had not yet experienced any myocardial necrosis. We selected a cut point of 3 mg/L as the upper limit of normal, based on our original 1981 study of 468 healthy volunteer blood donors in whom this was the 90th centile of the CRP distribution. 4 In both the ECAT and the unstable angina studies, increased baseline CRP values were associated with significantly increased risk of future coronary events. 5,6 Subsequently several groups showed independently that baseline CRP measurements are associated with future coronary events in general populations, without known preexisting coronary artery disease. 7–10 In 2000 we reported with Danesh and colleagues the results from the British Regional Heart Study comprising 506 coronary events, 2 as many as in any other such study up to that time, together with a meta-analysis of all previous studies.11 This showed that the relative risk of having a coronary event among individuals with a baseline CRP value in the upper compared with the lower tertile of the CRP distribution was 2.0. In 2004 the Reykjavik Study, comprising 2459 coronary events, showed this relative risk to be 1.45 (95% CI, 1.25 to 168), and meta-analysis of all previously published general populations studies, comprising 7068 patients with coronary events, gave a similar result. 12 The results from this now quite rigorously

To evaluate and compare the clinical implications of common inflammatory markers in systemic rheumatic diseases (SRDs). We investigated the profiles of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and white blood cell (WBC) count in treatment-naïve patients with SRDs, osteoarthritis and pneumonia diagnosed at Seoul National University Hospital during 2004-2016. SRDs included rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), systemic sclerosis (SSc), idiopathic inflammatory myopathy (IIM) and adult-onset Still's disease (AOSD). Associations between inflammatory markers were evaluated using Pearson's correlation and regression analysis. ROC curve analysis was performed to examine the predictive value of inflammatory markers for SRD diagnosis. We identified a total of 1191 patients. Leukocytosis was present in < 20% SRD patients. There was marked variability in ESR and CRP levels among different SRDs. The highest mean CRP levels (mean ± SD, mg/dL) were observed in AOSD (11.3 ± 7.9), followed by RA (2.0 ± 3.3), IIM (1.8 ± 3.5), SLE (1.5 ± 3.1), SSc (0.6 ± 1.3) and AS (0.08 ± 0.1). Mean ESR (mm/h) was also highest in AOSD (71.2 ± 31.0), followed by SLE (47.3 ± 34.2), RA (45.5 ± 30.6), IIM (40.8 ± 24.8) and SSc (27.8 ± 26.0). All SRDs showed significant positive correlations between ESR and CRP: greatest in RA (r = 0.53, p < 0.001) and weakest in SLE (r = 0.20, p = 0.03). WBC correlated weakly with CRP but not with ESR in most SRDs. While the AUC for WBC count was less than that of ESR or CRP, the AUC for ESR and CRP were similar in SRD. The optimal cuff-off values for inflammatory markers predicting SRD were within or slightly above the normal limit. ESR, CRP and WBC are not always elevated in treatment-naïve patients with SRD. Individual SRDs have a unique profile of inflammatory markers. However, routine inflammatory markers should still be interpreted with caution when diagnosing and assessing disease activity in those with SRD. Key Points •Leukocytosis and elevation of ESR and CRP are not always present in all systemic rheumatic diseases. •Inflammatory markers are often dissociated and they are not specific for disease diagnosis. •Better biomarkers, which measure disease-specific local and systemic inflammation, are needed.

Use of C-Reactive Protein in Children with Newly Diagnosed Inflammatory Bowel Disease

Purpose: Formulas such as the Crohn's Disease Activity Index and Harvey Bradshaw Index rely on subjective criteria and have had poorly documented relationships to inflammation in the gut and extraintestinal tissues. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) levels, however, have served as objective measures of IBD activity. If CRP and ESR forecast severity of disease, then a prolonged hospital stay might be expected. We sought to determine if CRP and ESR were correlated with length of hospital stay (LOS) in IBD patients and if there was a difference in those with Crohn's disease (CD) compared to ulcerative colitis (UC). Methods: IRB-approved retrospective study of 35 IBD patients admitted for an IBD flare in the past 10 years. Inclusion criteria were age >18, diagnosis of UC or CD,ESR and/or CRP taken within the first 2 days of admission, and an admission for an IBD flare. Statistical analysis done using SAS version 9.2. Results: All patients were of AfroCaribbean descent. Seventeen patients had CD and 18 patients had UC. Fourteen patients had IBD for more than 5 years. Mean age was 38 years. Fifteen patients had extraintestinal manifestations (EIM). For all IBD patients, mean CRP level was 62.0 mg/L (normal value <0.4) and mean ESR was 58.7 mm/hr (normal value 0-20). Average LOS was 8.1 days. Correlation of CRP with LOS was r=0.21 (p=0.29) and ESR with LOS r=0.271 (p=0.13). Stronger correlations were found with males (CRP r=0.40 and ESR r=0.48 in males; CRP r=0.22 and ESR r=0.23 in females). No difference was found in those with >5 years of IBD compared to <5 years (p=0.43). No difference was found in those with EIM compared to those without (p=0.79). In UC patients, mean CRP was 56.7 mg/L and ESR was 58 mm/hr, with a mean LOS of 8.9 days. Correlation of CRP with LOS was r=0.36 (p=0.18) and ESR with LOS being r=0.30 (p=0.22). In CD patients, mean CRP was 69 mg/L and ESR was 59 mm/hr, with the mean LOS being 7.2 days. Correlation of CRP with LOS was r=0.02 (p=0.94) and with ESR and LOS r= 0.26(p=0.38). Conclusion: We found no correlation between inflammatory markers and LOS. Differences may not have been seen due to our small sample size. In addition, our results come solely from AfroCaribbeans, an often under-reported group of IBD patients. Whether our findings can be applied to other ethnic IBD populations remain to be seen. No data have been available correlating inflammatory markers and LOS in ethnic populations. We question if stronger correlations could found among other ethnicities given that racial differences in phenotypic expression of IBD have been previously reported. In the meantime, though CRP and ESR have been correlated with disease activity, we do not encourage the use of these markers in forecasting LOS.

Introduction: Tuberculosis (TB) is a common infectious disease caused by Mycobacterium tuberculosis (MTB). Although no other current test is more reliable for determining the activity of PTB than culture growth of bacilli, some biochemical parameters that reflect the inflammation present in patients with this condition may provide guidance at the diagnostic stage. The mean platelet volume (MPV) reflects the size of platelets. It has been shown to be inversely correlated with level of the inflammation in some chronic inflammatory diseases. Aim of the Work: This study aims to evaluate the role of some inflammatory markers in patients with active pulmonary tuberculosis (PTB) and to investigate the relationship between the inflammatory markers with each other as well as with the sputum smear positivity for TB bacilli. Methods: This cross sectional study included 50 patients who presented to the outpatient clinic of Qena general chest hospital and were diagnosed with active pulmonary tuberculosis and 50 healthy subjects(control group) who presented to the outpatient clinic for routine examination and presented no disease during the period between April 2017 to October 2017. Complete blood count, C-reactive protein (CRP) level, Erythrocyte sedimentation rate(ESR), ferritin level, and albumin level were compared between the two groups. In the PTB group, the relationship between inflammatory markers with each other as well as with sputum smear positivity for TB bacilli were investigated. Results: The MPV was 7.46±0.71 fl in the PTB group and 8.02±0.56 fl in the control group(p=.000). The blood platelets count, CRP levels, ESR and ferritin levels were significantly higher in the active PTB group than in the control group(p=.000). In the PTB group, CRP levels(p=.012) and platelets count(p=.026) but not ESR(p=.565) and MPV(p=.392) were significantly correlated with the sputum smear positivity for TB bacilli. Conclusions: The MPV was lower in patients with PTB than in healthy controls but the difference was limited. The MPV does not reflect the severity of the disease. The use of MPV as an inflammatory marker and a negative acute phase reactant in PTB does not seem to be reliable. The ESR and CRP proved to be good markers for the severity of pulmonary tuberculosis. However CRP showed more significant results than ESR in determining the disease severity.

Background: The mean platelet volume (MPV) reflects the size of platelets. It has been shown to be inversely correlated with level of the inflammation in some chronic inflammatory diseases. This prospective study aims to show the usability of MPV as an inflammation marker in patients with active pulmonary tuberculosis (PTB) by comparison with healthy controls. In addition, its relationships with other inflammatory markers such as C-reactive protein (CRP) and the erythrocyte sedimentation rate (ESR) as well as with the radiological extent of disease were examined. Methods: This study included 82 patients with active PTB and 95 healthy subjects (control group). Whole blood counts, CRP level, and ESR were compared between the two groups. In the PTB group, the relationships between the radiological extent of disease and the MPV and other inflammation markers were investigated. Results: The MPV was 7.74 ± 1.33/μL in the PTB group and 8.20 ± 1.13/μL in the control group (p = 0.005). The blood platelet count, CRP level, and ESR were significantly higher in the active PTB group than in the control group (p &lt; 0.0001). In the PTB group, CRP levels (r = 0.26, p = 0.003) and ESR (r = 0.39, p = 0.003), but not MPV (p = 0.80), were significantly correlated with the radiologic extent of the disease. Conclusions: The MPV was lower in patients with PTB than in healthy controls, however, the difference was limited. The MPV does not reflect the severity of the disease. The use of MPV as an inflammation marker and a negative acute-phase reactant in PTB does not seem to be reliable.

AB0270 Can Alkaline Phosphatase and Gamma-Glutamyl Transferase be Used as Inflammatory Markers in Patients with Rheumatoid Arthritis?

Elevated serum globulin gap as a highly reliable marker of elevated erythrocyte sedimentation rate in patients with systemic rheumatic diseases

SAT0271 Hepatosplenomegaly: A Complication of Persistent Subclinical Inflammation in Children with Familial Mediterranean Fever?