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Background: Red cell distribution width (RDW) is a recently found marker of inflammation in acute and chronic conditions such as heart attack (myocardial infarction), heart failure, angina-pectoris, peripheral vascular disease, inflammatory conditions, and metabolic disorders such as diabetes. The literature suggests that both C-reactive protein (CRP) and RDW are elevated in hypertensive patients almost simultaneously. Hypertension is a state of chronic inflammation. Several studies have shown increased levels of inflammation markers such as CRP, high-sensitive CRP (hs-CRP), Interleukin, and IL-1β in hypertension. hs-CRP was found to predict the changes in inflammation quite earlier. Aim: A few studies have been conducted on RDW in secondary hypertensives, but none in recent hypertensives or patients with hypertension for 2 years. Hence, this study aimed to explore whether cost-efficient RDW can be considered as an alternative to CRP to assess the inflammation levels in hypertensive, pre-hypertensive, and normotensive subjects. Methods: Ethical clearance was obtained from Chettinad Medical College and Research Institute, Chennai, India, and consent was obtained from both patients and controls. This is a case-control study that included 120 individuals, who were subdivided into three groups: normotensive, 40; pre-hypertensive, 40; and hypertensive, 40. Hypertensive patients were categorized into two groups based on the duration of hypertension: recently diagnosed hypertensive patients (who were diagnosed with hypertension for less than 6 months) and those on antihypertensive medication for less than or equal to 2 years. CRP, hs-CRP analysis, was performed based on the enzyme-linked immunosorbent assay principle. Results: Pearson’s χ2 test gave a p value of 0.002, suggesting a strong association between RDW and CRP. Conclusion: Further study is required to establish cost-effective parameters, such as RDW, for the early assessment of inflammatory changes in the pre-hypertensive stage and to understand the correlation between RDW and blood pressure.

C-reactive protein (CRP) is well-recognized as a sensitive biomarker of inflammation. Association of elevations in plasma/serum CRP level with disease state has received considerable attention, even though CRP is not a specific indicator of a single disease state. Circulating CRP levels have been monitored with a varying degree of success to gauge disease severity or to predict disease progression and outcome. Elevations in CRP level have been implicated as a useful marker to identify patients at risk for cardiovascular disease and certain cancers, and to guide therapy in a context-dependent manner. Since even strong associations do not establish causality, the pathogenic role of CRP has often been over-interpreted. CRP functions as an important modulator of host defense against bacterial infection, tissue injury and autoimmunity. CRP exists in conformationally distinct forms, which exhibit distinct functional properties and help explaining the diverse, often contradictory effects attributed to CRP. In particular, dissociation of native pentameric CRP into its subunits, monomeric CRP, unmasks “hidden” pro-inflammatory activities in pentameric CRP. Here, we review recent advances in CRP targeting strategies, therapeutic lowering of circulating CRP level and development of CRP antagonists, and a conformation change inhibitor in particular. We will also discuss their therapeutic potential in mitigating the deleterious actions attributed to CRP under various pathologies, including cardiovascular, pulmonary and autoimmune diseases and cancer.

[This corrects the article DOI: 10.3389/fimmu.2026.1743603.].

Systemic inflammation, diagnostically ascribed by measuring serum levels of the acute phase reactant C-reactive protein (CRP), has consistently been correlated with poor outcomes across cancer types. CRP exists in two structurally and functionally distinct isoforms, circulating pentameric CRP (pCRP) and the highly pro-inflammatory monomeric isoform (mCRP). The aim of this pilot study was to map the pattern of mCRP distribution in a previously immunologically well-defined colon cancer (CC) cohort and explore possible functional roles of mCRP within the tumor microenvironment (TME). Formalin-fixed, paraffin-embedded (FFPE) tissue samples from 43 stage II and III CC patients, including 20 patients with serum CRP 0-1 mg/L and 23 patients with serum CRP >30 mg/L were immunohistochemically (IHC) stained with a conformation-specific mCRP antibody and selected immune and stromal markers. A digital analysis algorithm was developed for evaluating mCRP distribution within the primary tumors and adjacent normal colon mucosa. mCRP was abundantly present within tumors from patients with high serum CRP (>30 mg/L) diagnostically interpreted as being systemically inflamed, whereas patients with CRP 0-1 mg/L exhibited only modest mCRP positivity (median mCRP per area 5.07‰ (95%CI:1.32-6.85) vs. 0.02‰ (95%CI:0.01-0.04), p<0.001). Similarly, tissue-expressed mCRP correlated strongly with circulating pCRP (Spearman correlation 0.81, p<0.001). Importantly, mCRP was detected exclusively within tumors, whereas adjacent normal colon mucosa showed no mCRP expression. Double IHC staining revealed colocalization of mCRP with endothelial cells and neutrophils. Intriguingly, some tumor cells also colocalized with mCRP, suggesting a direct interaction or mCRP expression by the tumor itself. Our data show that the pro-inflammatory mCRP isoform is expressed in the TME of CC, primarily in patients with high systemic pCRP values. This strengthens the hypothesis that CRP might not only be an inflammatory marker but also an active mediator within tumors.

Eating disorders are important psychiatric conditions with serious implications for physical and mental health. These disorders may be seen in all age groups ages but are more common in adolescents and young adults. Anorexia nervosa, bulimia nervosa, and binge-eating disorder are the main eating disorders. These disorders are triggered by acute stress regarding distorted body image and identified by persistent changes in eating behaviors. Each eating disorder involves different clinical features, but they all share some common risk factors, including genetic predisposition, environmental factors, and psychological triggers. Inflammation is a core mechanism that underlies the pathophysiology of eating disorders. This editorial essay will discuss the evidence linking inflammatory markers to eating disorders' etiology, diagnosis, and treatment.

Peripheral low-grade inflammation in depression is increasingly seen as a therapeutic target. We aimed to establish the prevalence of low-grade inflammation in depression, using different C-reactive protein (CRP) levels, through a systematic literature review and meta-analysis. We searched the PubMed database from its inception to July 2018, and selected studies that assessed depression using a validated tool/scale, and allowed the calculation of the proportion of patients with low-grade inflammation (CRP >3 mg/L) or elevated CRP (>1 mg/L). After quality assessment, 37 studies comprising 13 541 depressed patients and 155 728 controls were included. Based on the meta-analysis of 30 studies, the prevalence of low-grade inflammation (CRP >3 mg/L) in depression was 27% (95% CI 21-34%); this prevalence was not associated with sample source (inpatient, outpatient or population-based), antidepressant treatment, participant age, BMI or ethnicity. Based on the meta-analysis of 17 studies of depression and matched healthy controls, the odds ratio for low-grade inflammation in depression was 1.46 (95% CI 1.22-1.75). The prevalence of elevated CRP (>1 mg/L) in depression was 58% (95% CI 47-69%), and the meta-analytic odds ratio for elevated CRP in depression compared with controls was 1.47 (95% CI 1.18-1.82). About a quarter of patients with depression show evidence of low-grade inflammation, and over half of patients show mildly elevated CRP levels. There are significant differences in the prevalence of low-grade inflammation between patients and matched healthy controls. These findings suggest that inflammation could be relevant to a large number of patients with depression.

Objective: To evaluate the prognostic accuracy of the C-reactive protein (CRP)/albumin ratio in predicting severe acute pancreatitis (SAP) and its correlation with clinical complications. Methods: This retrospective observational study included 40 adult patients diagnosed with acute pancreatitis between January and August 2024. Patients were categorized by severity using the Revised Atlanta Classification into moderately severe or severe groups. Laboratory data, clinical characteristics, and imaging findings were compared. Receiver operating characteristic (ROC) analysis with Youden’s Index evaluated the CRP/albumin ratio predictive performance and logistic regression identified independent predictors of SAP. Results: The CRP/albumin ratio was significantly higher in SAP patients (median 5.0 [IQR 0.93–12.62]) compared to non-SAP (1.58 [IQR 0.28–8.6], p = 0.0187). ROC analysis showed an area under the curve (AUC) of 0.809 for the CRP/albumin ratio, superior to CRP alone (AUC 0.479) and comparable to the Ranson score (AUC 0.88). An optimal cut-off value of 4.22 provided 76.9% sensitivity and 85.2% specificity. Multivariable logistic regression identified absence of intestinal transit (p = 0.033) and splenic vein thrombosis (p = 0.026) as independent predictors of SAP. The CRP/albumin ratio correlated significantly with both these complications. Conclusions: The CRP/albumin ratio is a valuable, non-invasive, and readily available prognostic marker for early identification of severe acute pancreatitis. Its predictive accuracy is comparable to established scoring systems and may aid in triage and clinical decision-making.

Abstract Cyclic AMP (cAMP) is a ubiquitous second messenger synthesized by most living organisms. In bacteria, it plays highly diverse roles in metabolism, host colonization, motility, and many other processes important for optimal fitness. The main route of cAMP perception is through transcription factors from the diverse and versatile CRP–FNR protein superfamily. Since the discovery of the very first CRP protein CAP in Escherichia coli more than four decades ago, its homologs have been characterized in both closely related and distant bacterial species. The cAMP-mediated gene activation for carbon catabolism by a CRP protein in the absence of glucose seems to be restricted to E. coli and its close relatives. In other phyla, the regulatory targets are more diverse. In addition to cAMP, cGMP has recently been identified as a ligand of certain CRP proteins. In a CRP dimer, each of the two cyclic nucleotide molecules makes contacts with both protein subunits and effectuates a conformational change that favors DNA binding. Here, we summarize the current knowledge on structural and physiological aspects of E. coli CAP compared with other cAMP- and cGMP-activated transcription factors, and point to emerging trends in metabolic regulation related to lysine modification and membrane association of CRP proteins. This review summarizes the current knowledge on CRP transcription factors allosterically activated by cAMP or cGMP to control highly diverse regulons in a broad range of bacteria.

Background: Type 2 diabetes mellitus (T2DM) is a growing global health concern characterized by chronic hyperglycemia, insulin resistance and associated complications. Serum ferritin an iron storage protein and inflammatory marker has been linked to poor glycemic control and may provide insight into the interplay between iron metabolism, inflammation and diabetes management. Objective: To assess the correlation of glycemic control with serum ferritin levels. Methods: This comparative cross-sectional study was performed at the Department of Pathology and Endocrinology, Fauji Foundation Hospital, Rawalpindi from December 2023 to May 2024. Data of patients attending the diabetic clinic were included and distributed into two groups: Group A (patients with good glycemic control) and Group B (patients with poor glycemic control). Blood samples from patients included in this study were collected and analyzed for the levels of serum ferritin, CRP and HbA1C. Descriptive variables were presented as frequency, percentages and median accordingly. Results: In this study of 160 participants, divided based on glycemic control, group A had a lower median HbA1C of 5.70% compared to 8.10% in group B. Group B also had a higher median serum ferritin level (348.00 µg/L versus 161.5 µg/L). Additionally, group A had lower levels of C-reactive protein (0.3 mg/dL) compared to group B (0.4 mg/dL). Higher serum ferritin and CRP levels were strongly correlated to increased HbA1C levels. Conclusion: Increased ferritin and CRP levels are strongly related to poorly controlled T2DM. Monitoring ferritin levels in glycemic care can enhance patient outcomes by allowing for better risk assessment ...