# Hemoglobin-to-Red Cell Distribution Width Ratio and Vitamin D Status as Early Predictors of Cardiovascular Risk in Primary Sjögren’s Syndrome

**Authors:** Francesca Coppi, Francesco Sbarra, Aurora Vicenzi, Cecilia Campani, Martina Moretti, Dilia Giuggioli, Caterina Vacchi, Amelia Spinella, Daniela Aschieri, Anna Vittoria Mattioli, Francesco Fedele, Alessio Baccarani, Marcello Pinti, Alessandra Dei Cas, Federica Fantuzzi, Leila Bigdelu, Gianluca Pagnoni, Susan Darroudi

PMC · DOI: 10.3390/life16020190 · 2026-01-23

## TL;DR

This study explores how blood markers like hemoglobin-to-RDW ratio and vitamin D levels can predict heart risks in patients with Sjögren’s syndrome.

## Contribution

The study introduces HRR as a novel composite biomarker for early cardiovascular risk in primary Sjögren’s syndrome.

## Key findings

- Lower HRR is linked to higher pulmonary artery pressures and poorer right heart function in pSS patients.
- The association between HRR and heart function is stronger in patients with low vitamin D levels.
- HRR reflects the interplay between anemia, inflammation, and cardiovascular health in pSS.

## Abstract

Introduction: Primary Sjögren’s (pSS) is an autoimmune disease that affects several organs, especially the heart, and raises cardiovascular risk. Investigating the associations of hemoglobin-to-red cell distribution width (RDW) ratio (HRR), vitamin D status, and cardiac function could provide valuable insights and biomarkers regarding early cardiovascular risk in patients with pSS. Method: This cross-sectional study involved 61 patients diagnosed with pSS based on ACR/EULAR criteria. Data on demographics, hematological (Hb, RDW), echocardiography, and serum vitamin D levels were collected. Echocardiograms were conducted by trained cardiologists following established guidelines, while vitamin D levels were measured using ELISA. Statistical analyses, including univariate linear regression, were performed with SPSS in order to identify whether HRR tertiles were related to cardiac function and vitamin D status. Results: A study of 61 pSS patients (mean age 59.8 years, 89% female) revealed that patients with a lower hemoglobin-to-RDW ratio (HRR ≤ 0.98) had significantly higher pulmonary artery pressures (PAPs) and lower values for the tricuspid annular plane systolic excursion (TAPSE)/PAPs ratio, contributing to poor right heart function. These associations were particularly strong in patients with insufficient levels of vitamin D (<30 ng/mL), while differences in other echocardiographic parameters remained nonsignificant between HRR groups. Conclusions: These findings underscore the clinical value of HRR as a composite biomarker that reflects the interplay between anemia, inflammation, and cardiovascular health in primary Sjögren’s disease. They also suggest that vitamin D status may be an important therapeutic consideration to mitigate cardiopulmonary risks in this population.

## Full-text entities

- **Genes:** EPO (erythropoietin) [NCBI Gene 2056] {aka DBAL, ECYT5, EP, MVCD2}, HAMP (hepcidin antimicrobial peptide) [NCBI Gene 57817] {aka HEPC, HFE2B, LEAP1, PLTR}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** cardiovascular abnormalities (MESH:D018376), anemia of chronic disease (MESH:D002908), pulmonary hypertension (MESH:D006976), endothelial (MESH:D005642), heart failure (MESH:D006333), conduction disturbances (MESH:C563984), coronary artery disease (MESH:D003324), cardiac involvement (MESH:D006331), cardiac remodeling (MESH:D020257), ILD (MESH:D017563), chronic renal failure (MESH:D007676), cardiomyocyte hypertrophy (MESH:D006984), right ventricular dysfunction (MESH:D018497), CVD (MESH:D002318), microvascular impairment (MESH:D017566), Anemia (MESH:D000740), atherosclerosis (MESH:D050197), hematologic disturbances (MESH:D006402), hypertension (MESH:D006973), hematologic alterations (MESH:D019337), hypoxia (MESH:D000860), autoimmune disease (MESH:D001327), arrhythmias (MESH:D001145), obesity (MESH:D009765), impaired erythropoiesis (MESH:C563479), D (MESH:D014808), myocardial injury (MESH:D009202), endothelial dysfunction (MESH:D014652), diabetes (MESH:D003920), Primary Sjogren's syndrome (MESH:D012859), vit D insufficiency (MESH:D000309), DM (MESH:D009223), cardiopulmonary impairment (MESH:D006323), fibrosis (MESH:D005355), injury to (MESH:D014947), Chronic systemic inflammation (MESH:D007249), acute coronary syndrome (MESH:D054058), erythrocyte dysfunction (MESH:D012010), dyslipidemia (MESH:D050171)
- **Chemicals:** PAPs (-), 25-hydroxyvitamin D (MESH:C104450), iron (MESH:D007501), Vit D (MESH:D014807), oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941808/full.md

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Source: https://tomesphere.com/paper/PMC12941808