Aggravated Systemic Inflammation and Atherogenicity in African Patients Living With Type 2 Diabetes and Hypertension Comorbidity.

Clin Med Insights Endocrinol Diabetes

Department of Molecular Medicine and Haematology, School of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.

Published: July 2024

Objective: To explore routinely measured markers of systemic inflammation in hypertension (HTN) and type 2 diabetes (T2D) comorbidity, and their association with atherogenicity.

Methods: This study included a total of 70 patients with T2D which were categorised into 2 groups, that is with T2D and with HTN comorbidity (T2D + HTN) (n = 35/group). All measured laboratory parameters were determined using standardised methods.

Results: The neutrophil/lymphocyte ratio (NLR) was elevated in patients with T2D + HTN when compared to those with T2D ( = .0494). This was also the case with C-reactive protein (CRP) levels ( < .0001) and systemic immune-inflammation (SII) index ( = .0298). Notably, the majority of patients with T2D + HTN [63% (n = 22)] were classified as having an intermediate or high atherogenic index of plasma (AIP). The correlation analysis of systemic inflammation showed significant associations between CRP and age (r = .24,  = .0477); CRP and red blood cell count (r = -.4,  = .0455), and SII and systolic blood pressure (SBP) (r = .33,  = .0056). However, there was no association between inflammatory profiles and lipograms ( > .05). We further assessed predictors for an elevated AIP using mutivariable regression model adjusted for age, SBP, CRP and SII. Only NLR was a significant predictor of AIP (β = .287, SE: 0.1,  = .0046).

Conclusion: HTN comorbidity in T2D is associated with exacerbated levels of inflammation and atherogenicity. NLR is a significant independent risk factor for increased atherogenicity in patients with T2D. Therefore, the use of therapeutic strategies that target and alleviate inflammation in patients with T2D and HTN comorbidity is imperative in reducing the initiating and progression of cardiovascular events (CVEs).

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11287731PMC
http://dx.doi.org/10.1177/11795514241263298DOI Listing

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