RESUMEN
Background: Hypothyroidism can predispose systolic and diastolic cardiac dysfunction, increased peripheral vascular resistance, endothelial dysfunction, altered coagulopathy, and dyslipidemia resulting in atherosclerosis. Thyroid hormones can influence homocysteine metabolism by regulating the methylenetetrahydrofolate reductase (M THR). So, this study aimed to compare the markers homocysteine, high sensitive C-reactive protein (hs-CRP), and Atherogenic Indices (AI) between newly diagnosed hypothyroid and euthyroid premenopausal women. Methods: 80 Female patients between 20 and 45 years were enrolled in this study and were equally divided into cases and controls group. Laboratory tests included: i) Serum T3, T4, TSH was measured using electrochemiluminescence, ii) lipid profile, homocysteine, and hs-CRP were measured for all the participants. Atherogenic indices: Castelli risk indices I&II, Atherogenic coefficient (AEC), and Atherogenic Index of Plasma (AIP) were calculated using formulas. A comparison between the study groups was made by using the Independent t-test and Mann-Whitney U test. p-value < 0.05 was considered significant. Results: The hypothyroid group had significantly higher levels of homocysteine (p= 0.014), and hs-CRP (hs-CRP> 3.0 mg/L, 70% of participants have intermediate to high risk for a cardiovascular event) and elevated BMI compared to participants in the euthyroid group. Atherogenic indices (p< 0.001) was significantly increased in the hypothyroid participants' group. TC, TG , and LDL were significantly elevated in the hypothyroid group but did not show any association with systolic and diastolic blood pressure. Conclusions: Premenopausal women with hypothyroidism have a greater predisposition for cardiovascular disease compared to euthyroid.
RESUMEN
Inflammation plays a critical role in the development and progression of chronic diseases like type 2 diabetes mellitus, coronary artery disease, and chronic obstructive pulmonary disease. Inflammatory responses are indispensable for pathogen control and tissue repair, but they also cause collateral damage. A chronically activated immune system and the resultant immune dysregulation mediated inflammatory surge may cause multiple negative effects, requiring tight regulation and dampening of the immune response to minimize host injury. While chronic diseases are characterized by systemic inflammation, the mechanistic relationship of neutrophils and lymphocytes to inflammation and its correlation with the clinical outcomes is yet to be elucidated. The neutrophil to lymphocyte ratio (NLR) is an easy-to-measure laboratory marker used to assess systemic inflammation. Understanding the mechanisms of NLR perturbations in chronic diseases is crucial for risk stratification, early intervention, and finding novel therapeutic targets. We investigated the correlation between NLR and prevalent chronic conditions as a measure of systemic inflammation. In addition to predicting the risk of impending chronic conditions, NLR may also provide insight into their progression. This review summarizes the mechanisms of NLR perturbations at cellular and molecular levels, and the key inflammatory signaling pathways involved in the progression of chronic diseases. We have also explored preclinical studies investigating these pathways and the effect of quelling inflammation in chronic disease as reported by a few in vitro, in vivo studies, and clinical trials.