Objective: Homozygous familial hypercholesterolemia (FH) is an extremely rare (1/1,000,000) condition characterized by markedly increased LDL cholesterol levels and a significantly increased risk of premature coronary heart disease (CHD). We aimed to evaluate the levels of high-sensitivity C-reactive protein (hs-CRP) and proinflammatory cytokines, which are known to be associated with atherogenesis, in patients with this condition.
Method And Results: A total of 10 patients with homozygous FH (5 women and 5 men, mean age 17.0 +/- 6.9 years, body mass index (BMI) (18.8 +/- 1.9 kg/m2) and 16 healthy controls were included. hs-CRP levels, proinflammatory cytokine levels and lipid parameters were measured and compared between patients and control subjects. Homozygous FH patients had significantly higher total cholesterol, LDL-cholesterol and Lp(a) levels and significantly lower triglyceride and HDL cholesterol levels, compared to controls (P = 0.0001, for all). Serum hs-CRP (3.7 +/- 1.3 mg/L vs. 0.6 +/- 0.6 mg/L) and IL-1beta, IL-2R, IL-6, IL-8, IL-10, TNF-alpha levels were all significantly higher in the homozygous FH group, compared to controls (P = 0.0001, for all).
Conclusions: Homozygous FH patients have significantly higher levels of hs-CRP and circulating proinflammatory cytokines, which may explain their increased risk of atherosclerotic disease. hs-CRP is an important biomarker that may be helpful in the identification of asymptomatic CHD in FH patients.
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http://dx.doi.org/10.2143/AC.64.5.2042689 | DOI Listing |
Mol Nutr Food Res
January 2025
2nd Abdominal Surgery Department, Jiangxi Cancer Hospital, The Second Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, People's Republic of China.
This study investigated the protective effects of the dietary polyphenol vanillic acid (VA) on dextran sulfate sodium-induced acute ulcerative colitis (UC) in mice, focusing on its impact on the gut microbiota and inflammatory responses. VA was supplemented following dextran sulfate sodium administration, and key indicators, including body weight, disease activity index, colon length, spleen index, and inflammatory markers, were assessed. VA supplementation significantly alleviated UC symptoms, preserved intestinal barrier integrity, and reduced pro-inflammatory cytokine levels.
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January 2025
Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Background Severe acute pancreatitis (SAP) manifests as a critical state marked by acute abdominal symptoms, often associated with intestinal barrier dysfunction, exacerbating SAP retroactively. Ganoderic acid A (GAA) demonstrates anti-inflammatory properties in various inflammatory disorders. Nonetheless, its potential therapeutic impact on SAP and the underlying mechanisms remain unexplored.
View Article and Find Full Text PDFJID Innov
March 2025
Small Animal Clinic, École Nationale Vétérinaire de Toulouse, University of Toulouse, Toulouse, France.
Our objectives were to explore epidermal barrier defects in dogs with atopic dermatitis and to determine whether the defects are genetically determined or secondary to skin inflammation. First, the expression of filaggrin, corneodesmosin, and claudin1, analyzed using indirect immunofluorescence in skin biopsies collected from 32 healthy and 32 dogs with atopic dermatitis, was weaker in the atopic skin ( .003).
View Article and Find Full Text PDFMater Today Bio
February 2025
Scientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Sepsis is a serious and life-threatening condition, which can lead to organ failure and death clinically. Abnormally increased cell-free DNA (cfDNA) and inflammatory cytokines are involved in the development and progression of sepsis. Thus, cfDNA clearance and down-regulation of inflammatory factors are essential for the effective treatment of sepsis.
View Article and Find Full Text PDFHeliyon
January 2025
Wolfson Sensory, Pain and Regeneration Centre, King's College London, London, United Kingdom.
Neuropathic pain following peripheral nerve injury results from maladaptive changes in neurons and immune cells contribution to mechanisms underlying chronic pain. Specifically, in dorsal root ganglia (DRG), sensory neuron cell bodies release extracellular vesicles (EVs) which promote pro-inflammatory macrophage accumulation that facilitates nociceptive signalling. Here, we show that macrophages shuttle EVs to neurons.
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