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arthritis/triglyceride

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OBJECTIVE We investigated the effect of Infliximab, an anti TNF-alpha antibody, on plasma lipids and lipoproteins in patients with rheumatoid arthritis and psoriatic arthritis. METHODS Five male and 10 female patients with a mean age of 56.7 years were included in this study. Seven of the patients
The levels of plasma cortisol, blood glucose, serum triglycerides (TG) and total cholesterol (TC) were estimated in 175 human subjects (50 normal controls, 65 having essential hypertension and 60 suffering from rheumatoid arthritis. The results showed a significant elevation in the levels of plasma

Infliximab induces increase in triglyceride levels in psoriatic arthritis patients.

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OBJECTIVE To evaluate lipid profile changes after anti-TNF therapy in patients with psoriatic arthritis (PsA). METHODS Fifteen PsA patients (eight polyarticular, four oligoarticular, two axial, and one mutilating) under infliximab were included. None had dyslipoproteinemia or previous statin use.
BACKGROUND The interactions between inflammation and lipid profile in rheumatoid arthritis (RA) are poorly understood. The lipid profile study in RA has been biased toward lipoprotein levels, whereas those of triglycerides (TGs) and lipoprotein functionality have been underestimated. OBJECTIVE Since

Infliximab but not methotrexate induces extra-high levels of VLDL-triglyceride in patients with rheumatoid arthritis.

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OBJECTIVE Tumor necrosis factor (TNF-alpha), a pivotal inflammatory cytokine, is known to induce proatherogenic changes in the lipid profile and may increase the cardiovascular risk of patients with rheumatoid arthritis (RA). We examined the effects of anti-TNF-alpha antibody (infliximab, IFX)

Increase in serum triglyceride was associated with coronary plaque vulnerability in a patient with rheumatoid arthritis.

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Rates of morbidity and mortality from cardiovascular disease are high in patients with rheumatoid arthritis (RA); however, the mechanisms and biomarkers that reflect coronary plaque vulnerability have not yet been established. We present a case of acute coronary syndrome (ACS) presumably caused by

Serum total, HDL, LDL cholesterol, and triglyceride levels in patients with rheumatoid arthritis.

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Patients with rheumatoid arthritis are at risk of increased prevalence of coronary heart disease. In general, the plasma level of high density lipoprotein cholesterol (HDL) correlates with the risk of incidence of ischemic heart disease. The levels of total, HDL, low density (LDL) cholesterol, and
Insulin resistance (IR) is frequently observed in patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). In clinical practice, IR assessment is limited to a low proportion of patients due to cost and equipment and technical expertise requirements. The surrogate
OBJECTIVE Rheumatoid arthritis (RA) is associated with an excess mortality from cardiovascular disease which is likely attributed to an atherogenic lipid profile. Among nutritional factors vitamin K has been recently focused as a pivotal nutrient in improvement of lipid related markers. Thus, this

Glucocorticoids improve endothelial function in rheumatoid arthritis: a study in rats with adjuvant-induced arthritis.

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To determine the effect of glucocorticoids (GCs) on endothelial dysfunction (ED) and on traditional cardiovascular (CV) risk factors in the adjuvant-induced arthritis (AIA) rat model. At the first signs of AIA, a high dose (HD) [10 mg/kg/day, intraperitoneally (i.p.), GC-HD] or low dose (LD) (1
OBJECTIVE To analyze lipid changes in patients with rheumatoid arthritis (RA) and patients with spondyloarthritis (SpA) treated with biologic agents or tofacitinib in randomized clinical trials (RCTs). METHODS A systematic literature search was performed, using the Medline, Embase, Cochrane Library,
Background: MicroRNAs have been implicated in the pathogenesis of rheumatoid arthritis (RA), obesity, and altered metabolism. Although RA is associated with both obesity and altered metabolism, expression of RA-related microRNA in the setting of these cardiometabolic comorbidities is unclear.
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