Association between Genes for Inflammatory Factors and Neuroticism, Anxiety, and Depression in Men with Ischemic Heart Disease
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01.10.2018 |
Golimbet V.
Volel’ B.
Korovaitseva G.
Kasparov S.
Kondrat’ev N.
Kopylov F.
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Neuroscience and Behavioral Physiology |
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0 |
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© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Objectives. To study the relationship between the immune system and depression, as well as its endophenotypes (neuroticism and trait anxiety), in patients with ischemic heart disease (IHD). Materials and methods. Studies were performed in a group of men with IHD and depression (78 patients) and without depression (91 patients), as well as in healthy male volunteers (127 subjects). Polymorphisms of the interleukin-4 (IL-4 –589C/T), interleukin-6 (IL-6 –174G/C), tumor necrosis factor α (TNF-α –308G/A), and C-reactive protein (CRP –717A/G) genes were studied. Results. An association between the IL-6 –174G/C polymorphism with depression comorbid with IHD was found (p = 0.01, OR = 2.3, 95% CI = 1.2–4.3), which was apparent as an increase in the frequency of the highly expressed G allele in the group of patients with depression. The IL-4 –589C/T polymorphism was associated with IHD: the frequency of the CC IL-4 –589C/T genotype was greater in this group of patients than in the control group regardless of the presence of depression (p = 0.007, OR = 2.1, 95% CI = 1.2–3.4). The TNF-α –308G/A and CRP –717A/G polymorphisms were not associated with depression in IHD. There were no signifi cant differences in the expression of neuroticism or trait anxiety in carriers of different genotypes at the IL-4 –589C/T, IL-6 –174G/C, TNF-α –308G/A, or CRP –717A/G loci. Conclusions. The association between the IL-6 –174G/C polymorphism with depression comorbid with IHD is consistent with published data on the role of IL-6 in the depression of depression in cardiology patients.
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C-reactive protein is linked to disease activity, impact, and response to treatment in patients with chronic spontaneous urticaria
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01.04.2018 |
Kolkhir P.
Altrichter S.
Hawro T.
Maurer M.
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Allergy: European Journal of Allergy and Clinical Immunology |
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9 |
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© 2017 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd. Background: Elevated levels of C-reactive protein (CRP), a sensitive marker of inflammation, have been consistently reported in chronic spontaneous urticaria (CSU). Here, we retrospectively analyzed data from 1253 CSU patients from 2 centers to answer the following questions: (i) What is the prevalence of elevated levels of CRP in CSU? (ii) Why do CSU patients show elevated levels of CRP? (iii) Are elevated CRP levels relevant?. Methods: Serum levels of CRP were measured by the nephelometric method. We collected information regarding various laboratory tests including ESR, CBC with differential, D-dimer, fibrinogen, C3, C4, IL-6, etc. For most patients, we also collected data on age, gender, duration of CSU, presence of angioedema, activity (UAS at the time of blood sampling and for 7 days), quality of life (CU-Q2oL and/or DLQI), comorbidities and possible causes of CSU, and autologous serum skin test (ASST) response. The efficacy of second-generation antihistamines was evaluated on the day of blood collecting. Results: One-third of CSU patients had elevated levels of CRP. Higher levels of CRP were associated with ASST positivity (P =.009) and arterial hypertension (P =.005), but not with other possible causes or comorbidities of CSU. C-reactive protein correlated with urticaria activity (P <.001), quality of life impairment (P =.026), and inflammatory and coagulation markers (P <.001). C-reactive protein levels were significantly higher in nonresponders to antihistamines as compared to responders (P <.001). Conclusion: Elevated levels of CRP are common and relevant in CSU patients. The assessment of CRP levels may help to optimize the management of patients with CSU.
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Metabolic syndrome: Development of the issue, main diagnostic criteria
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01.01.2018 |
Belenkov Y.
Privalova E.
Kaplunova V.
Zektser V.
Vinogradova N.
Ilgisonis I.
Shakaryants G.
Kozhevnikova M.
Lishuta A.
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Rational Pharmacotherapy in Cardiology |
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1 |
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© 2018 Stolichnaya Izdatelskaya Kompaniya. All rights reserved. Obesity is one of the leading and the most serious risk factors of cardiovascular diseases. Overweight provokes many metabolic and hemodynamic disorders. About 30% of inhabitants of the planet have overweight and prevalence of obesity increases by 10% every 10 years according to the WHO data. The probability of arterial hypertension in obese patients is 50% higher than in people with normal body mass. Framingham study showed that obesity is an independent, significant risk factor of ischemic heart disease, myocardial infarction, cerebral stroke and diabetes mellitus. The most dangerous is the central obesity with the preferential fat deposition in the abdomen. Combination of visceral obesity, violation of carbohydrate and lipid metabolism, arterial hypertension, and close pathogenic relationship between these factors underlie the isolated symptom complex known as metabolic syndrome. J. Vague was the first to describe relationship between abdominal obesity with cardiovascular disease and mortality in 1947. In our country G.F. Lang noticed common combination of arterial hypertension with obesity, lipid and carbohydrate metabolism disorders. Thus, metabolic syndrome significantly increases risk and severity of cardiovascular disease. Within last decades criteria of metabolic syndrome stays constant. The factors of insulin resistance and endothelial dysfunction as stages of the pathogenesis of the metabolic syndrome have been studied in detail. The mechanisms of insulin resistance and endothelial dysfunction are discussed in detail in this article as well as inflammatory markers and the significance of highly sensitive C-reactive protein.
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Possible mechanisms of cognitive dysfunction in patients with chronic forms of cerebrovascular diseases
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01.01.2018 |
Voskresenskaya O.
Zakharova N.
Tarasova Y.
Tereshkina N.
Perepelov V.
Perepelova E.
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Nevrologiya, Neiropsikhiatriya, Psikhosomatika |
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1 |
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© 2018 Ima-Press Publishing House. All rights reserved. Cognitive impairment (CI) is a basis for the clinical presentation of chronic cerebral ischemia (CCI). However, the role of the mechanisms of inflammation and angiogenesis in the origin of CI is unclear, as is its relationship to the number and localization of foci during a neuroimaging examination. Objective: to investigate the relationship between the presence of CI, focal brain tissue changes, and the plasma and serum levels of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) in patients with CCI. Patients and methods. Examinations were made in 59 patients with CCI and in 20 apparently healthy individuals. The investigators evaluated the cognitive status using the Mini-Mental State Examination (MMSE) and the clock drawing test), performed brain magnetic resonance imaging (MRI), duplex scanning of cerebral vessels, and determined laboratory indicators: the serum levels of MCP-1 and C-reactive protein, and the serum and plasma concentrations of VEGF. Results. The patients with CI were found to have higher values of inflammatory markers, lower serum and plasma concentrations of angiogenic factors, and a greater number of focal changes on MRI than those without CI (5.06±0.23 and 2.36±0.3 scores, respectively; p(0.05). Imbalance of angiogenic and antiangiogenic factors can cause disease progression and moderate vascular CI in patients with CCI.
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