Article

Serum interleukin-6 and hemoglobin as physiological correlates in the geriatric syndrome of frailty: a pilot study.

Division of Geriatric Medicine and Gerontology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Journal of the American Geriatrics Society (Impact Factor: 4.22). 08/2002; 50(7):1268-71. DOI: 10.1046/j.1532-5415.2002.50315.x
Source: PubMed

ABSTRACT To determine specific physiological correlates of the geriatric syndrome of frailty that warrant further investigation.
Population-based case-control study.
General Clinical Research Center at Johns Hopkins Bayview Medical Center.
Community-dwelling adults aged 74 and older from Baltimore, Maryland.
Frailty status was determined using a recently validated screening tool that consists of weight loss, fatigue, low levels of physical activity, and measurements of grip strength and walking speed. Serum interleukin-6 (IL-6) was measured using enzyme-linked immunosorbent assay, and standard complete blood count was performed using a Coulter counter.
Eleven frail and 19 nonfrail subjects with mean age +/- standard deviation of 84.9 +/- 6.7 vs 81.3 +/- 4.1 years, respectively, completed the study. The frail subjects had significantly higher serum IL-6 levels and significantly lower hemoglobin and hematocrit than the nonfrail subjects (4.4 +/-2.9 vs 2.8 +/- 1.6 pg/mL, 12.1 +/- 1.1 vs 13.9 +/- 1.0 g/dL, and 35.8% +/- 3.1% vs 40.6% +/- 2.8%, respectively). No significant difference was observed in mean corpuscular volume, red blood cell distribution width, or white blood cell and platelet counts between the frail and nonfrail groups. Furthermore, there was an inverse correlation between serum IL-6 level and hemoglobin (Pearson's correlation coefficient: -0.46) and hematocrit (-0.48) in the frail group but not in the nonfrail group.
These results suggest that frail subjects have evidence of inflammation and lower hemoglobin and hematocrit levels. This subclinical anemia is normocytic and is hence unlikely due to myelosuppression or iron deficiency and is potentially related to the increased chronic inflammatory state marked by serum IL-6 elevation. Further studies are indicated to better characterize the immune and hematological changes that underlie frailty.

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    ABSTRACT: Sokołowski Remigiusz, Ciesielska Natalia, Czajkowska Agnieszka, Bentryn Dominika, Węgrzyn Edyta, Oleksy Patrick, Zukow Walery. Patogeneza zespołu kruchości = Patogenesis of Frailty Syndrome. Journal of Health Sciences. 2014;4(9):197-204. ISSN 1429-9623 / 2300-665X. Retrieved from http://journal.rsw.edu.pl/index.php/JHS/article/view/2014%3B4%289%29%3A197-204. DOI: 10.13140/2.1.4322.4327 http://dx.doi.org/10.13140/2.1.4322.4327 The journal has had 5 points in Ministry of Science and Higher Education of Poland parametric evaluation. Part B item 1107. (17.12.2013). © The Author (s) 2014; This article is published with open access at Licensee Open Journal Systems of Radom University in Radom, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. Conflict of interest: None declared. Received: 10.06.2014. Revised 07.08.2014. Accepted: 05.09.2014. Patogeneza zespołu kruchości Patogenesis of Frailty Syndrome Remigiusz Sokołowski1, Natalia Ciesielska1, Agnieszka Czajkowska1, Dominika Bentryn1, Edyta Węgrzyn1, Patrick Oleksy1, Walery Zukow2 1Department and Clinic of Geriatrics, Nicolaus Copernicus University Collegium Medicum, Bydgoszcz, Poland 2 Wydział Kultury Fizycznej, Zdrowia i Turystyki, Uniwersytet Kazimierza Wielkiego w Bydgoszczy, Polska Słowa klucze: zespół kruchości, słabość, patogeneza, stan zapalny, IL-6, starzenie. Key words: frailty syndrom, weakness, patogenesis, inflammation, IL-6, aging. Streszczenie Wstęp. Zespół kruchości (Frailty Syndrome – FS) jest szeroko występującym zespołem geriatrycznym charakteryzującym się fizjologicznym obniżeniem odporności na czynniki stresogenne. W ostatnich latach poczyniono znaczny postęp w rozumieniu patogenezy FS. Prawdopodobnie kluczowym procesem patogenetycznym jest stan przewlekłego zapalenia, które wpływa na układy: mięśniowo- szkieletowy, dokrewny, sercowo-naczyniowy i krwiotwórczy. Cel. Przedstawienie najnowszych doniesień dotyczących patogenezy FS i szersze omówienie najbardziej istotnych mechanizmów patogenetycznych. Materiał i metody. Posługując się słowami kluczowymi: zespół kruchości (frailty syndrom), słabość (weakness), patogeneza (patogenesis), stan zapalny (inflammation), IL-6, starzenie (aging), przeszukano elektroniczne polskie oraz zagraniczne pełnotekstowe bazy bibliograficzne: Polska Bibliografia Lekarska, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct oraz Medline oraz przeanalizowano 40 publikacji nawiązujących do patogenezy FS. Wyniki. Badania wykazały, że podłożem zespołu kruchości jest proces zapalny różnych układów i narządów. U pacjentów z zespołem kruchości odnotowano zwiększony poziom prozapalnych cytokin, takich jak IL- 6, IL- 1 oraz zwiększony poziom leukocytów, głównie limfocytów T oraz monocytów i neutrofili. Zauważono obniżanie się poziomu hormonów steroidowych i IGF-1 prowadzące do sarkopenii oraz osteopenii. Wpływa to w sposób znaczący na objawy FS u starszego pacjenta. Wnioski. Patogeneza zespołu kruchości jest wieloczynnikowa. Jej podłożem jest przewlekle toczący się proces zapalny, który dotykając poszczególnych układów i narządów organizmu, prowadzi do dysfunkcji, takich jak sarkopenia, osteopenia, zaburzenia funkcji poznawczych, anoreksja, zaburzenia endokrynologiczne. Należy zwiększyć skuteczności diagnostyki oraz opracować programy leczenia wczesnych zaburzeń FS. Abstract Introduction. Frailty Syndrome (FS) is a widely common geriatric syndrome characterized by a decrease in resistance to physiological stressors. In recent years there has been considerable progress in understanding the pathogenesis of FS. Probably the key pathogenetic process is a state of chronic inflammation that affects the systems: musculoskeletal, endocrine, cardiovascular and hematopoietic. Purpose. Presentation of the latest reports on the pathogenesis of FS and wider discussion of the most important pathogenetic mechanisms. Material and methods. Using the key words: frailty syndrome, weakness, pathogenesis, inflammation, IL-6, and aging, searched Polish and foreign electronic full-text bibliographic databases: Polish Medical Bibliography, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct and Medline and analyzed 40 publications referring to the pathogenesis of FS. Results. Studies have shown that the basis of FS is inflammation of various systems and organs. In patients with FS reported an increase of proinflammatory cytokines such as IL-6, IL-1, and increased levels of leukocytes, especially T lymphocytes as well as monocytes and neutrophils. It was observed the decrease of the steroid hormone and IGF-1 leads to sarcopenia and osteopenia. This effects in a significant way the symptoms of FS an elderly patient. Conclusions. Pathogenesis of fragility is multifactorial. The basis is a chronic ongoing inflammatory process that effects various systems and organs of the body, leading to dysfunction, such as sarcopenia, osteopenia, cognitive disorders, anorexia, endocrine disorders. Increasing the efficiency of diagnosis and developing treatment programs for early disorders of FS is required.
    Journal of Health Sciences 09/2014; 4(9):197-204.
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    ABSTRACT: Objectives: To compare the impact of HIV infection and healthy ageing on monocyte phenotype and function and determine whether age-related changes induced by HIV are reversed in antiretroviral treated individuals. Design: A cross sectional study of monocyte ageing markers in viremic and virologi-cally suppressed HIVþ males aged 45 years and age-matched and elderly (!65 years) HIV-uninfected individuals. Methods: Age-related changes to monocyte phenotype and function were measured in whole blood assays ex vivo on both CD14 þþ CD16 À (CD14 þ) and CD14 variable CD16 þ (CD16 þ) subsets. Plasma markers relevant to innate immune acti-vation were measured by ELISA. Results: Monocytes from young viremic HIVþ males resemble those from elderly controls and show increased expression of CD11b (p < 0.0001 on CD14 þ and CD16 þ subsets), and decreased expression of CD62L and CD115 (p ¼ 0.04 and 0.001 respectively on CD14 þ monocytes) when compared to young uninfected con-trols. These changes were also present in young virologically suppressed HIVþ males. Innate immune activation markers neopterin, sCD163 and CXCL10 were elevated in both young viremic (p < 0.0001 for all) and virologically suppressed (p ¼ 0.0005, 0.003 and 0.002 respectively) HIVþ males with levels in suppressed individuals resembling those observed in elderly controls. Like the elderly, CD14 þ monocytes from young HIVþ males exhibited impaired phagocytic function (p ¼ 0.007) and telomere short-ening (p ¼ 0.03) as compared to young uninfected controls. Conclusions: HIV infection induces changes to monocyte phenotype and function in young HIVþ males that mimic those observed in elderly uninfected individuals, suggesting HIV may accelerate age-related changes to monocytes. Importantly, these defects persist in virologically suppressed HIVþ individuals.