Nursing Assignment Sample Online

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Assignment Question

Is there a causal link between the Metabolic Syndrome and the development and/or progression of Osteoarthritis?

Assignment Solution

Osteoarthritis (OA) is a prevalent chronic joint disease generally affecting either the knees, hands, spine or hips. Ageing and an obesity-induced increased mechanical load of joints are reported to be the risk factors contributing to the development of OA. However, obesity is also seen as a risk factor in osteoarthritis affecting the non-weight bearing joints like hands, suggesting that not only mechanical load but even metabolic factors may play an important role in the obesity and osteoarthritis link. This has contributed to a keen interest amongst researchers to establish any causal relationship between the Metabolic Syndrome (MetS) and OA. Metabolic syndrome is a phenotype characterised by central obesity and a combination of metabolic dysfunctions such as hypertension, hyperglycaemia, and dyslipidaemia (low HDL and triglyceridemia).

Metabolic factors- risk markers in Osteoarthritis

A lot of published literature indicates that metabolic change augments the chances of developing osteoarthritis. . Metabolites involved in energy, lipid and carbohydrate metabolism in the OA patients were reported to be significantly altered compared with those with little or no evidence of the disease (Qingming Zhang et al., 2015). The involvement of pro-inflammatory adipokines in the onset and progression of OA was reported suggesting additional metabolic factors are involved rather than just mechanical stress on the joints (Javier et al., 2013, L.K.Kinget al.,2015). Synovial cells can also be triggered by oxidized LDL to release growth factors and proinflammatory cytokines which cause cartilage destruction and bone deformations in OA (Wouter de Munteret al., 2016).

Additionally, lipid builds up in the cartilage can impair cholesterol efflux in chondrocytes, hence inducing OA (Tsezouet al., 2010). As parts of the metabolic syndrome, insulin resistance, hyperglycaemia, and hyperinsulinemia are also strongly related to OA pathogenesis. Georg Schettet al.,(2013) conducted a population-based cohort study followed over a period of 20 years in which diabetes is an independent predictor of osteoarthritis. Oxidative damage, endothelial dysfunction, inflammation and altered metabolism are pointed out to be the shared pathophysiological channels in osteoarthritis as well as MetS. (J. Sellam and F. Berenbaum ,2013) (Q. Zhuo et al.,2012) (D. M. Findlay,2007) (T. Simopoulouet al., 2007).The above studies not only establish a connection between the components of MetS and OA but also suggest its involvement in the progression of the disease.

However, the causal link will hold significance only if the obesity-related load to some extent is adjusted for while assessing the influence of metabolic syndrome and its components on OA. Hussain et al.(2014) found that abdominal obesity and hypertension, independent of BMI were associated with a high prevalence of knee osteoarthritis, and also stated that the accumulation of MetS components in an individual increase the risk of OA. However, the same correlation could not be established for hip osteoarthritis in both the above studies In contrast, some studies revealed that all MetS components had a strong connection with knee OA but after adjustment for BMI, almost all of these links became insignificant. (JingboNiu et al.,2017) .

Yoshimura et al. (2012) also reported that the association of systolic blood pressure and hyperlipidaemia with Knee OA proved to be trivial after adjusting for BMI. Moreover, this study also confirmed that the gradual build-up of MetS components increases the occurrence of Knee OA. DoosupShin (2014) established the relationship between MetS and knee OA on the basis of excessive weight only and not by insulin resistance, the key pathophysiology of MetS. As in the previous studies, in this study also, the association of other MetS components, abdominal obesity and high BP with knee OA became nonsignificant after adjusting for weight or BMI.

Osteoarthritis - is another component of metabolic syndrome (MetS)

OA is also one of the cluster components of MetS, as hypothesised by a few researchers (VelasquezMTand Katz JD, 2010). Q.Zhuoet al. (2012) examined the likely shared pathogenesis between the Mets and knee OA that supports the inclusion of OA as a component of MetS. Available evidence supports that the accumulation of components of MetS increases the risk for knee osteoarthritis. Thus, metabolic factors contribute greatly to the pathogenesis of the heterogeneous condition, osteoarthritis. Also, all evidence was related to knee Osteoarthritis, and no studies established a firm link with hand, hip or spine osteoarthritis. However, as there are contrasting results with a positive relation between MetS components and OA, after adjusting for BMI, no direct causal link can be established between the two.

BIBLIOGRAPHY

1. M. Findlay (2007) ‘Vascular pathology and osteoarthritis’, Rheumatology, vol. 46, no. 12, pp. 1763–1768.
2. Shin, (2014) ‘Association between metabolic syndrome, radiographic knee osteoarthritis, and intensity of knee pain: results of a national survey’, The Journal of Clinical Endocrinology & Metabolism, vol. 99, no. 9, pp. 3177–3183,
3. Schett G1, Kleyer A, Perricone C, Sahinbegovic E, Iagnocco A, Zwerina J, Lorenzini R, Aschenbrenner F, Berenbaum F, D'Agostino MA, Willeit J, Kiechl (2013) ‘Diabetes is an independent predictor for severe osteoarthritis: results from a longitudinal cohort study’, Diabetes Care, vol. 36, no. 2, pp. 403– 409,
4. Hussain SM, Wang Y, Cicuttini FM, Simpson JA, Giles GG, N. Graves S, and W.Anita (2014) ‘Incidence of total knee and hip replacement for osteoarthritis in relation to the metabolic syndrome and its components: a prospective cohort study’,Seminars in Arthritis and Rheumatism ,43: pp 429–36.
5. Yoshimura, S. Muraki, H. Oka, Tanaka S, Kawaguchi H, Nakamura K, Akune T. (2012), ‘Accumulation of metabolic risk factors such as overweight, hypertension, dyslipidaemia, and impaired glucose tolerance raises the risk of occurrence and progression of knee osteoarthritis: a 3-year follow-up of the ROAD study’, Osteoarthritis and Cartilage, vol. 20, no. 11, pp. 1217–1226.
6. Conde, M. Scotece, V. L´opez Gómez R, Lago F, Pino J, Gómez-Reino JJ, Gualillo O (2013). ‘Adipokines: novel players in rheumatic diseases’, Discovery Medicine, vol. 15, no. 81, pp. 73–83
7. Sellam and F. Berenbaum,(2013) ‘Is osteoarthritis a metabolic disease?’, Joint Bone Spine, vol. 80, no. 6, pp. 568–573
8. JingboNiu, Margaret Clancy, PiranAliabadi, Ramachandran Vasan, and David T. Felson,(2017) ‘Metabolic Syndrome, Its Components, and Knee Osteoarthritis’ , Arthritis & Rheumatology 69, No. 6, pp 1194–1203
9. K.King ,H.Henneicke,M. J. Seibel ,L .March, andA. Ananda coomarasmy,(2015) ‘Association of adipokines and joint biomarkers with cartilage-modifying effects of weight loss in obese subjects’, Osteoarthritis and Cartilage, vol. 23, no. 3, pp. 397–404.
10. Zhang, H. Li, Z. Zhang, F. Yang, and J. Chen, (2015) ‘Serum metabolites as potential biomarkers for diagnosis of knee osteoarthritis’,Disease Markers, vol., Article ID 684794,
11. Zhuo,W. Yang, J. Chen, and Y.Wang, (2012), ‘Metabolic syndrome meets osteoarthritis’, Nature Reviews Rheumatology, vol. 8, no. 12, pp. 729–737.
12. Simopoulou, K. N. Malizos, D. IliopoulosStefanou N, Papatheodorou L, Ioannou M, Tsezou A. (2007), ‘Differential expression of leptin and leptin’s receptor isoform (Ob-Rb) mRNA between advanced and minimally affected osteoarthritic cartilage; effect on cartilage metabolism’, Osteoarthritis and Cartilage, vol. 15, no. 8, pp. 872–883,
13. Tsezou, D. Iliopoulos, K. N. Malizos, and T. Simopoulou,(2010) ‘Impaired expression of genes regulating cholesterol efflux in human osteoarthritic chondrocytes’, Journal of OrthopaedicResearch, vol. 28, no. 8, pp. 1033–1039.
14. Velasquez MT and (2010) ‘Osteoarthritis :another component of metabolic syndrome?’ MetabSyndrRelatDisord ;8:295–305.
15. de Munter, P. M. van der Kraan, W. B. van den Berg, and P. L. van Lent, (2016) ‘High systemic levels of low-density lipoprotein cholesterol: fuel to the flames in inflammatory osteoarthritis?’,Rheumatology, vol. 55, no. 1, pp. 16–24.

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