Podiatry Rhuematoid Arthritis
Introduction
Throughout this essay I shall critique the available evidence regarding rheumatoid arthritis (RA); particularly concerning the conclusions on its aetiology, diagnosis techniques, pharmacological management, physical therapeutics and surgical treatment interventions. I shall explore the expected prognosis and the key developments we can expect in the future.
Aetiology and Prevalence RA is a chronic, systemic and inflammatory disease that progressively impacts peripheral joints (Panayi 2011).The damage that occurs is predominantly symmetrical and polyarthropathic (Rindfleisch & Muller 2005). It affects the host’s joint synovial membranes, tendon sheaths and bursae and causes stiffness, pain and swelling to the joints and affected tissues (NRAS 2011).
There are 400,000 people with RA in the UK with 12,000 people developing the disease per year. 1.5 men to every 3.6 to women per 10,000 develop RA annually. The peak age of incidence is 70 (NICE 2009 and Panayi 2011).
Evidence explaining aetiology of RA is broad-spectrum and multifactorial, and many sources quote its cause as unknown (Adams et al.2008, Maggi 2012). Genetic (tabulated in Figure.1) and environmental factors (for example smoking and pathogenic bacterium) interact (Klareskog 2006, Too 2012).
Genetic Involvement
Author/s
Critique of Literature
Genes associated with expression Major Histocompatability Complex (MHC)
Presence of the human leukocyte antigens or (HLA) ‘share-epitope’ alleles
Newton et al 2004, Plenge et al 2007, Steer 2009, Too et al 2012
Strong evidence behind HLA involvement in inflammatory RA, play pivotal role in individual producing anti-cyclic citrullinated peptide (CCP) serum that will increase risk of RA. HLA-DRB1 variation is more common in malaysian multi-ethnic population of Asian descent; allele not common in Caucasians. HLA-DRA variant is significantly commoner among Caucasian suffers.
Presence of protein tyrosine phosphatase 22 (PTPN22)
Throughout this essay I shall critique the available evidence regarding rheumatoid arthritis (RA); particularly concerning the conclusions on its aetiology, diagnosis techniques, pharmacological management, physical therapeutics and surgical treatment interventions. I shall explore the expected prognosis and the key developments we can expect in the future.
Aetiology and Prevalence RA is a chronic, systemic and inflammatory disease that progressively impacts peripheral joints (Panayi 2011).The damage that occurs is predominantly symmetrical and polyarthropathic (Rindfleisch & Muller 2005). It affects the host’s joint synovial membranes, tendon sheaths and bursae and causes stiffness, pain and swelling to the joints and affected tissues (NRAS 2011).
There are 400,000 people with RA in the UK with 12,000 people developing the disease per year. 1.5 men to every 3.6 to women per 10,000 develop RA annually. The peak age of incidence is 70 (NICE 2009 and Panayi 2011).
Evidence explaining aetiology of RA is broad-spectrum and multifactorial, and many sources quote its cause as unknown (Adams et al.2008, Maggi 2012). Genetic (tabulated in Figure.1) and environmental factors (for example smoking and pathogenic bacterium) interact (Klareskog 2006, Too 2012).
Genetic Involvement
Author/s
Critique of Literature
Genes associated with expression Major Histocompatability Complex (MHC)
Presence of the human leukocyte antigens or (HLA) ‘share-epitope’ alleles
Newton et al 2004, Plenge et al 2007, Steer 2009, Too et al 2012
Strong evidence behind HLA involvement in inflammatory RA, play pivotal role in individual producing anti-cyclic citrullinated peptide (CCP) serum that will increase risk of RA. HLA-DRB1 variation is more common in malaysian multi-ethnic population of Asian descent; allele not common in Caucasians. HLA-DRA variant is significantly commoner among Caucasian suffers.
Presence of protein tyrosine phosphatase 22 (PTPN22)
References: Boers M (2001) Rheumatoid arthritis. Treatment of early disease. Rheumatolgy Disorder Clinical North America 1(27):405–14 Botting RM & Botting JH (2011) C14 Non-steroidal anti-inflammatory drugs. Principles of Immunopharmacology 23(4) 573-584 Firestein, G. S. (2003). Evolving concepts of rheumatoid arthritis. Nature,423(6937), 356-361. Hennessy K, Woodburn J, & Steultjens MP (2012) Custom foot orthoses for rheumatoid arthritis: A systematic review. Arthritis Care & Research 64(3):311-320. Landorf KB and Burns J (2009) Health outcome assessment IN: Yates B (ed) Merrimans assessment of the lower limb (3rd edition) Edinburgh: Elsevier. 33-51 Loveday DT, Jackson GE and Geary NPJ (2012) The rheumatoid foot and ankle: Current evidence Muller S & Roddy E A rasch analysis of the Manchester foot pain and disability index. J Foot Ankle Res. 2009 Oct 30;2:29. Newton JL, Harney SMJ, Wordsworth BP & Brown MA (2004) "A review of the MHC genetics of rheumatoid arthritis."Genes and immunity 5(3):151-157.