Smoking and Rheumatoid arthritis
Just published in Arthritis Research and Therapy is the latest work from Dr Paul Hessian’s Dunedin laboratory entitled Dendritic cells provide a potential link between smoking and inflammation in rheumatoid arthritis.
The work carried out by Department of Physiology PhD student, Marina Kazantseva (who is about to graduate in December), deals with an aspect of the puzzle that associates smoking with increased risk of getting rheumatoid arthritis (RA) and with increased severity of established disease. Dendritic cells (DCs) are very important cells in the immune system, normally tasked with surveillance and response to infection. There is also a critical role for these cells in diseases like RA. The results of this study show that a subgroup of the DCs in joint tissue are extremely sensitive to at least one of the chemical compounds found in cigarette smoke, a polycyclic aromatic hydrocarbon. The smoke exposure activates the aryl hydrocarbon receptor (AHR) transcription factor system in DCs and reduces the production of a key cytokine, intereleukin-6, used by DCs for signalling to the immune system. There is more to work out about the consequences of DC responding to cigarette smoke. However a very practical outcome is that in RA patients who have quit smoking, this effect on the synovial DCs is rapidly lost. So while the work does not yet explain the lasting effect of smoking on increasing the risk of getting RA, it does show that stopping smoking will have some immediate impact on inflammation in the very tissues targeted by rheumatoid inflammation. That has to have some additional benefit for patients.
Barriers to smoking cessation in rheumatoid arthritis
The reason people develop rheumatoid arthritis (RA) is still not entirely clear. Research has revealed two things that seem to add up to make someone at risk of developing RA: an inherited weakness in your body’s immune system that can be triggered by smoking. A bigger issue is that continuing to smoke after developing RA tends to make the symptoms of the disease more severe and can stop the medicines used to treat RA from working. We also know that smoking contributes to the increased risk of heart disease, which is already increased in people with RA because of the inflammation that RA causes. Giving up smoking is therefore one of the most important ways a smoker with RA can help themselves. However, we know that quitting smoking can be particularly difficult when living with a painful disease like RA.
A PhD student in the group has focused on talking to patients with RA to see if there are any specific factors that makes stopping smoking more difficult. Five main issues were identified that make it more difficult to quit smoking when you have RA. Firstly, patients were unaware of the link between smoking and having worse RA so they hadn’t been previously been motivated by the fact their RA might be better controlled if they quit smoking. Secondly, interviewees had trouble managing their pain – it wasn’t that they were using smoking to control their pain but the difficulty of being in pain and unable to control it added to people continuing to smoke, for example on the many sleepless nights when the pain is bad. Thirdly, interviewees also had difficulty exercising because of their joint pain – this also added to people continuing to smoke. Fourthly, lacking support and finally, coping strategies to help give up. The results of this study have recently been published in Arthritis Research and Therapy
From this research, we have developed a RA-specific smoking cessation programme with the help of Arthritis New Zealand. It is also important for the family and whānau or people with RA to be aware of the risks of continuing to smoke if you have RA. Support is important in making steps towards giving up smoking such as having a smoke-free house or car, and eventually having a smoke-free life.
Prevalence of HLA-B27 in the New Zealand population: effect of age and ethnicity
HLA-B27 genotyping is commonly used to support a diagnosis of ankylosing spondylitis (AS). A recent study has suggested that HLA-B27 may adversely affect longevity. The objectives of this study were to determine, for the first time, the prevalence of HLA-B27 in the New Zealand population, and to test whether HLA-B27 prevalence declines with age.
117 Caucasian controls, 111 New Zealand Māori controls, and 176 AS patients were directly genotyped for HLA-B27 using PCR-SSP. These participants and a further 1103 Caucasian controls were genotyped for the HLA-B27 tagging single nucleotide polymorphisms (SNPs) rs4349859 and rs116488202. All AS patients testing positive for HLA-B27 of New Zealand Māori ancestry underwent high resolution typing to determine sub-allele status.
HLA-B27 prevalence was 9.2% in New Zealand Caucasian controls and 6.5% in Māori controls. No decline in HLA-B27 prevalence with age was detected in Caucasian controls (p = 0.92). Concordance between HLA-B27 and SNP genotypes was 98.7-99.3% in Caucasians and 76.9-86% in Māori. Of the 14 AS patients of Māori ancestry, 1 was negative for HLA-B27, 10 were positive for HLAB*2705, and 3 positive for HLAB*2704. All cases of genotype discordance were explained by the presence of HLAB*2704.
HLA-B27 prevalence in New Zealand Caucasians is consistent with that of Northern European populations and did not decline with increasing age. In Māori with AS who were HLA-B27 positive, 76.9% were positive for HLA-B*2705, suggesting that genetic susceptibility to AS in Māori is primarily due to admixture with Caucasians.