We investigated the association between cigarette smoking and the risk of developing rheumatoid arthritis (RA) in the Malaysian population. A total of 1,056 RA patients and 1,416 matched controls aged 18-70 years within a defined area of Peninsular Malaysia were evaluated in a case-control study between August 2005 and December 2009. A case was defined as a person with early diagnosed RA using the 1987 American College of Rheumatology criteria for RA. Controls were randomly selected matched for sex, age, and residential area. Cases and controls answered a questionnaire on a broad range of issues, including lifestyle factors and smoking habits wherein current and former smoking was classified as ever-smoking. The presence of anti-citrullinated peptide antibodies (ACPA) was determined for cases and controls. We found that ever-smokers had an increased risk of developing ACPA-positive RA [odds ratio (OR) = 4.1, 95% confidence interval (CI) 1.9-9.2] but not ACPA-negative RA (OR = 0.7, 95% CI 0.3-2.0), compared with never-smokers. A significant dose-response relationship between cumulative dose of smoking and risk of ACPA-positive RA was observed (<20 pack-years OR = 3.3, 95% CI 1.1-9.8; at least 20 pack-years OR = 5.2, 95% CI 1.6-17.6). Hence, smoking is associated with an increased risk of ACPA-positive RA in the Malaysian population, in which the genetic context is similar to several other Asian countries.

We investigated the association between cigarette smoking and the risk of developing rheumatoid arthritis (RA) in the Malaysian population. A total of 1,056 RA patients and 1,416 matched controls aged 18-70 years within a defined area of Peninsular Malaysia were evaluated in a case-control study between August 2005 and December 2009. A case was defined as a person with early diagnosed RA using the 1987 American College of Rheumatology criteria for RA. Controls were randomly selected matched for sex, age, and residential area. Cases and controls answered a questionnaire on a broad range of issues, including lifestyle factors and smoking habits wherein current and former smoking was classified as ever-smoking. The presence of anti-citrullinated peptide antibodies (ACPA) was determined for cases and controls. We found that ever-smokers had an increased risk of developing ACPA-positive RA [odds ratio (OR) = 4.1, 95% confidence interval (CI) 1.9-9.2] but not ACPA-negative RA (OR = 0.7, 95% CI 0.3-2.0), compared with never-smokers. A significant dose-response relationship between cumulative dose of smoking and risk of ACPA-positive RA was observed (<20 pack-years OR = 3.3, 95% CI 1.1-9.8; at least 20 pack-years OR = 5.2, 95% CI 1.6-17.6). Hence, smoking is associated with an increased risk of ACPA-positive RA in the Malaysian population, in which the genetic context is similar to several other Asian countries.

Background: Food-borne biogenic amines (BAs), namely, histamine, putrescine, cadaverine, tyramine, spermine and spermidine are known for their contributions as fish-based food freshness biomarkers to determine level of contamination. The remaining food–borne BAs (phenylethylamine, tryptamine and agmatine) effects on promoting inflammation are yet to be investigated. The effect of these compounds on induction of inflammation in macrophages was investigated using Principal Component Analysis (PCA) from independent (BAs at 1, 10 and 100 µg/ml, food extract and its standard mixture solution) and dependent variables [cell viability, nitric oxide (NO) and tumor necrosis factor-α (TNF-α) secretion]. Nine individual BAs and keropok lekor extracts were exposed to RAW 264.7 macrophages for 18-24 hr at 37oC with 5% carbon dioxide environment. Cell viability, NO and TNF-α secretion were determined using MTS assay kit, Greiss Reagent System and Enzyme-linked Immunosorbent Assay (ELISA) kits, respectively. Results: Q2V values were not equal to Q2 (an estimate of the predictive ability of the model) values for individual variables because the eigenvalues values were more than 0.5, indicating a good model. All variance (R2VX) values were > 0.9, suggesting goodness of fit. Conclusions: PCA is thus proven as an effective tool to discriminate between inflammogenic and non-inflammogenic food-borne BAs.

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