Metformin-treated diabetics (MTD) showed a decrease in cobalamin, a rise in homocysteine, and methylmalonic acid, leading to accentuated diabetic peripheral neuropathy (DPN). This study aimed to determine whether or not metformin is a risk factor for DPN. We compared MTD to non-metformin-treated diabetics (NMTD) clinically using the Toronto Clinical Scoring System (TCSS), laboratory (methylmalonic acid, cobalamin, and homocysteine), and electrophysiological studies. Median homocysteine and methylmalonic acid levels in MTD vs. NMTD were 15.3 vs. 9.6 µmol/l; P < 0.001 and 0.25 vs. 0.13 µmol/l; P = 0.02, respectively with high statistical significance in MTD. There was a significantly lower plasma level of cobalamin in MTD than NMTD. Spearman’s correlation showed a significant negative correlation between cobalamin and increased dose of metformin and a significant positive correlation between TCSS and increased dose of metformin. Logistic regression analysis showed that MTD had significantly longer metformin use duration, higher metformin dose > 2 g, higher TCSS, lower plasma cobalamin, and significant higher homocysteine. Diabetics treated with metformin for prolonged duration and higher doses were associated with lower cobalamin and more severe DPN.

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The aim of the present work was to study the effect of tobacco smoking on disease progression in rheumatoid arthritis patients and its relation to anti-cyclical citrullinated peptide (anti-CCP) antibodies. The study included 54 patients; 20 non-smokers, 9 ex-smokers, 14 mild to moderate smokers and 11 heavy smokers. Fifteen normal volunteers were also studied as controls. Disease stage was clinically and radiologically determined, rheumatoid factor (RF) and anti-CCP antibodies were measured in serum. Higher percentage of severe disease (stage III) was seen in heavy smoker patients than mild to moderate smokers (54.6% versus 35.7%) and in moderate smokers than ex-smokers (35.7% versus 33.6%). Lowest percentage of severe disease was seen in non-smokers (15%). RF and anti-CCP were significantly higher in smoker than non-smoker and in heavy than mild to moderate smoker patients (p < 0.01, p < 0.05 and p < 0.01, p < 0.001, respectively). In smoker patients, both RF and anti-CCP antibodies correlated significantly and positively with smoking index (r = 0.581, p < 0.001; r = 0.661, p < 0.001). Also, smoking index and anti-CCP correlated significantly and positively with disease stage (r = 0.424, p < 0.05; r = 0.523, p < 0.01). It appears from our results that, tobacco smoking mostly play a role in progression of rheumatoid arthritis through tissue protein citrullination. So all rheumatoid arthritis patients must quit completely to achieve a good control.

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