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Context: Acitretin increases serum lipids. Data on its effects on insulin resistance and glucose metabolism are sparse and contradicting. Aims: The aim of this study is to investigate the effects of acitretin on insulin resistance, glucose metabolism, and lipids. Methods: Dermatology clinic in a public tertiary hospital. A cross sectional study involving chronic plaques psoriasis patients on acitretin plus topical therapy or topical therapy alone was performed. Fasting blood glucose (FBG), serum lipids, serum insulin, and glucose tolerance test (GTT) were performed. Homeostatic model of insulin resistance (HOMA-IR) was calculated. Psoriasis severity was evaluated using Psoriasis Area and Severity Index. Chi square and t-tests determined differences between cases and controls. Pearson's correlation coefficient test determined the relationship between continuous variables. Results: A total of 60 patients participated, 30 were on acitretin while 30 were on topical therapy. Psoriasis duration, disease severity, BMI, presence of metabolic syndrome, and other comorbidities between the two groups were similar. There were no significant differences in GTT, FBG, HOMA-IR, and serum lipids. Patients on acitretin >25 mg daily had lower FBG [4.4 (0.8) versus 4.9 (0.9), P = 0.04] and triglyceride [1.05 (0.33) versus 1.57 (1.03), P = 0.02] compared with doses ≤25 mg. Higher acitretin dose correlated with lower FBG (r = −0.36, P = 0.05) and triglycerides (r = −0.37, P = 0.05) while longer therapy duration correlated with lower total cholesterol (r = −0.37, P = 0.05). HOMA-IR showed inverse correlation with acitretin dose and duration (r = −0.10, P = 0.61 and r = −0.12, P = 0.53, respectively). Conclusion: Acitretin therapy resulted in increased triglyceride. The effect of acitretin on glucose metabolism and insulin resistance maybe dependent on the dose and duration of therapy.

Background: Although a variety of strategies have been employed for managing articular cartilage defects in the knee, overall outcomes have not been satisfactory. An alternative option may be autologous chondrocyte transplantation (ACT). However, as this method is still under investigation, here we assessed the efficacy of ACT for human knee defect cartilage repair. Methods: In a randomized clinical trial study, eleven patients (mean age 31.09 years) were enrolled in the study with full thickness cartilage defects in the knee. Arthroscopically, healthy cartilage was obtained, chondrocytes expanded for 2-3 weeks and ACT performed. Clinical status was evaluated before ACT, 6 and 12 months after ACT using the Brittberg-Peterson functional assessment and modified Cincinnati rating score. Magnetic resonance imaging (MRI) findings were evaluated based on the scoring systems used by Sally Roberts and by Henderson. Results: Modified Cincinnati rating indicated significant improvement of clinical score before ACT compared to 6 (p = 0.000) and 12 (p = 0.000) months after ACT (from 2.73 before ACT to 7.27, 8.36 and 9.5 at 6, 12, and 48 months after ACT, respectively). Brittberg-Peterson functional assessment indicated a decline from 79.27 to 25.82 and 19.27 at 6 and 12 months post ACT. Further, statistical test demonstrated significant differences 6, 12 and 48 months post ACT (p = 0.007). Evaluation of MRI revealed a score of 6.5 for Henderson criteria and a score of 2.5 for Robert criteria. Conclusions: Our study demonstrated that ACT of the knee provides an excellent treatment for full thickness cartilage defects with outstanding clinical and radiological outcomes.