ABSTRACT
Purpose: Hyperhomocysteinemia has been postulated as a potential risk factor for the development and progression of diabetic retinopathy. The aim of this study was to determine the association of hyperhomocysteinemia with proliferative diabetic retinopathy (PDR). Methods: This was a hospital-based, case–control study, conducted at a tertiary care ophthalmic center in South India. Thirty-nine patients with proliferative diabetic retinopathy were enrolled as cases, and 39 age- and gender-matched patients with no diabetic retinopathy (No DR) were enrolled as controls. Fasting serum homocysteine estimation, as well as baseline investigations, were done in all participants. Data regarding demographic profile and risk factors were documented. Data were analyzed using Chi-square test and independent t-test, as appropriate. Results: The prevalence of hyperhomocysteinemia was higher in PDR (59%) compared to “No DR” (48.7%); however, this difference was not statistically significant (P = 0.36). Similarly, the mean serum homocysteine level in cases was higher than in controls, but this was not statistically significant (17.98 + 6.26 ?mol/L vs. 17.71 + 8.17 ?mol/L; P = 0.87). Longer duration of diabetes, hypertension, anemia, and renal dysfunction were found to be significantly associated with PDR. Conclusion: The prevalence of hyperhomocysteinemia as well as the mean serum levels of homocysteine were found to be higher in the cases with PDR, compared to the controls with No DR, although the difference was not statistically significant. Longer duration of diabetes, hypertension, anemia, and renal dysfunction were significantly associated with PDR.
ABSTRACT
INTRODUCTION: We performed retrospective analysis of 106 patients with lung cancer for which formalin‑fixed paraffin‑embedded tissues was available. Their epidermal growth factor receptor (EGFR) mutation status and treatment outcomes are described. MATERIALS AND METHODS: All patients with confirmed non–small cell lung cancer (NSCLC) during Jan 2008 to Dec 2010 were included. EGFR sequencing was performed with ABI PRISM 310 genetic analyzer. RESULTS: Forty‑two (39.6%) patients had mutation in one of the four exons characterized. Patients whose EGFR mutational status was not available at presentation before the start of treatment were started on chemotherapy, n = 46 (43.39%). If EGFR mutational analysis was available and mutations were present, the patients were started on either upfront tyrosine kinase inhibitor (TKI), n = 15 (14.15%) or if on chemotherapy arm were allowed to finish six cycles and then start with maintenance TKIs, n = 26 (24.52%). The median progression free survival for patients with and without mutations was 11 months (95% CI,7-14) and 9 months (95% CI,7-10) respectively. A median PFS of 14 months (95%CI, 12-16) was seen in the mutation‑positive group that received both chemotherapy followed by switch maintenance with TKIs versus 8 months (95%CI, 7-8 months) in the group that received only TKI. CONCLUSION: The prevalence of EGFR mutations in this population of NSCLC patients was 39.6% with exon 19 mutation being the most common. The observed benefit of addition of chemotherapy over TKI in EGFR mutation‑positive group raises the question, can we offer the therapy of chemotherapy–TKI combination to EGFR mutation‑positive lung cancer patients as shown in the present study.