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Aim: To compare the efficiency of canagliflozin (C1) 100mg vs. canagliflozin (C3) 300mg on highly sensitive C reactive protein (hs-CRP) and other cardio-renal (CR) biomarkers. Methodology: Between July and Sept 2018, a cohort of 190 T2DM patients aged 18-75 yrs, irrespective of baseline A1c, receiving SGLTi C1 or C3 were identified. A propensity score 1:1 matching was done for both the groups with variables that could affect treatment outcomes and to minimise confounding. Patients were evaluated every 2-3months for CR biomarkers (body mass index (BMI), A1c, systolic (S) BP, diastolic (D) BP, Lipid profile (TC, LDL, TG, HDL), Hs-CRP, creatinine, eGFR and urinary albumin/creatinine ratio {UACR}). NT-ProBNP was evaluated at 12 months. T2DM with history of IHD, revasularisation, major surgery, hyperkalemia >5.5Meq/L and eGFR Results: 44 patients were identified in C1 gr and 44 in C3 gr. Baseline characters were well matched in both gr except, SBP (mean±SD) (C1 129.05±17.54 vs. C3 138.05±22.22, P-0.38).C1 gr (baseline to 12m): there was a S reduction in hs-CRP, A1c, BMI, SBP, DBP, TC, TG, LDL. C3 gr (baseline to 12m): there was a S reduction in hs-CRP, A1c, BMI, SBP, DBP, TC, LDL. Difference between C1 and C3 at 12m: There was no difference in hs-CRP mg/L {C1 1.88±0.43 vs. C3 1.31±0.46, p-0.371}, A1c% {C1 1.27±0.19 vs. C3 1.44±0.34, p-0.666}, BMI kg/m2 {C1 1.24±0.27 vs. C3 1.23± 0.25, p-0.988}, NT-ProBNP pg/ml {C1 63.95±65.52 vs. C3 61.53±61.71, p-0.864} eGFR {C1 6.39±3.37 vs. C3 0.99±3.20, p-0.952}, UACR mg/gm {C1 25.48±10.86 vs. C3 9.61±7.87, p-0.240}, Lipid profile, SBP and DBP between both gr. Conclusion: Canagliflozin 100mg is as good as canagliflozin 300mg in reduction of hs-CRP and CR markers. Disclosure V. Gupta: None. V. Teli: None. A. Patel: None.

Aim: The aim is to describe a very rare case of idiopathic granulomatous hypophysitis presenting as panhypopituitarism on the background of chronic renal failure and type 2 diabetes mellitus. The patient presented with fatigue and episodes of self-terminated hypoglycemia (while on sulfonylurea) as the sole manifestation of panhypopituitarism. The case also highlights the difficulties of identifying patients with hypophysitis in the setting of chronic renal failure. Results: We describe a middle-aged man who presented to us with the sole complaints of early morning fatigue and hypoglycemia (while on glimepiride), with a background history of type 2 diabetes and chronic renal failure. Before visiting our practice, he was repeatedly evaluated for decompensation of renal and cardiovascular disease without much success. When we saw the patient there was no obvious evidence of any endocrine disturbance, especially as the blood pressure was high without any postural drop. It was only when the patient persistently complained of an impaired quality of life due to the fatigue that we decided to chase an endocrine cause for the same. On endocrine evaluation, we diagnosed panhypopituitarism secondary to idiopathic granulomatous hypophysitis. Conclusion: Idiopathic granulomatous hypophysitis is a very rare form of inflammatory pituitary disease. Fewer than 35 cases of biopsy-proven idiopathic granulomatous hypophysitis have been reported in medical literature. This is only the third case of biopsy-proven idiopathic granulomatous hypophysitis reported from India.