LAUSR

It is estimated that up to 14% of patients with HIV have diabetes mellitus (DM), which is a determinant risk factor for the development of cardiovascular disease [1]. The therapeutic regimen is the same as that recommended in clinical practice guidelines such as the American Diabetes Association (ADA) and the European Diabetes Association (EASD) [2]. At the moment, one option for treatment are sodium and potassium cotransporter inhibitors type 2 (ISGLT2), glycosuric drugs that improve glycosylated hemoglobin between 0–8 and 1% and can produce weight loss, decreased systolic blood pressure, not producing hypoglycemia [3,4]. Nowadays, canagliflozin, empagliflozin and dapagliflozin can be used. The experience of use in patients with HIV infection is poor, and there is lack of information about safety of these drugs in people using antiretrovirals. A prospective observational study in HIV patients with poorly controlledDM2estimatedasHbA1cN7%overweightor obese (BMIN27kg/m) after 24 weeks of treatment with canagliflozin was conducted. The patients are part of the cohort of 800 HIV patients on follow-up at the Costa del Sol Hospital (Marbella, Spain). The following variables were collected: glycosylated hemoglobin (HbA1C), weight, body mass index (BMI), lipid and renal profile, canagliflozin discontinuations due to adverse effect or any other cause, antiretroviral modifications due to toxicity or interactions. Quantitative variables are presented as medians with interquartile amplitude. Non-parametric tests (UMann-Whitney)were used to compare the medians of the baseline values and the week 24. Treatment with canagliflozin was instituted in 8 patients (6 men, 2 women), all of whom completed 24 weeks of follow-up. Median age was 56.5 ± 4.5 years. Median time with DM2 diagnosis was 8 ± 2.1 years. None had micro or macrovascular complications derived from the disease. Seven were obese and one was overweight, median BMI being 35.50 ± 7.12 kg/m. Waist circumference was 124.12 ± 24.6 cm. Three patients were receiving hypotensives and statins. Only one was smoking. Glycemic control was inadequate, being median fasting glycemia 190.37 ± 41, 24 mg/dL and HbA1c of 8.57 ± 1.34%. As baseline therapy for DM2, all patients were treated with metformin, sulphonylureas and incretinic for as long as 5 years and two receiving basal insulin. None had a detectable viral load. The CD4 count was 1074.5± 837.75 cells/μL at the beginning of follow-up. Two patients received tenofovir/emtricitabine/raltegravir, two abacavir/lamivudine/efavirenz, one tenofovir/emtricitabine/rilpivirine, one etravirine/darunavir-ritonavir/raltegravir, another darunavir-ritonavir/raltegravir and another darunavir-ritonavir monotherapy. In no case was the ART changed during the follow-up of the patients. Lifestyle improvements were proposed and the sulphonylureas and incretinics were discontinued replacing them with 100 mg/d canagliflozin,