Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are drugs that act by maintaining glycosuria. Recent studies have shown promising effects of these in the treatment of type 2 diabetes mellitus (DM2). However, there may be an increased risk of developing urinary tract infections (UTIs) in patients treated with these. Our study aims to analyze the association between the risk of UTI in patients treated with SGLT2i. A systematic review of the literature was carried out by randomized clinical trials, totalizing at the end of the selection 23 articles that were statistically evaluated. The incidence of UTI was generally demonstrated in articles and in different subgroups: patients on SGLT2i monotherapy or on combination therapy; according to specific comorbidities of each sample or according to the drug used. They noticed an increase in the chance of UTI in the SGLT2i groups compared to the control groups on placebo or other oral antidiabetic agents. This increased chance was found predominantly with the use of Dapagliflozin, Canagliflozin, and Tofogliflozin, regardless of the dosing. Lastly, stands out that the dimension of UTI chances for DM2 patients who use SGLT2i remains to be more strictly determined.

SUMMARY Hepatopulmonary Syndrome (HPS) is a complication of cirrhosis that worsens the disease's prognosis, pre and post liver transplant. The objective of this study is to analyze the prevalence of HPS in cirrhotic patients at our service and to correlate it with oxygen saturation (SatO2) using a pulse oximeter to evaluate if this is useful as a screening test for HPS. A prospective study was conducted in patients with hepatic cirrhosis conventionally selected from 2014 to 2016. All the patients underwent an echocardiogram with microbubbles and oxygen saturation measurement by pulse oximetry. Those with intrapulmonary shunt were submitted to arterial blood gas analysis. The relationship between oxygen saturation and HPS was assessed by the multivariate model of binary logistic regression. We analyzed 77 patients, and 23.3% (18 patients) had all criteria for HPS. The relationship between HPS and SatO2 did not show statistical significance, even after the variables were adjusted for sex, age, and smoking. Oxygen saturation alone was not able to detect HPS in the sample of cirrhotic patients. More accurate methods for screening and diagnosis of the syndrome should be used.

A Deficiência de Alfa-1 Antitripsina é um distúrbio genético autossômico recessivo, na qual existem alelos de deficiência no locus dos inibidores de proteases (Pi), localizados no braço longo do cromossomo 14. Dentre todas as variantes relacionadas à doença clínica, a mutação Z é a mais comum e deriva da substituição de ácido glutâmico por lisina na posição 342 do gene SERPINA1. No fígado, o acúmulo da proteína mutante nos hepatócitos pode levar à colestase neonatal, hepatopatia crônica, cirrose hepática e carcinoma hepatocelular. O diagnóstico da doença requer, além da medição dos níveis séricos de alfa-1 antitripsina, reconhecimento do padrão clínico, exame físico, história familiar, identificação e interpretação dos resultados dos exames com realização de fenotipagem/genotipagem. O relato tem como objetivo abordar o caso de um paciente portador de Deficiência de Alfa-1 Antitripsina que evoluiu com cirrose hepática e carcinoma hepatocelular identificado no explante hepático, bem como discutir os achados laboratoriais, clínicos, de imagem e histológicos, identificando a repercussão da doença nos indivíduos, complicações e a melhor abordagem diagnóstica e terapêutica.