SUMÁRIOO tratamento do diabetes gestacional é importante para evitar a morbimortalidade materno--fetal. O objetivo deste artigo é descrever o tratamento atualmente disponível para o manejo otimizado da hiperglicemia na gestação e sugerir um algoritmo de tratamento multidisciplinar. A terapia nutricional é a primeira opção de tratamento para as gestantes, e a prática de exercício físico leve a moderado deve ser estimulada na ausência de contraindicações obstétricas. O tratamento medicamentoso está recomendado quando os alvos glicêmicos não são atingidos ou na presença de crescimento fetal excessivo à ultrassonografia. O tratamento tradicional do diabetes gestacional é a insulinoterapia, embora mais recentemente a metformina venha sendo considerada uma opção segura e eficaz. A monitorização do tratamento é realizada com aferição da glicemia capilar e com avaliação da circunferência abdominal fetal por meio de ultrassonografia obstétrica a partir da 28 a semana de gestação. INTRODUÇÃOO diabetes gestacional é definido como qualquer grau de redução da tolerância à glicose, cujo início ou detecção ocorre durante a gravidez (1,2). Sua prevalência é variável, dependendo dos critérios diagnósticos empregados e da população estudada (1). No Brasil, em torno de 7% das gestações são complicadas pela hiperglicemia gestacional (3).Habitualmente, o diagnóstico do diabetes gestacional é realizado por busca ativa, com testes provocativos que empregam sobrecarga de glicose, a partir do segundo trimestre da gestação. Mais recentemente, tem-se recomendado a triagem precoce de gestantes de alto risco na primeira consulta pré-natal, o que permite identificar casos de diabetes preexistente e que não devem, portanto, ser rotulados como diabetes gestacional (1,4).

Asthma and chronic obstructive pulmonary disease (COPD) are chronic respiratory diseases that share some common characteristics. Asthma is associated with airway hyperresponsiveness, airway inflammation and airflow limitation that is reversible [1]. COPD is characterised by persistent and progressive airflow limitation and airway inflammation [2]. In recent years, there has been an ongoing discussion of whether asthma and COPD are different diseases, since a significant proportion of patients with symptoms of obstructive lung disease has features of both asthma and COPD [3-5]. In this respect, the most clinically significant phenotypes are COPD patients with asthmatic features and asthmatic patients that smoke. These patients may necessitate different therapeutic approaches and, therefore, there is a great need for diagnostic criteria that would allow proper diagnosis and treatment [6, 7]. Histological analysis has been previously suggested as a tool to identify and understand overlapping clinical and physiological phenotypes, thereby helping to better design treatments and plan long-term management [8]. However, there are few studies that have examined the histological patterns of patients who may be characterised as having asthma-COPD overlap. The present study is a pilot to provide data to inform the design and size of a study to test whether there are consistent histological differences between COPD patients with asthmatic features and asthma patients who have smoked. We included patients drawn from a cohort of COPD patients (total n=147) who underwent diagnostic bronchoscopy for clinical indications such as coin lesions (27%), evaluation of bronchoscopical or surgical low volume reduction procedures (25%), infiltrates (16%) and haemoptysis (8%). COPD patients had an average forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) ratio post-bronchodilation of 0.4 (range 0.3-0.5) and a smoking history of 43 pack-years (range 30-60). We also included a cohort of asthma patients (total n=19), with severe to very severe disease, that underwent bronchial thermoplasty. Diagnosis of COPD and asthma was based on European Respiratory Society/American Thoracic Society guidelines, according to Global Initiative for Chronic Obstructive Lung Disease and Global Initiative for Asthma criteria.

Although inhaled corticosteroids (ICS) are highly effective in asthma, they provide significant but modest clinical benefit in COPD. Here, we tested the hypothesis that high bronchial airway smooth muscle (ASMC) area in COPD is associated to ICS responsiveness.In this investigator-initiated and –driven, double-blind, randomised, placebo-controlled trial (HISTORIC), 190 COPD patients, GOLD stage B-D, underwent bronchoscopy with endobronchial biopsy. Patients divided in groups A and B with high ASMC area (HASMC: >20% of the bronchial tissue area) and with low ASMC area (LASMC: ≤20% of the bronchial tissue area), respectively and followed a run-in period of 6 weeks on open-label triple inhaled therapy with aclidinium/formoterol/budesonide (ACL/FOR/BUD:400/12/400 mcg/bid). Subsequently, patients were randomised to receive either ACL/FOR/BUD or ACL/FOR/Placebo and followed for 12 months. The primary end point of the study was the difference in post-bronchodilator FEV1over 12 months between patients with LASMC and HASMC receiving or not receiving ICS.In patients with LASMC, ACL/FOR/BUD did not significantly improve FEV1over 12 months, as compared to ACL/FOR/placebo p=0.675. In patients with HASMC, however, ACL/FOR/BUD significantly improved FEV1, as compared to ACL/FOR/placebo p=0.020. Over 12 months, the difference of FEV1change between the group of ACL/FOR/BUD and the group of ACL/FOR/placebo was 50.6 mL·year−1within the group of patients with LASMC and 183.0 mL·year−1within the group of patients with HASMC.COPD patients with ΗASMC respond better to ICS than patients with LASMC, suggesting that this type of histological analysis may predict ICS responsiveness in COPD patients receiving triple therapy.

Pulmonary infections are common complications in immunocompromised patients and are associated with high morbidity and mortality. Differentiating between infectious and noninfectious complications remains challenging. [1][2][3] BAL in critically ill patients often occurs following initiation of antibiotics, hampering the TABLE 1 ] Demographic Characteristics of 522 Immunocompromised Patients Undergoing BAL for Suspicion of Pneumonia Characteristic Value Age, y 57.63 AE 14.73 Male sex 306 (58.6) Hospitalization (IQR), d 11 (3; 25) Symptoms and signs Cough 300 (57.5) Dyspnea 124 (23.8) Sputum 118 (22.6) Fever 108 (20.7) Decrease in FEV 1 % predicted 59 (11.3) Reasons for immunosuppression a Allogenic HSCT 112 (21.5) Lung transplantation 83 (15.9) Other hematologic therapies 79 (15.1) Interstitial lung disease 59 (11.3) Connective tissue disease 52 (10.0) Chemotherapy 37 (7.1

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