68 Ga-DOTA-FAPI-04 is a promising PET agent for tumor imaging. However, inflammatory lesions can also show increased FAPI uptake. Herein, we reported a 52-year-old woman who underwent total thyroidectomy for thyroid papillary carcinoma 1 year ago and underwent adjuvant radioiodine therapy 1 month later. After 131 I therapy, she began to develop pain and swelling in bilateral cheeks, which developed into oral dryness. The patient was diagnosed with radioactive iodine-induced parotitis. 68 Ga-DOTA-FAPI-04 PET/CT showed the density of bilateral parotid glands increased, and the volume decreased with intense tracer uptake. 99m TcO 4 − salivary gland scintigraphy showed decreased tracer uptake in the bilateral parotid glands.

Background. The offspring of pregnant women with gestational diabetes mellitus (GDM) are vulnerable to be glucometabolic disorders. However, to date, few current studies focused on the associations of maternal accumulated glucose exposure before delivery with neonatal glucometabolic disorders and large for gestational age (LGA) infants. This study is aimed at exploring the associations of maternal fructosamine (FMN) before delivery in GDM pregnant women with neonatal glucometabolic disorders in the first 3 days of life and LGA infants. Methods. The study subjects were the GDM pregnant women, who gave birth in our hospital from September 1, 2018 to January 31, 2021, and their newborns. The maternal FMN adjusted by serum albumin (FMNALB) before delivery was selected as exposure factors. A multivariate logistical regression model was used to calculate the odds ratios (OR) for neonatal glucometabolic disorders, hypoglycemia needing intervention (<2.6 mmol/L), and glucose intolerance (>7.0 mmol/L) in the first 3 days and LGA infants. Results. In GDM pregnant women, the newborns in the maternal FM N ALB ≥ 75 th   percentile (≥5.89 mmol/g) group had higher risks in neonatal glucometabolic disorders (aOR 2.50, 95% CI 1.34-4.65, P = 0.004 ) and hypoglycemia (aOR 2.18, 95% CI 1.16-4.10, P = 0.016 ). However, FM N ALB ≥ 75 th   percentile seemed to be not predictive of the glucose intolerance (aOR 1.76, 95% CI 0.82-3.79, P = 0.149 ) and LGA (aOR 1.56, 95% CI 0.81-3.02, P = 0.185 ). Further, in the sensitivity analysis, the newborns in the maternal FM N ALB ≥ 90 th   percentile (≥6.40 mmol/g) group also had higher risks in neonatal glucometabolic disorders (aOR 5.70, 95% CI 2.18-14.89, P < 0.001 ) and hypoglycemia (aOR 3.72, 95% CI 1.48-9.31, P = 0.005 ). Conclusions. The maternal FMNALB before delivery in GDM pregnant women was a useful biomarker to identify the offspring with high risk of neonatal glucometabolic disorders. However, the association between maternal FMNALB and the risk of LGA infants was not so strong.

Acute respiratory distress syndrome (ARDS) is an acute respiratory failure syndrome caused by non-cardiogenic pulmonary edema of various etiologies.[1](#ref-0001) When the fetus encounters asphyxia, acidosis, infection, meconium inhalation, et al. during childbirth, the inflammatory pathway will be activated. The systemic inflammatory response can remove pathogens, but the excessive inflammatory response will prompt pulmonary surfactant (PS) inactivation and increase the permeabilities of alveolar epithelial and endothelial cells, resulting in the accumulation of edema fluid in the alveoli and eventually leading to severe hypoxemia, respiratory distress and decreased lung compliance.[1,2](#ref-0001) Population-based studies in the United States, Australia, Europe, and New Zealand reported that the incidence of ARDS in children is 2.0-12.8 per 100000 person-years,[3](#ref-0003) and according to the interim report of the International Neonatal ARDS Multicenter Study, the mortality of neonatal ARDS (NARDS) is approximately 20%.[4](#ref-0004) Due to the high mortality of NARDS, the researchers try to explore potential new treatments to limit the incidence and mortality of NARDS. Systemic inflammatory response plays a significant role in the occurrence and development of NARDS, budesonide, a non-halogenated corticosteroid, has a potent local pulmonary anti-inflammatory effect, therefore, it may be an effective treatment option for NARDS. This article reviews the evolution of ARDS definition and diagnosis, pathophysiological mechanisms of NARDS, and gives an outlook on the application of budesonide in NARDS.