Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin–angiotensin–aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Additionally, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

The purpose of this study is to define the impact of early brain growth trajectory in very low birth weight infants (VLBWI) on neurological prognosis at 2 years, assessed using sequential ultrasound (US) scans. This is a prospective cohort study with consecutive inclusion of VLBWI ≤ 32 weeks gestational age and ≤ 1500 g at birth. Total brain volume (TBV) was assessed using sequential 3D-US from birth to discharge. Prognosis at 2 years (corrected age) was assessed using the Bayley Scales of Infant and Toddler Development Third Edition. TBV showed slower growth with postmenstrual age (PMA) in those VLBWI who had an adverse cognitive prognosis compared to those with good cognitive prognosis (mean difference in TBV between prognostic groups from 4.56 cm³ at 28 weeks to 42.58 cm³ at 43 weeks) as well as in those with adverse language prognosis (mean difference in TBV from 2.21 cm³ at 28 weeks to 26.98 cm³ at 43 weeks) although other variables showed more impact than TBV on language prognosis (gestational age at birth, brain injury at term, and socioeconomic status). No association was found between TBV and motor prognosis. Brain growth rate was also significantly higher in those VLBWI who presented good cognitive scores (18.78 + (0.33 × (PMA-33)) cm³/week) compared to those with adverse cognitive outcome (13.73 + (0.64 × (PMA-33)) cm³/week).  Conclusion: Early altered brain growth is associated with poor cognitive prognosis at 2 years of age. Using sequential US monitoring, we can detect early brain growth deviation in patients who will have adverse cognitive outcomes. What is known:• The prediction of neurodevelopmental outcome of VLBWI is mostly based on the presence of brain injury in US and structural magnetic resonance imaging (MRI) at term. • Some studies have related brain volume measured on MRI at term with neurodevelopment outcome. What is new:• VLBWI with adverse cognitive prognosis at two years of age present smaller brain volumes detectable by sequential US during NICU admission.• Brain volume can be estimated from 2D and 3D US and has prognostic value in VLBWI.

Glycemic control in very-low-birth-weight preterm infants is challenging due to the immaturity of glucose homeostasis during the early postnatal period. The first two weeks of life represent a critical window of metabolic adaptation, characterized by high variability and gradual stabilization of glucose levels; continuous monitoring during this period is therefore essential to capture clinically relevant trends. We aimed to describe daily glucose patterns and variability during the first 14 days and to generate gestational-age–specific reference percentiles for clinically stable preterm infants. A prospective observational study was conducted in a tertiary neonatal intensive care unit (2021–2024), with continuous glucose monitoring during the first 14 days of life. Of 203 eligible infants, 103 clinically stable preterm infants without major comorbidities were included and classified into three gestational age groups (24–26, 27–29, and 30–32 weeks). The median number of glucose readings per infant was 2,557 [1,681–2,959]. Mean glucose concentrations declined over the first two weeks in all groups, with the largest decrease during the initial 72 hours. Infants born at 24–26 weeks had higher mean glucose on day 1 (156.5 ± 47.2 mg/dL) and day 14 (121.4 ± 21.8 mg/dL), and greater variability than those born at 27–29 and 30–32 weeks. Reference percentiles reflected these differences: on day 1, the fifth to ninety-fifth percentiles were 92–245 mg/dL for 24–26 weeks, 65–168 mg/dL for 27–29 weeks, and 67–148 mg/dL for 30–32 weeks; by day 14, they were 73–185, 67–150, and 58–136 mg/dL, respectively.In summary, glucose concentrations and variability decreased with postnatal age, and the least mature infants exhibited higher and more variable values. These gestational-age–specific reference percentiles, derived from continuous monitoring may support individualized glucose management in neonatal intensive care.

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin-angiotensin-aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Also, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.