Molecular and cellular pediatrics最新文献

{"title":"Red blood cell transfusion is not associated with lymphocyte subpopulation counts in very low birthweight infants.","authors":"Niclas Oßmann, Mats Ingmar Fortmann, Kirstin Faust, Julia Pagel, Martin Demmert, Christoph Härtel, Alexander Humberg","doi":"10.1186/s40348-026-00266-9","DOIUrl":"10.1186/s40348-026-00266-9","url":null,"abstract":"<p><strong>Background: </strong>Very low birthweight (VLBW) infants frequently require red blood cell (RBC) transfusions. Transfusions may modulate immune responses, but their impact on immune development remains incompletely understood.</p><p><strong>Methods: </strong>120 VLBW infants participating in the prospective \"Immune Regulation of the Newborn Study\" (IRON study) were analyzed during the first 42 postnatal days with serial immune phenotyping. Infants were stratified by RBC transfusion exposure. Determinations were assigned to six nominal time points by their actual day of life. Associations were estimated with linear mixed models with a random intercept per infant, with exposure defined both as ever transfused and as the number of red blood cell (RBC) units received before the respective measurement and corrected by the Benjamini-Hochberg procedure. A falsification analysis modelled exposure occurring only after the measurement.</p><p><strong>Results: </strong>23 of 120 infants received at least one RBC unit within the first 42 days. Transfused infants were more premature, smaller, more anemic and had higher morbidity. RBC transfusion was not significantly associated with alterations in leukocyte subpopulations (e.g. CD8 + T-cell counts (β = -0.161, 95% CI - 0.359 to 0.036, p = 0.11)). No subpopulation reached significance after correction for multiple comparisons. Transfusion occurring only after the measurement gave a coefficient of larger magnitude (β = -0.137) than actual exposure.</p><p><strong>Conclusions: </strong>RBC transfusion exposure during the first six postnatal weeks was not associated with the counts of any lymphocyte subpopulation examined. The falsification analysis indicates that residual differences reflect the condition of infants selected for transfusion rather than an effect of transfusion.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149208303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acquired hypothalamic obesity as α-MSH deficiency syndrome: a paradigm shift with therapeutic impact.","authors":"Martin Wabitsch, Kim Ulrich, Christian Denzer","doi":"10.1186/s40348-026-00260-1","DOIUrl":"10.1186/s40348-026-00260-1","url":null,"abstract":"<p><p>Recent findings by Miller et al. ( https://doi.org/10.1056/NEJMoa2512275 ) suggest a fundamental shift in the understanding of acquired hypothalamic obesity (aHO), proposing that this condition should be viewed as an α-melanocyte-stimulating hormone (α-MSH) deficiency syndrome. Building on these observations, we discuss the proposed underlying pathophysiological mechanisms and argue that aHO can be conceptualized as an injury-induced loss of melanocortin tone, analogous to an α-MSH deficiency. The marked clinical response to setmelanotide in affected individuals indicates that downstream melanocortin-4 receptor (MC4R)-dependent pathways remain functionally intact, supporting the concept of a hormone deficiency-like state. We further explore the implications of this paradigm change, highlighting how this new framework may fundamentally change the diagnosis and management of patients with aHO.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal Stem Cell (MSC)-based therapies for neonatal lung and brain injury - one size fits all?","authors":"U Felderhoff-Müser, J Herz, I Bendix, J Behnke, Y Dong, H Ehrhardt","doi":"10.1186/s40348-026-00262-z","DOIUrl":"10.1186/s40348-026-00262-z","url":null,"abstract":"<p><p>MSC-based therapies have emerged as a highly promising approach for two of the most devastating consequences of perinatal insults such as extreme prematurity and perinatal asphyxia: bronchopulmonary dysplasia (BPD) and neonatal brain injury. Both conditions share a common pathophysiological basis of inflammation, oxidative stress, and disrupted progenitor cell function in critical windows of organ development. Exogenous MSC act primarily through their secretome, releasing extracellular vesicles, growth factors, and immunomodulatory mediators that attenuate injury and support organ development. Despite compelling preclinical evidence and early clinical feasibility and safety data, neither indication has yet achieved definitive proof of therapeutic efficacy in adequately powered randomised trials. This review summarises the current state of knowledge for MSC-based therapies for neonatal chronic lung disease and subsequently for brain injury, highlighting shared mechanisms, organ-specific considerations, and the path towards clinical implementation.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Durable treatment response to Trastuzumab deruxtecan in two patients with recurrent grade III anaplastic ependymoma.","authors":"Dietmar Krex, Irina A Kerle, Arne Grey, Stephanie Pleißner, Stephan Richter, Christoph Heining, Stefan Fröhling, Hanno Glimm, Martin Bornhäuser, Gunnar Folprecht, Andy Göbel, Cornelia S Link-Rachner","doi":"10.1186/s40348-026-00263-y","DOIUrl":"10.1186/s40348-026-00263-y","url":null,"abstract":"<p><strong>Background: </strong>Anaplastic ependymoma is a rare and aggressive central nervous system malignancy for which effective systemic treatment options are limited. Trastuzumab deruxtecan (T-DXd), an antibody-drug conjugate targeting human epidermal growth factor receptor 2 (HER2), has demonstrated intracranial activity in patients with HER2-positive solid tumors. We report two patients with recurrent, heavily pretreated anaplastic ependymoma and molecular evidence of HER2 activation who received T-DXd as off-label therapy.</p><p><strong>Methods: </strong>Both patients underwent comprehensive molecular profiling, including whole-genome and transcriptome sequencing and proteomic analyses. HER2 expression was subsequently assessed by immunohistochemistry. Treatment response was evaluated by serial magnetic resonance imaging (MRI), while clinical benefit and treatment-related toxicities were documented longitudinally.</p><p><strong>Results: </strong>Both patients had multiply recurrent anaplastic ependymoma and had exhausted conventional local and systemic treatment options. Molecular profiling identified elevated ERBB2 expression at the transcriptomic and/or proteomic level, with HER2 immunohistochemical positivity in approximately 80% and 15% of tumor cells, respectively. The first patient received T-DXd and achieved sustained disease stabilization after an initial mixed radiographic response, with ongoing disease control for 26 months. The second patient initially received temozolomide plus lapatinib but experienced progressive disease. Following treatment with T-DXd disease stabilization was achieved and maintained for 14 months at the most recent follow-up. Treatment-related hematologic and hepatic toxicities were manageable with supportive measures, dose modification, and temporary treatment interruption.</p><p><strong>Conclusions: </strong>These two cases demonstrate durable disease stabilization with T-DXd in heavily pretreated patients with recurrent anaplastic ependymoma and molecular evidence of HER2 activation. The clinical benefit observed, including after failure of lapatinib-based HER2-targeted therapy, supports further investigation of T-DXd in molecularly selected patients with recurrent ependymoma. Comprehensive molecular profiling may help identify patients who could benefit from HER2-directed treatment in this rare and therapeutically challenging disease.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Menin inhibition in pediatric UBTF-TD myelodysplastic syndrome: molecular rationale and clinical observation.","authors":"Franziska Rummel, Tabea Blessing, Triantafyllia Brozou, Sujal Ghosh, Roland Meisel, Maximilian Seidl, Arndt Borkhardt","doi":"10.1186/s40348-026-00264-x","DOIUrl":"10.1186/s40348-026-00264-x","url":null,"abstract":"<p><strong>Background: </strong>UBTF tandem duplications (UBTF-TD) define a recently recognized high-risk subtype of pediatric myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). UBTF-TD myeloid neoplasms are driven by a HOX/MEIS1 transcriptional program that depends on the interaction between menin and KMT2A. Preclinical studies have shown sensitivity to menin inhibition, but clinical experience in children with MDS remains scarce.</p><p><strong>Results: </strong>We report a ten-year-old girl with MDS with excess blasts harboring UBTF-TD together with NRAS and WT1 mutations. During the first cycle of azacitidine and venetoclax, blood counts did not improve, and the patient remained dependent on platelet and red blood cell transfusions. Revumenib was added to the ongoing treatment. Within two weeks, platelet counts and hemoglobin increased markedly, the patient became transfusion independent, and bone marrow blasts cleared. UBTF-TD also became undetectable by molecular testing. The patient subsequently underwent allogeneic hematopoietic stem cell transplantation and remains in complete remission with full donor chimerism one year after transplantation.</p><p><strong>Conclusions: </strong>The rapid hematologic recovery and clearance of both bone marrow blasts and detectable UBTF-TD after initiation of revumenib provide clinical evidence that the menin dependency of UBTF-TD myeloid neoplasms can be therapeutically exploited. The timing and depth of the clinical and molecular response were remarkable.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The lung microbiome in childhood-onset severe neuromuscular disease with respiratory insufficiency: rationale, current evidence, and opportunities for oxford nanopore long-read sequencing.","authors":"Sebahattin Cirak, Vivien Grieshaber, Philip Müller, Cho-Ming Chao","doi":"10.1186/s40348-026-00261-0","DOIUrl":"10.1186/s40348-026-00261-0","url":null,"abstract":"<p><p>In severe childhood-onset neuromuscular disease (NMD), ventilatory muscle weakness and ineffective airway clearance drive recurrent infections and chronic colonization that is often culture-negative, polymicrobial, or both. The lung microbiome framework offers a unifying model: altered microbial immigration, elimination, and growth can produce dysbiosis with pathobiont expansion and antimicrobial resistance (AMR). We propose that pediatric NMD may follow a distinct developmental trajectory in which early-life secretion stasis, viral insults, and frequent antibiotics perturb immune-microbiome crosstalk during lung growth, potentially \"imprinting\" long-term community structure. However, NMD-specific airway microbiome data remain sparse because most studies rely on culture or upper-airway sampling. Oxford Nanopore Technologies (ONT) long-read sequencing enables real-time metagenomics with AMR gene detection and can deliver same-day profiles (as short as ~ 6 h from sample to result in optimized workflows), but requires robust low-biomass controls and, in some settings, polishing or hybrid strategies to mitigate higher per-read error. A major limitation of metagenomic sequencing of respiratory samples is the high proportion of host DNA, bacterial reads may account for only about 1-5% of the total sequencing reads. We review microbiome principles relevant to pediatric NMD, summarize current evidence, and outline ONT-enabled study designs and translational priorities.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal metformin treatment in obese pregnant dams normalizes neonatal sensory-motor reflexes.","authors":"Elena Müller-Limberger, Bettina Frederick, Sebastian Hansen, Maria Wohlfarth, Ruth Janoschek, Esther Mahabir, Pascal Fischer, Dirk Gründemann, Simone Kalis, Miguel A Alejandre Alcázar, Jörg Dötsch, Eva Hucklenbruch-Rother, Sarah Appel","doi":"10.1186/s40348-026-00259-8","DOIUrl":"10.1186/s40348-026-00259-8","url":null,"abstract":"<p><strong>Background: </strong>Maternal overweight and obesity have reached epidemic proportions over recent decades, with detrimental effects on offspring metabolism and neurodevelopment. Metformin, commonly used to treat type 2 diabetes mellitus and gestational diabetes, is being investigated for use in maternal obesity due to its weight-loss-promoting, glucose-lowering, and insulin-sensitizing effects. Metformin may improve maternal metabolic state and support early sensory-motor development in offspring.</p><p><strong>Methods: </strong>Three-week-old female C57BL/6NCrl mice were fed either a standard diet (SD, 9 kJ% fat, low sucrose content; CO group) or a Western-style diet (WSD, 45 kJ% fat, high sucrose content; OB group) from weaning through mating, gestation, and lactation. A subgroup of pregnant WSD-fed mice received metformin hydrochloride (target dose 380 mg/kg/d; OB + M group), dissolved in drinking water during gestation. At mid-gestation, a small cohort of pregnant dams was assessed for their metabolic profile. After delivery, pups were culled to six per litter at postnatal day (P) 2, and reflex ontogeny - such as righting, negative geotactic, and cliff-avoidance responses - was evaluated until P9 as a measure of early neurodevelopment.</p><p><strong>Results: </strong>Feeding a WSD resulted in approximately 20% heavier dams in the OB group by the time of mating. Metformin administration led to gestational weight gain of about 56%, compared to OB weight gain of approximately 64%. Plasma leptin levels, perigonadal white adipose tissue, fasting glucose, and HbA1c in OB + M dams were numerically intermediate between OB and CO at mid-gestation, without reaching statistical significance, while glucose tolerance remained impaired to a similar extent as in OB dams. Metformin reduced placental weight in female fetuses and increased the fetal-to-placental weight ratio compared with the CO group. Metformin had no effect on neonatal survival but accelerated postnatal weight gain in both sexes and improved sensory-motor reflex maturation compared to OB neonates, most consistently for the geotactic reflex in both sexes and the cliff avoidance reflex in females.</p><p><strong>Conclusions: </strong>Metformin did not restore maternal metabolic parameters at mid-gestation, despite the numerically intermediate phenotype across several markers, but it significantly attenuated gestational weight gain. Although neonatal survival was not improved, gestational metformin was associated with accelerated postnatal weight gain and improved sensory-motor reflex maturation in offspring, though effects varied across reflex types. Accelerated postnatal weight gain warrants cautious interpretation and long-term follow-up, as it is a risk factor for childhood obesity and metabolic disorders in later life.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13582716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breastfeeding type is associated with urinary metabolic changes in early life: influence of sex and early weight gain in healthy term infants.","authors":"Pere Bibiloni, Jean-Charles Martin, Pilar Cobo, María De Lucas, María Victoria Jiménez-Cabanillas, Catherine Tardivel, Catalina Picó, Francisca Serra, Juana Sánchez","doi":"10.1186/s40348-026-00258-9","DOIUrl":"10.1186/s40348-026-00258-9","url":null,"abstract":"<p><strong>Background: </strong>Perinatal factors are key modulators of neonatal metabolism and may contribute to long-term health trajectories. However, the metabolic adaptations underlying these early-life influences remain poorly characterized. In this study, we comprehensively characterized neonatal urinary metabolic profiles associated with multiple perinatal factors in full-term, healthy, breastfed infants at one month of age.</p><p><strong>Methods: </strong>Ninety-six urine samples from full-term, healthy, breastfed infants at one month of age were analyzed using liquid chromatography-mass spectrometry (LC-MS) and nuclear magnetic resonance (NMR). Exploratory multivariate analyses identified the maternal and infant factors most strongly associated with urinary metabolic variation, followed by multiblock integration to characterize the biological functions associated with the identified metabolic signatures.</p><p><strong>Results: </strong>Breastfeeding type (exclusive, n = 79; mixed, n = 17) emerged as the factor most associated with urinary metabolic variability and was associated with differences in metabolites related to carbohydrate and lipid metabolism, gut microbiota, oxidative status, and vitamin handling, among others. Infant sex was also associated with metabolic differences, particularly affecting steroid metabolism, amino acid profiles, and mitochondrial-related compounds. In addition, weight gain during the first month of life was associated with variation in metabolites related to amino acid metabolism, gut-microbiota and antioxidant pathways.</p><p><strong>Conclusions: </strong>Urinary metabolomics revealed distinct metabolic signatures associated with early-life exposures. Among the factors studied, breastfeeding type (mixed vs. exclusive) was associated with the most pronounced differences in the urinary metabolome. These findings highlight the potential of urinary metabolomics for investigating early-life metabolic adaptations and provide a basis for future studies exploring the relationship between infant feeding and metabolic programming.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13578156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148978437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of preterm birth and gestational diabetes on innate lymphoid cells (ILCs) in human breast milk.","authors":"Malgorzata Raché, Larissa Lükewille, Antje Vogelgesang, Anja Lange, Till Ittermann, Matthias Heckmann, Johanna Ruhnau","doi":"10.1186/s40348-026-00255-y","DOIUrl":"10.1186/s40348-026-00255-y","url":null,"abstract":"<p><strong>Background: </strong>Breastfeeding provides key immunological and metabolic benefits for newborns, reducing complications of preterm birth and long-term risks associated with maternal gestational diabetes mellitus (GDM). However, the mechanisms underlying these protective effects, particularly the role of maternal immune cells in breast milk, remain incompletely understood. This study aimed to investigate how preterm birth and GDM influence the composition of breast milk-derived innate lymphoid cells (ILCs) during early lactation and to explore whether these maternal cells affect neonatal immune characteristics in vitro using cord blood T cells as a model system.</p><p><strong>Results: </strong>Breast milk samples (colostrum and transitional milk) were collected within the first two weeks postpartum from mothers of term and preterm infants. Flow cytometric analysis revealed that total ILC frequencies decreased over time, with no significant differences between term and preterm deliveries. Colostrum from GDM mothers, however, contained significantly higher ILC frequencies compared with samples from normoglycemic controls, indicating that maternal metabolic status alters the immunological composition of breast milk. Cord blood T cells from GDM pregnancies showed elevated expression of the sphingosine-1-phosphate receptor 1 (S1PR1), suggesting an enhanced migratory phenotype. Co-culture experiments with breast milk-derived ILCs did not further increase S1PR1 expression or modify T cell activation markers (CD25, CD69, CTLA-4, PD-1). We emphasize that all functional assays were conducted in vitro using coculture systems with umbilical cord blood cells and were not performed directly on newborns.</p><p><strong>Conclusions: </strong>Maternal GDM modifies the composition of breast milk-derived ILCs and is associated with altered receptor expression on neonatal cord blood T cells. Nevertheless, in vitro exposure to breast milk ILCs did not enhance T cell activation, suggesting that breastfeeding may help maintain neonatal immune balance despite maternal metabolic stress. These results highlight a potential regulatory role of breast milk immune cells at the maternal-infant interface and underscore the importance of breastfeeding in mitigating pro-inflammatory programming in infants of GDM mothers.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148876909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pediatric intensive care follow-up in Germany is rarely established and highly heterogeneous: a nationwide survey of 20 PICUs.","authors":"Sarah C Goretzki, Richard Biedermann, Sebastian Brenner, Anna Daniels, Christian Dohna-Schwake, Kai Fiedler, Ingmar Fortmann, Hans Fuchs, Stefanie Giese, Konrad Heimann, Christoph Härtel, Stefanie Hort, Sarah Irlbeck, Sarah Lampe, Victoria Lieftüchter, Katja Masjosthusmann, Michael Merker, David Overberg, Irwin Reiss, Christiaan P Sentner, Janina Soler Wenglein, Ingeborg van den Heuvel, Anne Vierzig, Gert Warncke, Jens H Westhoff, Nadine Mand, Nora Bruns","doi":"10.1186/s40348-026-00257-w","DOIUrl":"10.1186/s40348-026-00257-w","url":null,"abstract":"<p><strong>Background: </strong>Survival after pediatric critical illness has improved substantially, but many survivors and their families experience long-term physical, neurocognitive, psychological and social sequelae, summarized as post-intensive care syndrome in pediatrics and in families. Structured follow-up care after discharge from a pediatric intensive care unit (PICU) is considered essential, yet its implementation in Germany has not been described systematically. We therefore assessed the current structures, organizational forms and barriers of PICU follow-up care in Germany.</p><p><strong>Methods: </strong>A structural survey was conducted among 20 German PICUs collaborating within the Section of Pediatric Intensive Care and Emergency Medicine of the German Interdisciplinary Association of Intensive Care and Emergency Medicine and the Pediatric Intensive Care Unit Admissions Network. One representative per center reported basic unit characteristics, the availability and organization of follow-up services, the disciplines and components involved, the timing of assessments, and perceived barriers to implementation.</p><p><strong>Results: </strong>Nineteen of the 20 participating centers were university hospitals. Structured follow-up care was established in four centers (20%) and planned in seven (35%). Follow-up relied largely on existing ambulatory structures, most frequently social pediatric centers and academic outpatient clinics, and was led by pediatric intensive care specialists in most centers. A core set of disciplines was involved in nearly all programs, while the broader team composition, the components of care and the timing of assessments varied considerably; most consultations took place within four months after discharge, without predefined later timepoints. 90% of centers rated the need for structured follow-up as high or very high. The most frequent barriers were lack of personnel, logistic challenges, lack of financing and limited therapeutic capacities.</p><p><strong>Conclusions: </strong>Structured PICU follow-up care in Germany is rarely established and highly heterogeneous, despite a uniformly high perceived need. Nationwide minimum standards linked to a harmonized outcome set, interdisciplinary coordination and sustainable financing are required to translate this need into routine care.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":"13 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13522329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148842420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}