Azoicai Alice Nicoleta, Lupu Ancuta, Trandafir Laura Mihaela, Alexoae Monica Mihaela, Alecsa Mirabela, Starcea Iuliana Magdalena, Cuciureanu Magdalena, Knieling Anton, Salaru Delia Lidia, Hanganu Elena, Mocanu Adriana, Lupu Vasile Valeriu, Ioniuc Ileana
Pediatrics, "Grigore T. Popa" University of Medicine and Pharmacy, Iasi, Romania.
Faculty of Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, Iasi, Romania.
Front Pediatr. 2024 May 10;12:1393193. doi: 10.3389/fped.2024.1393193. eCollection 2024.
Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). In 1949, it's been identified as a monogenic disease and was thought to primarily affect individuals of Northern European descent. It was the most prevalent autosomal recessive disease that shortens life. With the availability of multiple testing methodologies nowadays, there is a chance to create novel and enhanced treatment options. Even in the absence of a high sweat chloride test (SCT) result, the discovery of two causal mutations is diagnostic for cystic fibrosis (CF). For a CF diagnosis, however, at least two positive E sweat chloride tests are still required. In order to achieve early and active intervention to manage cystic fibrosis (CF) and its comorbidities, treatment regimens for pediatric patients should be evaluated, improved, and closely monitored. New developments in the treatment of cystic fibrosis (CF) have led to the development of medications derived from molecules that target the pathogenetic pathway of the illness. These options are very efficient and allow pediatric patients to receive individualized care. However, in order to better direct patient care and enhance patient outcomes, it is crucial to research uncommon CF mutations, which can provide crucial information about the prognosis of the disease and the relationships between genotype and phenotype. To ensure the success of creating novel, safer, and more efficient treatment approaches, a deeper understanding of the pathogeny of the illness is required. In the age of customized medicine, genetic research will be essential to improving patient care and quality of life for those with uncommon mutations.
囊性纤维化(CF)是一种常染色体隐性疾病,由编码囊性纤维化跨膜传导调节因子(CFTR)的基因突变引起。1949年,它被确定为一种单基因疾病,当时认为主要影响北欧血统的个体。它是缩短寿命的最常见的常染色体隐性疾病。如今有了多种检测方法,就有机会创造新的和更好的治疗方案。即使没有高汗液氯化物测试(SCT)结果,发现两个致病突变也可诊断为囊性纤维化(CF)。然而,对于CF诊断,仍至少需要两次汗液氯化物测试呈阳性。为了实现对囊性纤维化(CF)及其合并症的早期积极干预,应评估、改进并密切监测儿科患者的治疗方案。囊性纤维化(CF)治疗的新进展导致了从针对该疾病致病途径的分子衍生而来的药物的开发。这些选择非常有效,使儿科患者能够接受个性化护理。然而,为了更好地指导患者护理并改善患者预后,研究罕见的CF突变至关重要,这可以提供有关疾病预后以及基因型与表型之间关系的关键信息。为确保创造新的、更安全和更有效的治疗方法取得成功,需要更深入地了解该疾病的发病机制。在个性化医疗时代,基因研究对于改善罕见突变患者的护理和生活质量至关重要。