Journal of Clinical Research in Pediatric Endocrinology最新文献

{"title":"A 13-Year-Old Girl with Congenital Hyperinsulinemic Hypoglycemia Due to an <i>ABCC8</i> Mutation and Recent Onset of Diabetes Mellitus: A Case Report and Literature Review.","authors":"Aikaterini Kantzavelou, Ekaterini Siomou, Anny Mertzanian, Amalia Sertedaki, Christina Kanaka-Gantenbein, Stelios Tigas, Anastasios Serbis","doi":"10.4274/jcrpe.galenos.2026.2025-10-21","DOIUrl":"https://doi.org/10.4274/jcrpe.galenos.2026.2025-10-21","url":null,"abstract":"<p><p>Congenital hyperinsulinism (HI) is the most prevalent cause of persistent hypoglycemia in infancy and childhood and comprises a heterogeneous group of genetic disorders affecting insulin secretion. The most common etiology involves inactivating mutations in the <i>ABCC8</i> and <i>KCNJ11</i> genes, which encode the SUR1 and Kir6.2 subunits of the pancreatic β-cell ATP-sensitive potassium (KATP) channel. Variants in these genes are associated with a broad phenotypic spectrum, ranging from asymptomatic macrosomia and mild diazoxide-responsive disease to severe, persistent hyperinsulinemic hypoglycemia unresponsive to medical therapy. In some individuals, the clinical course may evolve over time, with progression from early hyperinsulinism to impaired glucose regulation and eventual diabetes mellitus. We describe a 13-year-old girl with diazoxide-unresponsive congenital hyperinsulinism caused by a heterozygous de novo <i>ABCC8</i> variant (c.2147G>A, p.Gly716Asp) who later developed insulin-deficient diabetes mellitus. She was treated with octreotide from 2 months until 7 years of age, when therapy was discontinued after gradual remission of hypoglycemia. At 11 years, evaluation revealed impaired fasting glucose and impaired glucose tolerance, and glibenclamide was initiated. After being lost to follow-up, she presented at 13 years with hyperglycemia and was diagnosed with antibody-negative, insulin-deficient diabetes mellitus. Basal insulin therapy led to progressive normalization of glycemic levels. To our knowledge, this is the first report linking the <i>ABCC8</i> p.Gly716Asp variant to transition from congenital hyperinsulinism to adolescent-onset diabetes, underscoring the phenotypic continuum of ABCC8-related disorders and the necessity for lifelong metabolic surveillance.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147677323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early-Onset Multiple Necrobiosis Lipoidica in a Child with Type 1 Diabetes Mellitus.","authors":"Emel Gül Açıkgöz, Özge Yanık, Şeyma Koca, Tuğba Kontbay Çetin, Gökhan Şahin","doi":"10.4274/jcrpe.galenos.2026.2026-1-1","DOIUrl":"https://doi.org/10.4274/jcrpe.galenos.2026.2026-1-1","url":null,"abstract":"<p><p>Necrobiosis lipoidica is uncommon in childhood, and a multifocal presentation early in the course of type 1 diabetes mellitus appears to be infrequently reported. In our patient, multiple lesions developed within 3 years of diabetes diagnosis, despite the absence of overt microvascular complications. The persistence of lesions alongside recurrent episodes of ketoacidosis may suggest a potential association between suboptimal metabolic control and cutaneous microangiopathic changes; however, causality cannot be established on the basis of a single case. Early recognition of such lesions may be clinically relevant, as they may prompt careful metabolic evaluation and closer follow-up in affected children.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149070282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short Stature and Growth Hormone Deficiency in POMC Deficiency: An Unexpected Clinical Association.","authors":"Uğur Cem Yılmaz, Deniz Özalp Kızılay, Damla Gökşen, Samim Özen","doi":"10.4274/jcrpe.galenos.2026.2025-10-19","DOIUrl":"https://doi.org/10.4274/jcrpe.galenos.2026.2025-10-19","url":null,"abstract":"<p><p>Proopiomelanocortin (POMC) deficiency is a rare monogenic obesity syndrome typically characterized by early-onset obesity, red hair, and hypopigmentation, while linear growth is usually preserved. We report an adolescent girl with genetically confirmed POMC deficiency who developed short stature with biochemically confirmed growth hormone deficiency (GHD). She was diagnosed at 3.5 years of age with a homozygous c.64delA (p.Thr22Leufs*29) variant. Progressive growth deceleration became apparent after 12 years of age. At 13 years, her weight was 56.7 kg (+0.8 SDS), height was 143.0 cm (-2.5 SDS), and BMI was 27.1 kg/m² (+2.0 SDS). Growth velocity was 1.64 cm/year (-1.61 SDS), and pubertal stage was Tanner I. At 14 years of age, bone age was 10 years. IGF-1 was low at 82.8 µg/L (SDS: -2.28), and IGFBP-3 was 2.3 mg/L (SDS: -3.84). After euthyroidism had been achieved and estrogen priming had been completed, GH stimulation testing with L-DOPA and clonidine showed peak GH levels of 0.52 and 1.0 µg/L, respectively. Pituitary MRI was normal. Recombinant GH therapy (0.035 mg/kg/day) was initiated at 14 years 3 months. After 9 months, height increased to 150.2 cm (-1.95 SDS), BMI was 26.51 kg/m² (+1.79 SDS), and growth velocity improved to 11.29 cm/year, with no adverse events during follow-up. This case expands the clinical spectrum of POMC deficiency by demonstrating short stature with biochemically confirmed GHD and a notable early growth response to GH therapy. Further studies are needed to clarify the underlying mechanisms and to guide follow-up and management.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147475912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Late-Onset and Recurrent Agranulocytosis During Low-Dose Methimazole Therapy in an Adolescent with Graves' Disease.","authors":"Betül Demircan Coşkun, Şebnem Yılmaz, Balahan Bora, Ayhan Abacı, Ece Böber, Korcan Demir","doi":"10.4274/jcrpe.galenos.2026.2025-12-3","DOIUrl":"https://doi.org/10.4274/jcrpe.galenos.2026.2025-12-3","url":null,"abstract":"<p><p>Graves' disease (GD) is the most common cause of thyrotoxicosis in the pediatric population. Methimazole (MMI) is the first-line therapy; however, it may rarely cause agranulocytosis, a potentially life-threatening adverse effect. Recurrent or delayed-onset agranulocytosis presents diagnostic and therapeutic challenges due to the scarcity of reported cases. This report aims to describe a pediatric case with recurrent MMI-induced agranulocytosis and to discuss potential mechanisms and management strategies. We describe a 16-year-old female with GD who developed recurrent MMI-induced agranulocytosis. The initial episode was identified during routine monitoring at the 16th month of treatment, in the absence of clinical signs of infection. MMI was promptly discontinued, and infection precautions were implemented. Treatment with granulocyte colony-stimulating factor (G-CSF) led to rapid neutrophil recovery. However, intermittent neutropenia recurred, requiring repeated G-CSF administration. Despite persistent thyroid-stimulating immunoglobulin (TSI) positivity, the patient remained euthyroid and did not require further antithyroid therapy during 20 months of follow-up. Autoimmune serology revealed positive antinuclear antibody (ANA) and anti-centromere protein B (anti-CENP-B) antibodies, while bone marrow and genetic analyses were unremarkable. This case illustrates the complex and variable course of methimazole-induced agranulocytosis in pediatric GD. Recurrent neutropenia may occur even after initial resolution, emphasizing the need for individualized management. Persistent TSI positivity alone may not necessarily reflect ongoing disease activity or justify continued antithyroid therapy.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147469748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Obesity and Overweight with Early Puberty in Boys: A Meta Analysis","authors":"Xiou Wang, Yi Song, Ziqin Liu","doi":"10.4274/jcrpe.galenos.2025.2025-4-8","DOIUrl":"10.4274/jcrpe.galenos.2025.2025-4-8","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the published associations between obesity, overweight, and central obesity and the risk of early puberty in boys.</p><p><strong>Methods: </strong>A comprehensive systematic search was conducted in accordance with PRISMA guidelines using the Web of Science and PubMed databases up to December 31, 2024. Study quality was assessed using the Newcastle-Ottawa Scale. Statistical analyses were performed using R software (version 4.4.2), with odds ratios (ORs) and 95% confidence intervals (CIs) calculated.</p><p><strong>Results: </strong>A total of 15,452 studies were initially identified, of which six high-quality studies (n=64,485) met the inclusion criteria after screening. The analysis found that obesity [defined by body mass index (BMI)] was significantly associated with an increased risk of testicular enlargement (OR=1.27, 95% CI: 1.19-1.36). Overweight also increased the risk of testicular enlargement (OR=1.20, 95% CI: 1.11-1.29). Obesity was significantly associated with an increased risk of pubarche (OR=1.37, 95% CI: 1.23-1.53). Funnel plots and sensitivity analyses indicated no significant publication bias, and the results remained robust.</p><p><strong>Conclusion: </strong>This study demonstrated that obesity and overweight are reported to be associated with an increased risk of early puberty in boys. Childhood obesity appears to be an important determinant of earlier pubertal onset, though the relationship may follow a non-linear pattern at extreme BMI levels. The potential implications for adult reproductive health warrant further investigation.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"58-65"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144754938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic Value of Peak-to-Basal Difference or Ratio of Growth Hormone in Children with Growth Hormone Deficiency","authors":"Özge Köprülü, Elif Gökçe Basa, İbrahim Mert Erbaş, Fatma Yavuzyılmaz Şimşek, Özlem Nalbantoğlu, Hüseyin Anıl Korkmaz, Behzat Özkan","doi":"10.4274/jcrpe.galenos.2025.2025-10-26","DOIUrl":"10.4274/jcrpe.galenos.2025.2025-10-26","url":null,"abstract":"<p><strong>Objective: </strong>Growth hormone (GH) deficiency (GHD) is a rare but important cause of short stature in children. Although GH stimulation tests remain the gold standard for diagnosis, establishing a definitive diagnosis continues to be challenging. Our aim was to evaluate the diagnostic performance of the peak-to-basal ratio and difference for identifying GHD in children.</p><p><strong>Methods: </strong>Patients with short stature who were evaluated for GHD with GH stimulation tests were retrospectively assessed. ΔGH was defined as the difference between peak and basal GH levels. The GH ratio was calculated as the ratio of peak to basal GH levels.</p><p><strong>Results: </strong>Data were collected from 265 patients (182 prepubertal) with a median age at presentation of 10.6 years (interquartile range: 6.13-12.42), of whom 46.7% were female. In total, 146 patients met the diagnostic criteria for GHD. ΔGH and GH ratio during the L-Dopa and Clonidine stimulation tests were significantly lower in the GHD group (p<0.001). A ΔGH cut-off of ≤7.08 in the clonidine test demonstrated excellent discriminative ability, with both sensitivity and specificity above 80%, and an area under the curve close to 0.9, suggesting that this parameter may may provide supportive diagnostic information for GHD.</p><p><strong>Conclusion: </strong>To the best of our knowledge, ΔGH has been explored only in a limited number of studies. This study investigated diagnostic accuracy of difference (ΔGH) or ratio of peak-to-basal GH on a large cohort of children with short stature. The supportive diagnostic performance observed in our cohort suggests that ΔGH is clinically useful in routine practice.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"138-144"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145858651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-World Experience from Türkiye: Genetic and Therapeutic Insights in Pediatric Heterozygous Familial Hypercholesterolemia","authors":"Havva Yazıcı, Esra Er, Fehime Erdem, Ayşe Yüksel Yanbolu, Sakina Mammadova, Sedef Alpdoğan, Merve Yoldaş Çelik, Yasemin Atik Altınok, Ebru Canda, Ayça Aykut, Haluk Akın, Sema Kalkan Uçar, Mahmut Çoker","doi":"10.4274/jcrpe.galenos.2025.2025-7-15","DOIUrl":"10.4274/jcrpe.galenos.2025.2025-7-15","url":null,"abstract":"<p><strong>Objective: </strong>Familial hypercholesterolemia (FH) is an inherited metabolic disorder that increases cardiovascular risk from childhood. Despite its frequency, pediatric diagnosis and treatment remain limited, particularly in developing countries.</p><p><strong>Methods: </strong>Retrospective analysis of pediatric patients with genetically confirmed heterozygous FH (HeFH). Genetic testing included sequencing of the genes <i>LDLR</i>, <i>APOB</i>, and <i>PCSK9</i>. Clinical features, treatment responses, statin use, and adverse events were assessed and a comparative analysis was conducted between different statin types.</p><p><strong>Results: </strong>Among the cohort of 124 patients only 28.2% of patients were diagnosed via routine lipid screening, though 90.3% had a positive family history. After diagnosis, 16.1% declined treatment and 41.1% were lost to follow-up. Most genetic diagnoses involved pathogenic <i>LDLR</i> variants; only a few cases involved APOB and PCSK9. Three novel <i>LDLR</i> variants were identified. Among treated patients, atorvastatin led to a greater median low density lipoprotein-cholesterol (LDL-C) reduction. A higher (though not statistically significant) proportion of pitavastatin users achieved LDL-C targets. LDL-C reduction was positively correlated with baseline LDL-C levels. For the majority of patients, statins were well tolerated; five patients had transient creatine kinase elevations that resolved with treatment interruption.</p><p><strong>Conclusion: </strong>This is the first large pediatric HeFH cohort study from Türkiye and provides data on both genetic background and treatment outcome. Despite genetic confirmation, significant gaps remain in early diagnosis, treatment acceptance, and long-term follow-up. Both atorvastatin and pitavastatin proved to be safe and effective. These results suggest a need for national screening programmes, family education, dietary counselling, and consistent follow-up.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"74-84"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine Implications of Congenital Disorders of Glycosylation","authors":"Yağmur Ünsal, Zeynep Alev Özön","doi":"10.4274/jcrpe.galenos.2025.2024-10-7","DOIUrl":"10.4274/jcrpe.galenos.2025.2024-10-7","url":null,"abstract":"<p><p>Glycosylation, attachment of monosaccharides or glycans to specific residues of proteins and lipids, is the most common post-translational modification. Defects among glycoprotein synthesis or modification pathways result in a genetically and clinically heterogenous group of metabolic disorders, congenital disorders of glycosylation (CDGs) with an estimated prevalence of 1/10,000. CDGs have multisystem involvement in which significant neurological dysfunction is frequent, with variable impairment of other organ functions. Most of the proteins responsible for endocrine homeostasis are essentially glycoproteins so disorders of glycosylation have an impact on hormone secretory pathways, changing hormone and carrier protein stability, circulatory half-live and abundance, alternating receptor configuration, activation, hormone-substrate affinity, and resetting endocrine control and feedback loops. Endocrine implications of CDGs are extensive and are described in up to 55% of all patients with CDGs during the natural course of the disease. This frequency is increased up to 85% in some CDG subgroups. Impacts on growth and growth factors, thyroid hormones, hypothalamo-pituitary-adrenal axis, hypothalamo-pituitary-gonadal axis, glucose metabolism, bone health and prolactin have been reported, yet clinical studies are scarce, with data mostly derived from case series. The aim of this review is to describe the current understanding of the endocrine implications of CDGs, focusing on both preclinical and clinical studies, highlighting the broad spectrum of findings. Clinical and laboratory findings of CDGs and the effect of current treatment strategies on endocrine function will be briefly discussed.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"11-29"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperinsulinemia in Sotos Syndrome with a <i>de novo NSD1</i> Deletion","authors":"Elena Lundberg, Magnus Burstedt, Irina Golovleva","doi":"10.4274/jcrpe.galenos.2024.2023-5-15","DOIUrl":"10.4274/jcrpe.galenos.2024.2023-5-15","url":null,"abstract":"<p><p>Sotos syndrome belongs to the group of diseases characterised by features such as facial dysmorphism, intellectual disability, hypotonia and overgrowth. Usually, Sotos syndrome is caused by heterozygous mutations in the <i>NSD1</i> gene at chromosome 5q35 or by large genomic deletions of the same region. Genotype-phenotype correlations have mainly been reported as an association of significant or major abnormalities and presence of 5q35 deletions rather than intragenic deletions or point mutations in <i>NSD1</i>. Congenital hyperinsulinemic hypoglycaemia (CHI) has been described as an uncommon feature in the presentation of Sotos syndrome. Most of the patients with Sotos syndrome and transient CHI were carriers of 5q35 deletions, while persistent CHI has been recently reported in individuals with point mutations or small <i>NSD1</i> deletions. We report the clinical features and medical treatment in a new-born child with Sotos syndrome and CHI that was present for almost two years. Genetic cause of Sotos syndrome in this case was a novel, large genomic deletion encompassing 24 Online Mendelian Inheritance in Man genes including the entire <i>NSD1</i> gene and six other potentially morbid genes. Our report describes challenges in diagnosis and management of this rare genetic condition. We propose, that in neonatal diagnostics, the phenotypic spectrum of Sotos syndrome should include CHI as a characteristic feature and molecular genetic testing should be done by whole genome analysis.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"161-168"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139724608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of Urinary Metabolites of Parabens and Bisphenol a with Premature Thelarche among a Sample of Iranian Girls","authors":"Nafiseh Mozafarian, Mahin Hashemipour, Mohammad Reza Maracy, Hamid Galehdari, Roya Kelishadi","doi":"10.4274/jcrpe.galenos.2025.2025-3-22","DOIUrl":"10.4274/jcrpe.galenos.2025.2025-3-22","url":null,"abstract":"<p><strong>Objective: </strong>Endocrine-disrupting chemicals may influence the process of puberty including the development of premature thelarche (PT). Our aim was to investigate the relationship between exposure to bisphenol A (BPA) and parabens with PT among a sample of Iranian girls.</p><p><strong>Methods: </strong>This case-control study was conducted in 2022-2023 on girls with a mean (standard deviation) age of 7.5 (0.6) years in Isfahan, Iran. Participants were 90 newly diagnosed PT cases and 114 healthy controls. Spot urine samples were collected from both groups to measure the levels of BPA and paraben metabolites. Analyses of BPA and paraben metabolites included methyl paraben (MeP), ethyl paraben (EtP), propyl paraben, and butyl paraben and benzyl paraben and were performed by gas chromatography-mass spectrometry. The association between concentrations of creatinine-standardized urinary BPA and parabens and PT was analyzed with multiple logistic regression models, after adjusting for potential confounders.</p><p><strong>Results: </strong>The results showed that individuals in the highest quartile of MeP [odds ratio (OR)=4.3, 95% confidence interval (CI): 1.2-14.9, p=0.023], EtP (OR=4.7, 95% CI: 1.3-17.2, p=0.018) and BPA (OR=5.03, 95% CI: 1.4-17.9, p=0.013) had a significantly higher odds for PT compared to those in the lowest quartile.</p><p><strong>Conclusion: </strong>The findings of this study suggest that exposure to BPA, MeP and EtP is related to increased odds of early breast development in girls. Limiting the exposure to these chemicals may help to reduce the risk of PT.</p>","PeriodicalId":48805,"journal":{"name":"Journal of Clinical Research in Pediatric Endocrinology","volume":" ","pages":"85-96"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}