Objective Accidental traumatic brain injury (TBI) can lead to severe complications such as endocrine abnormalities and long-term morbidities and can negatively impact patient lives. These conditions are also associated with a high cost of treatment over a lifetime, a significant concern in low-to-middle-income countries (LMICs). In Pakistan, the prevalence of children with endocrine abnormalities secondary to TBI remains largely unexplored. We conducted a retrospective cross-sectional study to estimate the burden of endocrine abnormalities due to TBI among children in our population. Methods Twenty patients previously admitted with head injury between September and October 2019 were retrospectively reviewed with tests for baseline serum sodium, plasma osmolality, cortisol, adrenocorticotropin (ACTH), free thyroxine (fT4), growth hormone (GH), insulin growth factor-1 (IGF-1), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), prolactin, estradiol, and testosterone. Data were collated from the electronic Health and Information Management System (HIMS) and analyzed using SPSS v25. Chi-square and t-tests were used to identify associations between variable groups. Outcomes of interest included correlations between hormonal levels and demographic factors, interventions and hormonal levels, and complication rates and hormonal levels. Results Our study reports three (15% of the total cohort) patients with pituitary hormone deficits (two with low IGF-1 and one with low TSH). High serum IGF-1 and ACTH levels were also observed in three (15%) children. High IGF-1 was associated with female gender (p=0.007), mechanical ventilation (p=0.038), and falls (p=0.028). IGF-1 (p=0.035) and GH (p=0.049) levels were associated with improvement in Extended Glasgow Outcome Scale (GOS-E) score. Testosterone was positively correlated with a high percentile for height (p=0.005) and GOS-E scores on follow-up (p=0.030). High testosterone levels (592.12 ± 102.28 ng/dl) were associated with good functional outcomes in post-pubescent patients (p<0.05). Serum fT4 was linked with a high GOS-E score at discharge in prepubescent patients (p=0.034). Neurosurgical decompression was the only risk factor for hormone deficiency, comprising 67% of the group with hormone deficiencies (p=0.028). The learning difficulties were observed exclusively in children with hormonal deficiencies (7 patients, p=0.000). Conclusion Hormonal dysfunction due to TBI in children can lead to poor outcomes. High serum IGF-1, testosterone, and free T4 levels were associated with improved functional outcomes in children with TBI. Limited follow-up and resources in LMICs are significant barriers to addressing the morbidity associated with these conditions and need to be addressed at a health policy level.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9947722 | PMC |
http://dx.doi.org/10.7759/cureus.34131 | DOI Listing |
Clin Ther
December 2024
Department of Clinical Research, Hindu Mission Hospital, Tambaram, Chennai, Tamil Nadu, India. Electronic address:
Purpose: Clinical trials are advancing the treatment of polycystic ovary syndrome (PCOS), an endocrine disorder affecting 8-13% of women. Lifestyle interventions, including nutritional plans, physical activity, and stress management, can improve reproductive hormones and metabolic health. Novel pharmacotherapies targeting hormonal, metabolic, and reproductive abnormalities are being explored for individualized treatment.
View Article and Find Full Text PDFReprod Toxicol
December 2024
Laboratory of Animal Endocrine and Reproductive Physiology, Department of Physiology, Federal University of Paraná, Curitiba-Brazil. Electronic address:
The endocannabinoid system (ECS) plays a pivotal role in reproductive physiology, including gonadal development, though its influence on testis and ovary development has only recently gained attention. The ECS comprises lipid-derived ligands such as anandamide (AEA) and 2-arachidonoylglycerol (2-AG), along with cannabinoid receptors CB1 and CB2, which are expressed in various gonadal cells. Emerging research indicates that ECS signaling is critical for testosterone synthesis and gonadal cell proliferation and differentiation.
View Article and Find Full Text PDFEndocrine
December 2024
Department of Endocrinology and Metabolism, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Purpose: Iodine nutrition during pregnancy plays an important role in fetal development and maternal outcomes. Iodine deficiency has been proved to be associated with maternal thyroid dysfunction, adverse fetal outcomes and neurodevelopmental disorders in offspring. At present, there are few studies concentrate on the effects of iodine excess during pregnancy on thyroid function, maternal and neonatal outcomes, and the results are still controversial.
View Article and Find Full Text PDFSteroids
December 2024
Laboratory of Endocrinology, Department of Bioscience, Barkatullah University, Bhopal, Madhya Pradesh 462026, India.
Background: Besides ovarian dysfunction and infertility, individuals with polycystic ovarian syndrome (PCOS) also present a number of systemic disturbances including functional derangements in the adipose tissue which possibly aggravates the endocrinometabolic abnormality in PCOS. Epigenetic changes have been implicated in metabolic-related disorders including PCOS. However, its pathogenic involvement in adipose-ovarian dysfunction is unclear.
View Article and Find Full Text PDFTissue Cell
December 2024
Medical Physiology Department, Faculty of Medicine, Zagazig University, P.O. Box 44519, Zagazig, Egypt. Electronic address:
Endocrine multisystem defect polycystic ovary syndrome (PCOS) causes hyperandrogenism and infertility. Half of PCOS women have (non-alcoholic fatty liver disease) NAFLD, which increases metabolic disease risk. We tested decorin's effect on NAFLD and related processes in PCOS.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!