PubMed Health⌕ Search

PubMed · 11480445

Multiple marker second trimester serum screening for pre-eclampsia.

Abstract

OBJECTIVE: To investigate whether an appropriate combination of maternal serum inhibin A, free beta-human chorionic gonadotropin (free beta-hCG), unconjugated estriol (uE3), and alpha-fetoprotein (AFP) may be an effective means of screening for pre-eclampsia in the second trimester of pregnancy. SETTING: Women who attended an antenatal clinic in Oxford, from whom serum samples were stored, 19 of whom subsequently developed pre-eclampsia. METHODS: Serum inhibin A, free beta-hCG, uE3, and AFP were measured in 32 serum samples collected from the 19 women who developed pre-eclampsia and, for each sample, in three control samples collected from women with unaffected pregnancies matched for gestational age and maternal age. RESULTS: In pregnancies that developed pre-eclampsia the median inhibin A value was raised (1.7 multiples of the median (MoM) for unaffected pregnancies (95% confidence interval (95% CI) 1.1 to 2.7 MoM), the median free beta-hCG was raised (2.1, 1.4 to 3.3 MoM) and the median uE3 was lowered (0.8, 0.6 to 0.98 MoM) after 19 completed weeks of gestation and at least 2 weeks before the onset ofproteinuria. Values of AFP were similar in affected and unaffected pregnancies. Combining the values ofinhibin A, free beta-hCG, and uE3 to form a screening test would detect an estimated 55% of affected pregnancies with a false positive rate of 5%. CONCLUSIONS: Inhibin A, free beta-hCG, and uE3 in combination may be a useful screening test during the second trimester for pre-eclampsia.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

N J Wald, J K Morris. 2001. Multiple marker second trimester serum screening for pre-eclampsia.. https://doi.org/10.1136/jms.8.2.65

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Genomic and Transcriptomic Correlates of Deep PSA Response in Patients with Metastatic Androgen Pathway Modulation-Sensitive Prostate Cancer.

BACKGROUND: Despite advances in metastatic androgen pathway modulation-sensitive prostate cancer (mAPMS) treatment, outcomes remain heterogeneous. Achieving a post-treatment undetectable prostate specific antigen (PSA) is a strong prognostic marker. We aimed to identify genomic and transcriptomic determinants of PSA response in a real-world clinical-genomic cohort. PATIENTS AND METHODS: Patients with mAPMS who underwent DNA (Tempus xT) and, in a subset, RNA (Tempus xR) sequencing were identified from the Tempus Lens database. Inclusion required stage IV disease within 90 days of sample collection and samples obtained within 12 months before or 3 months after treatment initiation. Patients with PSA at 6 months (n&#x2009;=&#x2009;525) were classified as PSA-low (<0.1&#x2009;ng/mL, n&#x2009;=&#x2009;240) or PSA-high (&#x2265;0.1&#x2009;ng/mL, n&#x2009;=&#x2009;285). Overall survival (OS) was assessed by 6-month landmark analysis with delayed-entry adjustment. Logistic and Cox models were adjusted for clinical variables. Sensitivity analyses used a relative definition of&#x2009;>&#x2009;95% PSA decline from baseline. RESULTS: Baseline PSA was lower in PSA-low versus PSA-high patients (24 vs 36&#x2009;ng/mL, p&#x2009;=&#x2009;0.01). SPOP (17% vs 11%) and ZFHX3 (2.5% vs 6%) alterations differed between groups, but neither persisted after adjustment. Using the relative definition, ZMYM3 and JAK1 alterations were independently associated with failure to achieve a deep PSA response. Expression of PSMA, TROP2, B7-H3, and STEAP1 did not differ between groups. PSA-low status was independently associated with improved OS, as was deep relative response. CONCLUSION: Deep PSA response at 6 months correlates with improved OS in mAPMS. Integrating molecular markers with PSA response may inform treatment intensification or de-escalation strategies.

Biomarkers↗

Systemic treatment of advanced pancreatic cancer: A Comprehensive Review.

IMPORTANCE: Pancreatic adenocarcinoma (PDAC) is an uncommon but potentially catastrophic diagnosis with historically poor prognosis. It is the tenth most prevalent cancer in the US & UK. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, with a five-year survival rate of approximately 10%. Despite increasing understanding of its molecular biology, systemic treatment options for advanced disease remain limited, and survival outcomes have improved only modestly over the past decade. OBSERVATIONS: This narrative review traces the evolution of systemic therapy for advanced PDAC from gemcitabine monotherapy through the landmark FOLFIRINOX (PRODIGE trial) and gemcitabine/nab-paclitaxel (MPACT trial) combination regimens, which remain the standard of care. Second-line options including liposomal irinotecan plus 5-FU/LV (NAPOLI-1) and maintenance olaparib for germline BRCA1/2-mutated disease (POLO) are also reviewed. Emerging data on sequential treatment strategies (SEQUENCE trial), biomarker-driven treatment selection (PRIMUS-001, PASS-01), and precision medicine approaches targeting actionable molecular subgroups, including dMMR/MSI-H, NTRK fusions, and homologous recombination deficiency are discussed. Real-world evidence comparing FOLFIRINOX and gemcitabine/nab-paclitaxel is critically appraised, including the challenges of patient selection, tolerance, and applicability outside clinical trial settings. CONCLUSION AND RELEVANCE: Despite incremental progress, the treatment landscape of advanced PDAC remains challenging. Molecular stratification and biomarker-driven precision oncology represent the most promising path forward. This review serves as a clinical reference for physicians managing advanced pancreatic cancer, highlighting current evidence, evidence limitations, and future research priorities including prospective biomarker-driven trials and improved access to genomic testing.

Biomarkers↗

Blood-based biomarkers of Alzheimer's disease and neurodegeneration in an indigenous African cohort using both Simoa and NULISA platforms.

In low- and middle-income countries, Alzheimer's disease (AD) constitutes a growing public health burden. However, AD biomarkers research remains underrepresented in African populations. This study assesses core biomarkers of AD and their relevance in the African context as potential aid in clinical diagnosis. Nigerian older adults from VALIANT cohort (n&#x2009;=&#x2009;967) underwent biomarker quantification in plasma (p-tau217, GFAP, NfL, A&#x3b2;42 and A&#x3b2;40) employing both the Single Molecule Assay (Simoa, Quanterix) and Nucleic acid-Linked Immuno-Sandwich Assay (NULISA, Alamar). Biomarkers were associated with disease severity in clinical-diagnostic and clinical-biological groups, with stepwise increases of p-tau217, NfL and GFAP from cognitively unimpaired to dementia (p&#x2009;<&#x2009;0.05). Results were consistent across platforms. Comparison between sexes showed higher biomarker levels in male participants across diagnostic groups. A significant effect of apoE-E4 proteotype on p-tau217 levels, after adjusting for age and sex was identified. These findings support the application of plasma AD biomarkers in the African context and the relevance of further AD biomarker research in diverse populations.

Biomarkers↗