Mechanisms of Disease: genetic causes of familial hypercholesterolemia
By A. Soutar, R. Naoumova. Nature Clinical Practice Cardiovascular Medicine, 2007
617 citations recorded by the source corpus.
Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Surgery
View Paper: https://www.semanticscholar.org/paper/1e67909a54bced7a59bd58350f5a6d1ca4e9cd17
Citations in the corpus
- Atherosclerotic Cardiovascular Disease and Heart Failure in Type 2 Diabetes – Mechanisms, Management, and Clinical Considerations (2016, neutral): “Diabetes mellitus is diagnosed based on fasting plasma glucose ≥126 mg/dL (7.0 mmol/L), 2-hour glucose after 75-g oral glucose load ≥200 mg/dL (11.1 mmol/L), hemoglobin A 1c (HbA 1c ) ≥6.5% (48 mmol/mol), or random plasma glucose ≥200 mg/dL confirmed by repeat testing in the absence of signs or symp”
- Homozygous familial hypercholesterolaemia: new insights and guidance for clinicians to improve detection and clinical management. A position paper from the Consensus Panel on Familial Hypercholesterolaemia of the European Atherosclerosis Society (2014, neutral): “Other sources of variability in the HoFH phenotype may arise from small effect genetic variants (common single nucleotide polymorphisms), gene–gene and gene–environment interactions, and non-Mendelian and epigenetic influences.(6,9,10) Greater access and wider clinical application of next generation”
- Guidelines on the Use of Therapeutic Apheresis in Clinical Practice – Evidence‐Based Approach from the Writing Committee of the American Society for Apheresis: The Eighth Special Issue (2019, neutral): “References [349–466]”