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Pathophysiology of Severe Familial Hypercholesterolemia
S4
Journal of Clinical Lipidology, Vol 6, No 6, December 2012
Disclosure of Unlabeled Use and Investigational Product This educational activity may include discussion of uses of agents that are investigational and/or unapproved by the FDA. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings.
prematurely compared with individuals who inherit heterozygous FH. This Journal of Clinical Lipidology open-access eCME activity (accessed at http://multimedia. lipidjournal.com/2012/SevereFH/) underscores that the pathophysiology of severe heterozygous FH is not different from the pathophysiology of other forms of atherosclerosis; it simply manifests more severely and decades earlier, requiring physicians to be aware of the lipid markers for this condition and of the necessity for an aggressive therapeutic response. McGowan MP. J Clin Lipidol. 2012;6(6). Accessible at http://lipidjournal.com.
Disclosure Declaration It is the policy of NLA to ensure independence, balance, objectivity, scientific rigor, and integrity in all of its continuing education activities. The faculty must disclose to the participants any significant relationships with commercial interests whose products or devices may be mentioned in the activity or with the commercial supporter of this continuing education activity. Identified conflict of interest is resolved by NLA prior to accreditation of the activity. NLA planners and reviewers have no relevant financial relationships to disclose. Disclaimer This course is designed solely to provide the healthcare professional with information to assist in his/her practice and professional development and is not to be considered a diagnostic tool to replace professional advice or treatment. The course serves as a general guide to the healthcare professional, and therefore, cannot be considered as giving legal, nursing, medical, or other professional advice in specific cases. The NLA specifically disclaims responsibility for any adverse consequences resulting directly or indirectly from information in the course, for undetected error, or through reader’s misunderstanding of content. Release date: November 15, 2012. Expiration date: November 15, 2013.
Hardware/Software Requirements To view this educational activity you will need a web browser with Javascript and either Flash or HTML5 enabled. Nearly all modern web browsers will work.
eCME Multimedia Activity Pathophysiology of Severe Familial Hypercholesterolemia
http://dx.doi.org/10.1016/j.jacl.2012.10.008
eCME Multimedia Activity Therapeutic Strategies for Optimizing Outcomes in the Severe Familial Hypercholesterolemia Patient James A. Underberg, MD, MS, FNLA
ABSTRACT Familial hypercholesterolemia (FH), in both its homozygous and heterozygous inheritance forms, is both underrecognized and undertreated in the United States and elsewhere. This is an important gap in current evidencebased clinical practice, for new recommendations from the NLA underscore the importance of early detection and treatment if the morbidity and mortality associated with FH is to be reduced. As discussed in this Journal of Clinical Lipidology open-access eCME activity (accessed at http://multimedia.lipidjournal.com/2012/SevereFH/), efforts to understand and address this gap are especially important at this point because after decades of relying on an established armamentarium of drugs for treating the severe elevations in low-density lipoprotein cholesterol and early cardiovascular heart disease that are caused by FH, several new classes of drugs show additional therapeutic benefit as possible future agents for treating FH. Underberg JA. J Clin Lipidol. 2012;6(6). Accessible at http://lipidjournal.com. http://dx.doi.org/10.1016/j.jacl.2012.10.009
Mary P. McGowan, MD, FNLA
ABSTRACT Familial hypercholesterolemia (FH) is a commonly inherited autosomal-dominant disorder. As discussed in this presentation, the four principal defects occur as mutations in the genes encoding for the low-density lipoprotein cholesterol receptors, ApoB, PCSK9, or LDL RAP1, or in other as-yet unidentified genes. Severe heterozygous FH occurs in between 1 in 10,000 and 1 in 50,000 people in the United States, with the pathology resulting in lifelong elevations of the serum low-density lipoprotein cholesterol levels and in patients developing coronary heart disease
eCME Multimedia Activity Strategies for Early Detection: The Role of Genetic Testing in Patients with Severe Hypercholesterolemia Daniel J. Rader, MD, FNLA
ABSTRACT Familial hypercholesterolemia (FH) is a genetically determined disorder of lipid metabolism, which raises the question of whether genetic testing or screening may be of
Journal of Clinical Lipidology, Vol 6, No 6, December 2012
Disclosure of Unlabeled Use and Investigational Product This educational activity may include discussion of uses of agents that are investigational and/or unapproved by the FDA. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings.
prematurely compared with individuals who inherit heterozygous FH. This Journal of Clinical Lipidology open-access eCME activity (accessed at http://multimedia. lipidjournal.com/2012/SevereFH/) underscores that the pathophysiology of severe heterozygous FH is not different from the pathophysiology of other forms of atherosclerosis; it simply manifests more severely and decades earlier, requiring physicians to be aware of the lipid markers for this condition and of the necessity for an aggressive therapeutic response. McGowan MP. J Clin Lipidol. 2012;6(6). Accessible at http://lipidjournal.com.
Disclosure Declaration It is the policy of NLA to ensure independence, balance, objectivity, scientific rigor, and integrity in all of its continuing education activities. The faculty must disclose to the participants any significant relationships with commercial interests whose products or devices may be mentioned in the activity or with the commercial supporter of this continuing education activity. Identified conflict of interest is resolved by NLA prior to accreditation of the activity. NLA planners and reviewers have no relevant financial relationships to disclose. Disclaimer This course is designed solely to provide the healthcare professional with information to assist in his/her practice and professional development and is not to be considered a diagnostic tool to replace professional advice or treatment. The course serves as a general guide to the healthcare professional, and therefore, cannot be considered as giving legal, nursing, medical, or other professional advice in specific cases. The NLA specifically disclaims responsibility for any adverse consequences resulting directly or indirectly from information in the course, for undetected error, or through reader’s misunderstanding of content. Release date: November 15, 2012. Expiration date: November 15, 2013.
Hardware/Software Requirements To view this educational activity you will need a web browser with Javascript and either Flash or HTML5 enabled. Nearly all modern web browsers will work.
eCME Multimedia Activity Pathophysiology of Severe Familial Hypercholesterolemia
http://dx.doi.org/10.1016/j.jacl.2012.10.008
eCME Multimedia Activity Therapeutic Strategies for Optimizing Outcomes in the Severe Familial Hypercholesterolemia Patient James A. Underberg, MD, MS, FNLA
ABSTRACT Familial hypercholesterolemia (FH), in both its homozygous and heterozygous inheritance forms, is both underrecognized and undertreated in the United States and elsewhere. This is an important gap in current evidencebased clinical practice, for new recommendations from the NLA underscore the importance of early detection and treatment if the morbidity and mortality associated with FH is to be reduced. As discussed in this Journal of Clinical Lipidology open-access eCME activity (accessed at http://multimedia.lipidjournal.com/2012/SevereFH/), efforts to understand and address this gap are especially important at this point because after decades of relying on an established armamentarium of drugs for treating the severe elevations in low-density lipoprotein cholesterol and early cardiovascular heart disease that are caused by FH, several new classes of drugs show additional therapeutic benefit as possible future agents for treating FH. Underberg JA. J Clin Lipidol. 2012;6(6). Accessible at http://lipidjournal.com. http://dx.doi.org/10.1016/j.jacl.2012.10.009
Mary P. McGowan, MD, FNLA
ABSTRACT Familial hypercholesterolemia (FH) is a commonly inherited autosomal-dominant disorder. As discussed in this presentation, the four principal defects occur as mutations in the genes encoding for the low-density lipoprotein cholesterol receptors, ApoB, PCSK9, or LDL RAP1, or in other as-yet unidentified genes. Severe heterozygous FH occurs in between 1 in 10,000 and 1 in 50,000 people in the United States, with the pathology resulting in lifelong elevations of the serum low-density lipoprotein cholesterol levels and in patients developing coronary heart disease
eCME Multimedia Activity Strategies for Early Detection: The Role of Genetic Testing in Patients with Severe Hypercholesterolemia Daniel J. Rader, MD, FNLA
ABSTRACT Familial hypercholesterolemia (FH) is a genetically determined disorder of lipid metabolism, which raises the question of whether genetic testing or screening may be of