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2. Cardiovascular outcomes in patients with homozygous familial hypercholesterolaemia on lipoprotein apheresis initiated during childhood: long-term follow-up of an international cohort from two registries

Author

Reijman, M Doortje, Tromp, Tycho R, Hutten, Barbara A, Hovingh, G Kees, Blom, Dirk J, Catapano, Alberico L, Cuchel, Marina, Dann, Eldad J, Gallo, Antonio, Hudgins, Lisa C, Raal, Frederick J, Ray, Kausik K, Sadiq, Fouzia, Soran, Handrean, Groothoff, Jaap W, Wiegman, Albert, and Kusters, D Meeike

Published
2024
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3. Clinical practice recommendations on lipoprotein apheresis for children with homozygous familial hypercholesterolaemia: An expert consensus statement from ERKNet and ESPN

Author

Reijman, M. Doortje, Kusters, D. Meeike, Groothoff, Jaap W., Arbeiter, Klaus, Dann, Eldad J., de Boer, Lotte M., de Ferranti, Sarah D., Gallo, Antonio, Greber-Platzer, Susanne, Hartz, Jacob, Hudgins, Lisa C., Ibarretxe, Daiana, Kayikcioglu, Meral, Klingel, Reinhard, Kolovou, Genovefa D., Oh, Jun, Planken, R. Nils, Stefanutti, Claudia, Taylan, Christina, Wiegman, Albert, and Schmitt, Claus Peter

Published
2024
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7. Worldwide experience of homozygous familial hypercholesterolaemia: retrospective cohort study

Author

Tromp, Tycho R., Hartgers, Merel L., Hovingh, G. Kees, Vallejo-Vaz, Antonio J., Ray, Kausik K., Soran, Handrean, Freiberger, Tomas, Bertolini, Stefano A., Harada-Shiba, Mariko, Pang, Jing, Watts, Gerald F., Greber-Platzer, Susanne, Mäser, Martin, Stulnig, Thomas M., Ebenbichler, Christoph F., Bin Thani, Khalid, Cassiman, David, Descamps, Olivier S., Rymen, Daisy, Witters, Peter, Santos, Raul D., Brunham, Liam R., Francis, Gordon A., Genest, Jacques, Hegele, Robert A., Kennedy, Brooke A., Ruel, Isabelle, Sherman, Mark H., Jiang, Long, Wang, Luya, Reiner, Željko, Blaha, Vladimir, Ceska, Richard, Dvorakova, Jana, Dlouhy, Lubomir, Horak, Pavel, Soska, Vladimir, Tichy, Lukas, Urbanek, Robin, Vaverkova, Helena, Vrablik, Michal, Zemek, Stanislav, Zlatohlavek, Lukas, Emil, Sameh, Naguib, Tarek, Reda, Ashraf, Béliard, Sophie, Bruckert, Eric, Gallo, Antonio, Elisaf, Moses S., Kolovou, Genovefa, Cohen, Hofit, Durst, Ronen, Dann, Eldad J., Elis, Avishay, Hussein, Osama, Leitersdorf, Eran, Schurr, Daniel, Setia, Nitika, Verma, Ishwar C., Alareedh, Mohammed D., Al-Khnifsawi, Mutaz, Abdalsahib Al-Zamili, Ali F., Rhadi, Sabah H., Shaghee, Foaad K., Arca, Marcello, Averna, Maurizio, Bartuli, Andrea, Bucci, Marco, Buonuomo, Paola S., Calabrò, Paolo, Calandra, Sebastiano, Casula, Manuela, Catapano, Alberico L., Cefalù, Angelo B., Cicero, Arrigo F.G., D'Addato, Sergio, D'Erasmo, Laura, Di Costanzo, Alessia, Fasano, Tommaso, Gazzotti, Marta, Giammanco, Antonina, Iannuzzo, Gabriella, Ibba, Anastasia, Negri, Emanuele A., Pasta, Andrea, Pavanello, Chiara, Pisciotta, Livia, Rabacchi, Claudio, Ripoli, Carlo, Sampietro, Tiziana, Sbrana, Francesco, Sileo, Fulvio, Suppressa, Patrizia, Tarugi, Patrizia, Trenti, Chiara, Zenti, Maria G., Hori, Mika, Ayesh, Mahmoud H., Azar, Sami T., Bitar, Fadi F., Fahed, Akl C., Moubarak, Elie M., Nemer, Georges, Nawawi, Hapizah M., Madriz, Ramón, Mehta, Roopa, Cupido, Arjen J., Defesche, Joep C., Reijman, M. Doortje, Roeters-van Lennep, Jeanine E., Stroes, Erik S.G., Wiegman, Albert, Zuurbier, Linda, Al-Waili, Khalid, Sadiq, Fouzia, Chlebus, Krzysztof, Bourbon, Mafalda, Gaspar, Isabel M., Lalic, Katarina S., Ezhov, Marat V., Susekov, Andrey V., Groselj, Urh, Charng, Min-Ji, Khovidhunkit, Weerapan, Aktan, Melih, Altunkeser, Bulent B., Demircioglu, Sinan, Kose, Melis, Gokce, Cumali, Ilhan, Osman, Kayikcioglu, Meral, Kaynar, Leyla G., Kuku, Irfan, Kurtoglu, Erdal, Okutan, Harika, Ozcebe, Osman I., Pekkolay, Zafer, Sag, Saim, Salcioglu, Osman Z., Temizhan, Ahmet, Yenercag, Mustafa, Yilmaz, Mehmet, Yilmaz Yasar, Hamiyet, Mitchenko, Olena, Lyons, Alexander R.M., Stevens, Christophe A.T., Brothers, Julie A., Hudgins, Lisa C., Nguyen, Christina, Alieva, Rano, Shek, Aleksandr, Do, Doan-Loi, Kim, Ngoc-Thanh, Le, Hong-An, Le, Thanh-Tung, Nguyen, Mai-Ngoc T., Truong, Thanh-Huong, Blom, Dirk J., Raal, Frederick J., Cuchel, Marina, Tromp, Tycho R, Hartgers, Merel L, Hovingh, G Kees, Vallejo-Vaz, Antonio J, Ray, Kausik K, Bertolini, Stefano, Blom, Dirk J, and Raal, Frederick J

Published
2022
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17. The impact of the COVID-19 pandemic on different aspects of the delivery of physical therapy after total hip or knee surgery

Author

Groot, L., Vlieland, T.P.M.V., Peter, W.F.H., Yildiz, U., Reijman, M., Gademan, M.G.J., and PaTIO Study Grp

Subjects
Nursing (miscellaneous), COVID-19, Physical Therapy, Sports Therapy and Rehabilitation, rehabilitation, Physical Therapists, Rheumatology, Humans, Orthopedic Procedures, Orthopedics and Sports Medicine, Chiropractics, Pandemics, Physical Therapy Modalities, physiotherapy, orthopaedics
Published
2022
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31. Lipoprotein(a) levels in children with homozygous familial hypercholesterolaemia: A cross-sectional study.

Author

de Boer, Lotte M., Reijman, M. Doortje, Hutten, Barbara A., and Wiegman, Albert

Subjects
ATHEROSCLEROSIS risk factors, LIPOPROTEINS, CARDIOVASCULAR diseases risk factors, HOMOZYGOUS familial hypercholesterolemia, CONFIDENCE intervals, CROSS-sectional method, RISK assessment, COMPARATIVE studies, DESCRIPTIVE statistics
Abstract

• 29 HoFH children were matched to 101 HeFH and 102 unaffected children. • Children with HoFH had the highest Lp(a) levels. • A gene-dose increase (zero, one, two pathogenic LDLR variants) in Lp(a) was found. • We recommend to measure Lp(a) in HoFH children to minimize (potential) ASCVD risk. Homozygous familial hypercholesterolaemia (HoFH) is a life-threatening disorder characterized by extremely elevated low-density lipoprotein cholesterol (LDL-C) levels. Untreated, severe atherosclerotic cardiovascular disease (ASCVD), including aortic valve stenosis (AVS), may already occur in childhood. Another important genetic risk factor for ASCVD and AVS is elevated lipoprotein(a) [Lp(a)], which is highly prevalent in the general paediatric population. However, data on Lp(a) in children with HoFH are scarce. Therefore, we performed a cross-sectional study to evaluate Lp(a) levels in children with HoFH and compared them to children with heterozygous FH (HeFH) and unaffected children. Adjusted least-square mean (95% CI) Lp(a) levels in HoFH (n=29), HeFH (n=101) and unaffected children (n=102) were 18.7 (12.0-29.1), 15.3 (11.8-19.8) and 10.5 (8.3-13.2) mg/dL, respectively (p-for-trend=0.007). Lp(a) levels in children with HoFH were higher than in children with HeFH and in unaffected children. Given the very high ASCVD risk with HoFH, identifying other risk factors such as elevated Lp(a) in these children is important. Therefore, Lp(a) levels should be measured at least once in all children with HoFH. [ABSTRACT FROM AUTHOR]

Published
2023
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34. Counseling couples at risk of having a child with homozygous familial hypercholesterolemia – Clinical experience and recommendations.

Author

Tromp, Tycho R., Reijman, M. Doortje, Wiegman, Albert, Hovingh, G. Kees, Defesche, Joep C., van Maarle, Merel C., and Mathijssen, Inge B.

Subjects
RISK-taking behavior, FAMILIAL hypercholesterolemia, GENETIC testing, ABORTION, GENOTYPES, GENETIC counseling, PARENTS, PRECONCEPTION care
Abstract

• HoFH requires prompt diagnosis and intensive treatment to prevent CVD in childhood. • Couples both carrying an FH variant run a 25% chance of having a child with HoFH. • Prenatal genetic counseling for HoFH should be performed on a case-by-case basis. • Clinicians should discuss all available diagnostic and reproductive options. • Discuss treatment outlook considering FH genotype and weighing parental preferences. Homozygous familial hypercholesterolemia (HoFH) is a rare, potentially life-limiting, inherited disorder of lipoprotein metabolism characterized by extremely high low-density lipoprotein cholesterol levels. When both parents have heterozygous FH, there is a 25% chance they will conceive a child with HoFH. Here we describe our clinical experience with two such prospective parent couples who were counseled regarding reproductive options and prenatal testing for HoFH. These cases showcase how, in consultation with a molecular geneticist and pediatric cardiologist, parents may be informed of the prognosis and treatment outlook of HoFH based on the FH-variants carried, to ultimately make personal decisions on reproductive options. One couple opted for prenatal testing and termination of pregnancy in case HoFH was found, while the other accepted the risk without testing. We review the available literature on preconception counseling for HoFH and provide practical guidance to clinicians counseling at-risk couples. Optimal counseling of prospective parents may help prevent future physical and psychological problems for both parent and child. [ABSTRACT FROM AUTHOR]

Published
2023
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50. The Long-Term Efficacy and Safety of Evinacumab in Pediatric Patients with Homozygous Familial Hypercholesterolemia.

Author

Greber-Platzer, Susanne, Ali, Shazia, Waldron, Alpana, Reijman, M. Doortje, Brinton, Eliot, Charng, Min-Ji, Srinivasan, Shubha, Baker-Smith, Carissa, Baum, Seth, Brothers, Julie, Hartz, Jacob, Moriarty, Patrick, Banerjee, Poulabi, George, Richard, Hirshberg, Boaz, Pordy, Robert, and Wiegman, M. Albert

Subjects
THERAPEUTIC use of monoclonal antibodies, HOMOZYGOUS familial hypercholesterolemia, PATIENT safety, CLINICAL trials, CONFERENCES & conventions, DRUG efficacy, CHILDREN
Abstract

Regeneron Pharmaceuticals, Inc. Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder caused primarily by mutations in the low-density lipoprotein (LDL) receptor gene and characterized by severely elevated levels of LDL cholesterol (LDL-C), leading to early-onset atherosclerotic cardiovascular disease. Currently, few treatments are available to lower LDL-C levels in pediatric patients with HoFH. In Part B of a three-part open-label study (NCT04233918), the addition of evinacumab, an angiopoietin-like-3 inhibitor, to background lipid-lowering therapies (LLTs) reduced LDL-C from baseline to Week 24 by 48% in patients with HoFH aged 5-11 years. Evaluate the long-term (up to 72 weeks) efficacy and safety of evinacumab in pediatric patients with HoFH. This open-label, three-part study enrolled patients aged 5-11 years with LDL-C >130 mg/dL on optimized LLT, including apheresis and lomitapide. Part A was a Phase 1b, single-dose, 16-week study including six patients who received intravenous (IV) evinacumab 15 mg/kg. Part B was a Phase 3, 24-week open-label treatment study including 14 patients who had not participated in Part A. Part C was a Phase 3, 48-week open-label extension study, with an optional 24-week follow-up period, which included all 20 patients from both Parts A and B. In Parts B and C, patients received IV evinacumab 15 mg/kg every 4 weeks. We report data pooled from Parts B and C that includes results from Part A patients who participated in Part C and had 48 weeks of evinacumab treatment, and Part B patients who participated in Parts B and C and had a total treatment duration of 72 weeks. All 20 patients completed Part C. Mean (standard deviation [SD]) LDL-C at baseline was 301.9 (149.1) mg/dL. Evinacumab reduced mean LDL-C by 44.6% (mean [SD] reduction of 131.1 [90.2] mg/dL) and 40.7% (mean [SD] reduction of 115.8 [101.2] mg/dL) from baseline to Weeks 48 (n=16) and 72 (n=14), respectively. Evinacumab reduced mean apolipoprotein B (Week 48: 38.3%; Week 72: 34.0%), non-high-density lipoprotein cholesterol (Week 48: 45.3%; Week 72: 41.6%), total cholesterol (Week 48: 44.7%; Week 72: 42.2%), and median lipoprotein(a) (Week 48: 17.3%; Week 72: 15.7%). Treatment-emergent adverse events (TEAEs) occurred in all 20 patients. Serious TEAEs occurred in two (10.0%) patients (tonsilitis [n=1]; aortic valve stenosis [n=1]), both were unrelated to the study drug. No treatment discontinuations or deaths were reported. In pediatric patients with HoFH, evinacumab demonstrated substantial and durable reductions in LDL-C and other atherogenic lipids, and was generally well tolerated. [ABSTRACT FROM AUTHOR]

Published
2024
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