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3. Synopsis of an integrated guidance for enhancing the care of familial hypercholesterolaemia: an Australian perspective

Author

Ademi, Zanfina, Ardill, Justin J, Barnett, Wendy, Bates, Timothy R, Beilin, Lawrence J, Bishop, Warrick, Black, J Andrew, Brown, Alex, Burnett, John R, Bursill, Christina A, Colley, Alison, Clifton, Peter M, Ekinci, Elif I, Figtree, Gemma A, Forge, Brett H, Garton-Smith, Jacquie, Graham, Dorothy F, Hamilton-Craig, Ian, Hamilton-Craig, Christian R, Heal, Clare, Hespe, Charlotte M, Hooper, Amanda J, Howes, Laurence G, Ingles, Jodie, Janus, Edward D, Kangaharan, Nadarajah, Keech, Anthony C, Kirke, Andrew B, Kritharides, Leonard, Kyle, Campbell V, Lacaze, Paul, Li, Stephen CH, Maticevic, Stjepana, McQuillan, Brendan M, Mirzaee, Sam, Mori, Trevor A, Morton, Allison C, Colquhoun, David M, Moullin, Joanna C, Nestel, Paul J, Nowak, Kristen J, O'Brien, Richard C, Pachter, Nicholas, Page, Michael M, Psaltis, Peter J, Radford, Jan, Reid, Nicola J, Robertson, Elizabeth N, Ryan, Jacqueline DM, Sarkies, Mitchell N, Schultz, Carl J, Scott, Russell S, Semsarian, Christopher, Simons, Leon A, Spinks, Catherine, Tonkin, Andrew M, van Bockxmeer, Frank, Waddell-Smith, Kathryn E, Ward, Natalie C, White, Harvey D, Wilson, Andrew M, Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J, Brett, Peter, Elias, Luke, Malan, Wynand, Irvin, John, Lambert, Kirsten, Pedrotti, Annette, Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., and Pang, Jing

Published
2021
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4. Integrated Guidance for Enhancing the Care of Familial Hypercholesterolaemia in Australia

Author

Ademi, Zanfina, Ardill, Justin J., Barnett, Wendy, Bates, Timothy R., Beilin, Lawrence J., Bishop, Warrick, Black, J. Andrew, Brett, Peter, Brown, Alex, Burnett, John R., Bursill, Christina A., Colley, Alison, Clifton, Peter M., Ekinci, Elif I., Elias, Luke, Figtree, Gemma A., Forge, Brett H., Garton-Smith, Jacquie, Graham, Dorothy F., Hamilton-Craig, Ian, Hamilton-Craig, Christian R., Heal, Clare, Hespe, Charlotte M., Hooper, Amanda J., Howes, Laurence G., Ingles, Jodie, Irvin, John, Janus, Edward D., Kangaharan, Nadarajah, Keech, Anthony C., Kirke, Andrew B., Kritharides, Leonard, Kyle, Campbell V., Lacaze, Paul, Lambert, Kirsten, Li, Stephen C.H., Malan, Wynand, Maticevic, Stjepana, McQuillan, Brendan M., Mirzaee, Sam, Mori, Trevor A., Morton, Allison C., Colquhoun, David M., Moullin, Joanna C., Nestel, Paul J., Nowak, Kristen J., O'Brien, Richard C., Pachter, Nicholas, Page, Michael M., Pedrotti, Annette, Psaltis, Peter J., Radford, Jan, Reid, Nicola J., Robertson, Elizabeth N., Ryan, Jacqueline D.M., Sarkies, Mitchell N., Schultz, Carl J., Scott, Russell S., Semsarian, Christopher, Simons, Leon A., Spinks, Catherine, Tonkin, Andrew M., van Bockxmeer, Frank, Waddell-Smith, Kathryn E., Ward, Natalie C., White, Harvey D., Wilson, Andrew M., Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J., Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., and Pang, Jing

Published
2021
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5. Gaps in the Care of Familial Hypercholesterolaemia in Australia: First Report From the National Registry

Author

Pang, Jing, Sullivan, David R., Hare, David L., Colquhoun, David M., Bates, Timothy R., Ryan, Jacqueline D.M., Bishop, Warrick, Burnett, John R., Bell, Damon A., Simons, Leon A., Mirzaee, Sam, Kostner, Karam M., Nestel, Paul J., Wilson, Andrew M., O’Brien, Richard C., Janus, Edward D., Clifton, Peter M., Ardill, Justin J., Chan, Dick C., van Bockxmeer, Frank, and Watts, Gerald F.

Published
2021
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6. Tackling cardiometabolic risk in the Asia Pacific region

Author

Li, Jian-Jun, Yeo, Khung Keong, Tan, Kathyrn, Ako, Junya, Krittayaphong, Rungroj, Tan, Ru San, Aylward, Philip E., Lam, CarolynS.P., Baek, Sang Hong, Dalal, Jamshed, Fong, Alan, Li, Yi-Heng, O’Brien, Richard C., Koh, Si Ya Natalie, Scherer, Daniel J., Tada, Hayato, Kang, Vernon, Butters, Julie, and Nicholls, Stephen J.

Published
2020
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8. Improved metabolic parameters of people with diabetes attending an Aboriginal health service in regional Victoria

Author

Eer, Audrey S., primary, Hearn, Tracey, additional, Atkinson‐Briggs, Sharon, additional, Drake, Shannon, additional, Singh, Satpal, additional, Neoh, Sandra, additional, Pyrlis, Felicity, additional, Hachem, Mariam, additional, Zajac, Jeffrey D., additional, Burchill, Luke J., additional, O'Brien, Richard C., additional, and Ekinci, Elif I., additional

Published
2022
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9. Improved metabolic parameters of people with diabetes attending an Aboriginal health service in regional Victoria.

Author

Eer, Audrey S., Hearn, Tracey, Atkinson‐Briggs, Sharon, Drake, Shannon, Singh, Satpal, Neoh, Sandra, Pyrlis, Felicity, Hachem, Mariam, Zajac, Jeffrey D., Burchill, Luke J., O'Brien, Richard C., and Ekinci, Elif I.

Subjects
INDIGENOUS Australians, GLYCOSYLATED hemoglobin, OBESITY, BIOCHEMISTRY, ALBUMINS, HEALTH services accessibility, HEMOGLOBINS, KIDNEY function tests, ANTILIPEMIC agents, AGE distribution, GLYCEMIC control, ACE inhibitors, HYPOGLYCEMIC agents, TYPE 2 diabetes, COMPARATIVE studies, SYMPTOMS, PLATELET aggregation inhibitors, BODY mass index, VASCULAR diseases, BLOOD pressure measurement, SECONDARY care (Medicine), MEDICAL care of indigenous peoples, MEDICAL specialties & specialists, LIPIDS, CREATININE, DISEASE complications
Abstract

Background: Aboriginal and Torres Strait Islander people have higher rates of diabetes and its complications than non‐Aboriginal people. Rumbalara Aboriginal Co‐operative is the major primary healthcare provider for Aboriginal people in the Greater Shepparton region. Aims: To evaluate the baseline metabolic parameters and presence of diabetes complications in people with type 2 diabetes attending Rumbalara Aboriginal Co‐operative in 2017 and compare it with other Aboriginal and Torres Strait Islander studies and Australian specialist diabetes services. Methods: Clinical and biochemical characteristics, including diabetes type, age, weight, body mass index (BMI), blood pressure, micro‐ and macrovascular complications, glycosylated haemoglobin (HbA1c), haemoglobin, renal function, lipid profile, urine albumin:creatinine ratio, diabetes medications, renin angiotensin system inhibition therapies, HMG‐CoA reductase inhibitors and antiplatelet agents, were determined. Results: One hundred and twenty‐six individuals had diabetes, 121 had type 2 diabetes. One hundred and thirteen identified as Aboriginal and/or Torres Strait Islander. Median age was 57.5 (48–68) years, median HbA1c was 7.8% (6.8–9.6) and median BMI was 33.4 kg/m2 (29–42.3). Compared with other Australian Aboriginal and Torres Strait Islander populations, this population was older and had more obesity, but with better glycaemia management. Compared with specialist diabetes services, this population was of similar age, with greater BMI but comparable HbA1c. Conclusions: Aboriginal people living with type 2 diabetes attending this regional Aboriginal health service have comparable glycaemic management to specialist diabetes services in Australia, managed largely by primary care physicians with limited access to specialist care for the past 5 years. [ABSTRACT FROM AUTHOR]

Published
2023
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11. Synopsis of an integrated guidance for enhancing the care of familial hypercholesterolaemia: An Australian perspective

Author

Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., Pang, Jing, Ademi, Zanfina, Ardill, Justin J., Barnett, Wendy, Bates, Timothy R., Beilin, Lawrence J., Bishop, Warrick, Black, J. Andrew, Brown, Alex, Burnett, John R., Bursill, Christina A., Colley, Alison, Clifton, Peter M., Ekinci, Elif I., Figtree, Gemma A., Forge, Brett H., Garton-Smith, Jacquie, Graham, Dorothy F., Hamilton-Craig, Ian, Hamilton-Craig, Christian R., Heal, Clare, Hespe, Charlotte M., Hooper, Amanda J., Howes, Laurence G., Ingles, Jodie, Janus, Edward D., Kangaharan, Nadarajah, Keech, Anthony C., Kirke, Andrew B., Kritharides, Leonard, Kyle, Campbell V., Lacaze, Paul, Li, Stephen C. H., Maticevic, Stjepana, McQuillan, Brendan M., Mirzaee, Sam, Mori, Trevor A., Morton, Allison C., Colquhoun, David M., Moullin, Joanna C., Nestel, Paul J., Nowak, Kristen J., O'Brien, Richard C., Pachter, Nicholas, Page, Michael M., Psaltis, Peter J., Radford, Jan, Reid, Nicola J., Robertson, Elizabeth N., Ryan, Jacqueline D. M., Sarkies, Mitchell N., Schultz, Carl J., Scott, Russell S., Semsarian, Christopher, Simons, Leon A., Spinks, Catherine, Tonkin, Andrew M., van Bockxmeer, Frank, Waddell-Smith, Kathryn E., Ward, Natalie C., White, Harvey D., Wilson, Andrew M., Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J., Brett, Peter, Elias, Luke, Malan, Wynand, Irvin, John, Lambert, Kirsten, Pedrotti, Annette, FH Australasia Network Consensus Working Group, Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., Pang, Jing, Ademi, Zanfina, Ardill, Justin J., Barnett, Wendy, Bates, Timothy R., Beilin, Lawrence J., Bishop, Warrick, Black, J. Andrew, Brown, Alex, Burnett, John R., Bursill, Christina A., Colley, Alison, Clifton, Peter M., Ekinci, Elif I., Figtree, Gemma A., Forge, Brett H., Garton-Smith, Jacquie, Graham, Dorothy F., Hamilton-Craig, Ian, Hamilton-Craig, Christian R., Heal, Clare, Hespe, Charlotte M., Hooper, Amanda J., Howes, Laurence G., Ingles, Jodie, Janus, Edward D., Kangaharan, Nadarajah, Keech, Anthony C., Kirke, Andrew B., Kritharides, Leonard, Kyle, Campbell V., Lacaze, Paul, Li, Stephen C. H., Maticevic, Stjepana, McQuillan, Brendan M., Mirzaee, Sam, Mori, Trevor A., Morton, Allison C., Colquhoun, David M., Moullin, Joanna C., Nestel, Paul J., Nowak, Kristen J., O'Brien, Richard C., Pachter, Nicholas, Page, Michael M., Psaltis, Peter J., Radford, Jan, Reid, Nicola J., Robertson, Elizabeth N., Ryan, Jacqueline D. M., Sarkies, Mitchell N., Schultz, Carl J., Scott, Russell S., Semsarian, Christopher, Simons, Leon A., Spinks, Catherine, Tonkin, Andrew M., van Bockxmeer, Frank, Waddell-Smith, Kathryn E., Ward, Natalie C., White, Harvey D., Wilson, Andrew M., Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J., Brett, Peter, Elias, Luke, Malan, Wynand, Irvin, John, Lambert, Kirsten, Pedrotti, Annette, and FH Australasia Network Consensus Working Group

Abstract

Introduction Familial hypercholesterolaemia (FH) is a common, heritable and preventable cause of premature coronary artery disease, with significant potential for positive impact on public health and healthcare savings. New clinical practice recommendations are presented in an abridged guidance to assist practitioners in enhancing the care of all patients with FH. Main recommendations Core recommendations are made on the detection, diagnosis, assessment and management of adults, children and adolescents with FH. There is a key role for general practitioners (GPs) working in collaboration with specialists with expertise in lipidology. Advice is given on genetic and cholesterol testing and risk notification of biological relatives undergoing cascade testing for FH; all healthcare professionals should develop skills in genomic medicine. Management is under-pinned by the precepts of risk stratification, adherence to healthy lifestyles, treatment of non-cholesterol risk factors, and appropriate use of low-density lipoprotein (LDL)-cholesterol lowering therapies, including statins, ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Recommendations on service design are provided in the full guidance. Potential impact on care of FH These recommendations need to be utilised using judicious clinical judgement and shared decision making with patients and families. Models of care need to be adapted to both local and regional needs and resources. In Australia new government funded schemes for genetic testing and use of PCSK9 inhibitors, as well as the National Health Genomics Policy Framework, will enable adoption of these recommendations. A broad implementation science strategy is, however, required to ensure that the guidance translates into benefit for all families with FH.

Published
2021

12. Integrated guidance for enhancing the care of familial hypercholesterolaemia in Australia

Author

Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., Pang, Jing, Ademi, Zanfina, Ardill, Justin J., Barnett, Wendy, Bates, Timothy R., Beilin, Lawrence J., Bishop, Warrick, Black, J. Andrew, Brett, Peter, Brown, Alex, Burnett, John R., Bursill, Christina A., Colley, Alison, Clifton, Peter M., Ekinci, Elif I., Elias, Luke, Figtree, Gemma A., Forge, Brett H., Garton-Smith, Jacquie, Graham, Dorothy F., Hamilton-Craig, Ian, Hamilton-Craig, Christian R., Heal, Clare, Hespe, Charlotte M., Hooper, Amanda J., Howes, Laurence G., Ingles, Jodie, Irvin, John, Janus, Edward D., Kangaharan, Nadarajah, Keech, Anthony C., Kirke, Andrew B., Kritharides, Leonard, Kyle, Campbell V., Lacaze, Paul, Lambert, Kirsten, Li, Stephen C. H., Malan, Wynand, Maticevic, Stjepana, McQuillan, Brendan M., Mirzaee, Sam, Mori, Trevor A., Morton, Allison C., Colquhoun, David M., Moullin, Joanna C., Nestel, Paul J., Nowak, Kristen J., O'Brien, Richard C., Pachter, Nicholas, Page, Michael M., Pedrotti, Annette, Psaltis, Peter J., Radford, Jan, Reid, Nicola J., Robertson, Elizabeth N., Ryan, Jacqueline D. M., Sarkies, Mitchell N., Schultz, Carl J., Scott, Russell S., Semsarian, Christopher, Simons, Leon A., Spinks, Catherine, Tonkin, Andrew M., van Bockxmeer, Frank, Waddell-Smith, Kathryn E., Ward, Natalie C., White, Harvey D., Wilson, Andrew M., Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J., FH Australasia Network Consensus Working Group, Watts, Gerald F., Sullivan, David R., Hare, David L., Kostner, Karam M., Horton, Ari E., Bell, Damon A., Brett, Tom, Trent, Ronald J., Poplawski, Nicola K., Martin, Andrew C., Srinivasan, Shubha, Justo, Robert N., Chow, Clara K., Pang, Jing, Ademi, Zanfina, Ardill, Justin J., Barnett, Wendy, Bates, Timothy R., Beilin, Lawrence J., Bishop, Warrick, Black, J. Andrew, Brett, Peter, Brown, Alex, Burnett, John R., Bursill, Christina A., Colley, Alison, Clifton, Peter M., Ekinci, Elif I., Elias, Luke, Figtree, Gemma A., Forge, Brett H., Garton-Smith, Jacquie, Graham, Dorothy F., Hamilton-Craig, Ian, Hamilton-Craig, Christian R., Heal, Clare, Hespe, Charlotte M., Hooper, Amanda J., Howes, Laurence G., Ingles, Jodie, Irvin, John, Janus, Edward D., Kangaharan, Nadarajah, Keech, Anthony C., Kirke, Andrew B., Kritharides, Leonard, Kyle, Campbell V., Lacaze, Paul, Lambert, Kirsten, Li, Stephen C. H., Malan, Wynand, Maticevic, Stjepana, McQuillan, Brendan M., Mirzaee, Sam, Mori, Trevor A., Morton, Allison C., Colquhoun, David M., Moullin, Joanna C., Nestel, Paul J., Nowak, Kristen J., O'Brien, Richard C., Pachter, Nicholas, Page, Michael M., Pedrotti, Annette, Psaltis, Peter J., Radford, Jan, Reid, Nicola J., Robertson, Elizabeth N., Ryan, Jacqueline D. M., Sarkies, Mitchell N., Schultz, Carl J., Scott, Russell S., Semsarian, Christopher, Simons, Leon A., Spinks, Catherine, Tonkin, Andrew M., van Bockxmeer, Frank, Waddell-Smith, Kathryn E., Ward, Natalie C., White, Harvey D., Wilson, Andrew M., Winship, Ingrid, Woodward, Ann Marie, Nicholls, Stephen J., and FH Australasia Network Consensus Working Group

Abstract

Familial hypercholesterolaemia (FH) is a dominant and highly penetrant monogenic disorder present from birth that markedly elevates plasma low-density lipoprotein (LDL)-cholesterol concentration and, if untreated, leads to premature atherosclerosis and coronary artery disease (CAD). There are approximately 100,000 people with FH in Australia. However, an overwhelming majority of those affected remain undetected and inadequately treated, consistent with FH being a leading challenge for public health genomics. To further address the unmet need, we provide an updated guidance, presented as a series of systematically collated recommendations, on the care of patients and families with FH. These recommendations have been informed by an exponential growth in published works and new evidence over the last 5 years and are compatible with a contemporary global call to action on FH. Recommendations are given on the detection, diagnosis, assessment and management of FH in adults and children. Recommendations are also made on genetic testing and risk notification of biological relatives who should undergo cascade testing for FH. Guidance on management is based on the concepts of risk re-stratification, adherence to heart healthy lifestyles, treatment of non-cholesterol risk factors, and safe and appropriate use of LDL-cholesterol lowering therapies, including statins, ezetimibe, proprotein convertase subtilisin/kexin type 9 inhibitors and lipoprotein apheresis. Broad recommendations are also provided for the organisation and development of health care services. Recommendations on best practice need to be underpinned by good clinical judgment and shared decision making with patients and families. Models of care for FH need to be adapted to local and regional health care needs and available resources. A comprehensive and realistic implementation strategy, informed by further research, including assessments of cost-benefit, will be required to ensure that this new guidance benefits

Published
2021

13. Synopsis of an integrated guidance for enhancing the care of familial hypercholesterolaemia: an Australian perspective

Author

Watts, Gerald F., primary, Sullivan, David R., additional, Hare, David L., additional, Kostner, Karam M., additional, Horton, Ari E., additional, Bell, Damon A., additional, Brett, Tom, additional, Trent, Ronald J., additional, Poplawski, Nicola K., additional, Martin, Andrew C., additional, Srinivasan, Shubha, additional, Justo, Robert N., additional, Chow, Clara K., additional, Pang, Jing, additional, Ademi, Zanfina, additional, Ardill, Justin J, additional, Barnett, Wendy, additional, Bates, Timothy R, additional, Beilin, Lawrence J, additional, Bishop, Warrick, additional, Black, J Andrew, additional, Brown, Alex, additional, Burnett, John R, additional, Bursill, Christina A, additional, Colley, Alison, additional, Clifton, Peter M, additional, Ekinci, Elif I, additional, Figtree, Gemma A, additional, Forge, Brett H, additional, Garton-Smith, Jacquie, additional, Graham, Dorothy F, additional, Hamilton-Craig, Ian, additional, Hamilton-Craig, Christian R, additional, Heal, Clare, additional, Hespe, Charlotte M, additional, Hooper, Amanda J, additional, Howes, Laurence G, additional, Ingles, Jodie, additional, Janus, Edward D, additional, Kangaharan, Nadarajah, additional, Keech, Anthony C, additional, Kirke, Andrew B, additional, Kritharides, Leonard, additional, Kyle, Campbell V, additional, Lacaze, Paul, additional, Li, Stephen CH, additional, Maticevic, Stjepana, additional, McQuillan, Brendan M, additional, Mirzaee, Sam, additional, Mori, Trevor A, additional, Morton, Allison C, additional, Colquhoun, David M, additional, Moullin, Joanna C, additional, Nestel, Paul J, additional, Nowak, Kristen J, additional, O'Brien, Richard C, additional, Pachter, Nicholas, additional, Page, Michael M, additional, Psaltis, Peter J, additional, Radford, Jan, additional, Reid, Nicola J, additional, Robertson, Elizabeth N, additional, Ryan, Jacqueline DM, additional, Sarkies, Mitchell N, additional, Schultz, Carl J, additional, Scott, Russell S, additional, Semsarian, Christopher, additional, Simons, Leon A, additional, Spinks, Catherine, additional, Tonkin, Andrew M, additional, van Bockxmeer, Frank, additional, Waddell-Smith, Kathryn E, additional, Ward, Natalie C, additional, White, Harvey D, additional, Wilson, Andrew M, additional, Winship, Ingrid, additional, Woodward, Ann Marie, additional, Nicholls, Stephen J, additional, Brett, Peter, additional, Elias, Luke, additional, Malan, Wynand, additional, Irvin, John, additional, Lambert, Kirsten, additional, and Pedrotti, Annette, additional

Published
2021
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14. Disparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathy

Author

Tan, Adeline L.Y., Sourris, Karly C., Harcourt, Brooke E., Thallas-Bonke, Vicki, Penfold, Sally, Andrikopoulos, Sofianos, Thomas, Merlin C., O'Brien, Richard C., Bierhaus, Angelika, Cooper, Mark E., Forbes, Josephine M., and Coughlan, Melinda T.

Subjects
Diabetic nephropathies -- Development and progression, Diabetic nephropathies -- Genetic aspects, Diabetic nephropathies -- Diet therapy, Gene expression -- Research, Glycosylation -- Observations, Advanced glycation end products -- Properties, Biological sciences
Abstract

Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) generate ROS, and therefore this study evaluated the effects of RAGE deletion, decreasing AGE accumulation, or lowering dietary AGE content on oxidative parameters in diabetic nephropathy (DN). Control and diabetic male wild-type and RAGE-deficient ([RAGE.sup.-/-]) mice were fed high- or low-AGE diets, with two groups given the inhibitor of AGE accumulation, alagebrium chloride, and followed for 24 wk. Diabetic [RAGE.sup.-/-] mice were protected against albuminuria, hyperfiltration, glomerulosclerosis, decreased renal mitochondrial ATP production, and excess generation of both mitochondrial and cytosolic superoxide. Whereas glomerulosclerosis, tubulointerstitial expansion, and hyperfiltration were improved in diabetic mice treated with alagebrium, there was no effect on urinary albumin excretion. Both diabetic [RAGE.sup.-/-] and alagebrium-treated mice had an attenuation of renal RAGE expression and decreased renal and urinary AGE (carboxymethyllysine) levels. Low-AGE diets did not confer renoprotection, lower the AGE burden or renal RAGE expression, or improve cytosolic or mitochondrial superoxide generation. Renal uncoupling protein-2 gene expression and mitochondrial membrane potential were attenuated by all therapeutic interventions in diabetic mice. In the present study, diverse approaches to block the AGE-RAGE axis had disparate effects on DN, which has potential clinical implications for the way this axis should be targeted in humans. advanced glycation; advanced glycation end products; receptor of advanced glycation end products doi:10.1152/ajprenal.00591.2009

Published
2010

15. Integrated Guidance for Enhancing the Care of Familial Hypercholesterolaemia in Australia

Author

Watts, Gerald F., primary, Sullivan, David R., additional, Hare, David L., additional, Kostner, Karam M., additional, Horton, Ari E., additional, Bell, Damon A., additional, Brett, Tom, additional, Trent, Ronald J., additional, Poplawski, Nicola K., additional, Martin, Andrew C., additional, Srinivasan, Shubha, additional, Justo, Robert N., additional, Chow, Clara K., additional, Pang, Jing, additional, Ademi, Zanfina, additional, Ardill, Justin J., additional, Barnett, Wendy, additional, Bates, Timothy R., additional, Beilin, Lawrence J., additional, Bishop, Warrick, additional, Black, J. Andrew, additional, Brett, Peter, additional, Brown, Alex, additional, Burnett, John R., additional, Bursill, Christina A., additional, Colley, Alison, additional, Clifton, Peter M., additional, Ekinci, Elif I., additional, Elias, Luke, additional, Figtree, Gemma A., additional, Forge, Brett H., additional, Garton-Smith, Jacquie, additional, Graham, Dorothy F., additional, Hamilton-Craig, Ian, additional, Hamilton-Craig, Christian R., additional, Heal, Clare, additional, Hespe, Charlotte M., additional, Hooper, Amanda J., additional, Howes, Laurence G., additional, Ingles, Jodie, additional, Irvin, John, additional, Janus, Edward D., additional, Kangaharan, Nadarajah, additional, Keech, Anthony C., additional, Kirke, Andrew B., additional, Kritharides, Leonard, additional, Kyle, Campbell V., additional, Lacaze, Paul, additional, Lambert, Kirsten, additional, Li, Stephen C.H., additional, Malan, Wynand, additional, Maticevic, Stjepana, additional, McQuillan, Brendan M., additional, Mirzaee, Sam, additional, Mori, Trevor A., additional, Morton, Allison C., additional, Colquhoun, David M., additional, Moullin, Joanna C., additional, Nestel, Paul J., additional, Nowak, Kristen J., additional, O'Brien, Richard C., additional, Pachter, Nicholas, additional, Page, Michael M., additional, Pedrotti, Annette, additional, Psaltis, Peter J., additional, Radford, Jan, additional, Reid, Nicola J., additional, Robertson, Elizabeth N., additional, Ryan, Jacqueline D.M., additional, Sarkies, Mitchell N., additional, Schultz, Carl J., additional, Scott, Russell S., additional, Semsarian, Christopher, additional, Simons, Leon A., additional, Spinks, Catherine, additional, Tonkin, Andrew M., additional, van Bockxmeer, Frank, additional, Waddell-Smith, Kathryn E., additional, Ward, Natalie C., additional, White, Harvey D., additional, Wilson, Andrew M., additional, Winship, Ingrid, additional, Woodward, Ann Marie, additional, and Nicholls, Stephen J., additional

Published
2021
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17. Statin intolerance: an updated, narrative review mainly focusing on muscle adverse effects

Author

Li, Jian-Jun, primary, Liu, Hui-Hui, additional, Wu, Na-Qiong, additional, Yeo, Khung Keong, additional, Tan, Kathryn, additional, Ako, Junya, additional, Krittayaphong, Rungroj, additional, Tan, Ru San, additional, Aylward, Philip E, additional, Baek, Sang Hong, additional, Dalal, Jamshed, additional, Fong, Alan Yean Yip, additional, Li, Yi-Heng, additional, O’Brien, Richard C, additional, Lim, Tien Siang Eric, additional, Koh, Si Ya Natalie, additional, Scherer, Daniel J, additional, Tada, Hayato, additional, Kang, Vernon, additional, Butters, Julie, additional, and Nicholls, Stephen J, additional

Published
2020
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18. Systemic arterial compliance is reduced in young patients with IDDM

Author

Berry, Karen L., Skyrme-Jones, R. Andrew P., Cameron, James D., O'Brien, Richard C., and Meredith, Ian T.

Subjects
Type 1 diabetes -- Research, Arteries -- Research, Diabetics -- Research, Biological sciences
Abstract

Research was conducted to examine the hypothesis that young patients with insulin-dependent diabetes mellitus (IDDM) have reduced arterial compliance before developing endothelial dysfunction or overt micro- and macrovascular disease. An analysis of endothelium-dependent flow-mediated vasodilation and systemic arterial compliance in 25 individuals with uncomplicated IDDM was performed and the relationship between the endothelial function and arterial compliance was investigated. Results suggest that compliance was not related to the integrity of endothelial vasodilator function, degree of glycemic control or disease duration.

Published
1999

20. Lipoprotein apheresis and PCSK9 inhibitors for severe familial hypercholesterolaemia: Experience from Australia and New Zealand.

Author

Page, Michael M, Ekinci, Elif I, Burnett, John R, Hooper, Amanda J, Reid, Nicola, Bishop, Warrick, Florkowski, Chris M, Scott, Russell, O'Brien, Richard C, and Watts, Gerald F

Subjects
FAMILIAL hypercholesterolemia, QUALITY of life, CAREGIVERS
Abstract

Introduction: Severe familial hypercholesterolaemia (FH) causes premature disability and death due to atherosclerotic cardiovascular disease and is refractory to standard lipid‐lowering therapies. Lipoprotein apheresis (LA) has long been a standard of care for patients with severe FH, but is invasive, expensive and time‐consuming for patients and their caregivers. Newer drug therapies, including the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, may reduce the need for LA. Materials and methods: We audited the records of 16 patients (eight homozygous, eight heterozygous) treated with LA in Australia and New Zealand, 14 of whom subsequently commenced PCSK9 inhibitor therapy. LA was performed by cascade filtration in all centres. Results: LDL‐cholesterol was acutely lowered by 69 ± 7% in patients with homozygous FH and by 72 ± 9% in those with heterozygous FH, representing time‐averaged reductions of 36 ± 12% and 34 ± 5%, respectively. LA was well‐tolerated, and patients reported comparable quality of life to population and disease‐related norms. After commencement of PCSK9 inhibitors, four of seven patients with homozygous FH had meaningful biochemical responses, with a reduction in the frequency of LA permitted in one patient and complete cessation in another. Four of seven patients with heterozygous FH were able to be managed without LA after commencing PCSK9 inhibitors. Conclusion: While PCSK9 inhibitors have reduced the need for LA, some patients with severe FH continue to require LA, and will require it for the foreseeable future. However, emerging therapies, including angiopoetin‐like 3 inhibitors, may further reduce the need for LA. [ABSTRACT FROM AUTHOR]

Published
2021
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21. The effects of perindopril and triple therapy in a normotensive model of diabetic nephropathy

Author

O'Brien, Richard C., Cooper, Mark E., Jerums, George, and Doyle, Austin E.

Subjects
ACE inhibitors -- Evaluation, Diabetic nephropathies -- Development and progression -- Drug therapy, Hypertension -- Drug therapy -- Development and progression, Health, Drug therapy, Evaluation, Development and progression
Abstract

The effect of the angiotensin-converting enzyme inhibitor, perindopril, on functional and structural parameters of diabetic nephropathy has been compared with triple therapy (hydralzine, reserpine, and hydrochlorothiazide) in normotensive, STZ-induced diabetic [...]

Published
1993

23. Nephropathy in model combining genetic hypertension with experimental diabetes: enalapril versus hydralazine and metoprolol therapy

Author

Cooper, Mark E., Allen, Terri J., O'Brien, Richard C., Papazoglou, Dimitria, Clarke, Belinda E., Jerums, George, and Doyle, Austin E.

Subjects
Metoprolol -- Physiological aspects, Enalapril -- Physiological aspects, Diabetic nephropathies -- Models, Hypertension -- Complications, Antihypertensive drugs -- Physiological aspects, Diabetic nephropathies -- Prevention, Hypertension -- Drug therapy, Hydralazine -- Physiological aspects, Health
Abstract

The effects of enalapril (an angiotensin-converting enzyme inhibitor), hydralazine and metoprolol (conventional antihypertensive drugs) on kidney function; the urinary excretion of the blood protein albumin; and the structure of glomeruli (the filtering units of the kidney) were assessed in experimental hypertensive rats with and without diabetes. Spontaneously hypertensive rats (SHR; a special breed of rats with high blood pressure) were made diabetic with the agent streptozocin, which destroys the insulin-secreting beta cells in the pancreas. The antihypertensive drugs were given to the rats in their drinking water. Enalapril and hydralazine plus metoprolol produced similar decreases in blood pressure. The blood levels of creatinine (an indicator of kidney function) increased in untreated diabetic SHR rats after 32 weeks, but not in treated, diabetic and treated, nondiabetic SHR rats. Both drug regimens caused similar decreases in albuminuria (urinary excretion of albumin), thickening of the glomerular basement membrane, and glomerular volume. These findings show that antihypertensive treatment delays the development of albuminuria, glomerular basement thickening, and glomerular overgrowth in SHR rats with and without diabetes. Enalapril did not appear to have additional benefit over the conventional antihypertensive agents in these models of hypertension-related kidney disease. Studies examining the effects of different types of antihypertensive agents on kidney function, albuminuria, and glomerular structure in humans are needed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

24. Design of the Familial Hypercholesterolaemia Australasia Network Registry: Creating Opportunities for Greater International Collaboration

Author

Bellgard, Matthew I, primary, Walker, Caroline E, additional, Napier, Kathryn R, additional, Lamont, Leanne, additional, Hunter, Adam A, additional, Render, Lee, additional, Radochonski, Maciej, additional, Pang, Jing, additional, Pedrotti, Annette, additional, Sullivan, David R, additional, Kostner, Karam, additional, Bishop, Warrick, additional, George, Peter M, additional, O’Brien, Richard C, additional, Clifton, Peter M, additional, Bockxmeer, Frank M Van, additional, Nicholls, Stephen J, additional, Hamilton-Craig, Ian, additional, Dawkins, Hugh JS, additional, and Watts, Gerald F, additional

Published
2017
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25. Comparison of effects of diabetes mellitus on an EDHF-dependent and an EDHF-independent artery

Author

WIGG, SUSAN J., TARE, MARIANNE, TONTA, MARY A., O'BRIEN, RICHARD C., MEREDITH, IAN T., and PARKINGTON, HELENA C.

Subjects
Diabetes -- Physiological aspects, Endothelium -- Research, Biological sciences
Abstract

Comparison of effects of diabetes mellitus on an EDHF-dependent and an EDHF-independent artery. Am J Physiol Heart Circ Physiol 281: H232-H240, 2001.--The hypothesis tested in this study is that diabetes has a different impact on an artery in which endothelium-dependent responses derive from both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) compared with responses in which NO predominates and EDHF is absent. The streptozotocin-treated rat model of diabetes was used, and the arteries were mounted on a wire myograph. In mesenteric arteries depolarized and constricted with phenylephrine, acetylcholine evoked hyperpolarization (31 [+ or -] 2 mV) and complete relaxation; these responses were attributed to EDHF and NO. In femoral arteries, acetylcholine evoked a small, NO-mediated hyperpolarization (5 [+ or -] 1 mV) and incomplete relaxation. Bradykinin evoked NO-dependent responses in mesenteric arteries. Whereas diabetes significantly impaired the EDHF-dependent hyperpolarization and relaxation in mesenteric arteries, NO-dependent responses in femoral and mesenteric arteries were preserved, 1-Ethyl-2-benzimidazolinone evoked hyperpolarization and relaxation in mesenteric arteries, and this was impaired in diabetes. In conclusion, NO-dependent responses are preserved in diabetes, whereas endothelial responses-dependent upon EDHF appear to be impaired. The putative channels responsible for mediating the EDHF response may be altered in diabetes. hyperpolarization and relaxation; nitric oxide; endothelium-derived hyperpolarizing factor; mesenteric artery; femoral artery

Published
2001

31. Welcome to the fifth year of economic expansion, a record breaker

Author

Qualls, John, Lashinsky, Bernie, O'Brien, Richard C., and Corrigan, Thomas D.

Subjects
United States economic conditions -- Forecasts and trends, Purchasing -- Forecasts and trends, Inflation (Finance) -- Forecasts and trends, Balance of trade -- Forecasts and trends, Business, Business, general
Published
1987

41. Diabetic dyslipidaemia

Author

Best, James D, primary, Jerums, George, additional, Newnham, Harvey H, additional, and O'Brien, Richard C, additional

Published
1995
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42. Microalbuminuria in diabetes

Author

Jerums, George, primary, Cooper, Mark E, additional, Gilbert, Richard E, additional, O'Brien, Richard C, additional, and Taft, Jonathan L, additional

Published
1994
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49. Clinical Thiazolidinediones as PPARγ Ligands with the Potential for the Prevention of Cardiovascular Disease in Diabetes

Author

de Dios, Stephanie T., O'Brien, Richard C., and Little, Peter J.

Abstract

Thiazolidinediones (TZDs) are PPARγ ligands and the newest class of agents in routine clinical practice for the treatment of hyperglycemia in type 2 diabetes. The prime reason for treating hyperglycemia and related aspects of the metabolic syndrome is to prevent accelerated cardiovascular disease (CVD) in diabetes. The formation and subsequent rupture of atherosclerotic "plaques", establishes CVD as the major cause of premature mortality in diabetes. Metabolically, TZDs act as insulin sensitizers resulting in improved glucose uptake, lower blood glucose and reduced hyperinsulinemia, however, they also appear to have beneficial direct vascular actions. TZDs have a range of actions directly on vascular cells and the predominance of the reported actions is potentially beneficial. TZDs inhibit vascular smooth muscle cell proliferation, inhibit the expression of adhesion molecules and modify the structure of vascular proteoglycans in a manner that results in reduced lipid binding. These actions manifest as reduced lipid deposition in the vessels of animals with experimental diabetes and atherosclerosis. Early clinical data indicates that TZDs may prevent or delay CVD including atherosclerosis and restenosis following coronary angiography. TZDs may be the first class of oral hypoglycemic agents with significant anti-atherogenic effects to combat one of the major complications of diabetes.

Published
2006

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