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Alberto M Pereira - One of the best experts on this subject based on the ideXlab platform.
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Cabergoline and cardiac valve disease in prolactinoma patients additional studies during long term treatment are required
European Journal of Endocrinology, 2008Co-Authors: Marleen Kars, Alberto M Pereira, J J Bax, Johannes A RomijnAbstract:The increased risk of cardiac valve disease in patients treated for Parkinson's disease with Cabergoline has raised concerns about the safety of treatment with ergot-derived dopamine agonists in patients with endocrine diseases, especially prolactinoma. Six cross-sectional studies have been published recently, of which five studies do not show an association between the treatment of prolactinoma with Cabergoline during 45-79 months and clinically relevant valvular regurgitation in a total of 413 patients. Nonetheless, concern is raised because the use of Cabergoline was associated in one study with an increased prevalence of moderate tricuspid regurgitation, and in two other studies with mild tricuspid regurgitation. Furthermore, the use of Cabergoline was associated with increased frequencies of valvular thickening, calcifications and increased mitral tenting area. At present, the clinical relevance of these findings is still uncertain, but concern is raised with respect to the safety of the use of Cabergoline in the long-term treatment of prolactinomas. Echocardiographic evaluation should be considered in patients, who require long-term treatment with Cabergoline, especially in high doses. There is a need for larger, preferably prospective, studies with careful echocardiographic assessment and with longer durations of follow-up than the currently available studies.
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aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma
The Journal of Clinical Endocrinology and Metabolism, 2008Co-Authors: Marleen Kars, Johannes A Romijn, Victoria Delgado, Eduard R Holman, Richard A Feelders, Johannes W A Smit, Jeroen J Bax, Alberto M PereiraAbstract:Objective: Treatment with ergot-derived dopamine agonists, pergolide, and Cabergoline has been associated with an increased frequency of valvular heart disease in Parkinson’s disease. The aim of the present study was to assess the prevalence of valvular heart disease in patients treated with dopamine agonists for prolactinomas. Design: This was a cross-sectional study. Patients: We performed two-dimensional and Doppler echocardiography in 78 consecutive patients with prolactinoma (mean age 47 ± 1.4 yr, 26% male, 31% macroprolactinoma) treated with dopamine agonists for at least 1 yr (mean 8 ± 0.6 yr) and 78 control subjects. Patients were classified according to treatment: patients treated with Cabergoline (group 1: n = 47) and patients not treated with Cabergoline (group 2: n = 31). Results: Clinically relevant valvular heart disease was present in 12% of patients (nine of 78) vs. 17% of controls (13 of 78) (P = 0.141) and 17% (eight of 47) of patients treated with Cabergoline vs. 3% (one of 31) of patie...
Johannes A Romijn - One of the best experts on this subject based on the ideXlab platform.
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Cabergoline and cardiac valve disease in prolactinoma patients additional studies during long term treatment are required
European Journal of Endocrinology, 2008Co-Authors: Marleen Kars, Alberto M Pereira, J J Bax, Johannes A RomijnAbstract:The increased risk of cardiac valve disease in patients treated for Parkinson's disease with Cabergoline has raised concerns about the safety of treatment with ergot-derived dopamine agonists in patients with endocrine diseases, especially prolactinoma. Six cross-sectional studies have been published recently, of which five studies do not show an association between the treatment of prolactinoma with Cabergoline during 45-79 months and clinically relevant valvular regurgitation in a total of 413 patients. Nonetheless, concern is raised because the use of Cabergoline was associated in one study with an increased prevalence of moderate tricuspid regurgitation, and in two other studies with mild tricuspid regurgitation. Furthermore, the use of Cabergoline was associated with increased frequencies of valvular thickening, calcifications and increased mitral tenting area. At present, the clinical relevance of these findings is still uncertain, but concern is raised with respect to the safety of the use of Cabergoline in the long-term treatment of prolactinomas. Echocardiographic evaluation should be considered in patients, who require long-term treatment with Cabergoline, especially in high doses. There is a need for larger, preferably prospective, studies with careful echocardiographic assessment and with longer durations of follow-up than the currently available studies.
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aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma
The Journal of Clinical Endocrinology and Metabolism, 2008Co-Authors: Marleen Kars, Johannes A Romijn, Victoria Delgado, Eduard R Holman, Richard A Feelders, Johannes W A Smit, Jeroen J Bax, Alberto M PereiraAbstract:Objective: Treatment with ergot-derived dopamine agonists, pergolide, and Cabergoline has been associated with an increased frequency of valvular heart disease in Parkinson’s disease. The aim of the present study was to assess the prevalence of valvular heart disease in patients treated with dopamine agonists for prolactinomas. Design: This was a cross-sectional study. Patients: We performed two-dimensional and Doppler echocardiography in 78 consecutive patients with prolactinoma (mean age 47 ± 1.4 yr, 26% male, 31% macroprolactinoma) treated with dopamine agonists for at least 1 yr (mean 8 ± 0.6 yr) and 78 control subjects. Patients were classified according to treatment: patients treated with Cabergoline (group 1: n = 47) and patients not treated with Cabergoline (group 2: n = 31). Results: Clinically relevant valvular heart disease was present in 12% of patients (nine of 78) vs. 17% of controls (13 of 78) (P = 0.141) and 17% (eight of 47) of patients treated with Cabergoline vs. 3% (one of 31) of patie...
Marleen Kars - One of the best experts on this subject based on the ideXlab platform.
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Cabergoline and cardiac valve disease in prolactinoma patients additional studies during long term treatment are required
European Journal of Endocrinology, 2008Co-Authors: Marleen Kars, Alberto M Pereira, J J Bax, Johannes A RomijnAbstract:The increased risk of cardiac valve disease in patients treated for Parkinson's disease with Cabergoline has raised concerns about the safety of treatment with ergot-derived dopamine agonists in patients with endocrine diseases, especially prolactinoma. Six cross-sectional studies have been published recently, of which five studies do not show an association between the treatment of prolactinoma with Cabergoline during 45-79 months and clinically relevant valvular regurgitation in a total of 413 patients. Nonetheless, concern is raised because the use of Cabergoline was associated in one study with an increased prevalence of moderate tricuspid regurgitation, and in two other studies with mild tricuspid regurgitation. Furthermore, the use of Cabergoline was associated with increased frequencies of valvular thickening, calcifications and increased mitral tenting area. At present, the clinical relevance of these findings is still uncertain, but concern is raised with respect to the safety of the use of Cabergoline in the long-term treatment of prolactinomas. Echocardiographic evaluation should be considered in patients, who require long-term treatment with Cabergoline, especially in high doses. There is a need for larger, preferably prospective, studies with careful echocardiographic assessment and with longer durations of follow-up than the currently available studies.
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aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma
The Journal of Clinical Endocrinology and Metabolism, 2008Co-Authors: Marleen Kars, Johannes A Romijn, Victoria Delgado, Eduard R Holman, Richard A Feelders, Johannes W A Smit, Jeroen J Bax, Alberto M PereiraAbstract:Objective: Treatment with ergot-derived dopamine agonists, pergolide, and Cabergoline has been associated with an increased frequency of valvular heart disease in Parkinson’s disease. The aim of the present study was to assess the prevalence of valvular heart disease in patients treated with dopamine agonists for prolactinomas. Design: This was a cross-sectional study. Patients: We performed two-dimensional and Doppler echocardiography in 78 consecutive patients with prolactinoma (mean age 47 ± 1.4 yr, 26% male, 31% macroprolactinoma) treated with dopamine agonists for at least 1 yr (mean 8 ± 0.6 yr) and 78 control subjects. Patients were classified according to treatment: patients treated with Cabergoline (group 1: n = 47) and patients not treated with Cabergoline (group 2: n = 31). Results: Clinically relevant valvular heart disease was present in 12% of patients (nine of 78) vs. 17% of controls (13 of 78) (P = 0.141) and 17% (eight of 47) of patients treated with Cabergoline vs. 3% (one of 31) of patie...
Sophie Vallette - One of the best experts on this subject based on the ideXlab platform.
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Cabergoline therapy for prolactinomas is valvular heart disease a real safety concern
Expert Review of Cardiovascular Therapy, 2010Co-Authors: Sophie Vallette, Karim Serri, Omar SerriAbstract:Dopamine agonists (DAs) are the first-line therapy for the treatment of hyperprolactinemia, with Cabergoline, an ergot-derived selective D2-receptor agonist, being the preferred and most widely used drug. Recent studies reported cardiac valve regurgitations in patients with Parkinson’s disease treated with high doses of DA, raising concerns about the safety of Cabergoline in patients with hyperprolactinemia. To date, seven case–control studies have examined the potential association between cardiac valvular abnormalities and Cabergoline therapy in patients with hyperprolactinemia. Overall, a total of 463 patients exposed to low doses of Cabergoline (mean cumulative doses: 204–443 mg) for a mean duration of 45–79 months have been included in these studies. Patients in all the studies were asymptomatic without clinical signs of cardiac disease. Six studies did not show any association between Cabergoline therapy and clinically relevant valvular regurgitation, whereas one study found an increased rate of mod...
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Long-term Cabergoline therapy is not associated with valvular heart disease in patients with prolactinomas
Pituitary, 2009Co-Authors: Sophie Vallette, Karim Serri, Juan Rivera, Patricia Santagata, Sophie Delorme, Natasha Garfield, Nora Kahtani, Hugues Beauregard, Nahla Aris-jilwan, Ghislaine HoudeAbstract:Ergot-derived dopamine receptor agonists, especially pergolide and Cabergoline, have been associated with an increased risk of valvular heart disease in patients treated for Parkinson’s disease. Cabergoline at lower doses than those employed in Parkinson’s disease is widely used in patients with prolactinomas, because of its high efficacy and tolerability; however, its safety with regard to cardiac valve disease is unknown. In order to assess the prevalence of cardiac valve regurgitation in patients with prolactinomas treated with long-term Cabergoline, we performed a prospective and multicentric study including four university centers in the province of Quebec. A transthoracic echocardiogram was performed in 70 patients with prolactinomas treated with Cabergoline for at least 1 year (duration of treatment, 55 ± 22 months; cumulative dose 282 ± 271 mg, mean ± SD) and 70 control subjects matched for age and sex. Valvular regurgitation was graded according to the American Society of Echocardiography recommendations as mild, moderate, or severe. Moderate valvular regurgitation was found in four patients (5.7%) and five control subjects (7.1%) ( P = 0.73). No patient had severe valvular regurgitation. There was no correlation between the presence of significant heart-valve regurgitation and Cabergoline cumulative dose, duration of Cabergoline treatment, prior use of bromocriptine, age, adenoma size, or prolactin levels. Our results show that low doses of Cabergoline seem to be a safe treatment of hyperprolactinemic patients. However, in patients with prolonged Cabergoline treatment, we suggest that echocardiographic surveillance may be warranted.
Hiroshi Kunugi - One of the best experts on this subject based on the ideXlab platform.
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Cabergoline, Dopamine D2 Receptor Agonist, Prevents Neuronal Cell Death under Oxidative Stress via Reducing
2016Co-Authors: Haruki Odaka, Tadahiro Numakawa, Naoki Adachi, Yoshiko Ooshima, Shingo Nakajima, Yusuke Katanuma, Takafumi Inoue, Hiroshi KunugiAbstract:Several lines of evidence demonstrate that oxidative stress is involved in the pathogenesis of neurodegenerative diseases, including Parkinson’s disease. Potent antioxidants may therefore be effective in the treatment of such diseases. Cabergoline, a dopamine D2 receptor agonist and antiparkinson drug, has been studied using several cell types including mesencephalic neurons, and is recognized as a potent radical scavenger. Here, we examined whether Cabergoline exerts neuroprotective effects against oxidative stress through a receptor-mediated mechanism in cultured cortical neurons. We found that neuronal death induced by H2O2 exposure was inhibited by pretreatment with Cabergoline, while this protective effect was eliminated in the presence of a dopamine D2 receptor inhibitor, spiperone. Activation of ERK1/2 by H2O2 was suppressed by Cabergoline, and an ERK signaling pathway inhibitor, U0126, similarly protected cortical neurons from cell death. This suggested the ERK signaling pathway has a critical role in Cabergoline-mediated neuroprotection. Furthermore, increased extracellular levels of glutamate induced by H2O2, which might contribute to ERK activation, were reduced by Cabergoline, while inhibitors for NMDA receptor or L-type Ca2+ channel demonstrated a survival effect against H2O2. Interestingly, we found that Cabergoline increased expression levels of glutamate transporters such as EAAC1. Taken together, these results suggest that Cabergoline has a protective effect on cortical neurons via a receptor-mediated mechanism includin
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Cabergoline, Dopamine D2 Receptor Agonist, Prevents Neuronal Cell Death under Oxidative Stress via Reducing Excitotoxicity
2014Co-Authors: Haruki Odaka, Tadahiro Numakawa, Naoki Adachi, Yoshiko Ooshima, Shingo Nakajima, Yusuke Katanuma, Takafumi Inoue, Hiroshi KunugiAbstract:Several lines of evidence demonstrate that oxidative stress is involved in the pathogenesis of neurodegenerative diseases, including Parkinson's disease. Potent antioxidants may therefore be effective in the treatment of such diseases. Cabergoline, a dopamine D2 receptor agonist and antiparkinson drug, has been studied using several cell types including mesencephalic neurons, and is recognized as a potent radical scavenger. Here, we examined whether Cabergoline exerts neuroprotective effects against oxidative stress through a receptor-mediated mechanism in cultured cortical neurons. We found that neuronal death induced by H2O2 exposure was inhibited by pretreatment with Cabergoline, while this protective effect was eliminated in the presence of a dopamine D2 receptor inhibitor, spiperone. Activation of ERK1/2 by H2O2 was suppressed by Cabergoline, and an ERK signaling pathway inhibitor, U0126, similarly protected cortical neurons from cell death. This suggested the ERK signaling pathway has a critical role in Cabergoline-mediated neuroprotection. Furthermore, increased extracellular levels of glutamate induced by H2O2, which might contribute to ERK activation, were reduced by Cabergoline, while inhibitors for NMDA receptor or L-type Ca2+ channel demonstrated a survival effect against H2O2. Interestingly, we found that Cabergoline increased expression levels of glutamate transporters such as EAAC1. Taken together, these results suggest that Cabergoline has a protective effect on cortical neurons via a receptor-mediated mechanism including repression of ERK1/2 activation and extracellular glutamate accumulation induced by H2O2.
