Rev Bras Ginecol Obstet 2016; 38(11): 580-582
DOI: 10.1055/s-0036-1594305
Letter to the Editor
Thieme Publicações Ltda Rio de Janeiro, Brazil

Comment On: Peripartum Cardiomyopathy Treatment with Dopamine Agonist and Subsequent Pregnancy with a Satisfactory Outcome

Comentários sobre Tratamento da miocardiopatia periparto com agonista dopaminérgico e subsequente gestação com resultado satisfatório
Jakob Triebel
1  Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, Nuremberg General Hospital & Paracelsus Medical University, Nuremberg, Germany
,
Carmen Clapp
2  Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Campus UNAM-Juriquilla, Querétaro, México
,
Thomas Bertsch
1  Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, Nuremberg General Hospital & Paracelsus Medical University, Nuremberg, Germany
› Author Affiliations
Further Information

Address for correspondence

Jakob Triebel, MD
Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine
Nuremberg General Hospital & Paracelsus Medical University, Prof.-Ernst-Nathan-Str. 1, 90419 Nuremberg
Germany   

Publication History

25 September 2016

24 October 2016

Publication Date:
22 November 2016 (online)

 

Medeiros e Melo et al report a case of a patient with pre-eclampsia and peripartum cardiomyopathy (PPCM) successfully treated with the dopamine receptor D2 agonist cabergoline.[1] Treatment with the dopamine receptor agonist bromocriptine is currently being evaluated in a multicenter clinical trial[2] (NCT00998556) that is based on the concept of dopamine agonists inhibiting the enzymatic generation of prolactin-fragments (etiologically linked to PPCM) by substrate depletion, that is, the inhibition of pituitary prolactin secretion. These prolactin-fragments are termed vasoinhibins, and represent a family of hormones with effects on the angiogenesis-mediated growth of reproductive and non-reproductive organs, and in the pathogenesis of a variety of diseases, such as pre-eclampsia, PPCM, and diabetic retinopathy.[3] [4] [5] [6] [7] In PPCM, vasoinhibins cause heart failure by impairing coronary microvascular growth and function.[3]

While the report by Medeiros e Melo et al is consistent with the above-mentioned concept, it lacks important information for claiming a similar mechanism. The authors refer to vasoinhibins as “products of prolactin degradation”, thereby contradicting their role as key pathological mediators. Furthermore, the work does not contain any information on the serum levels of prolactin nor of vasoinhibins. While vasoinhibin serum levels are difficult to evaluate due to the lack of a quantitative vasoinhibin-assay, prolactin levels should have been measured throughout the course of the treatment. It is puzzling that starting the treatment with cabergoline on the 39th day post-abdominal delivery was effective, since, in the absence of lactation, prolactin levels return to the non-pregnant level within the first few weeks. Did the authors check for prolactinoma evidence? Additionally, monitoring of cardiac markers as natriuretic peptides and troponin serum levels would be of interest. In view of the scarce data about prolactin serum levels before, during, and after PPCM with or without dopamine receptor agonists, we recommend strict monitoring of prolactin serum levels throughout the course of the disease.


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Address for correspondence

Jakob Triebel, MD
Institute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine
Nuremberg General Hospital & Paracelsus Medical University, Prof.-Ernst-Nathan-Str. 1, 90419 Nuremberg
Germany