We sincerely thank Dr Jolobe for the response to our paper1 and very much appreciate the interesting addition2 to the discussion on this difficult topic. It is true that autoimmunity has been proposed to play a role in the aetiology of Peripartum Cardiomyopathy (PPCM), as we mention in our introduction. Furthermore, it is indeed well known that congestive heart failure due to (dilated) cardiomyopathy can occur in patients with hypopituitarism or acute pituitary failure,3 4 as well as in adrenal insufficiency3 and thyroid dysfunction.5 However, there are numerous case reports supporting that this is certainly not exclusive to a peripartum onset.6–8 According to the latest definition from the Heart Failure Association of the European Society of Cardiology (ESC) Working Group on PPCM, PPCM is defined as an idiopathic cardiomyopathy presenting with heart failure secondary to left ventricular systolic dysfunction towards the end of pregnancy or in the months following delivery, where no other cause of heart failure is found.9 We therefore believe that the women Dr Jolobe mentions in the response, while very interesting and certainly worth discussing in the context of our paper, did not suffer from PPCM. Of course, the endocrine system and specifically the pituitary will undergo major changes during pregnancy, and many cases of acute heart failure due to Sheenan syndrome and postpartum haemorrhage have been reported in the literature.3 10 11 However, cardiomyopathy secondary to Sheenan syndrome is just that. While the peripartum onset mimics PPCM and thus poses a diagnostic dilemma, it is important to make the distinction for, as Dr Jolobe rightly points out, patients may not benefit from conventional heart failure therapy.11 We therefore wholeheartedly agree with Dr Jolobe that in women with peripartum-onset heart failure of unknown cause, evaluation of the endocrine status is mandatory.