PPCM and type II autoimmune polyglandular syndrome

While it is true that “there is no single diagnostic test for peripartum cardiomyopathy (PPCM)” [ ], over and above echocardiographic evaluation [ ], patients with this diagnosis should also receive the benefit of endocrinological evaluation. The rationale is that PPCM may occur in association with either anterior pituitary failure [ , , ] or primary hypoadrenalism [ ], arguably, in some cases, on the basis of autoimmunity. One of the earliest examples was a 37 year old woman in whom isolated adrenocorticotrophic hormone (ACTH) deficiency coexisted with PPCM, the latter occurring two months after uneventful child birth [ ]. A year after the publication of that case report isolated ACTH deficiency was reported as a manifestation of postpartum lymphocytic hypophysitis [ ]. Lymphocytic hypophysitis was also presumed to be the associated disorder in a 37 year old woman with PPCM and complete anterior pituitary failure who presented a week after normal and uneventful child birth [ ]. An autoimmune basis for PPCM is suggested by the fact that sera from PPCM patients contain high titers of autoantibodies against normal cardiac tissue proteins 37, 33, and 25 kD that are not present in the sera of patients with idiopathic cardiomyopathy [ ]. Therefore, according to one view, it might be hypothesised that a patient with PPCM has “a severe autoimmune condition … affecting multiple organs concomitantly” [ ]. However, even when pituitary failure is of presumed ischaemic aetiology, as is the case after postpartum haemorrhage, PPCM may be the outcome [ ].