Eosinophilia II

This is a continuation of yesterday's case.

How do you go about approaching a bizarre case of constitutional symptoms, global weakness, eosinophilia, and multi-organ failure in a young man with only mild asthma? Of course, as the information comes in, we alight on different bits of data which take us down diverging pathways. As we realize the gravity of the situation, we begin to take a more shotgun approach, ordering any tests that might give us clarity of the situation. But unfortunately, such tests can often confound things.

Here, the outside hospital ordered a battery of tests, most of which came back negative. The following were normal: SPEP, anticardiolipin antibodies, treponema pallidum antibodies, B12, parvovirus B19, Sjogrens A and B, ANA, antithrombin III, lupus anticoagulant, HIV 1 and 2 antibodies, mycoplasma, ASO, Hep B panel (evidence of immunization, no infection), Hep C, Hep A, TSH. The following were abnormal: IgE elevated, RF elevated, ESR and CRP mildly elevated, protein C slightly low (protein S normal).

Of course a patient like this gets pan-consulted, running the risk of too many cooks in the kitchen. Specialized tests and procedures get thrown about and each specialist interprets the data slightly differently. As rheumatology, heme/onc, and neurology weighed in, we got more tests: negative myeloperoxidase, anti-proteinase 3, HTLV, and BCR/abl. A C3 was slightly low and C4 was normal.

The way I approached this case was figuring out cause and effect. As things began to unfold, we reasoned that the altered mental status was likely a result of the multiple embolic strokes; these emboli, it turns out, were coming from the heart. The liver failure was likely from congestive hepatopathy and the renal failure was likely from decreased perfusion due to cardiac injury. Thus, in our minds, the case whittled down to a bizarre eosinophilia with cardiac dysfunction.

Further imaging began to elucidate the picture. A CT chest showed four-chamber enlargement with sub-endocardial irregularity and low attenuation in the apices of both ventricles. Bulky lymphadenopathy and patchy peripheral ground glass opacity and consolidation were also seen. A transthoracic echocardiogram showed severe left ventricular hypertrophy, normal systolic function, and endocardial thickening with obliteration of the left apex. There was involvement of the posterior mitral valve leaflet with mitral regurgitation. All of these were suggestive of something I'd never heard of: Loeffler endocarditis, a restrictive cardiomyopathy associated with eosinophilia.