If I had to pick a theme for this week’s issue, it would be ‘Things I Thought I Didn’t Need To Worry About But Apparently Do.’ Eosinophilia, for starters.
Eosinophilia apparently falls into three broad categories – reactive, clonal, and hypereosinophilic syndrome. Reactive eosinophilia (also known as non-clonal or secondary eosinophilia) is most usually to parasitic infections, drugs, or allergies, but can occasionally be due to Churg-Strauss Syndrome, connective tissue and auto-immune disease, and other types of infections (bacterial, fungal). Remember to ask about travel, medication history, rashes, and contact with animals. Clonal eosinophilia is rare but can occur in chronic myeloid leukaemia or chronic eosinophilic leukaemia. It may also be present in Hodgkins or T-cell lymphoma. On hypereosinophilic syndrome, we’re given no details other than that it accounts for less than 1% of all eosinophilias (which, incidentally, themselves show up on about 1 – 1.5% of all blood counts).
Appropriate intions include: Repeat FBC within a week or two, with blood film (to look at the morphology of the eosinophils, which is likely to be normal in reactive eosinophilia and abnormal in primary eosinophilia). PV/CRP. Immunoglobulins. Autoantibodies – nuclear, ENA, DNA, RF, and antineutrophil cytoplasmic antibodies. CXR. If the patient has a history of foreign travel, you may need to check three hot stool specimens taken on separate occasions (for ova, cysts, and parasites), strongyloides serology, and serology relevant to the particular area of travel. Personally, I think it would be reasonable to start with a repeat FBC, PV/CRP, possibly a blood film depending on the level of the eosinophilia, and then have a chat with the haematologist and possibly microbiologist as to where to go from there.
Next, scalp cysts. If there’s one type of lesion I’m happy to pronounce benign, it’s a cyst, so it was rather a blow to learn that scalp cysts can occasionally prove malignant. All the lesions described in the case reports in this article were rare, slow-growing, took several years to diagnose, and were cured by removal even after that time, so that’s reassuring. Still, we’re supposed to bear the possibility in mind with lesions that are painful or increasing in size. Frankly, I could have done with a bit more guidance on which ones to refer.
And, finally, a study has shown that using PPIs in patients post-MI makes aspirin less effective, increasing the MI risk by around half. When I read this I did actually think of what seemed like a good reason at the time why this might have been due to confounding factors, but it is now completely escaping me. Oh, well.
On the plus side, there is apparently now another trial showing that PPIs do not, in fact reduce the anti-MI effect of clopidogrel to any clinically important extent. This was reported in an editorial that finished up by advising us to use ranitidine or pantoprazole anyway where possible. C’mon, guys – even I think there’s such a thing as being too cautious.