Greetings from Paris and the Charcot Task Force

Greetings from the Salpetriere Hospital in Paris and the ADA/APMA Task Force on Charcot Arthropathy. 

Much of the discussion is now focusing on acute inflammation as the root commonality between various clinical appearances of what has formerly been called Charcot Foot. We are now entertaining the thought of backing up a bit and defining the red hot swollen foot (in the absence of other causes) as an Inflammatory Charcot Syndrome. Perhaps something like: Neuropathic Inflammatory Charcot Syndrome (NICS). I'm sitting next to my long time friend and colleague Luigi Uccioli and much nomenclature is being bounced back and forth. Stay tuned! 
Members of the Task Force:
Lee C. Rogers
Robert Frykberg
Dane Wukich
Michael Edmonds
William Jeffcoate
Fran Game
Stephan Morbach
Alexandra Jirkovska
Agnes Hartemann
Michael Pinzur
William Morrison
Georges Ha Van
Dario Pitocco
Edward Jude
Andrew JM Boulton
Luigi Uccioli
David G. Armstrong
Lee J. Sanders
We also share you work from our colleagues Maya Huijberts and Nick Schaper regarding PET scan and inflammation in Charcot. Note it is not just bone that's inflamed!
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Clin Nucl Med. 2011 Jan;36(1):8-10.

F-18 FDG PET/CT scanning in charcot disease: a brief report.

Pickwell KMvan Kroonenburgh MJWeijers REvan Hirtum PVHuijberts MSSchaper NC.

Division of Endocrinology, Department of Internal Medicine, Maastricht University Medical Centre, CAPHRI Research School, Maastricht, The Netherlands. k.pickwell@mumc.nl

Abstract

PURPOSE: because of the increasing prevalence of diabetes, complications of diabetes will also become more prevalent. The pathophysiology of Charcot neuro-osteoarthropathy (Charcot disease) as a complication of diabetes is still enigmatic. As a consequence, the optimal diagnostic, follow-up, and therapeutic strategies are unclear. To obtain more insight into the relation between bony abnormalities and the (concurrent) inflammatory response in acute Charcot disease, thereby creating more insight into the pathophysiology of this disease, we performed F-18 FDG PET/CT scanning. Research design and methods: We performed F-18 FDG PET/CT and Tc-99m bone scintigraphy in 10 patients with Charcot disease. Bony abnormalities on CT-scan and areas of increased uptake on F-18 FDG PET and Tc-99m bone scintigraphy were assessed independently. Subsequently, fused PET/CT images were evaluated for number and location of PET lesions.

RESULTS: nine patients had increased uptake of F-18 FDG, indicating inflammation, in 25 areas of soft tissue and/or bone without concurrent bony abnormalities on CT.

CONCLUSIONS: presented F-18 FDG PET/CT data may indicate an inflammatory origin of Charcot disease, with secondary bone resorption, possibly due to decreased inhibitory neurogenic inflammatory responses as a result of small fiber neuropathy. If these findings can be confirmed in future studies, F-18 FDG PET/CT scanning may be added to the diagnostic arsenal in Charcot disease, and anti-inflammatory drugs may be added to the therapeutic arsenal.

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