Chelation billing. A cautionary tale.
In a recent ruling on medicare fraud In Georgia against a Dr Adams involving the False Claims Act. He and his practice was fined $27 million for filing 1.1 million $ for EDTA chelations for a variety of patient clinical symptoms, such as GI complaints and atherosclerosis, and listing the indication as lead toxicity.... Now tragically in a number of these billings this may have been correct. For example, Disodium Ca-EDTA has also been shown and FDA-sponsored trials currently ongoing as removing Ca in individuals with coronary artery disease, so using EDTA to remove arterial calcification is not necessarily a crazy idea, but not fully proven. Similarly many of the symptoms that were used to justify lead chelation actually do occur with lead toxicity (Lead Deposition Disease)..
The problem is multiple.. Everyone in the US, and perhaps around the world has lead in them.... everyone. I have mentioned before, like Gd, maybe only 1 in 10,000 to 1 in 100,000 actually have Lead Deposition Disease, the great majority have Lead Storage Condition (lead in them but not [clearly] sick from it). So I am convinced that the majority, maybe > 95% of individuals who undergo chelation with DMSA or EDTA for lead, lead is in the Storage Condition state (that is not symptomatic) and not the Deposition DIsease state (that is symptomatic).
Anticipating the future of billing for GDD. One has to keep in mind then what I have stated about GDD for several years. One has to pay close attention to that and record it.
Everyone who has a GBCA enhanced MRI performed has Gd left behind in their body. Everyone. Read an early blog on estimated amount. This means because Gd can be chelated out of the body, does not mean that the individual is sick from it.
These are the 3 commandments for the diagnosis of GDD: I. The subject received a GBCA enhanced imaging study. II. Shortly after the GBCA injection, within 1 month (there are exceptions, but there are reasons for the exceptions) the subject experiences new symptoms (see my blogs and recent papers on symptoms) associated with GDD. III. Following chelation with an effective chelator, the individual develops Flare symptoms IIIa early (immediate to 3 days post-chelation) Gd removal Flare, and IIIb late (generally 2.5 weeks +) Gd re-equilibration Flare. More work (that is a lot more money invested) to show distinguishing characteristics of cytokine release experienced by GDD vs GSC individuals. Both experience general cytokine increased release. Both also show evidence of serum markers for mitochondrial injury, in the future with more investment this likely can be distinguished.
As a footnote, one of the tragedies that can happen with correct chelation treatment of patients is that some individuals will stop chelation for the exact reason they should be continuing chelation: too strong Gd removal Flare and/or too strong Gd re-equilibration Flare (read earlier blogs on this subject. Note that this only applies to when chelation is done correctly, as we do it, and as described in prior blogs. Extreme Flares will be observed in poorly done chelation, and there is presently no excuse for poorly done chelation, as I have clearly written how it should be performed.
It is clear to me, that lack of knowledge regarding the biochemical effects and physiological responses of chelation for any heavy metal is not understood by virtually anyone doing these procedures. I will address this is an upcoming blog.
Richard Semelka, MD