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Was the term NSF created before or after Gd was found to be the cause, and other questions

The following represents answers to an outstanding collection of questions I have received in recent months. I will weave in my responses to the various questions.

Question: discuss why the terms NSF, GDD, and GSC have been used rather than simply calling illness from retained gadolinium "exposure to toxic heavy metal - gadolinium" (there is a diagnosis code for that)?

Answer: With essentially all diseases, there are subtypes that are worth separating out. So as I have written in many blogs, NSF, GDD, and GSC are all relatively distinct. But you are correct, they are all part of gadolinium toxicity (GT). Acute Hypersensitivity Reactions (AHR) have to be included under the umbrella of GT. I believe we will find that the dominant immune cells involved in the response distinguish these entities. There are ICD-10 and CPT codes that refer to toxicity of heavy metals (other), and also chelation of heavy metals (other) - which yes I think could/should be used - but it is not yet specifically subcategorized as Gd, beyond 'other'.

Question:Was the term NSF coined before or after it was discovered that gadolinium was the culprit?

Answer: Briefly, and I may be off by 1 year, here or there (without looking it up again). Dr Shawn Cowper, Yale pathologist, discovered a fibrotic skin condition that arose in renal dialysis patients, that was distinct from other entities (scleroderma, scleromyedema, etc) in 1998 (about). He called it NFD at the time (I won't name in full because I do not want the offchance of resurrecting that name). In 2000, he renamed it nephrogenic systemic fibrosis (NSF) as he then recognized it as a multisystem disorder and not just affecting skin. In 2006 Grobner intially, then Marckmann et al published series describing that NSF was associated with GBCA administration. With publications over the next 2 years or so 'association' became more certain as 'causation' as this relationship became more solid. So the term NSF arose 6 years before the Gd association, and the terminology has not been changed.

Question: have any cases of NSF occurred in gadolinium miners or others who work with gadolinium in industry?

Answer: My principal colleague in this research, has actually mentioned to me recently his concern about Gd being found in ground water, and what may arise from that. I think I posted in an earlier blog, Gd behaves very similar to lead in its toxicity profile, and there is lots of lead everywhere, and probably all of us have lead. I am not aware of any publications or studies on 'gadolinium-workers' of all kinds: one could also wonder about the individuals working with the products in contrast agent manufacturing plants. It does conjure up the image of 'radium dial painters' in the 1920s and 1930s. I could ofcourse be wrong, but I am not so worried about all these people, unless they have the genetics of GDD sufferers.

Question: has the definition of NSF been changed, since there have been a few cases in people with healthy kidneys?

Answer: I am not sure that patients with NSF have normal kidneys- I do not think so. I think patients considered to have NSF but have normal kidneys, actually have GDD, but with a pronounced fibrosis or aggressive behavior (I have categorized GDD in an earlier blog). My current opinion is that NSF primarily has chronic immune cells as the culprit (cd 34+ circulating fibrocytes) and other members of the bone marrow infiltrate team. GDD has the full range of immune cells involved, possibly centered on mid-activity cells (T cells elaborating cytokines). AHR has acute activity immune cells as the principles (mast cells, other granulocytes).I believe that GDD can occur in patients with renal failure, as it has such a broad activity of immune cell activation. Ultimately it may be the isolation of the principle immune cell combatants that determines what subcategory of gadolinium toxicity an individual has.

Just as with other heavy metals, the symptoms of gadolinium toxicity are quite varied...just as the possible adverse reactions listed on the GBCA package inserts are quite varied.

This is true, but GDD-deniers have focused on this variability, and the difficulty patients have to articulate their symptoms, to explain their view that GDD is not real and should be dismissed. So I am very cautious about saying this - I prefer to see the glass half full approach, and that is why I carefully documented the most common symptoms that patients experience in my description of GDD, and have specifically avoided the concept that anything can happen. But you are right, the symptoms are varied. But symptoms are varied in essentially all multisystem diseases: atherosclerosis as a classic example- arterial disease may predominantly affect the brain (stroke), the heart (heart attack), the legs (claudication), the male genitalia (impotence), the kidneys (renal failure), etc. We can do this same lay out with any multisystem disease: lupus for example. So I do not fall in the trap of everyone has different symptoms- yes there is variation but some symptoms are extremely common and consistent.

Question: It just seems to me that a person who undergoes an MRI with contrast and then immediately begins to experience all those admitted possible adverse reactions for years following that injection and is found to be excreting gadolinium years after the injection would have a clear case against the manufacturer of this product that was either of bad design or was defective.

Answer: As I have written in many blogs and many articles, this is the central point with GDD or any other disease that arises from some exposure or some activity. If new symptoms develop immediately after something happens, what could it possibly be but as a result from that exposure? So if a person is acutely sick immediately after a GBCA injection, with symptoms that were not pre-existent- what rational explanation is there other than that this disease arose from GBCA. I am not sure I like the legal words of bad design or defective - that are used for this type of reaction description. I don't think they are bad design or defective with many of these GBCA agents, but rather it is a logical possible adverse event that a patient may experience 'heavy metal toxicity' symptoms after receiving a heavy metal based drug.

Question:It seems the radiologists have a license to kill and maim and very few are willing to speak up for the victims.

Answer: As a radiologist I struggle with this point, and maybe how you have worded it, and it varies between radiologists who deny the existence of GDD. We see these same tendencies playing out in everything: national politics, etc. It would be the excellent subject on a book on human psychology. Probably most people, and radiologists are people, approach difficult subjects with the ostrich-strategy: head in the sand. It is a self-preservation approach often based on the healthy psychology of cowardice. If you avoid an issue completely, then it is easy to rationalize it does not exist. Most people fall into this category. But you can categorize further the deniers, in a Dante's levels of Hell analogy. I think most radiologists are in this, the 4th level of Hell category: which I find amusing the description: the gluttons and the squanderers. But you can descend further into lower levels of Hell, as the stake-holder ramps up their aggressiveness. I have heard patients describe how doctors have loudly told them to leave their office and not come back when they raise the question if they have gadolinium toxicity... These physicians are probably in the 7th level of Hell> and it gets worse than that, all heavily laden with dishonesty, aggressiveness, and hypocrisy- but let us move away from this subject. Most people, the great majority, do not get sick from GBCA - but the great tragedy is when patients keep getting more GBCA injections to investigate for, what actually turns out to be GDD, so they get worse with each injection. If you think you have GDD (based on my blog description) then never get another blog again.

Question: As for the judge saying there was insufficient evidence that the symptoms the patients experienced was from gadolinium,

Answer: the package inserts list those very symptoms. The manufacturers of these GBCAs already know and admitted in their package inserts that their products can cause those symptoms. In my blog, even though it has been very difficult for me as well, and it is very imperfect as I described> the best we have for 'proof' is peer-reviewed literature. So it is difficult to fault him on that.

I will take the opportunity to mention again, and I will have a separate blog (I have written on this before, but will write again) patients often ask me about this paper or that paper, that the authors may construe disputes claims that I have made, and hence makes the patient anxious. The findings of the study relate to just what is written in the study. This is true of all studies. So if a paper is based on a GBCA injected into the peritoneum in a rat, and imaged within 48 hours, the findings pertain to that circumstance: what would happen to a rat getting an intraperitoneal injection and then sacrificed at 48 hours. This is taking just a modified description from a paper, or any animal study where they are studied out to 1 week. The point is the findings relate to just what was done in the paper - and maybe nothing more than that (but maybe a little bit more can be extrapolated from that - but you have to have the expertise to know what is reasonable to extrapolate, and what is not). By no means am I intending to be disrespectful of serious researchers doing research on animals. A study that pertains to GDD patients, unfortunately right now can only be done on GDD patients - there is no animal model for GDD, no test tube, and no normal human analogue. It does not mean these studies(test tube or animal) do not have value, many do, but one has to understand how these findings then may relate to the subject of GDD, which may be very tangential, but none-the-less of some value. The critical missing link in animal and 'normal' human research is that they do not have the immunological or neurological response to Gd that GDD sufferers have- hence this most critical spect is missing.

So papers that would directly relate to GDD patients, are GDD-susceptible individuals receiving a GBCA injection, a single injection, but up to 20 over 10 years time or more. Then be studied for immune response, treatment with various approaches, perhaps years after the exposure. That kind of study you could say - this relates to me. But a rat study, a rat given something at time 0, then studied out to 1 week, probably has little correlation with the human GDD experience - but there are tidbits in it, that an expert would be able to process out, that may add a pebble to the construction of the monolith of knowledge that is required on GDD.

Richard Semelka MD Consulting Stay tuned on the latest advancements:

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