Our Wish List for additional research includes:
- A Retrospective Study of patients who have had contrast MRIs with a control group of patients who have only had non-contrast MRI. Their urine levels of Gadolinium would be determined through testing, and through a brief interview, their present symptoms and conditions would be detailed. The interview would be focused on symptoms for which no cause has been identified or conditions that have been diagnosed since their contrast MRI but whose underlying cause has not been determined (idiopathic conditions). The statistical significance of any differences would help understand the effects of Gadolinium Toxicity
- A Medical Examination Study of the participants in the Survey of the Chronic Effects of Retained Gadolinium from Contrast MRIs by a selected medical team or individual. When we describe our symptoms to medical personnel, they attempt to identify a known condition that would create those symptoms. Since Gadolinium Toxicity has not been studied and documented, our groupings of symptoms do not match anything the doctor has been trained to identify. With each of our doctors only seeing one patient with our symptoms, they conclude that our problem is just a bad set of idiopathic symptoms for which they try to provide relief. In this Study, a single doctor would be seeing many Gadolinium Toxic patients and the commonality of symptoms reported would help determine the credibility of Gadolinium Toxicity as a valid condition.
- A Retrospective Study of MR Images of the Brain and Spine of patients with normal renal function who had multiple doses of a Gadolinium-Based Contrast Agent. Two recent studies have reported a progressive increase of T1 signal intensity on non-contrast images of the brain in patients who received multiple doses of Omniscan. Based on early animal testing of Omniscan and Magnevist, it appears that when the blood-brain barrier was crossed the agents caused lesions in different parts of the brain and/or spinal cord. A retrospective study of patients with normal renal function who received multiple doses of only one GBCA is needed to determine if the various agents cause abnormalities in other areas of the brain and/or spinal cord. Subsequent non-contrast MRIs should be reviewed to determine long-term changes to T1-weighted signal intensity.
I want to see tissue based studies (in animals) to confirm what is making these recently reported MR signal changes in the brain, as well as some haematology input of where any free Gd+++ sits so that it is amenable to extraction by these simple chelations. Strong clear evidence will change attitudes fast.
Great addition to the wish list. That would be a huge step in the right direction. Thanks.
Great idea to ask for tissue studies. There are good arguments, that the gadolinium toxicity is caused by the exchange of iron by gadolinium within the inflammatory active ferritin. Look at following papers:
Zhang, Lei, “INTERACTION OF FERRITIN WITH TRANSITION METAL IONS AND CHELATES” (2011). Publicly accessible
Penn Dissertations. Paper 321.
Serum ferritin is an important inflammatory disease marker ….
Metallomics, 2014,
6, 748