The results of a 9 question survey about gadolinium exposure and related symptoms in patients with normal renal function were reported in an article by Burke et al titled Self-reported gadolinium toxicity: A survey of patients with chronic symptoms. The survey provides the initial description in the medical literature of patients with normal renal function who self-described toxicity related to administration of gadolinium-based contrast agents (GBCAs). There were 50 respondents to the anonymous online survey. All 50 respondents (100%) received gadolinium-based contrast with an average of 4.2 doses. All 50 attribute their symptoms to gadolinium exposure.
Thirty-three (66%) subjects described the onset of symptoms immediately following GBCA administration and 16 (32%) within 6 weeks. The most common symptoms included bone/joint pain and head/neck symptoms including headache, vision change, and hearing change. Headache and bone/joint pain was described by more than 75% of the cases. Skin changes were seen in approximately 60% of respondents.
Other symptoms reported include: flu-like symptoms (30.6%); digestive symptoms described as nausea, vomiting, diarrhea (46.9%); chest symptoms described as difficulty breathing (42.9%); generalized whole body symptoms (30.6%); and other (75.5%).
The findings of the survey showed that subjects with normal renal function might develop disease following administration of the majority of GBCAs including macrocyclic agents.
Despite the limitations of the survey, the authors said that it was their opinion “that there most likely is toxicity associated with GBCA administration in patients with normal renal function”. They concluded that, “at the very least, this study highlights the need to further investigate the subject of patients with normal renal function who complain of severe long-lasting symptomatology following GBCA administration”.
My thoughts –
When Hubbs Grimm and I released the findings of the online symptom survey that we conducted in early 2014, we noted that the results presented in our paper should stimulate further professional investigation into gadolinium retention in all patient populations including those with normal renal function. It is good to see that the medical community is now looking into the issue of gadolinium retention in patients with normal renal function further.
Our paper, Gadolinium Toxicity – A Survey of the Chronic Effects of Retained Gadolinium from Contrast MRIs can be found in the Research section of our website.
Burke, L. M. B., Ramalho, M., AlObaidy, M., Chang, E., Jay, M., & Semelka, R. C. (2016). Self-Reported Gadolinium Toxicity: A Survey of Patients with Chronic Symptoms. Magnetic Resonance Imaging. http://doi.org/10.1016/j.mri.2016.05.005
Important News for Patients who have retained gadolinium –
A recently published article by UNC Radiologist Dr. Richard Semelka and his colleagues proposes naming the histopathologically proven presence of gadolinium in brain tissue “gadolinium storage condition”, and it describes a new entity that represents symptomatic deposition of gadolinium in individuals with normal renal function, for which they propose the designation “gadolinium deposition disease”. The article titled: Gadolinium in Humans: A Family of Disorders, was published in AJR online.
The article is not freely available to the public at this time. Because of that, I will provide some important information from the article for patients and their doctors below.
Gadolinium Storage Condition –
“Gadolinium storage condition” is the term proposed for gadolinium tissue deposition. The authors said, “Even in patients with normal renal function, in vivo clinical exposure to gadolinium chelates results in gadolinium incorporation into body tissues such as bone matrix or brain tissues.” (See references below.)
It appears that gadolinium accumulation varies depending on the stability of the agent used. As with NSF, the least stable GBCAs appear to be most likely to result in gadolinium storage condition, and stable agents either do not cause it or cause it at a very low level. The clinical significance of gadolinium tissue deposition remains incompletely understood.
Gadolinium Deposition Disease –
“Gadolinium deposition disease” is the name proposed for a disease process observed in subjects with normal or near normal renal function who develop persistent symptoms that arise hours to 2 months after the administration of gadolinium-based contrast agents (GBCAs). In these cases, no preexistent disease or subsequently developed disease of an alternate known process is present to account for the symptoms.
The authors note that some of these patients are likely to have coexistent gadolinium storage condition, as described above, but gadolinium deposition disease is also described after a single administration of GBCA. The causal relationship has not been fully established, but it is under investigation.
The article references our MRI Gadolinium-Toxicity support group and notes that the group has reported symptoms it considers to be consistent with the known toxic effects of gadolinium. They also cite the results of our 2014 Symptom Survey which suggests an association between chronic effects and GBCA exposure.
The authors said, in their experience, “Symptoms of gadolinium deposition disease are similar but not identical to those observed in NSF”. They said that their preliminary investigation has convinced them that this phenomenon is a true disease process. (more…)
Editorial – Last December, I posted a Viewpoint titled “Gadolinium Retention – Is it all in my head?” When I wrote that, I believed I had retained gadolinium in my brain, thyroid gland, and various other parts of my body. I believed it, but I did not know it for sure. It is one thing to think it, but it causes totally different feelings when you have confirmation that you have retained a toxic metal in your body.
On April 8, 2015, I posted about the gadolinium found in my thyroid tissue that was removed 51 months after my 5th dose of a linear gadolinium-based contrast agent. In July, I learned that an analysis of my 2012 non-contrast brain MRI found evidence of gadolinium deposition in the globus pallidus; that MRI was performed exactly two years after my last dose of contrast. Because of recently published studies, I was not surprised that they detected residual gadolinium in my brain. At the time of my MRIs, except for hypertension and a past history of migraine headaches, I had no history of anything known to alter the blood-brain barrier. Then and now, I continue to have “normal” renal function with an eGFR >60, but yet, I have evidence of long-term retention of gadolinium in my body. If I only had gadolinium in my tissues and no symptoms, I might not worry about it as much, but that is not the case. (more…)
My first exposure to a Gadolinium-based Contrast Agent or GBCA took place in mid-2000. Of course, at that time I had no idea what they were injecting into me. All I knew was my doctor wanted me to have a brain MRI with contrast. Thankfully nothing abnormal was found, but in retrospect, I believe some of my symptoms that I thought were related to spine problems may have been caused by retained Gadolinium. From 2000 on, I began to experience periodic intense pain on the left-side of my head. In 2001, I developed a small section of hyperpigmented skin on the front of my neck that ran from just below the incision line for my first two anterior cervical fusions down to the base of my neck – it was centered directly over my thyroid gland.
It would be 8 more years before I had another MRI with contrast. In 2008, I had my 2nd and 3rd dose of a GBCA. My head pain intensified and started to happen more frequently after my second brain MRI with contrast.
By October of 2009, the pain on the left-side of my head, especially toward the top, became extremely intense and it lasted longer. My doctor ordered a brain MRA without contrast. Soon after the MRA unexplained things began to happen. (more…)