This question was poised to me by a patient who was worried about getting a GBCA-enhanced MRI to evaluate a liver lesion seen on ultrasound. This is a circumstance that patients are left to make their own risk-benefit analysis. The first thing to realize is that you don't have to receive anything you don't want to get. Perhaps this alone is a liberating thought, and I think many patients when confronted by an insistent physician feel they have no choice - but you do. If you don't want something don't get it. However, realize the down-side that maybe something important like a cancer can be missed. 1. Subjects at the highest risk for GDD, which is someone who had a GBCA injection and feel the

I have proposed a new informed consent for GBCA, as the first step of increased awareness of the disease GDD. A number of sufferers have felt that I have not gone far enough. I fully understand that sentiment, however in my position as a senior member of the Radiology and MRI community, I have to approach the subject in a measured step-wise fashion. I would lose all credibility if I rushed head-long in attacking GBCA use - in large measure because most of my colleagues would interpret it as rash, radical and ill-conceived, without there being sufficient peer-reviewed literature by a number of independent research teams. In focusing on patients who have previously received GBCA and have expe

Gadolinium Deposition Disease An expansion of described symptoms for GDD. Symptoms are categorized as "A Symptoms" which are symptoms distinctive for GDD (also other heavy metal toxicities), and "B Symptoms" which are symptoms that are commonly observed but may also be seen in a variety of other conditions. Timeline. For the present time the time of onset of disease following GBCA injection remains as onset between immediate post-injection to up to 1 month post-injection. A crucial aspect of diagnosis GDD is that distinctive symptoms arise shortly after contrast injection. If disease starts immediately after injection it is impossible to think that any other condition may be occurring. New S

A number of patients have described to me that they have developed a number of new skin or bone tumors that have appeared since GDD developed. I had to think about this for some time, and hear a number of reports before considering that there is likely a causal relationship and to postulate a mechanism. As I have written in earlier blogs describing the immune system reaction to Gd, circulating CD34+ fibrocytes and bone marrow cell infiltrates are marshalled to manage Gd. My opinion is that these cells function to a large extent to quarantine or isolate Gd into tissues that their presence can cause less damage to the overall health of the host than it would do in soft organs like liver, kidne

There are a number of individuals who have spoken to me about GDD developing in circumstances where small volume GBCA administration has occurred. Examples are GBCA-injected MR arthrography (administering GBCA into a joint space to look for cartilage injury or joint capsule disruption), and interstitial injection of GBCA due to a blown venous injection. MR arthrography is intentional, and interstitial injection unintentional. MR arthrography typically may inject 1- 2 ml of GBCA (compared to standard iv which is 10-15 ml of GBCA), and interstitial injections often may be caught at 5 ml of GBCA injected. It seems somehow improbably that so little GBCA can cause GDD, that may be as severe as G

This post looks at the subject of why patients react to GBCA either right away or after multiple GBCA administrations; and this is in response to this question submitted to me on Facebook: Can you help us to understand why some people get sick immediately after one MRI and for some it takes multiple doses before illness begins ? Could it be that the Gadolinium contrast agent that made us sick was unstable to begin with? I think it would be a good idea to scientifically take a second look at all the contrast agents for stability. This question really asks to look at again the subject of host immune response, which I have written an earlier blog on. The classic acute immune reaction is the a

Intraday and day to day variation in symptoms and severity of GDD is common. Disease often has diurnal variation (varying of severity of the symptoms over the course of the day) is very common. Actually diurnal variation may be most common. It turns out that perhaps virtually all physiologic functions show diurnal variation. Diurnal variation in hormone release has been known for decades. Other variations such as sCr (and by extension eGFR) only recently has been recognized. Tangentially, this is also why I recommend 24 hr urine Gd, because diurnal variation is certain to exist, but it is not clear at what times of the day Gd release from tissues and elimination in urine is highest, so sampl

A Flare reaction refers to worsening of symptoms, usually more intense of existing symptoms, but can also be, new symptoms, that are not due to administration of more GBCA, but focus on the rechelation of Gd with chelators. The proposed mechanism is that the host reacts to the remobilization of Gd in the vascular system, stimulating increased activity of host immune cells, which are often already in a high alert status. So Flare arises in the setting of treatment of the disease, when Gd is mobilized to remove it from the body. Flares are also observed when the host is in neutral status of Gd (not increased Gd or removal of Gd), such as increased symptoms that may arise during non contrast M