Gadolinium deposition disease

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Gadolinium deposition disease

Postby NHE » Thu Nov 10, 2016 1:06 am

Gadolinium deposition disease: Initial description of a disease that has been around for a while.
Magn Reson Imaging. 2016 Aug 13. pii: S0730-725X(16)30103-5.

    PURPOSE: To describe the clinical manifestations of presumed gadolinium toxicity in patients with normal renal function.

    MATERIALS AND METHODS: Participants were recruited from two online gadolinium toxicity support groups. The survey was anonymous and individuals were instructed to respond to the survey only if they had evidence of normal renal function, evidence of gadolinium in their system beyond 30days of this MRI, and no pre-existent clinical symptoms and/or signs of this type.

    RESULTS: 42 subjects responded to the survey (age: 28-69, mean 49.1±22.4years). The most common findings were: central pain (n=15), peripheral pain (n=26), headache (n=28), and bone pain (n=26). Only subjects with distal leg and arm distribution described skin thickening (n=22). Clouded mentation and headache were the symptoms described as persistent beyond 3months in 29 subjects. Residual disease was present in all patients. Twenty-eight patients described symptoms following administration of one brand of Gadolinium-Based Contrast Agent (GBCA), 21 after a single GBCA administration and 7 after multiple GBCA administrations, including: gadopentetate dimeglumine, n=9; gadodiamide, n=4; gadoversetamide, n=4; gadobenate dimeglumine, n=4; gadobutrol, n=1; gadoteridol, n=2; and unknown, n=4.

    CONCLUSIONS: Gadolinium toxicity appears to arise following GBCA administration, which appears to contain clinical features seen in Nephrogenic Systemic Fibrosis, but also features not observed in that condition.
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Re: Gadolinium deposition disease

Postby NHE » Thu Nov 10, 2016 1:10 am

New study adds to concerns about gadolinium deposition
http://www.auntminnie.com/index.aspx?se ... mID=113767

    March 24, 2016 -- A new study has found that deposition of gadolinium from MRI contrast in brain and bone tissue could be more common than previously thought. Researchers found traces of gadolinium in patients who received a class of MRI contrast agents that are more stable and thus were thought to be less prone to deposition.

    The findings contradict previous in vivo studies that showed no MRI signal increase from gadolinium in patients who received the more stable contrast agents, as opposed to the agents that previously have been associated with gadolinium deposition.

    The researchers from the University of Washington (UW) in Seattle confirmed minute traces of gadolinium from the more stable gadolinium-based contrast agents (GBCAs), with greater concentrations in cortical bone than in brain tissue. The question is what the findings actually mean, and whether they will affect the use of gadolinium contrast.

The article continues at the above link.
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Re: Gadolinium deposition disease

Postby NHE » Thu Nov 10, 2016 1:30 am

Intracranial Gadolinium Deposition after Contrast-enhanced MR Imaging
Neuroradiology. June 2015. 275(3):772-782.

    Purpose: To determine if repeated intravenous exposures to gadolinium-based contrast agents (GBCAs) are associated with neuronal tissue deposition.

    Materials and Methods: In this institutional review board–approved single-center study, signal intensities from T1-weighted magnetic resonance (MR) images and postmortem neuronal tissue samples from 13 patients who underwent at least four GBCA-enhanced brain MR examinations between 2000 and 2014 (contrast group) were compared with those from 10 patients who did not receive GBCA (control group). Antemortem consent was obtained from all study participants. Neuronal tissues from the dentate nuclei, pons, globus pallidus, and thalamus of these 23 deceased patients were harvested and analyzed with inductively coupled plasma mass spectrometry (ICP-MS), transmission electron microscopy, and light microscopy to quantify, localize, and assess the effects of gadolinium deposition. Associations between cumulative gadolinium dose, changes in T1-weighted MR signal intensity, and ICP-MS–derived tissue gadolinium concentrations were examined by using the Spearman rank correlation coefficient (ρ).

    Results: Compared with neuronal tissues of control patients, all of which demonstrated undetectable levels of gadolinium, neuronal tissues of patients from the contrast group contained 0.1–58.8 μg gadolinium per gram of tissue, in a significant dose-dependent relationship that correlated with signal intensity changes on precontrast T1-weighted MR images (ρ = 0.49–0.93). All patients in the contrast group had relatively normal renal function at the time of MR examination. Gadolinium deposition in the capillary endothelium and neural interstitium was observed only in the contrast group.

    Conclusion: Intravenous GBCA exposure is associated with neuronal tissue deposition in the setting of relatively normal renal function. Additional studies are needed to investigate the clinical significance of these findings and the generalizability to other GBCAs.

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Re: Gadolinium deposition disease

Postby 1eye » Thu Nov 10, 2016 7:56 am

I have had the skin thickening in my toes for a long time. The gadolinium probably settles there because it is a metal, and is heavier than blood. I suspect part of my MS symptoms, and perhaps my conversion to SPMS, has been caused by the contrast. If that is true we may never know whether some things work or not (such as the MBP that I was part of a trial of), because the MRI scans being done in the trial, actually make the MS worse. I had gadolinium every time I three months on that trial. The end of the trial for me was a heart attack. I was on placebo. I think if it were studied, the placebo group in that trial might be found to have gotten worse at a greater rate than untreated MS patients. That may have been the gadolinium. They were regularly given 9-hole, walking, and PASAT tests. The data might be useful. The vendor is probably going to keep it secret. Science triumphs again.
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