Gadolinium in gliomas, the adjacent tissue raises questions



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Finnish researchers found that gadolinium deposits were highest in gliomas with a marked contrast enhancement and in patients who received a linear GBCA, rather than a macrocyclic GBCA. Similar retention rates and the influence of GBCA type were also evident in normal brain tissue and necrosis samples.

"To our knowledge, this is the first study to provide quantitative data on gadolinium retention in gliomas and the neighboring normal brain regarding tumor enhancement and GBCA type." used, "wrote the researchers led by Dr. Aida Kiviniemi of the Turku University Hospital. "Levels of gadolinium in the tumor and the normal brain suggest a possible transit of gadolinium to brain injury."

Quantitative data

Many researches and writings have been devoted to gadolinium retention in recent years and its badociation with linear and macrocyclic GBCAs long after the administration of contrast agents. In contrast to previous studies, current research sought to provide quantitative data on gadolinium retention relative to glioma and adjacent normal brain tissue, as well as information on the role that could be played by the type of GBCA administered.

The retrospective study focused on 69 patients with a newly diagnosed primary glioma who underwent a contrast-enhanced MRI before surgery. Seven patients received a linear GBCA – either gadodiamide (Omniscan, GE Healthcare) or gadopentetate dimeglumine (Magnevist, Bayer HealthCare) – while the remaining 62 patients received a macrocyclic GBCA – gadobutrol (Gadovist, Bayer) or Gemotérotéglutine (Dotarem), Guerbet).

Gadolinium deposition was measured from histologically viable tumor samples in 69 patients, as well as 13 samples of normal brain tissue and necrosis samples from 14 glioblastomas. The amount of GBCA enhancement in the tumor has been badessed to be zero, minimal or noticeable. The researchers also noted differences in gadolinium retention relative to the type of GBCA.

Gadolinium was detected in 39 samples (57%) of glioma tumors, eight normal brain samples (62%) and 12 necrotic samples. The presence of linear gadodiamide and gadopentetate dimeglumine in linear GBCA resulted in a significantly higher presence of gadolinium in tumors, compared with GBCA gadotereic meglumine macrocyclic (p <0.01 and p <0.05, respectively).

Of the eight patients with gadolinium in normal brain tissue, two received gadadiamide GBCA linear, while six received gadotium meglumine macrocyclic GBCA. The concentration of gadolinium in normal brain tissue was significantly higher (p = 0.05) after exposure to linear gadodiamide, compared to macrocyclic meglumine gadoterate. Gadolinium exposure in necrosis samples was also significantly higher (p = 0.05) with linear gadodiamide, compared with macrocyclic gadoterate.

While one expects an increase in contrast in brain tumors, how and why is gadolinium found in adjacent normal brain tissue where contrast absorption is less likely? ? Previous studies have suggested that cerebrospinal fluid or the glymphatic system of the brain could provide this pathway.

"The exact mechanism behind the detention … remains unresolved," wrote Kiviniemi and his colleagues. "A weak but significant correlation between the amount of gadolinium in the tumor and the normal brain has been detected, involving the pbadage of gadolinium from the site of pathological brain injury.Additional studies are needed to confirm this badociation, an interesting question arises whether gadolinium crosses the area of ​​brain injury to nearby sites with other brain abnormalities such as ischemia, infection or multiple sclerosis ".

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