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Impact of Baseline Liver Function on the Dynamic Consumption of Fibrinogen During Double Filtration Plasmapheresis in Patients with Neuroimmune Diseases: A Retrospective Observational Study

This retrospective study demonstrates that while double filtration plasmapheresis causes significant, progressive fibrinogen consumption in neuroimmune patients, higher baseline alanine aminotransferase levels paradoxically correlate with a greater cumulative risk of severe hypofibrinogenemia during continuous therapy, despite the procedure's overall safety profile without exogenous supplementation.

Original authors: Tiantian Jiang, Yuhong Ma, Xiao Zhang, Shiya Zhang, Bin Liu, Fang Yan, Jingmei Sheng, Qiuping Zhu, Lu Wang, Shuxia Zheng, Yangtai Guan

Published 2026-08-19
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Original authors: Tiantian Jiang, Yuhong Ma, Xiao Zhang, Shiya Zhang, Bin Liu, Fang Yan, Jingmei Sheng, Qiuping Zhu, Lu Wang, Shuxia Zheng, Yangtai Guan

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

The human immune system is a powerful defense force, but sometimes it turns against the body, attacking its own tissues. In conditions known as neuroimmune diseases, the immune system produces harmful proteins called antibodies that damage the nervous system. To stop this attack, doctors can use a procedure called double filtration plasmapheresis. Imagine the blood as a river carrying both essential supplies and dangerous debris. This treatment acts like a sophisticated filter system that removes the harmful debris—the bad antibodies—while trying to keep the river flowing smoothly. However, the filters are not perfectly selective. Because the harmful antibodies and a vital blood-clotting protein called fibrinogen are similar in size, the machine often removes the good clotting protein along with the bad antibodies. If too much of this clotting protein is lost, the patient risks bleeding. The liver is the factory that makes this clotting protein, and doctors have long wondered if the factory's current health affects how quickly the protein runs out during treatment.

A team of researchers at Shanghai Punan Hospital and the 988th Hospital of the Joint Service Support Force set out to watch this process in real time. They looked back at the medical records of fifty patients with neuroimmune diseases who underwent this filtering treatment between June 2024 and March 2026. None of these patients received extra clotting protein from blood donations during their care, which allowed the researchers to see exactly how the body handled the loss on its own. The team tracked the levels of the clotting protein and the harmful antibodies before and after each treatment session, paying close attention to the patients' liver health, specifically measuring an enzyme called ALT that indicates how hard the liver is working.

The researchers found that the treatment worked as expected: with every session, the levels of both the harmful antibodies and the clotting protein dropped significantly. The clotting protein reached its lowest point after the fourth treatment session. What surprised the team was the role of the liver. Patients who started with slightly higher levels of the liver enzyme ALT, even though their levels were still within the normal range, showed a different pattern. After the very first treatment, these patients actually lost less clotting protein than those with lower enzyme levels. It appeared their livers were reacting quickly to the initial stress, perhaps by ramping up production to compensate for the loss.

However, this early advantage did not last. As the treatments continued over several days, the story changed. The group with the higher initial liver enzyme levels began to lose their clotting protein more rapidly and deeply than the other group. By the end of the treatment series, nearly two-thirds of the patients with higher baseline liver enzymes had dropped to dangerously low levels of clotting protein, a condition known as severe hypofibrinogenemia. In contrast, the group with lower initial liver enzymes was less likely to reach this critical low point. This suggests that while a liver that is slightly more active might handle the first hit well, it may struggle to keep up with the repeated demands of multiple treatment sessions, eventually running out of steam.

Despite these dramatic drops in clotting protein, the outcome for the patients was surprisingly safe. Even among those who reached the lowest levels, no one suffered from major bleeding events like internal hemorrhages. The only bleeding issues were minor oozing at the needle insertion sites, which were easily managed with simple pressure. This finding challenges the idea that doctors must routinely replace the lost clotting protein with blood products during these treatments. The study indicates that the body can often tolerate these temporary lows without catastrophic consequences, provided the medical team monitors the levels closely. The researchers conclude that checking a patient's liver health before starting treatment can help predict who might need extra vigilance, allowing doctors to tailor the care plan to keep patients safe without unnecessary transfusions.

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