When “blood washing” is discussed in relation to MS, this refers to certain plasma exchange procedures that can be used in severe MS relapses if cortisone has not produced sufficient effects.The lay term “blood washing” actually describes dialysis, a kidney replacement therapy that is used when the kidneys are no longer functioning properly due to various diseases. In this case, the detoxification function of the kidneys fails – the harmful/toxic substances for the body are then washed out of the blood by dialysis (blood washing).
The “blood washing” that can be used in MS is actually two different plasma exchange procedures, namely plasmapheresis and immunoadsorption. Technically, similar devices are used as in dialysis, but the objective is different than in dialysis.
In plasmapheresis, blood plasma (the liquid part of the blood) and blood cells (the erythrocytes = red blood cells) are separated from each other, the plasma is collected and replaced by a human albumin (a major protein of the blood plasma) solution, and then returned to the patient’s body along with the blood cells.
In immunoadsorption, too, blood cells and plasma are separated, and the plasma runs over a “column” that binds the so-called immunoglobulins (= antibodies) from the plasma (absorbs). The plasma, thus cleared of the immunoglobulin fraction, is then returned to the patient’s body along with the blood cells.
Both methods aim to remove the immunoglobulin fraction, i.e., the immunologically relevant antibodies, from the blood plasma of an MS patient. In plasmapheresis in a somewhat coarser way, because all other plasma proteins are lost in addition to the immunoglobulins, and in immunoadsorption in a more specific way, because the method is specifically aimed at removing the antibody fraction from the patient’s blood.
Why can these methods be useful in MS? In an acute MS relapse, the myelin sheath is attacked by various immune cells, but antibodies also play a role in the attack on the myelin sheath. Since the antibodies are directed against one’s own myelin sheath, we also speak of autoantibodies. While immune cells are “braked” in their activity by cortisone, cortisone has no effect on already existing autoantibodies. If a relapse does not respond well to cortisone, it is assumed that possibly autoantibodies play the decisive role – and these can be removed by the aforementioned plasma exchange procedures.
You can probably imagine that these plasma exchange procedures are technically quite complex. They are also not very comfortable for the patient, as all the blood must be taken out of the body and then returned. For this, a large-lumen catheter must be placed in the jugular vein, where it remains for the duration of the procedure (several days) – the method is therefore quite invasive, and such a venous catheter also carries the risk of complications.
It goes without saying that plasma exchange procedures are only considered as reserve therapy for severe relapses, i.e., when eyesight or walking ability is acutely threatened. For milder relapses, especially for the frequently occurring sensitive irritations or failures, even if the symptoms are unpleasant for the affected patient, a plasma exchange treatment would not be offered.
And even with severe relapses, we first start with a cortisone therapy and wait for about 2 weeks to see if there is a success before we start a plasma exchange treatment. The situation is different if it is known from the past that a plasma exchange treatment has worked well – then one can directly revert to this procedure – provided the symptoms justify the procedure. But it is of course even better if there are no further relapses because the long-term immune therapy has been adjusted accordingly.
