“Accelerated antibody depletion may be relevant in patients at high risk of rapid neurological function deterioration, because of high antibody titre and severe symptoms, related to immunological disorders.”

Neurology

Chronic inflammatory demielinating polyneuropathy (CIDP) and acute (AIDP)

Chronic and acute inflammatory demyelinating polyneuropathy are rare diseases with idiopathic aetiology, which is counted among immunomediated polyneuropathies because an autoimmune cause is suspected.
The disease affects the myelin, whose task is to promote the transmission of the nervous impulse along the nerve, as well as protect the nerves from external stimuli.

When the damage reaches the axon often the lesions become irreversible. Approximately 10% of patients have an acute onset, but the subsequent onset of relapse indicates that the disease has a chronic form that can evolve with relapses or progressive worsening. The main symptoms are represented by peripheral muscle weakness, disturbance of sensitivity, tingling and numbness, lack of balance and tremor. Treatment includes corticosteroids, immunoglobulins and plasmapheresis, with the aim of removing the antibodies involved from the bloodstream.

  • Molecules to be removed:
    Antibodies; plasma globulins; IgG, IgA, IgM; cytokines; inflammation mediators

  • Suggested therapies:
    PEX, DFPP, Cascade Filtration

Multiple sclerosis is a disease characterized by diffuse areas of demyelination in the brain and spinal cord. The most frequent symptoms are visual and oculomotor abnormalities, paraesthesia, weakness, spasticity, urinary disorders and mild cognitive symptoms. The pathogenesis of multiple sclerosis is supposed to involve an immunological mechanism.

An assumed cause is an infection caused by a latent virus (potentially a human herpesvirus such as the Epstein-Barr virus) which, once activated, induces a secondary autoimmune response. The therapy includes corticosteroids for relapses, immunomodulatory drugs to prevent them and plasmapheresis to remove the circulating antibodies involved.

  • Molecules to be removed:
    Immunoglobulins (IgA, IgG, IgM); immunocomplexes, cytokines

  • Suggested therapies:
    PEX, DFPP, Cascade Filtration

Guillain-barré syndrome is an acute inflammatory polyneuropathy characterised by muscle weakness and mild loss of distal sensitivity.

It is the most frequent form of acquired inflammatory neuropathy. Although the cause is not fully known, it is thought to be on an autoimmune basis. In some variants, predominates demyelination; in others, the axon is hit. The therapy includes immunoglobulins, plasmapheresis and, for the most serious cases, assisted ventilation.

Myasthenia gravis an autoimmune disease characterized by an improper transmission of the neuromuscular signal, caused by the presence in the circulation of specific anti-nicotinic muscle receptor antibodies (AchR). The standard therapy for the treatment of this disease is characterized by the administration of immunosuppressive drugs and surgical removal of the thymus (primary lymphoid organ used for the development of T lymphocytes).

Plasmopheresis may be applied in patients who do not respond to immunosuppressive therapy and who require mechanical ventilation. The objective is to remove immunoglobulins containing anti-acetylcholine receptor antibodies (AchR) from plasma in a semi-selective manner in order to improve the patient’s muscle tone and symptoms.

Go to the Plasmapher Apherlungs system