Recruiting
Study Start: May, 2020
Study Completion: December, 2026
NCT03993262

Trial to Evaluate Efficacy and Safety of Bortezomib in Patients With Severe Autoimmune Encephalitis (Generate-Boost)

Keywords:
Autoimmune encephalitis
Autoimmune disease

Brief Summary

Autoimmune Encephalitis is a disorder of the central nervous system caused by bodily substances, called antibodies. Antibodies normally help the body to prevent infections. However, in this disorder, the antibodies turn against the body itself and especially against cells in the brain and disturb the normal brain function. They are therefore called autoantibodies.

There is no specific therapy for patients with autoimmune encephalitis so far. At the moment, the symptoms are treated with approved medications such as cortisone and immunotherapies also used in oncology. These therapies are unspecified and aim to reduce the number of autoantibodies and to contain the autoimmune process. In this trial we aim to test a new therapy option: in this therapy the body cells producing autoantibodies will be specifically targeted by a substance called bortezomib.

The trial addresses patients with severe autoimmune encephalitis. The aim of the trial is to evaluate the efficacy and safety of bortezomib in patients with severe autoimmune encephalitis.

Detailed Description

Autoimmune encephalitis is characterized by autoantibodies against neuronal surface antigens like the NMDA (N-methyl-D-aspartate) receptor or LGI1 (Leucin-rich glioma inactivated protein 1). So far, no specific therapy exists for this disease. Actual treatment includes combination therapies aiming for a reduction of pathogenic antibodies and containing the autoimmune process. In first line, patients are treated with plasmapheresis and cortisone. In second line, Rituximab and/or cyclophosphamide are administered. The response to these treatments are, however, often delayed and insufficient.

Therefore, we need a specific therapy aiming at the antibody-producing plasma cells.

Bortezomib is a proteasome inhibitor which interferes with NF-kB (nuclear factor kB) and the ubiquitin proteasome signaling pathway. Bortezomib acts preferably on cells with high protein synthesis - like plasma cells - and induces cell death in these cells. Bortezomib is used since more than a decade in chemotherapy of the multiple myeloma. Additionally, it is reported for systemic autoimmune diseases like lupus erythematodes that bortezomib leads to a depletion of plasma cells and therefore reduces the number of pathogenic antibodies and improves clinical outcome. The therapeutic potential of bortezomib for NMDAR encephalitis is described in a first case series with 5 patients.

Intervention / Treatment

01
Bortezomib
Drug
02
Placebo
Drug

Study Design

Primary Purpose

Treatment

Allocation

Randomized

Interventional Model

Parallel Assignment

Interventional Model Description

1:1 randomization will be done centrally and stratified by site. Block randomization of variable block sizes will be used.

Masking

Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)

Masking Description

The study drug will be provided blinded by the local pharmacy.

Arm Groups

Placebo Comparator: Placebo

1 to 3 cycles placebo (NaCl solution) s.c. + 20mg dexamethasone p.o. on days 1, 4, 8 and 11 (= 1 cycle)

Experimental: Interventional

1 to 3 cycles Bortezomib with 1,3mg/m2 body surface s.c. + 20mg dexamethasone p.o. on days 1, 4, 8 and 11 (= 1 cycle)

Eligibility Criteria

  • Clinically diagnosed severe autoimmune encephalitis (defined as mRS ≥ 3) with autoantibodies to neuronal surface proteins in cerebrospinal fluid and / or serum
  • Pretreatment with rituximab
  • Age ≥18 years
  • Signed informed consent
  • Women of childbearing potential (up to 2 years after menopause): negative pregnancy test

  • Pregnancy/breast-feeding
  • Acute infiltrative pulmonary and pericardial disease
  • Malignant tumor under current chemotherapy
  • Simultaneous participation in another intervention study
  • Previous participation in this study
  • Known hypersensitivity to an ingredient of the investigational product
  • Continued therapy with glucocorticoids / rituximab during the study duration (last dose must be administered before the first dose of the investigational product)

Outcome Measures

Primary Outcome Measures

Modified Rankin-Score (mRS)

Modified Rankin-Score from 0 = no symptoms to 6 = death

17 weeks after first administration of the study drug

Secondary Outcome Measures

Modified Rankin-Score (mRS)

Modified Rankin-Score from 0 = no symptoms to 6 = death

3, 6, 9 and 13 weeks after first administration of the study drug; GCS Score also 17 weeks after first administration of the study drug

Length of in-hospital stay / length of ICU stay

Number of days in hospital or on ICU for each patient from first administration of the study drug until 17 weeks after first administration of the study drug

Until 17 weeks after first administration of the study drug

Immune response

Antibody titer (in serum and liquor) and cellular immune response (FACS analysis of liquor)

At study start and 17 weeks after first administration of the study drug

Neurocognitive function assessed by Montreal Cognitive Assessment

Total score of the Montreal Cognitive Assessment (MoCA) (0 to max. 30 points = best possible result)

At study start and 17 weeks after first administration of the study medication

Neurocognitive function assessed by Mini-Mental Status Test

Total score of the Mini-Mental Status Test (MMST) (0 to max 30 points = best possible result)

At study start and 17 weeks after first administration of the study medication

Neurocognitive function assessed by Rey Auditory Verbal Learning Test

Total score of the Rey Auditory Verbal Learning Test (RAVLT) (memory performance assessed by 3 word lists which are read to the patient and should be recalled and repeated by the patient; different proceeding for the 3 word lists)

At study start and 17 weeks after first administration of the study medication

Neurocognitive function assessed by Neuropsychiatric Inventory Questionnaire

Total score of the Neuropsychiatric Inventory Questionnaire (NPI) (0 = best score to max 36 (patient) or 60 (caregiver)

At study start and 17 weeks after first administration of the study medication

Safety of Bortezomib regarding polyneuropathy, increase of liver enzymes and secondary infections

Number of polyneuropathy cases, number of increased liver enzymes, number of secondary infections

Until 17 weeks after first administration of the study drug

Safety of Bortezomib regarding polyneuropathy

Number of polyneuropathy cases

Until 17 weeks after first administration of the study drug

Safety of Bortezomib regarding increase of liver enzymes

Number of increased liver enzyme values

Until 17 weeks after first administration of the study drug

Secondary infections due to Bortezomib

Number of secondary infections

Until 17 weeks after first administration of the study drug

Hematotoxicity events due to Bortezomib

Number of hematotoxicity events

Until 17 weeks after first administration of the study drug

Gastrointestinal toxicity due to Bortezomib

Number of gastrointestinal toxicity events

Until 17 weeks after first administration of the study drug

Total Glasgow Coma Scale (GCS)

GCS from 3 to 15 points (sum of 3 subscores eye response (1 to 4 points), motor response (1 to 6 points), verbal response (1 to 5 points); highest score = best score; 1= worst score)

3, 6, 9, 13 and 17 weeks after first administration of the study drug

Destruction marker UCH-L1 (Ubiquitin carboxy-terminal hydrolase L1) in serum and liquor

Analysis of destruction marker UCH-L1 in serum and liquor

At baseline visit and 17 weeks after first administration of the study drug

Destruction marker Neurofilament light chain (in serum and liquor)

Analysis of destruction marker Neurofilament light chain in serum and liquor

At baseline visit and 17 weeks after first administration of the study drug

Destruction markers GFAP (glial fibrillary acidic protein) in serum and liquor

Analysis of destruction marker GFAP in serum and liquor

At baseline visit and 17 weeks after first administration of the study drug

Destruction marker TAU proteins in serum and liquor

Analysis of destruction marker TAU in serum and liquor

At baseline visit and 17 weeks after first administration of the study drug

Where is this study conducted?

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