Choroba związana z przeciwciałami białka mieliny oligodendrocytów (mogad)
Leczenie

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) to autoimmunologiczne schorzenie ośrodkowego układu nerwowego, charakteryzujące się ostrymi rzutami wymagającymi szybkiego leczenia glikokortykosteroidami (metyloprednizolon 1000 mg/dobę u dorosłych lub 20-30 mg/kg/dobę u dzieci przez 5 dni). W przypadku braku odpowiedzi stosuje się terapie drugiego rzutu, takie jak plazmafereza (stosowana przez 71,2% neurologów dorosłych) lub dożylne immunoglobuliny (IVIG, preferowane przez 45,5% neurologów dziecięcych). Wczesne wdrożenie immunoterapii w ciągu 7 dni od objawów zmniejsza ryzyko nawrotu 6,7-krotnie. Po ostrym rzucie kontynuacja kortykosteroidów przez około 3 miesiące (np. prednizon ≥12,5 mg/dobę lub 0,16 mg/kg u dzieci) redukuje ryzyko nawrotu o 88%. Długoterminowa terapia immunosupresyjna jest konieczna u 40-50% pacjentów, z najczęściej stosowanymi lekami: azatiopryną (30,8%), mykofenolanem mofetylu (25%), rytuksymabem (17,3%) oraz IVIG (54,5% u dzieci). IVIG wykazuje najwyższą skuteczność w zapobieganiu nawrotom, zmniejszając medianę rocznego wskaźnika nawrotów (ARR) z 2,16 do 0,51.

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) – leczenie i terapia

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), czyli choroba związana z przeciwciałami białka mieliny oligodendrocytów, to stosunkowo niedawno wyodrębniona jednostka chorobowa o charakterze autoimmunologicznym, atakująca ośrodkowy układ nerwowy. Obecnie nie istnieje metoda leczenia przyczynowego, a terapia skupia się głównie na trzech aspektach: leczeniu ostrych rzutów, zapobieganiu wczesnym nawrotom oraz długoterminowym prowadzeniu choroby12.

Leczenie ostrego rzutu choroby

Ataki MOGAD są zazwyczaj ciężkie i wymagają natychmiastowego leczenia, aby zapewnić jak najpełniejszy powrót do zdrowia3. Szybkie wdrożenie odpowiedniego leczenia jest kluczowe, gdyż badania sugerują, że wczesne zastosowanie glikokortykosteroidów może zmniejszyć ryzyko nawrotu i zapobiec trwałym uszkodzeniom1.

Podstawową metodą leczenia ostrego rzutu MOGAD jest zastosowanie wysokich dawek glikokortykosteroidów4. Zaleca się podawanie dożylne metyloprednizolonu w dawce 1000 mg u dorosłych lub 20-30 mg/kg/dobę u dzieci przez pięć kolejnych dni15. Glikokortykosteroidy redukują stan zapalny nerwów i szybko łagodzą objawy MOGAD3. Do potencjalnych działań niepożądanych należą: zaburzenia snu, podwyższone ciśnienie krwi, podwyższony poziom glukozy we krwi, wahania nastroju oraz zatrzymanie płynów3.

W przypadku braku odpowiedzi na leczenie glikokortykosteroidami lub przy bardzo ciężkim przebiegu choroby, stosuje się terapie drugiego rzutu36:

  • Plazmafereza (PLEX) – metoda polegająca na usunięciu osocza zawierającego przeciwciała z krwi pacjenta i zastąpieniu go płynem zastępczym78. Około 71,2% neurologów dorosłych stosuje plazmaferezę jako drugi rzut leczenia po niepełnej odpowiedzi na steroidy6.
  • Dożylne immunoglobuliny (IVIG) – terapia polegająca na podaniu przeciwciał od zdrowych dawców7. Ta metoda jest częściej preferowana przez neurologów dziecięcych (45,5%) niż plazmafereza6.

Badania wskazują, że wczesne wdrożenie immunoterapii (w ciągu 7 dni od wystąpienia objawów) wiąże się z 6,7-krotnie zmniejszonym ryzykiem nawrotu choroby5.

Leczenie podtrzymujące i zapobieganie nawrotom

Po ostrym rzucie MOGAD, około 55,8% lekarzy kontynuuje podawanie kortykosteroidów przez około 3 miesiące, choć rzadziej stosuje się tę praktykę u dzieci6. Dłuższe stosowanie kortykosteroidów w formie stopniowo zmniejszanej dawki (taper) przez co najmniej 5 tygodni wiąże się ze znacznie zmniejszonym ryzykiem nawrotu5. Niedawne badanie wykazało, że pacjenci leczeni dawką co najmniej 12,5 mg/dzień (0,16 mg/kg u dzieci) prednizonu przez co najmniej 3 miesiące mieli o 88% mniejsze ryzyko nawrotu w porównaniu do osób, które nie otrzymały takiego schematu leczenia9.

Ponieważ MOGAD jest chorobą nawracającą u około 40-50% pacjentów, często konieczne jest zastosowanie długoterminowej terapii immunosupresyjnej10. Po pierwszym incydencie około 60% lekarzy zazwyczaj rozpoczyna terapię podtrzymującą, a po drugim ataku wskaźnik ten wzrasta do 92,3%6.

Do najczęściej stosowanych leków immunosupresyjnych w leczeniu podtrzymującym MOGAD należą61011:

  • Azatiopryna (stosowana przez 30,8% neurologów dorosłych jako pierwsza linia leczenia)
  • Mykofenolan mofetylu (stosowany przez 25,0% neurologów)
  • Rytuksymab (stosowany przez 17,3% neurologów)
  • Dożylne immunoglobuliny (IVIG) – szczególnie preferowane u dzieci (54,5% neurologów dziecięcych wybiera IVIG jako pierwszą linię leczenia podtrzymującego)
  • Prednizon w niskich dawkach (stosowany częściej poza Stanami Zjednoczonymi)12

Skuteczność poszczególnych terapii w zapobieganiu nawrotom

Według badań retrospektywnych, różne terapie wykazują różną skuteczność w redukcji częstości nawrotów MOGAD13:

  • Prednizon zmniejsza nawroty o około 54%
  • Dożylne immunoglobuliny (IVIG) o około 87%
  • Deplecja komórek B (np. rytuksymab) o około 49%
  • Mykofenolan o około 78%

Dożylne immunoglobuliny okazują się najskuteczniejszą opcją w zapobieganiu nawrotom MOGAD, z około 70% pacjentów osiągających remisję14. Badanie prospektywne oceniające roczne wskaźniki nawrotów (ARR) i niepełnosprawność u 102 dzieci z MOGAD wykazało, że leczenie podtrzymujące z IVIG zmniejszyło medianę ARR z 2,16 do 0,5110.

Rytuksymab jest drugą najskuteczniejszą opcją, z około 50% pacjentów wolnych od nawrotów, następnie mykofenolan mofetylu (47%) i azatiopryna (39%)15. Badanie oceniające rytuksymab u pacjentów z MOGAD wykazało, że u trzech z dziewięciu pacjentów wystąpił spadek wskaźnika ARR, a większość nawrotów wystąpiła albo wkrótce po infuzji, albo pod koniec okresu dawkowania12.

Nowe kierunki w leczeniu MOGAD

Obecnie prowadzone są badania kliniczne nad nowymi lekami do leczenia MOGAD1516:

  • Tocilizumabprzeciwciało monoklonalne przeciwko receptorowi interleukiny-6 (IL-6), które odgrywa kluczową rolę w dojrzewaniu komórek B i produkcji przeciwciał15. Wydaje się być skuteczny w zmniejszaniu nawrotów nawet w przypadkach opornych na inne terapie17.
  • Satralizumab – przeciwciało monoklonalne blokujące działanie interleukiny-616. Trwają badania kliniczne fazy 3 oceniające skuteczność tego leku w MOGAD18.
  • Rozanolixizumab (Rozimab) – przeciwciało monoklonalne blokujące aktywność cząsteczki FcRN, która zwykle chroni przeciwciała we krwi przed zniszczeniem16. Jest to pierwszy lek testowany w badaniu klinicznym fazy 3 dla MOGAD19.

Metody monitorowania odpowiedzi na leczenie

Odpowiedź na leczenie w MOGAD monitorowana jest różnymi metodami6:

  • Rezonans magnetyczny (MRI) – stosowany przez 53,8% neurologów
  • Optyczna koherentna tomografia (OCT) – stosowana przez 23,1% neurologów
  • Miano przeciwciał MOG – monitorowane przez 36,5% neurologów

W MOGAD, oprócz monitorowania ostrości wzroku, do oceny upośledzenia funkcjonalnego mogą być również wykorzystywane pomiary pola widzenia20.

Potencjalne powikłania leczenia

Długotrwałe stosowanie niektórych leków immunosupresyjnych może prowadzić do potencjalnych powikłań21:

  • Infekcje
  • Chłoniaki lub nowotwory skóry
  • Spowolniony wzrost u dzieci
  • Bóle głowy
  • Niewydolność nerek

Istotnym aspektem jest również balansowanie korzyści z długoterminowej immunosupresji ze zwiększonym ryzykiem infekcji, szczególnie infekcji oportunistycznych, takich jak gruźlica, zwłaszcza u pacjentów z obniżoną odpornością22.

Leki niezalecane w MOGAD

Badania wykazały, że konwencjonalne leki stosowane w leczeniu stwardnienia rozsianego (SM) nie są skuteczne i mogą powodować działania niepożądane w MOGAD1223:

  • Interferon beta – może prowadzić do nasilenia aktywności choroby24
  • Octan glatirameru i natalizumab – nie wydają się być skuteczne25
  • Fingolimód lub alemtuzumab – istnieją doniesienia przeciwko ich stosowaniu24

W opisanym przypadku trzech pacjentów z MOGAD początkowo zdiagnozowanych jako SM i leczonych alemtuzumabem, u których wystąpiły liczne nawroty i pogorszenie niepełnosprawności, podkreślono, że alemtuzumab może być nieskuteczny w MOGAD26.

Rehabilitacja i leczenie objawowe

Oprócz leczenia immunomodulującego, ważnym elementem terapii MOGAD jest rehabilitacja i leczenie objawowe27:

Istotne jest również wsparcie psychologiczne oraz terapia zaburzeń poznawczych, emocjonalnych lub behawioralnych27.

Aktualne wyzwania i perspektywy w leczeniu MOGAD

Obecne leczenie MOGAD charakteryzuje się dużą zmiennością, co wskazuje na potrzebę opracowania wytycznych leczenia opartych na konsensusie, w oczekiwaniu na definitywne badania kliniczne6. Optymalne leczenie MOGAD pozostaje obszarem intensywnych badań, a brak jednolitych schematów terapeutycznych stanowi wyzwanie dla klinicystów28.

Chociaż nie ma leków zatwierdzonych przez FDA specjalnie do leczenia MOGAD, trwają obiecujące badania kliniczne, które mogą otworzyć nowe możliwości terapeutyczne dla pacjentów29. Kluczowe będzie również zidentyfikowanie biomarkerów, które ułatwią diagnozę i wykryją aktywność choroby, oraz określenie, którzy pacjenci z MOGAD wymagają długoterminowej immunoterapii30.

Dokładna i wczesna diagnoza MOGAD ma kluczowe znaczenie dla właściwego postępowania i lepszych wyników leczenia31. Wczesna identyfikacja pacjentów z MOGAD prezentujących pierwszy epizod demielinizacyjny i zagrożonych nawrotem umożliwia wczesne rozpoczęcie leczenia modyfikującego przebieg choroby, poprawiając tym samym rokowanie31.

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  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Treatment and prognosis – UpToDate
    https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-treatment-and-prognosis/print
    Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The treatment and prognosis of MOGAD are reviewed here. […] Treatment of MOGAD can be stratified by acute attack treatment and attack prevention strategies. […] Since acute attacks of MOGAD tend to be severe, almost all are treated. Starting acute treatment as quickly as possible is a good strategy, as some evidence suggests that early treatment of acute attacks with glucocorticoids may reduce the risk of relapse and prevent residual damage. […] We suggest initial treatment with high-dose intravenous (IV) methylprednisolone (1000 mg in adults, or 20 to 30 mg/kg per day in children) for five consecutive days.
  • #2 Advancing Expertise in the Understanding of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Masterclass Event Summary – European Medical Journal
    https://www.emjreviews.com/neurology/symposium/advancing-expertise-in-the-understanding-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-masterclass-event-summary-s110224/
    A masterclass initiated, organised, and funded by UCB, sought to advance understanding and expertise of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). […] The speakers explained that management has three main aims: resolving acute attacks, preventing early rebound attacks, and the long-term management of disease. Prompt intervention with an intravenous steroid after an acute attack significantly improves both visual and structural (peripapillary retinal nerve fibre layer) outcomes in patients with MOGAD. Other options for treatment for acute attacks are intravenous immunoglobulins and plasma exchange. A short follow-on treatment course, with an agent such as prednisolone, can reduce the risk of early relapse. A number of approaches can be employed for long-term relapse prevention. These include monthly maintenance intravenous immunoglobulins, conventional immunosuppressants, and rituximab. […] There is currently no approved treatment for MOGAD.
  • #3 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) – Diagnosis and treatment – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/mogad/diagnosis-treatment/drc-20560477
    There is no cure for MOGAD. Treatment typically focuses on speeding recovery from attacks, managing symptoms and reducing relapses. You meet with your healthcare team to come up with a treatment plan that fits your needs. […] Attacks for MOGAD are usually severe and should be treated right away for the most complete recovery. Treatment options may include: […] Corticosteroids are medicines used to reduce nerve inflammation and quickly reverse MOGAD symptoms. They are given at high doses and may be taken by mouth or given through an IV. Side effects may include trouble sleeping, increased blood pressure and blood glucose levels, mood swings, and fluid retention. […] Plasma exchange may be used if your symptoms are new, severe or haven’t responded to the corticosteroids. […] IV immune globulin can be used to prevent attacks because it suppresses the immune system. Other medicines such as rituximab and tocilizumab also may be given through an IV to help suppress the immune system.
  • #4 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Treatment and prognosis – UpToDate
    https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-treatment-and-prognosis
    Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Treatment and prognosis […] The treatment and prognosis of MOGAD are reviewed here. […] Treatment of MOGAD can be stratified by acute attack treatment and attack prevention strategies. […] Treatment of acute attacks — Since acute attacks of MOGAD tend to be severe, almost all are treated. Starting acute treatment as quickly as possible is a good strategy, as some evidence suggests that early treatment of acute attacks with glucocorticoids may reduce the risk of relapse and prevent residual damage. […] High-dose glucocorticoids – We suggest initial treatment with high-dose intravenous (IV) methylprednisolone (1000 mg in adults, or 20 to 30 mg/kg per day in children) for five consecutive days.
  • #5 Pediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) – EyeWiki
    https://eyewiki.org/Pediatric_Myelin_Oligodendrocyte_Glycoprotein_Antibody-Associated_Disease_(MOGAD)
    Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) is a demyelinating disease of the central nervous system associated with seropositivity of the MOG antibody. […] The diagnosis of MOGAD is important for counseling patients and their families on relapse risk and available treatments. […] The treatment of pediatric MOGAD in the acute setting is similar to that of adults although some specific considerations apply in children. […] A recent systemic review suggested that IVMP is the most commonly used acute treatment (88%) of cases and IVIG the next most common (66%). […] In the acute setting IV methylprednisolone (IVMP) is commonly used at a dose of 20-30mg/kg daily (max 1g/day) for 3 to 5 days. […] Most children are steroid responsive with a rapid improvement in visual acuity but a subset of patients do not respond to IVMP.
  • #5 Pediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) – EyeWiki
    https://eyewiki.org/Pediatric_Myelin_Oligodendrocyte_Glycoprotein_Antibody-Associated_Disease_(MOGAD)
    These patients should be rapidly escalated to intravenous immunoglobulins (IVIG) or plasma exchange (PLEX). […] In a retrospective review of 75 children with MOGAD, early initiation of immunotherapy (less than 7 days from symptom onset) was associated with a 6.7-fold reduced risk of relapse. […] The same study found that a longer steroid taper of 5 weeks or longer also associated with a significantly reduced risk of relapse. […] As with adults, azathioprine is one of the first line steroid-sparing immunosuppressive agents. […] An alternative first line agent is myocophenolate mofetil (MMF). […] The long-term risks of both steroid and steroid-sparing agents in pediatric patients is largely the same as those in adults. […] The treatment of pediatric patients especially in a condition such as MOGAD which often involves multiple and sometimes lengthy hospital stays has an important psychosocial impact on patients and can affect education.
  • #6 Treatment of MOG antibody associated disorders: results of an international survey
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7954658/
    While monophasic and relapsing forms of myelin oligodendrocyte glycoprotein antibody associated disorders (MOGAD) are increasingly diagnosed world-wide, consensus on management is yet to be developed. […] All treat acute attacks with high dose corticosteroids. If recovery is incomplete, 71.2% (37/52) proceed next to plasma exchange (PE). 45.5% (5/11) of paediatric neurologists use IV immunoglobulin (IVIg) in preference to PE. Following an acute attack, 55.8% (29/52) of respondents typically continue corticosteroids for 3 months; though less commonly when treating children. After an index event, 60% (31/51) usually start steroid-sparing maintenance therapy (MT); after 2 attacks 92.3% (48/52) would start MT. […] Commonly used first line MTs in adults are azathioprine (30.8%, 16/52), mycophenolate mofetil (25.0%, 13/52) and rituximab (17.3%, 9/52). In children, IVIg is the preferred first line MT (54.5%; 6/11). Treatment response is monitored by MRI (53.8%; 28/52), optical coherence tomography (23.1%; 12/52) and MOG antibody titres (36.5%; 19/52). Regardless of monitoring results, 25.0% (13/52) would not stop MT. […] Current treatment of MOGAD is highly variable, indicating a need for consensus-based treatment guidelines, while awaiting definitive clinical trials.
  • #7 MOGAD: What It Is, Diagnosis, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/myelin-oligodendrocyte-glycoprotein-antibody-disease-mogad
    Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune condition where your immune system attacks proteins in the protective cover around your nerves (myelin). Treatment options are available. […] Treatment for the sudden onset of MOGAD symptoms (acute) includes: Steroids (methylprednisolone), given intravenously (through a vein in your arm) for three to five days. Plasma exchange, where a machine will remove plasma from your blood, separate it from your blood cells and then return a plasma replacement liquid with your blood cells back into your body. Intravenous immunoglobulin (IVIG), which replaces antibodies in your blood with donor antibodies given through a vein in your arm. Immunosuppressant medications you take orally (by mouth). […] Long-term treatment to prevent MOGAD symptom relapses include: Immunosuppressant medications. Mycophenolate mofetil. Rituximab. Azathioprine. IVIG infusions or subcutaneous immunoglobulin injections. […] Each type of treatment comes with possible side effects. Your provider will explain how each treatment works and what to look out for before you begin treatment. […] There isnt a cure available for MOGAD at this time.
  • #8 MOG Antibody Disease Information – MyMyelitis
    https://mymyelitis.com/mog-antibody-disease/information/
    There are no Food and Drug Administration (FDA) or European Medicines Agency (EMA) approved treatments for MOG Antibody Disease. Medications approved for similar conditions may be prescribed 'Off Label”. […] Acute treatments for MOGAD involve stopping antibodies from attacking myelin in the central nervous system. The most common acute treatments for MOGAD are Intravenous and Oral steroids. […] A healthcare provider will likely treat an initial attack or relapse of MOG Antibody Disease with IV corticosteroids. IV steroids broadly reduce inflammation throughout the body and nervous system and are given via a cannula/IV into your bloodstream, generally for 3-5 days. […] If the IV steroids are unsuccessful, a healthcare professional may administer Plasma Exchange (PLEX) alongside the steroids. PLEX is often considered when a patient shows severe symptoms of demyelination.
  • #9 Oral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapse | Journal of Neurology, Neurosurgery & Psychiatry
    https://jnnp.bmj.com/content/95/11/1054
    Oral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapse. […] We sought to identify an optimal oral corticosteroid regimen at the onset of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), which would delay time to first relapse while minimising cumulative corticosteroid exposure. […] In this multicentre cohort study of 109 children and adults with MOGAD, there was evidence that patients treated with at least 12.5mg/day (0.16mg/kg in children) of oral prednisone for at least 3months had an 88% reduction in the risk of relapse compared with those who did not receive this regimen. […] This study highlights the need for effective early treatment after MOGAD onset to modify the long-term disease trajectory, and for the first time provides recommendations to clinicians on the corticosteroid dosing regimen and duration at disease onset to minimise relapsing disease, while minimising cumulative corticosteroid exposure. […] The optimal dose of 12.5mg of prednisone daily in adults (0.16mg/kg/day for children) for a minimum of 3months at the onset of MOGAD delays time to first relapse.
  • #10 MOG Antibody Disease (MOGAD) | Prognosis & Management | SRNA
    https://wearesrna.org/living-with-myelitis/disease-information/mog-antibody-disease/prognosis-management/
    Unlike AQP4 antibodies, MOG antibodies may decrease over time and may not be detectable early in the disease process or during remission, and this is especially the case for MOG antibody disease associated ADEM. About 40-50% of those with MOGAD only experience one attack. […] Those with MOG antibody disease should consider ongoing treatment with medications that suppress the immune system. There are no FDA-approved medications for maintenance in MOG antibody disease, so anything prescribed is done off-label. The primary therapies used in the US are mycophenolate mofetil (CellCept), rituximab (Rituxan), azathioprine (Imuran), and repeated IVIG infusions or subcutaneous immunoglobulin. […] IVIG has also been used as a maintenance treatment in MOG antibody disease. A prospective study looking at annualized relapse rates (ARRs) and disability in 102 children with MOG antibody disease found that maintenance treatment with IVIG reduced the median ARR from 2.16 to 0.51.
  • #11 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) – Diagnosis and treatment – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/mogad/diagnosis-treatment/drc-20560477
    Treatment options may include: Oral immunosuppressants. Medicines such as azathioprine, mycophenolate mofetil and prednisone can be taken orally. These medicines suppress the immune system so it stops attacking the myelin and causing damage. However, they can take up to a few months to work, so a relapse still may happen.
  • #12 MOG Antibody Disease (MOGAD) | Prognosis & Management | SRNA
    https://wearesrna.org/living-with-myelitis/disease-information/mog-antibody-disease/prognosis-management/
    A study looking at rituximab among those with MOG antibody disease found that three out of nine individuals experienced a decline in the ARR, and most relapses occurred either soon after an infusion or at the end-of-dose period. Rituximab treatment has been associated with reduced annualized relapse rates in MOGAD. […] Low-dose prednisone is used as well, more often outside of the United States. […] Studies have shown that conventional treatments for MS are not effective and may cause adverse reactions in AQP4-positive NMOSD. Since there is not enough information about their use in MOG antibody disease, and because they may not reduce relapse rates, or they may lead to adverse effects, treatments for MS are not recommended in MOG antibody disease.
  • #13 Treatment of Myelin Oligodendrocyte Glycoprotein–Associated Diseaselogo-32logo-40logo-60NEJM Journal WatchnejmJW_1L_RGB-b
    https://www.jwatch.org/na57153/2024/02/27/treatment-myelin-oligodendrocyte-glycoprotein-associated
    Treatment of Myelin Oligodendrocyte Glycoprotein–Associated Disease […] Myelin oligodendrocyte glycoprotein–associated disease (MOGAD) is increasingly recognized due to antibody testing, but no therapies have been approved. To evaluate relapses on various therapies, investigators conducted this single-center, retrospective study of 88 patients with MOGAD (59 adult-onset and 29 pediatric-onset) with a median of 6.7 years’ follow-up. […] Compared with a pretreatment annualized relapse rate of 1.05, prednisone reduced relapses by 54%, intravenous immunoglobulin (IVIG) by 87%, 49% for B-cell depletion (BCD), and mycophenolate by 78%. Results were similar in the pediatric MOGAD subgroup. […] This retrospective analysis confirms the prior report noted above on the benefit of IVIG in MOGAD, at a dose of 2g/kg/month. Whereas the prior study found mycophenolate to be comparable to BCD, in this study mycophenolate appeared superior. Prospective and randomized studies are needed, but these two studies suggest that BCD may not be the optimal approach. Studies are ongoing in MOGAD with the monoclonal antibodies satralizumab and rozanolixizumab.
  • #14 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
    https://www.mdpi.com/2073-4468/13/2/43
    Patients with severe symptoms can improve dramatically only after a short course of intravenous steroids. […] In severe cases, or in those who will not improve after 5 days, escalation to plasma exchange (5–7 cycles on alternative days), intravenous immunoglobulins (total of 2 g/kg over 2 or 5 days), or plasma exchange followed by intravenous immunoglobulins can be considered. […] Although randomized-controlled clinical trials have not been conducted, patients with MOGAD who are not considered high risk for relapse are given oral steroids (prednisolone 1g/kg/day) for 3 months followed by prolonged tapering (3 months). […] Data from retrospective studies have shown that intravenous immunoglobulin is the most effective preventive treatment option in MOGAD, with around 70% of the patients achieving remission.
  • #15 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
    https://www.mdpi.com/2073-4468/13/2/43
    Rituximab is the second most effective option, with 50% relapse-free patients, followed by mycophenolate mofetil (47%) and azathioprine (39%). […] New agents are currently being investigated for MOGAD. Tocilizumab, an anti-Interleukin-6 (IL-6) receptor monoclonal antibody, plays a crucial role in B cell maturation and antibody production.
  • #16 MOG Antibody Disease Information – MyMyelitis
    https://mymyelitis.com/mog-antibody-disease/information/
    Rituximab, also known as Rituxan, is a treatment given by IV that suppresses the immune system by depleting a type of white blood cell known as B-cells. […] Due to MOG Antibody Disease not having approved treatments, several clinical trials are ongoing to find beneficial preventative therapies. […] Rozanolixizumab also referred to as Rozimab, is a monoclonal antibody that blocks the activity of the FcRN molecule, which usually preserves antibodies in the bloodstream from being destroyed. […] Satralizumab is a monoclonal antibody, a protein designed to block the action of interleukin-6 (IL-6), a protein in the body that enhances inflammation.
  • #17 MS Minute: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease
    https://practicalneurology.com/articles/2024-nov/ms-minute-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
    The first line treatment for acute MOGAD attacks is high-dose intravenous methylprednisolone. In severe attacks, or in those refractory to intravenous steroids, plasma exchange or intravenous immunoglobulin (IVIg) can be used. Oral prednisone taper after acute treatment of the attack is typically recommended, although the optimal duration is unclear. Relapses can occur during steroid taper or shortly after discontinuation. A recent study showed reduced risk for relapse in people treated with at least 12.5 mg of prednisone for at least 3 months. […] Given that MOGAD can have a monophasic course, maintenance long-term immunosuppression to prevent new attacks is typically reserved for people with relapsing MOGAD. No data from randomized clinical trials are available; treatment has been based on retrospective studies and experience with other autoimmune disorders. Several immunosuppressive agents have been tried, such as azathioprine, mycophenolate mofetil, rituximab, and IVIg. Maintenance IVIg seems to have the lowest relapse rate when compared with rituximab, mycophenolate, and azathioprine. Although rituximab may be efficacious, some individuals with MOGAD experience relapse despite B-cell depletion. Interleukin-6 is elevated in CSF in individuals with MOGAD, and tocilizumab is increasingly used as it seems to be effective in reducing relapses even in refractory cases. […] Randomized placebo-controlled clinical trials are underway with rozanolixizumab, an anti-neonatal Fc receptor and satralizumab, an anti-interleukin-6 receptor. […] Symptomatic management of residual deficits such as sphincter dysfunction, neuropathic pain, and spasticity is essential.
  • #18 Clinical Trial – Myelin Oligodendrocyte Glycoprotein Anti…
    https://forpatients.roche.com/en/trials/autoimmune-disorder/mog-antibody-disease/a-study-to-evaluate-the-efficacy–safety–pharmacokinet-94806.html
    The main objective of the study is to evaluate the efficacy of satralizumab compared with placebo based on time from randomization to the first occurrence of an adjudicated MOGAD relapse in the double-blind (DB) treatment period. […] There is no approved, standard treatment for MOGAD. Medicines known as rescue therapy can be given during an attack or relapse that act fast to dampen or weaken the immune system. […] Satralizumab is a medicine that is approved in many countries for neuromyelitis optica spectrum disorder another condition affecting the optic nerves and spinal cord. Health authorities have yet to approve satralizumab for treating MOGAD on its own (as monotherapy) or in combination with current therapy (also known as background therapy). […] This clinical trial aims to compare the effects, good or bad, of satralizumab with placebo a drug that contains no active ingredients, alone or in combination with background therapy in people with MOGAD.
  • #19 Rozanolixizumab – A New Treatment for MOG Antibody Disease?
    https://mymyelitis.com/mog-antibody-disease/rozanolixizumab-mogad-trial/
    The first ever MOG Antibody Disease phase 3 clinical trial is now taking place. A new drug called Rozanolixizumab will be trialed with MOG Antibody Disease patients as a preventative treatment. If successful, this treatment will be the first-ever FDA-approved treatment for MOGAD and could be used as a preventive treatment to stop relapses. […] The trial aims to see whether Rozanolixizumab prevents relapses in MOG Antibody Disease. This trial is also the first phase 3 clinical trial for MOGAD. Phase 3 is the last testing phase to see if it is a safe, beneficial, and effective treatment. […] The trial is designed to prevent relapses but uses a placebo arm which could cause relapses as some participants would not be on any preventive treatment. However, patients are only allowed to have one relapse in the study.
  • #20 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
    https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease
    Myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) are a spectrum of idiopathic, inflammatory, demyelinating diseases affecting the central nervous system (CNS). […] MOGAD should be considered as an etiology in patients with undifferentiated optic neuritis as MOG antibodies can be detected in 2-5% of patients. […] In MOGAD in addition to visual acuity monitoring, visual field measurements could also be used to monitor functional impairment. […] We use varying slow taper regimens anywhere from 2-6 months depending on the severity of presentation and planned long term regimen and if applicable should be continued for approximately 1-2 months after initiation of long-term immunotherapy. […] Several studies have supported evidence for maintenance IVIG as an effective therapy to prevent relapses. […] At the Mellen center, we recommend long term immunotherapy with one of the above agents for all patients diagnosed with MOGAD although this decision should be individualized, depending on severity and recovery.
  • #21 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/mogad/symptoms-causes/syc-20560476
    There’s no cure for MOGAD. However, there are treatments to help speed the recovery from attacks, manage symptoms and reduce the likelihood of symptoms returning. […] Your healthcare team will work with you to decide which treatment options are the best and how long to continue them. […] Some MOGAD treatments also may cause complications. Long-term use of certain medicines may result in: Infection, Lymphoma or skin cancers, Slowed growth in children, Headaches, Kidney failure.
  • #22 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and Human Immunodeficiency virus infection: dilemmas in diagnosis and management: a case series | Journal of Medical Case Reports | Full Text
    https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-023-04191-7
    When managing autoimmune disorders in immunosuppressed patients, balancing the benefits of (long-term) immunosuppression with the increased risk of infections, particularly opportunistic infections such as tuberculosis, is an additional important consideration. […] Further studies investigating a possible association between HIV infection and MOGAD, and the role of immune dysregulation in the pathophysiology of MOGAD, are warranted.
  • #23 Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD) | American Journal of Neuroradiology
    https://www.ajnr.org/ajnr-case-collections-diagnosis/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
    Management of MOGAD attacks includes high-dose intravenous steroids followed by an oral steroid taper. […] Patients who do not respond adequately to steroids may be treated with intravenous immunoglobulin or plasma exchange. […] In patients with a relapsing disease course, maintenance therapy is recommended and includes the selection of specific therapeutic agents such as intravenous immunoglobulin, rituximab, azathioprine, or mycophenolate mofetil. […] Multiple sclerosis disease-modifying therapies do not appear to be efficacious for preventing MOGAD relapses.
  • #24 MOG antibody disease – Wikipedia
    https://en.wikipedia.org/wiki/MOG_antibody_disease
    MOG (myelin oligodendrocyte glycoprotein) antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. […] Acute therapy consists of high-dose corticosteroids, IVIG, or plasma exchange, and long-term immunosuppression may be necessary in recurrent cases. Anti-MOG positive patients should not be treated with interferons as these may worsen the disease course similar to those with NMOSD. MOG-ON is corticosteroid responsive. […] There are also anecdotal reports against using fingolimod or alemtuzumab.
  • #25 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management
    https://www.mdpi.com/1422-0067/22/1/100
    Unfortunately, the risk of worsening increased after steroid discontinuation or dose reduction. […] The number of reported second relapses was substantial. […] In another frequently cited study, relapses were noticed in as many as 80% of patients during a follow-up. […] Therapeutic strategies to prevent MOGAD attacks, which have been explored so far, involved mainly standard immunomodulating and immunosuppressive therapies, such as oral corticosteroids (OCS), rituximab (RTX), azathioprine (AZA), methotrexate (MTX), mycophenolate mofetil (MMF), and repeated cycles of IVIG. […] The efficacy of RTX is not constant. […] IVIG infusions gave promising results regarding effectiveness. […] Glatiramer acetate and natalizumab have both been shown to be ineffective, also interferon beta injections were not successful, moreover, it increased the disease activity.
  • #26 Failure of alemtuzumab therapy in three patients with MOG antibody associated disease | BMC Neurology | Full Text
    https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-022-02612-6
    Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) is most classically associated in both children and adults with phenotypes including bilateral and recurrent optic neuritis (ON) and transverse myelitis (TM), with the absence of brain lesions characteristic of multiple sclerosis (MS). […] We present three cases of anti-MOG encephalomyelitis initially diagnosed as MS and treated with alemtuzumab followed by multiple relapses and worsening disability on alemtuzumab. […] These cases highlight that (a) MOGAD can be misdiagnosed as MS and, (b) alemtuzumab may be ineffective in MOGAD. […] The development of novel autoimmune disorders following alemtuzumab therapy has been well reported. […] It is evident from our reports above that if a patient with suspected MS on natalizumab shows increased disease activity, as well as considering anti natalizumab neutralizing antibodies and possibility of progressive multifocal leukoencephalopathy (PML), one should also have high vigilance in revisiting the original diagnosis and considering NMOSD or MOGAD as alternatives. […] In conclusion, our cases demonstrate that alemtuzumab is ineffective in the management of MOGAD, but steroids, plasma exchange and IVIG are helpful.
  • #27 Pediatric anti-MOG antibody associated disorder (MOGAD) – Children’s Health Neurology
    https://www.childrens.com/specialties-services/conditions/antibody-associated-disorder
    IVIG therapy – IVIG in an infusible therapy that has been used extensively in pediatrics. IVIG is a collection of antibodies collected from blood donors and pooled together. When infused into patients the antibodies are thought to cause a reduction or blocking of the patients abnormal immune response. […] Rehabilitation – After completing this treatment, patients often require rehabilitation and symptom management. This can include physical therapy (PT), occupational therapy (OT), speech/language therapy, swallow therapy and management of bladder dysfunction. Rarely, patients may experience neuropathic pain that requires treatment. […] Psychosocial support or therapy – In addition to evaluation by a neuropsychologist for cognitive, emotional and/or behavioral problems, patients may also require psychosocial support or therapy to manage the impacts of inflammation in the brain.
  • #28 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad?embed_domain=hackmd.io%252525252F%2525252540yIPUAFeCSL2JsU8smR5nJQ%252525252Fbnjhjgjghjghjgh&lang=gb
    Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) represents a group of inflammatory demyelinating disorders united by the presence of IgG antibodies to myelin oligodendrocyte glycoprotein (MOG). […] Although treatment and prognosis remain to be fully understood, it appears that generally, individuals with anti-MOG antibodies have fewer relapses and less severe clinical course than individuals with anti-aquaporin 4 antibodies presenting with NMOSD. […] Acute management with intravenous methylprednisolone, plasma exchange, intravenous immunoglobulin or cyclophosphamide have been reported and appear to be efficacious. […] It remains unclear what, if any, long-term medications are required in individuals with a relapsing time course, although it seems that response to immunotherapeutic agents is different to multiple sclerosis and that some agents efficacious in the latter may actually worsen anti-MOG related diseases.
  • #29 Myelin oligodendrocyte glycoprotein antibody-associated disease – Overview of Information and Clinical Research
    https://clinicaltrials.eu/disease/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease/
    Despite the absence of a cure, rehabilitation programs and support networks play a vital role in enhancing the quality of life for patients. […] Additionally, ongoing Phase 3 clinical trials for drugs like Rozanolixizumab and Satralizumab hold promise for advancing treatment options and improving patient outcomes.
  • #30
    https://link.springer.com/article/10.1007/s00415-023-11737-8
    New diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) have recently been proposed, distinguishing this syndrome from other inflammatory diseases of the central nervous system. […] Key challenges to the current understanding of MOGAD are also highlighted, including uncertainty regarding the specificity and pathogenicity of MOG autoantibodies, the need to identify immunopathologic targets for future therapies, the quest to validate biomarkers that facilitate diagnosis and detect disease activity, and the importance of deciphering which patients with MOGAD require long-term immunotherapy. […] Treatment approaches for MOG-Ab-associated demyelination in children. […] The treatment of myelin oligodendrocyte glycoprotein antibody disease: a state-of-the-art review.
  • #31 The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children
    https://www.explorationpub.com/Journals/ent/Article/100469
    Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to cause a distinct disease called MOG antibody-associated disease (MOGAD). […] Although it was previously thought to be a milder demyelinating disorder and to have a monophasic course in the majority of patients, recent studies have shown that relapses occur in about half of the patients and sequelae develop in a significant proportion of them, especially in those with persistently high antibody titers, leukodystrophy-like magnetic resonance imaging (MRI) lesions, and spinal cord involvement. […] Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. […] In addition, early identification of MOGAD patients presenting with a first demyelinating event and at risk of relapse allows for early initiation of disease-modifying therapeutic agents, thereby improving prognosis.