Evidence map›Paper›PMID 28648664›Full record

ArticleMolecular genetics and metabolism2017

High dose IVIG successfully reduces high rhGAA IgG antibody titers in a CRIM-negative infantile Pompe disease patient.

Mugdha Rairikar, Zoheb B Kazi, Ankit Desai, Crista Walters, Amy Rosenberg, Priya S Kishnani

Registry-linked trialOpen access · greenAbstract readCase Reports
In one paragraph

Article in Molecular genetics and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01665326 (Determination of Cross-Reactive Immunological Material), which is not on this map. Cited by 11 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 4 pooled it
0.3field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT01665326 recruitingnot on this map

Determination of Cross-Reactive Immunological Material (CRIM) Status and Longitudinal Follow-up of Individuals With Pompe Disease

TypeobservationalSponsorDuke UniversityRan2009 to 2029Enrolled400ConditionsPompe DiseaseArmsObservational
3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 4 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. What's new and what's next for gene therapy in Pompe disease?Expert opinion on biological therapy · 2022
    Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Mugdha RairikarDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC, USA.
Zoheb B KaziDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC, USA.
Ankit DesaiDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC, USA.
Crista WaltersDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC, USA.
Amy RosenbergDivision of Therapeutic Proteins, Office of Biotechnology Products, Center for Drug Evaluation and Research, United States Food and Drug Administration, Bethesda, MD, USA.
Priya S KishnaniDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC, USA. Electronic address: priya.kishnani@duke.edu.
Duke Medical Center · USCenter for Drug Evaluation and Research · US

Funding

Training & EducationU54NS065768 · NINDS · UNIVERSITY OF MINNESOTA · PI WHITLEY, CHESTER B. · 2009 to 2024
$17.7M
NINDS NIH HHS U54 NS065768
6 · The paper itself

Abstract

Alglucosidase alfa (rhGAA) has altered the course of an otherwise fatal outcome in classic infantile Pompe disease (IPD), which presents with cardiomyopathy and severe musculoskeletal involvement. However, the response to therapy is determined by several factors including the development of high and sustained antibody titers (HSAT) to rhGAA. Cross-reactive immunologic material (CRIM) negative patients are at the highest risk for development of HSAT. Immune tolerance induction (ITI) with methotrexate, rituximab, and intravenous immunoglobulin (IVIG) has been largely successful in preventing the immune response and in achieving tolerance when done in conjunction with enzyme replacement therapy (ERT) initiation. Reducing antibody titers in cases with an entrenched immune response remains a challenge in the field despite the use of multiple immunomodulatory agents. Success has been shown with addition of bortezomib to the ITI regimen, yet the prolonged course and potential risks with the use of such agents' demands caution. We present here a 7-year-old CRIM-negative IPD patient who was not successfully tolerized by an ITI regimen with rituximab, methotrexate, and IVIG due to intolerability to the regimen and recurrent infections. She went on to develop HSAT, with significant clinical decline, loss of all motor abilities, and a fragile medical state, which made it challenging to institute the bortezomib based regimen to reduce HSAT. She had severe developmental delay, respiratory failure with invasive ventilation and tracheostomy, persistent hypotonia, ptosis of eyelids, diffuse severe osteopenia, contractures, and was completely G-tube fed. As a rescue mechanism, we treated her with high dose and high frequency IVIG in an attempt to reduce rhGAA IgG antibody titers (antibody titers; titers). Her titers saw a steady decline on weekly IVIG doses at 1g/kg for 20weeks. Subsequently when the IVIG regimen was altered to 1g/kg every month, rising titers were detected and therefore the regimen was changed to a biweekly regimen. High dose IVIG resulted in an eightfold decrease in antibody titers. Clinically, she showed improvement with partial recovery of previously lost motor abilities, especially hand movements and better head and neck control than before. The regimen was safely tolerated with no hospitalizations. The effectiveness of IVIG as a single agent, in this case with multiple comorbidities and fragile clinical status, was lifesaving and may represent an effective, perhaps lifesaving rescue approach to reduce antibody titers.

Indexed as

alpha-GlucosidasesAntibodiesChildCross ReactionsFemaleGlycogen Storage Disease Type IIHumansImmune ToleranceImmunoglobulins, IntravenousImmunomodulationMaleTreatment Outcomealpha-GlucosidasesAntibodiesGAA protein, humanImmunoglobulins, IntravenousAnti-rhGAA IgG antibodiesHigh dose IVIGImmunogenicityImmunomodulationPompe disease

Identifiers

PMID28648664
PMCPMC5612830
OpenAlexW2614861380

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.