Evidence map›Paper›PMID 9259176›Full record

ReviewDrugs & aging1997

Current and future therapies for myasthenia gravis.

Q Yi, A K Lefvert

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs & aging, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 30% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

2 authors at 2 institutions in 1 country.

Q YiImmunological Research Laboratory, Karolinska Hospital, Stockholm, Sweden. Qing.Yi@cmm.ki.se
A K Lefvert
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is undoubtedly the most thoroughly understood of all human autoimmune diseases. The basic defect in the disease is a decrease in the number of available acetylcholine receptors (AChR) at neuromuscular junctions caused by an antibody-mediated autoimmune attack. Current treatments aimed at restoring the available AChR, depleting the autoantibodies or suppressing the immune system have been so effective that most patients can lead normal lives. However, prolonged drug treatment is required, and this carries a potential risk of drug toxicity and, in the case of immunosuppressants, systemic immunosuppression. The ideal treatment for MG would eliminate only the abnormal autoimmune response without interfering with the immune system. During the past 20 years, impressive advances have been made in our understanding of the immunology and molecular biology of MG. Accordingly, it should be possible to design rational and immune-based therapies in the future. In this article, we briefly review the current treatment modalities for MG, and discuss the prospects for immunotherapy.

Indexed as

ThymectomyAutoantibodiesAutoimmune DiseasesCholinesterase InhibitorsHumansImmunoglobulins, IntravenousImmunosuppressive AgentsImmunotherapyMyasthenia GravisPlasma ExchangeT-LymphocytesAutoantibodiesCholinesterase InhibitorsImmunoglobulins, IntravenousImmunosuppressive Agents

Identifiers

PMID9259176
OpenAlexW2094776105

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.