Evidence map›Paper›PMID 20012975›Full record

ReviewZeitschrift fur Rheumatologie2010

[Pathogenesis and diagnosis of Sjögren's syndrome].

T Witte

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Zeitschrift fur Rheumatologie, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

T WitteKlinik für Immunologie und Rheumatologie, Carl-Neuberg-Str. 1, 30625 Hannover. witte.torsten@mh-hannover.de
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sjögren's syndrome is a common autoimmune disorder. Several genetic risk factors such as STAT-4, ILT6 and the haplotype HLA-B8/DR3 have been identified. In addition, there are environmental risk factors, possibly chronic viral infections. In the pathophysiology of Sjögren's syndrome T and B cells infiltrate the salivary and lacrimal glands. As a consequence of the destruction of glandular cells by cytotoxic T cells, production of cytokines and autoantibodies inhibiting glandular function, the production of saliva and tears is decreased. The feeling of dry eyes and mouth is frequently not noticed by the patients. Therefore, Sjögren's syndrome should also be considered when extraglandular manifestations such as vasculitis, polyneuropathy or arthritis occur, even when the patients do not complain of dry eyes and mouth. Establishing the diagnosis of Sjögren's syndrome requires verification of reduced glandular function, for example using Schirmer's test and the Saxon test. The confirmation of Sjögren's syndrome as a cause of sicca syndrome is subsequently performed by the detection of autoantibodies against Ro (SS-A) and La (SS-B) and/or by a salivary gland biopsy.

Indexed as

Environmental ExposureAutoantibodiesBiopsyB-LymphocytesCarrier ProteinsGenetic Predisposition to DiseaseHaplotypesHLA-B8 AntigenHLA-DR3 AntigenHumansKeratoconjunctivitis SiccaLacrimal ApparatusMicrofilament ProteinsReceptors, ImmunologicRisk FactorsSalivary GlandsAutoantibodiesCarrier ProteinsHLA-B8 AntigenHLA-DR3 AntigenLILRA3 protein, humanMicrofilament ProteinsReceptors, ImmunologicSpectrinSTAT4 protein, humanSTAT4 Transcription Factor

Identifiers

PMID20012975
OpenAlexW1496567072

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.