Evidence map›Paper›PMID 33201261›Full record

ReviewDer Internist2020

[Evidence-based treatment of cystic fibrosis].

F C Ringshausen, T Hellmuth, A-M Dittrich

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Internist, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 33% 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, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Review
  4. Review
  5. Article
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

3 authors at 1 institution in 1 country.

F C RingshausenKlinik für Pneumologie, OE 6870, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Straße 1, 30625, Hannover, Deutschland. Ringshausen.Felix@mh-hannover.de.
T HellmuthKlinik für Pädiatrische Pneumologie, Allergologie und Neonatologie, Medizinische Hochschule Hannover (MHH), Hannover, Deutschland.
A-M DittrichKlinik für Pädiatrische Pneumologie, Allergologie und Neonatologie, Medizinische Hochschule Hannover (MHH), Hannover, Deutschland.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucoviscidosis (cystic fibrosis [CF]) is the most common autosomal recessive inherited multisystem disease with fatal outcome. It is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which lead to a dysfunctional chloride channel and a defective CFTR protein. As a consequence, retention of insufficiently hydrated mucus affects multiple essential organs, mainly the lungs and airways, pancreas, liver, biliary tract and intestines. This leads to inflammation and infection, fibrosis and progressive tissue destruction. Respiratory failure is the major cause of mortality; however, in the no more than 30 years since the molecular characterization of the basic CFTR defect causing CF, tremendous success has been made with respect to the long-term prognosis of people with CF. This improvement in the prognosis was achieved by the cooperative spirit and networking of the very active and international CF research community and by establishing a multidisciplinary clinical CF team that implements the existing evidence in various aspects of standardized care together with the CF patient. This narrative review article presents the evidence in selected aspects of CF treatment, with special consideration of the most recent development of highly effective CFTR modulator treatment. This treatment will soon become available for more than 90% of the global CF patients and transform the pathophysiology as well as the course of disease towards a treatable chronic condition in internal medicine.

Indexed as

Precision MedicineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHumansLungMutationCystic Fibrosis Transmembrane Conductance RegulatorAntibacterial agentsAnti-inflammatory agentsCFTR modulatorsCystic fibrosis transmembrane conductance regulator (CFTR)Evidence-based medicine

Identifiers

PMID33201261
OpenAlexW3104867086

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.