Evidence map›Paper›PMID 11788559›Full record

Trial reportGut2002

Thalidomide reduces tumour necrosis factor alpha and interleukin 12 production in patients with chronic active Crohn's disease.

J Bauditz, S Wedel, H Lochs

Registry-linked trialOpen access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Gut, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04680195 (Prospective, Open Clinical Trial of Thalidomide in the Treatment of Chronic Radiation Proctitis With Intractable Bleeding), which is not on this map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
6.5field-weighted citation impact, top 3% 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.

NCT04680195 phase2unknown statusnot on this mapstarted 2020, after this paper: background citation

Prospective, Open Clinical Trial of Thalidomide in the Treatment of Chronic Radiation Proctitis With Intractable Bleeding

TypeinterventionalSponsorSixth Affiliated Hospital, Sun Yat-sen UniversityRan2020 to 2022Enrolled62ConditionsChronic Radiation ProctitisArmsThalidomide
3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Dually Efficacious Medicine Against Fibrosis and Cancer.Medical sciences (Basel, Switzerland) · 2019
    Review
  10. PPAR research · 2018
    Article
  11. Article
  12. Emerging biologics in inflammatory bowel disease.Journal of gastroenterology · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Inflammatory bowel disease: clinical aspects and treatments.Journal of inflammation research · 2014
    Review
  18. Article
  19. Article
  20. 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.

J BauditzCharité University Hospital, 4th Department of Medicine, Berlin, Germany. juergen.bauditz@charite.de
S Wedel
H Lochs
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThalidomide improves clinical symptoms in patients with therapy refractory Crohn's disease, as shown in two recent studies. The mechanism of this effect however is still unknown. Suppression of tumour necrosis factor alpha (TNF-alpha) by thalidomide has been suggested as a possible mechanism. However, effects on other cytokines have not been adequately investigated.

aimThe aim of our study was to investigate the effects of thalidomide on cytokine production in patients with inflammatory bowel disease (IBD).

methodsTen patients with therapy refractory IBD (nine Crohn's disease, one ulcerative colitis) received thalidomide 300 mg daily in a 12 week open label study. Production of TNF-alpha, interleukin (IL)-1 beta, IL-6, and IL-12 was investigated in short term cultures of stimulated colonic lamina propria mononuclear cells (LPMC) and peripheral blood monocytes (PBMC) before and after 12 weeks of treatment. LPMC were also cultured with graded doses of thalidomide.

resultsThree patients discontinued treatment because of sedative side effects. In the other patients, disease activity decreased significantly, with four patients achieving remission. Production of TNF-alpha and IL-12 decreased during treatment with thalidomide: LPMC (TNF-alpha: 42.3 (8.3) pg/ml v 16.4 (6.3); IL-12: 9.7 (3.3) v 5.0 (2.5); p<0.04) and PBMC (TNF-alpha: 62.8 (14.6) v 22.5 (9.2); p<0.02). Production of IL-1 beta and IL-6 did not change significantly. Culturing of LPMC with thalidomide showed a dose dependent decrease in TNF-alpha and IL-12 production.

conclusionThe clinical effects of thalidomide in Crohn's disease may be mediated by reduction of both TNF-alpha and IL-12.

Indexed as

AdultAnti-Inflammatory AgentsCells, CulturedColitisColitis, UlcerativeCrohn DiseaseDose-Response Relationship, DrugDrug ResistanceFatigueFemaleHumansInterleukin-12Intestinal MucosaLeukocytes, MononuclearMaleMiddle AgedAnti-Inflammatory AgentsInterleukin-12ThalidomideTumor Necrosis Factor-alpha

Identifiers

PMID11788559
PMCPMC1773116
OpenAlexW2122207878

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.