Evidence map›Paper›PMID 11096605›Full record

ArticleCurrent treatment options in gastroenterology2000

Alpha(1)-Antitrypsin Deficiency.

Perlmutter

Abstract read
PubMed Publisher
In one paragraph

Article in Current treatment options in gastroenterology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Increased expression or activation of TRPML1 reduces hepatic storage of toxic Z alpha-1 antitrypsin.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  4. Review
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.

PerlmutterDepartment of Pediatrics, Washington University School of Medicine, St. Louis Children's Hospital, 660 South Euclid Avenue, Box 8208, St. Louis, MO 63110, USA. perlmutter@kids.wustl.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most of the care of liver disease in alpha(1)-antitrypsin (alpha(1)-AT) deficiency involves supportive management for complications of chronic liver disease including gastrointestinal bleeding, ascites, edema, encephalopathy, coagulation disturbances, spontaneous bacterial peritonitis, and hepatorenal syndrome. Some of these patients will have manifestations of cholestatic injury, including pruritus, hypercholesterolemia, and steatorrhea with fat-soluble vitamin deficiencies. The major challenge for the clinician taking care of these patients is the timing of referral for liver transplantation therapy. Timing of such referral is a relatively straightforward decision in alpha(1)-AT-deficient patients with progressive liver dysfunction. Some patients have nonprogressive or slowly progressing liver disease even after the development of cirrhosis or portal hypertension. Timing of liver transplantation in these patients should not be based simply on the presence of cirrhosis, portal hypertension or mild liver synthetic dysfunction, but rather on the basis of a subjective judgment by the hepatologist, patient, and family that manifestations of liver disease are interfering with overall life functioning.

Identifiers

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.