Evidence map›Paper›PMID 26857124›Full record

ArticleMolecular and cellular pediatrics2016

The clinical consequences of sucrase-isomaltase deficiency.

Stanley A Cohen

Open access · goldAbstract read
In one paragraph

Article in Molecular and cellular pediatrics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Congenital Sucrase-Isomaltase Deficiency: Same Mutation with Different Clinical Presentations.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  4. Article
  5. Review
  6. Nutritional strategies to attenuate postprandial glycemic response.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  7. Review
  8. Article
  9. The patient journey to diagnosis and treatment of congenital sucrase-isomaltase deficiency.Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation · 2021
    Observational
  10. Article
  11. Article
  12. Article
  13. Food Intolerances.Nutrients · 2019
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Clinical medicine insights. Gastroenterology · 2018
    Review
  19. Article
  20. Molecular biology of the gut.Molecular and cellular pediatrics · 2016
    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

1 author at 1 institution in 1 country.

Stanley A CohenChildren's Center for Digestive Health Care, Children's Healthcare of Atlanta, 993D Johnson Ferry Road NE, Suite 440, Atlanta, GA, 30342, USA. stancohen@aol.com.
Children's Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary sucrase-isomaltase deficiency, originally thought to be a homozygous recessive disorder, has been found to have numerous genetic variants that alone or in combination (compound heterozygosity) express varying degrees of clinical illness, most commonly causing chronic diarrhea, abdominal pain, and bloating. These symptoms are also present with secondary sucrase-isomaltase deficiency. Recent investigations are providing evidence that sucrase-isomaltase deficiency is more prevalent and of greater clinical significance than previously suspected. Further research is required to correlate the specific genotypes and phenotypes with their clinical expressions and to determine the most appropriate treatment algorithm for these patients.

Indexed as

Genetic sucrase-isomaltase deficiencyHeterozygous carriersSacrosidaseSucraseSucrase-isomaltase deficiency

Identifiers

PMID26857124
PMCPMC4746203
OpenAlexW2298923378

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.