Evidence map›Paper›PMID 21102543›Full record

ReviewNature reviews. Rheumatology2011

Pathophysiology of articular chondrocalcinosis--role of ANKH.

Abhishek Abhishek, Michael Doherty

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
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  8. Pseudogout of the lumbar spine.Radiology case reports · 2023
    Article
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  14. Review
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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

2 authors at 2 institutions in 1 country.

Abhishek AbhishekDivision of Academic Rheumatology, Clinical Sciences Building, City Hospital Nottingham, Hucknall Road, Nottingham NG51PB, UK. docabhishek@gmail.com
Michael Doherty
Nottingham City Hospital · GBUniversity of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium pyrophosphate (CPP) crystal deposition (CPPD) is associated with ageing and osteoarthritis, and with uncommon disorders such as hyperparathyroidism, hypomagnesemia, hemochromatosis and hypophosphatasia. Elevated levels of synovial fluid pyrophosphate promote CPP crystal formation. This extracellular pyrophosphate originates either from the breakdown of nucleotide triphosphates by plasma-cell membrane glycoprotein 1 (PC-1) or from pyrophosphate transport by the transmembrane protein progressive ankylosis protein homolog (ANK). Although the etiology of apparent sporadic CPPD is not well-established, mutations in the ANK human gene (ANKH) have been shown to cause familial CPPD. In this Review, the key regulators of pyrophosphate metabolism and factors that lead to high extracellular pyrophosphate levels are described. Particular emphasis is placed on the mechanisms by which mutations in ANKH cause CPPD and the clinical phenotype of these mutations is discussed. Cartilage factors predisposing to CPPD and CPP-crystal-induced inflammation and current treatment options for the management of CPPD are also described.

Indexed as

AnimalsAnkylosisCalcium PyrophosphateChondrocalcinosisCrystallizationHumansHydroxychloroquineInterleukin-1MethotrexateMutationPhosphate Transport ProteinsRisk FactorsANKH protein, humanCalcium PyrophosphateHydroxychloroquineInterleukin-1MethotrexatePhosphate Transport Proteins

Identifiers

PMID21102543
OpenAlexW1997875330

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.