Evidence mapPaperPMID 20155993Full record

ArticleClinical drug investigation2010

Atorvastatin-induced prolonged cholestasis with bile duct damage.

Manuela Merli, Maria Consiglia Bragazzi, Federica Giubilo, Francesco Callea, Adolfo F Attili, Domenico Alvaro

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In one paragraph

Article in Clinical drug investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Statin-induced Liver Injury Patterns: A Clinical Review.Journal of clinical and translational hepatology · 2022
    Review
  2. Article
  3. Article
  4. Article
  5. Effects of statins on cholestasis: good, bad or indifferent?Journal of gastroenterology and hepatology · 2011
    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

6 authors.

Manuela MerliDivision of Gastroenterology, Department of Clinical Medicine, University of Rome 'Sapienza', Rome, Italy.
Maria Consiglia Bragazzi
Federica Giubilo
Francesco Callea
Adolfo F Attili
Domenico Alvaro

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We report a case of acute-onset, long-lasting cholestasis induced by atorvastatin. This antihyperlipidaemic drug was taken for 40 days by a 72-year-old male as a treatment for his mixed dyslipidaemia. At that point, the patient presented with asthenia, nausea, painless icterus, acholic stools and hyperchromic urine with biochemical analyses showing a dramatic increase in bilirubin (total bilirubin 22 mg/dL; direct bilirubin 21 mg/dL) and alkaline phosphatase (up to 4-fold over the normal level) with less marked increases in transaminases. Liver histology showed a pattern of cholestasis with evident signs of cholangiolitis and damage of the interlobular bile ducts. Serum transaminase and bilirubin levels returned to normal within 5 months after atorvastatin withdrawal while alkaline phosphatase normalized after only 8 months. Scores on both the Maria and Victorino clinical scale for the diagnosis of drug-induced hepatitis and the Naranjo Adverse Drug Reaction Probability Scale indicated that atorvastatin was the probable cause of prolonged cholestasis in this patient. This is a rare case of cholestasis probably caused by atorvastatin and unusually characterized by bile duct damage.

Indexed as

AgedAnticholesteremic AgentsAtorvastatinBile DuctsCholagogues and CholereticsCholangitisCholestasisDyslipidemiasHeptanoic AcidsHumansMalePyrrolesUrsodeoxycholic AcidAnticholesteremic AgentsAtorvastatinCholagogues and CholereticsHeptanoic AcidsPyrrolesUrsodeoxycholic Acid

Identifiers

What Socratic 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 Socratic graph.