Evidence map›Paper›PMID 38947766›Full record

ArticleOpen life sciences2024

Coexistence of hereditary spherocytosis with

Changwei Chi, Shenghao Wu, Wenjin Zhou, Yingying Hu, Yanwei Lu, Shanshan Weng

Abstract readCase Reports
In one paragraph

Article in Open life sciences, 2024. 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. Article
  3. [Expert consensus on the diagnosis and therapy of inherited hyperbilirubinemia (version 2025)].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  4. 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.

Changwei ChiDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.
Shenghao WuDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.
Wenjin ZhouDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.
Yingying HuDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.
Yanwei LuDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.
Shanshan WengDepartment of Hematology, The Dingli Clinical College of Wenzhou Medical University (The Second Affiliated Hospital of Shanghai University, Wenzhou Central Hospital), Wenzhou, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A congenital protein anomaly in the erythrocyte membrane skeleton causes a hereditary haemolytic illness known as hereditary spherocytosis (HS). The primary characteristic of HS is an increase in the number of tiny spherical red blood cells in the peripheral blood. The chief clinical features of HS include anaemia, jaundice, splenomegaly, spherical erythrocytosis in the blood, chronic anaemia with haemolysis, and recurrent acute attacks. Most patients have a family history; some have autosomal recessive inheritance, whereas most have autosomal dominant inheritance. In cases of severe hyperbilirubinemia disproportionate to haemolysis, other causes of hyperbilirubinemia should be considered. Gilbert syndrome (GS) is an autosomal dominant illness caused by the reduced activity of uridine diphosphate-glucuronosyl transferase lAl and is characterised by intermittent hyperbilirubinemia without any other signs or symptoms of liver disease. The possibility of the coexistence of HS and GS is very limited. Here we present the case of an elderly man with yellow skin and sclera recurring anaemia, and a final diagnosis of coexisting HS and GS.

Indexed as

Gilbert syndromehereditary spherocytosisjaundice

Identifiers

PMID38947766
PMCPMC11211870

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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.