Evidence map›Paper›PMID 41658631›Full record

ArticleCureus2026

Severe Pain Phenotype in Hemoglobin C (HbC)/Beta-Zero (β⁰) Thalassemia Without Hemoglobin S (HbS): A Clinical and Diagnostic Challenge.

Michael J Martinez, Benjamin N Friedland, Aayushi Jha, Tanya Zagoruychenko, Sesha Berman

Abstract readCase Reports
In one paragraph

Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Michael J MartinezInternal Medicine, St. Matthew's University, West Bay, CYM.
Benjamin N FriedlandInternal Medicine, Touro College of Osteopathic Medicine, New York, USA.
Aayushi JhaInternal Medicine, State University of New York (SUNY) Downstate Medical School, Brooklyn, USA.
Tanya ZagoruychenkoInternal Medicine, Brookdale University Hospital Medical Center, Brooklyn, USA.
Sesha BermanInternal Medicine, Brookdale University Hospital Medical Center, Brooklyn, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormalities in the synthesis or structure of globin chains are known as hemoglobinopathies, and they produce a wide range of clinical phenotypes. When both alleles of the same gene carry different hemoglobin variants, this results in compound heterozygosity. The condition described in this case report (hemoglobin C (HbC)/beta-zero (β⁰)-thalassemia) is one such example. On their own, neither HbC nor β⁰-thalassemia is typically associated with acute vaso-occlusive crises, and the combination of HbC/β⁰-thalassemia has not been well characterized. Limited reports indicate that this genotype is not known to cause pain episodes resembling those seen in HbSC disease. Here, we describe a 32-year-old woman with DNA-confirmed HbC/β⁰-thalassemia. She has chronic transfusion dependence, marrow expansion, and anemia, with a baseline hemoglobin of about 8 g/dL. Despite treatment with hydroxyurea and opioid therapy, she has persistent diffuse bone pain. During the current admission, she presented with worsening pain, nausea, and vomiting. Laboratory findings showed stable hemoglobin compared to her baseline, without leukocytosis or sickling, and imaging revealed no acute pathology. Her pain was managed with intravenous hydromorphone, with plans to transition to oral methadone and oxycodone as needed before discharge. This case illustrates the difficulty of managing severe pain in HbC/β⁰-thalassemia, particularly when symptoms occur with high intensity but without evidence of vaso-occlusion or acute hemolysis. While extramedullary hematopoiesis is a leading explanation for her pain, the degree of pain she experienced is unusual in the absence of acute sickling. Given the rarity of this genotype and the limited amount of published data, management remains challenging. Further research is needed to clarify the mechanisms of pain in HbC/β⁰-thalassemia and to distinguish organic causes from central sensitization in patients with chronic opioid use.

Indexed as

compound heterozygosityextramedullary hematopoiesishemoglobin ctransfusion-dependent anemiaβ⁰-thalassemiaβ-globin gene mutations

Identifiers

PMID41658631
PMCPMC12880838

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