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Cited by 256

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Peliosis Hepatis Associated with Androgenic-Anabolic Steroid Therapy: A Severe Form of Hepatic Injury

BAGHERI, SAEED A., BOYER, JAMES L.·1974·Annals of Internal Medicine

Abstract

Blood-filled cysts, characteristic of peliosis hepatis, developed within hepatic parenchyma in seven patients who were treated with androgenic-anabolic steroids for periods ranging from 2 to 27 months. Five patients had hematologic disorders, and two had malignancies. Although liver function was normal in all patients before therapy was started, all but one patient developed hepatomegaly or signs of hepatic toxicity. Two patients sustained intraperitoneal hemorrhages from the peliotic lesions, and one died from shock. Peliosis hepatis resulted in hepatic failure and death in three patients, with terminal renal failure supervening in two. The spectrum of histologic abnormalities in these patients suggested that the hemorrhagic cysts developed from focuses of hepatocellular necrosis. These studies indicate that peliosis hepatis can be a serious life-threatening complication of androgenic-anabolic steroid therapy in man.

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Authors
BAGHERI, S. A., & BOYER, J. L.
Venue
Annals of Internal Medicine
Published
1974-11-01
Volume
81
Issue
5
Pages
610-618
ISSN
  • 0003-4819 (ISSN-L)
  • 1539-3704
OpenAlex
W2049275648
Cited by
256
References
0
FWCI
9.98
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Peliosis Hepatis Associated with Androgenic-Anabolic Steroid Therapy: A Severe Form of Hepatic Injury. https://app.cochat.ai/papers/10.7326/0003-4819-81-5-610
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BAGHERI, S. A., & BOYER, J. L. (1974). Peliosis Hepatis Associated with Androgenic-Anabolic Steroid Therapy: A Severe Form of Hepatic Injury. Annals of Internal Medicine. https://doi.org/10.7326/0003-4819-81-5-610

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.