Fatty Lesions in Liver Induced by Alcohol Abuse in 3 Patients with Chronic Hepatic Porphyria, Case Report Suggests

Fatty Lesions in Liver Induced by Alcohol Abuse in 3 Patients with Chronic Hepatic Porphyria, Case Report Suggests

Three patients with multiple fat deposits in the liver caused by alcohol abuse were diagnosed with chronic hepatic porphyria (CHP), a case report describes.

In all three cases, a highly sensitive imaging technique called contrast-enhanced ultrasound (CEUS) was useful in confirming a diagnosis.

The report, “Multinodular fatty change in the liver in three patients with chronic hepatic porphyria: Contribution of sonography to the diagnosis,” appeared in the Journal of Clinical Ultrasound.

CHP is characterized by periportal inflammation — around the portal vein in the liver — deposits of an iron storage complex called hemosiderin, and fatty changes, or steatosis, referring to lipid accumulation in liver cells.

Multinodular fatty changes (MNFC) may occur in some CHP cases, mimicking liver tumors. Because of its high sensitivity, CEUS is expected to be able to differentiate between CHP-related MNFC and a true liver tumor.

Alcohol abuse and hepatitis viral infections have been reported as possible causes of hepatic steatosis in CHP patients.

In the three cases described in the report, CEUS was used to determine a diagnosis immediately after grayscale ultrasound, a technique that can potentially misdiagnose MNFC as liver tumors. In two of these cases, 2D shear-wave elastography (2DSWE), an ultrasound-based technique that assesses tissue stiffness, was then performed for the first time in this context, according to the researchers.

The first case was a 61-year-old man with chronic alcoholism (more than 50 g/day for 30 years), who was complaining of general fatigue that had lasted for two months. Biochemical parameters were normal, with negative results for tumor markers and antibodies for the hepatitis virus.

An abdominal ultrasound revealed well-defined masses, 1-3 cm in size, but no portal or hepatic vein displacement. CEUS results then suggested that the masses represented fatty changes, which was supported by a computed tomography (CT) scan. Ultrasound-guided biopsy of one lesion subsequently revealed focal fatty changes and minimal inflammatory infiltrates.

Urine analysis showed an excess amount of uroporphyrin — 270 mcg/g.Cr (upper normal limit is 36 mcg/g.Cr) — prompting a diagnosis of MNFC due to CHP. The man was advised to stop drinking alcohol to avoid progression into severe hepatic injury and was followed up by ultrasound every month. His multiple mass lesions gradually became less distinct and disappeared after three months.

The second case was also a 61-year-old man with chronic alcoholism (more than 30 g/day for 25 years), who was initially referred for detailed examination due to a slight liver dysfunction. Like the first patient, this man also had negative results for tumor markers and antibodies for HCV, and revealed multiple well-defined mass lesions of 1-3 cm in both lobes on an ultrasound, as well as no portal or hepatic vein displacement. Unlike the first case, the mass lesions in this patient showed a rim-like structure.

Although CEUS results suggested the masses were focal fatty changes, a CT scan did not support this. The patient refused to undergo ultrasound-guided biopsy.

Urine analysis showed a uroporphyrin level of 91 mcg/g.Cr, leading the clinicians to consider a diagnosis of MNFC due to CHP, also as a result of their experience in the first case. The patient was also advised to abstain from alcohol. His mass lesions disappeared after six months.

The third case was a 58-year-old woman also with chronic alcoholism (more than 40 g/day for 30 years) who was referred for detailed examination and treatment of mild liver dysfunction and multiple mass lesions. Ultrasound and CEUS results were similar to the first patient. No abnormalities in liver blood vessels or tissue were found.

Urine analysis showed an abnormally high level of coproporphyrin — 252 mcg/g.Cr, where the normal upper limit is 170 mcg/g.Cr — leading to a diagnosis of liver cirrhosis with MNFC due to CHP. She was also advised to abstain from alcohol. Her multiple mass lesions disappeared after three months.

Overall, the fact that the three patients were alcoholic, their mass lesions rapidly decreased upon abstinence from alcohol, and they were not infected with hepatitis B or C all supported alcohol abuse as the trigger of hepatic manifestations in these cases.

The scientists added that in cases of multiple mass lesions in alcoholic patients, “CHP-related MNFC should be considered, and observation of CEUS and close monitoring with grayscale US are recommended to confirm the diagnosis.”

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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