We read with interest the articles by Arena et al.1 and Sagir et al.,2 and the editorial by Cobbold and Taylor-Robinson3, pertaining to transient elastography (TE) and acute viral hepatitis (AVH) or acute liver damage (ALD). The study by Sagir et al. supports that TE is unreliable for the detection of cirrhosis in patients with ALD, and the study by Arena et al. supports that AVH increases liver stiffness values (LSVs) measured by TE. However, the LSVs found after the resolution of ALD correspond well to the histological degree of fibrosis2 and decrease with catabasis of aminotransferases.1
We agree with the observations of these investigators that AVH and ALD increase the LSVs (our unpublished data) and that liver stiffness measurements (LSMs) do not represent a reliable instrument to detect the presence of advanced fibrosis and cirrhosis in patients presenting concomitantly with a clinical picture of acute hepatitis and/or ALD. Coco et al.4 also previously noted increases in LSVs in patients with alanine aminotransferase flares whereas, during hepatitis exacerbations and in acute hepatitis, LSM values increased above the cutoff for significant fibrosis (≥F2).
TE seems to detect particular hepatic pathology other than fibrosis, and there is no clear explanation for this, although properties of the underlying histopathology have been recruited in an attempt to provide explanation.5–7
From our experience in using the FibroScan test in assessing chronic and acute hepatic liver disease in immunocompetent or immunosuppressed, monoinfected, dual-infected, and HIV-coinfected patients, we have come to deepen our understanding of the apparatus and its properties as used in clinical practice, and propose ways to take advantage of the properties of TE in the evaluation of these disease states, in order to use this technology efficiently.
Physicians do not rely on TE to diagnose ALD or hepatitis but can nevertheless use it along with, and even in parallel with, the traditional diagnostic tests, as an adjunct tool in assessing previously well patients with clinical features of acute hepatopathy, toward establishing the diagnosis and follow-up. A high LSV offers a baseline, so that reassessments on follow-up can indicate the disease evolution pattern, characterized by a worsening in the case of fulminant hepatitis or an improvement once in remission. Serial assessments by LSM can provide valuable information and follow-up on the efficacy of implemented therapy, whether it is supportive or specific as in antiviral treatment in chronic hepatitis B or C and in selected cases in acute/fulminant hepatitis B8 or C9, but also as a follow-up in recurrent HCV after orthotopic liver transplantation.10 TE can provide information on the demarcation of the end of the acute phase (where LSV returns to normal [<F2]); when a reduced but still high LSV that is compatible with significant fibrosis (≥F2) is obtained, this can indicate dual-infection/hepatopathy with a corresponding degree of fibrosis. Periodical long-term follow-up by TE can diagnose flare recurrence and/or fibrosis stage progression.
In conclusion, TE can still be used prudently to augment clinical evaluation and follow-up both in the setting of acute and chronic hepatopathy, provided that a clinico-laboratory diagnosis is made of the underlying condition according to standard medical practice.