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Perihepatic lymphadenopathy: a marker of response to interferon alpha in chronic hepatitis C
H Wedemeyer1, J Ockenga, H Frank
1Department of Gastroenterology and Hepatology, Medizinische Hochschule, Hannover, Germany.
Insights
Perihepatic lymphadenopathy (PHL) correlates with interferon alpha response in chronic hepatitis C. Monitoring PHL via ultrasound is a simple, non-invasive marker for treatment effectiveness.
Area of Science:
- Hepatology
- Virology
- Medical Imaging
Background:
- Perihepatic lymphadenopathy (PHL) has been linked to histological activity in chronic hepatitis C.
- The relationship between PHL and response to interferon alpha therapy was previously unexplored.
Purpose of the Study:
- To investigate the correlation between perihepatic lymphadenopathy (PHL) and response to interferon alpha treatment in patients with chronic hepatitis C.
- To assess PHL as a potential marker for predicting treatment outcomes.
Main Methods:
- 103 patients with chronic hepatitis C treated with interferon alpha were studied.
- High-resolution ultrasonography was used to assess PHL before and during treatment.
- A grading system (I, II, III) was established for PHL severity based on lymph node size and number.
Main Results:
- Hepatic inflammatory activity (Ishak score) was significantly higher in patients with grade III PHL compared to grades I and II (p=0.01).
- Initial response rates to interferon alpha were 45% for PHL grade I, 40% for grade II, and 33% for grade III.
- An increase in PHL during therapy was observed more frequently in non-responders than in primary responders (p=0.03).
Conclusions:
- Perihepatic lymphadenopathy (PHL) grading prior to treatment correlates with hepatic inflammatory activity.
- Monitoring PHL using abdominal ultrasonography can serve as a simple, non-invasive, and cost-effective additional marker for interferon alpha response in chronic hepatitis C.
Background/Aims:
Recently it was shown that perihepatic lymphadenopathy (PHL) correlates with histological activity in chronic hepatitis C. However, the question whether there is a correlation between the response to interferon alpha and PHL has not yet been raised.
Methodology:
We examined 103 patients who had been treated with interferon alpha for hepatitis C. Prior to treatment all patients had undergone high resolution ultrasonography. Thirty-six patients had follow up ultrasound scans during the course of the treatment. According to size and number of lymph nodes we introduced a grading of the PHL and determined grade I as minimal, grade II as medium and grade III as extensive PHL.
Results:
Classification of PHL prior to treatment revealed 40 patients with PHL I, 30 with grade II and 33 with grade III. Hepatic inflammatory activity according to the Ishak score was increased in patients with PHL III (9.1+/-2.4) compared to PHL II (6.7+/-2.9) and PHL I (7.3+/-3.1) (p=0.01). In patients with PHL grade I prior to treatment 45% were initial responder, patients with grade II or III showed response rates of 40% and 33%, respectively. During therapy we found an increase of PHL in one out of 13 primary responder vs. 10 out of 23 non-responder (p=0.03).
Conclusions:
In conclusion, monitoring of PHL by abdominal ultrasonography is a simple, non-invasive and cheap additional marker of response to interferon alpha.