ArticleJournal of clinical and experimental hepatology2012
HBsAg Quantification in Clinical Practice.
Article in Journal of clinical and experimental hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Answers to multiple choice questions.Journal of clinical and experimental hepatology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several standardized commercial assays for quantification of hepatitis B surface antigen (qHBsAg) are now available. Studies on HBsAg kinetics from Asia and Europe have demonstrated that HBsAg levels are highest during the immune-tolerant phase, become lower during immune-clearance phase and are the lowest in hepatitis B 'e' antigen (HBeAg)-negative inactive low-replicative phase with a rise during HBeAg-negative chronic hepatitis B (CHB). Combined use of hepatitis B virus-deoxyribonucleic acid (HBV-DNA) and HBsAg levels may help in differentiating true inactive carrier state from HBeAg-negative CHB. Several retrospective studies have demonstrated a role for decline in HBsAg level for predicting response and nonresponse to therapy. In HBeAg-positive patients treated with pegylated-interferon (PEG-IFN), a lack of decline of qHBsAg at week 12 predicts nonresponders while a decline of qHBsAg at week 24 predicts responders to PEG-IFN. In HBeAg-negative patients, if at week 12, there is no decline in qHBsAg and the HBV-DNA decline is < 2 log, the patient is unlikely to respond, then stopping of PEG-IFN should be considered. With nucleos(t)ide analogs, the decline in HBsAg is lower than that with PEG-IFN and more marked in patients with HBeAg-positive chronic hepatitis, with elevated alanine aminotransaminase (ALT), thus suggesting that active immune response against HBV is required to lower HBsAg. In patients with HBeAg-negative chronic hepatitis, fall in HBsAg may help in developing stopping rules to reduce the need for lifelong therapy. Information provided by HBsAg is complementary to HBV-DNA and cannot replace the same. Prospective studies on HBsAg kinetics from all regions of the world are required to define optimum time of testing and cutoff levels before stopping rules can be recommended.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.