ReviewPaediatric drugs2006
Current strategies for the treatment of hereditary tyrosinemia type I.
Review in Paediatric drugs, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 43 citations in OpenAlex.
- In vivo quantitative photoacoustic evaluation of the liver and kidney pathology in tyrosinemia.Photoacoustics · 2022Article
- Natural Protein Tolerance and Metabolic Control in Patients with Hereditary Tyrosinaemia Type 1.Nutrients · 2020Article
- Conditional targeting in mice reveals that hepatic homogentisate 1,2-dioxygenase activity is essential in reducing circulating homogentisic acid and for effective therapy in the genetic disease alkaptonuria.Human molecular genetics · 2019Article
- Fumarylacetoacetate Hydrolase Knock-out Rabbit Model for Hereditary Tyrosinemia Type 1.The Journal of biological chemistry · 2017Article
- Medical management of chronic liver diseases in children (part I): focus on curable or potentially curable diseases.Paediatric drugs · 2011Review
- Hereditary tyrosinemia type 1 from a single center in Egypt: clinical study of 22 cases.World journal of pediatrics : WJP · 2011Article
- Neonatal liver failure: aetiologies and management--state of the art.European journal of pediatrics · 2011Review
- Recent insights on risk factors of hepatocellular carcinoma.World journal of hepatology · 2009Article
- Detoxification reactions: relevance to aging.Ageing research reviews · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary tyrosinemia type I (HT-I) is the most common of the three known diseases caused by defects in tyrosine metabolism. This type of tyrosinemia is caused by a mutation in the gene coding for fumarylacetoacetate hydrolase; several mutations in this gene have been identified. The main clinical features of HT-I are caused by hepatic involvement and renal tubular dysfunction. Dietary intervention with restriction of phenylalanine and tyrosine together with supportive measures can ameliorate the symptoms, but given the high risk for hepatocellular carcinoma, a cure for these patients has so far been possible only with liver transplantation. Pharmacologic treatment with nitisinone, a peroral inhibitor of the tyrosine catabolic pathway, offers an improved means of treatment for patients with HT-I. However, longer follow-up periods are needed to establish the role of this drug in ultimately protecting patients from end-stage organ involvement and hepatocellular carcinoma. Experimental work in mice has provided some promise for the future management of tyrosinemia with gene therapy.
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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.