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      Suggested guidelines for the diagnosis and management of urea cycle disorders

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          Abstract

          Urea cycle disorders (UCDs) are inborn errors of ammonia detoxification/arginine synthesis due to defects affecting the catalysts of the Krebs-Henseleit cycle (five core enzymes, one activating enzyme and one mitochondrial ornithine/citrulline antiporter) with an estimated incidence of 1:8.000. Patients present with hyperammonemia either shortly after birth (~50%) or, later at any age, leading to death or to severe neurological handicap in many survivors. Despite the existence of effective therapy with alternative pathway therapy and liver transplantation, outcomes remain poor. This may be related to underrecognition and delayed diagnosis due to the nonspecific clinical presentation and insufficient awareness of health care professionals because of disease rarity. These guidelines aim at providing a trans-European consensus to: guide practitioners, set standards of care and help awareness campaigns. To achieve these goals, the guidelines were developed using a Delphi methodology, by having professionals on UCDs across seven European countries to gather all the existing evidence, score it according to the SIGN evidence level system and draw a series of statements supported by an associated level of evidence. The guidelines were revised by external specialist consultants, unrelated authorities in the field of UCDs and practicing pediatricians in training. Although the evidence degree did hardly ever exceed level C (evidence from non-analytical studies like case reports and series), it was sufficient to guide practice on both acute and chronic presentations, address diagnosis, management, monitoring, outcomes, and psychosocial and ethical issues. Also, it identified knowledge voids that must be filled by future research. We believe these guidelines will help to: harmonise practice, set common standards and spread good practices with a positive impact on the outcomes of UCD patients.

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          Survival after treatment with phenylacetate and benzoate for urea-cycle disorders.

          The combination of intravenous sodium phenylacetate and sodium benzoate has been shown to lower plasma ammonium levels and improve survival in small cohorts of patients with historically lethal urea-cycle enzyme defects. We report the results of a 25-year, open-label, uncontrolled study of sodium phenylacetate and sodium benzoate therapy (Ammonul, Ucyclyd Pharma) in 299 patients with urea-cycle disorders in whom there were 1181 episodes of acute hyperammonemia. Overall survival was 84% (250 of 299 patients). Ninety-six percent of the patients survived episodes of hyperammonemia (1132 of 1181 episodes). Patients over 30 days of age were more likely than neonates to survive an episode (98% vs. 73%, P<0.001). Patients 12 or more years of age (93 patients), who had 437 episodes, were more likely than all younger patients to survive (99%, P<0.001). Eighty-one percent of patients who were comatose at admission survived. Patients less than 30 days of age with a peak ammonium level above 1000 micromol per liter (1804 microg per deciliter) were least likely to survive a hyperammonemic episode (38%, P<0.001). Dialysis was also used in 56 neonates during 60% of episodes and in 80 patients 30 days of age or older during 7% of episodes. Prompt recognition of a urea-cycle disorder and treatment with both sodium phenylacetate and sodium benzoate, in conjunction with other therapies, such as intravenous arginine hydrochloride and the provision of adequate calories to prevent catabolism, effectively lower plasma ammonium levels and result in survival in the majority of patients. Hemodialysis may also be needed to control hyperammonemia, especially in neonates and older patients who do not have a response to intravenous sodium phenylacetate and sodium benzoate. Copyright 2007 Massachusetts Medical Society.
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            Histone deacetylase inhibitors.

            Histones are small basic proteins that, by complexing wtih DNA, form the nucleosome core. Repetitive units of this nucleosome led to the chromatin in which all the human genome is packaged. Histones can be in one of the two antagonist forms, acetylated or deacetylated, equilibrium regulated by the corresponding enzymes, histone acetylases and histones deacetylases (HDACs). Inhibition of HDACs represents a new strategy in human cancer therapy since these enzymes play a fundamental role in regulating gene expression and chromatin assembly. They are potent inducers of growth arrest, differentiation and apoptosis of tumor cells. A wide variety of HDACs of both natural and synthetic origin has been reported. Except depsispeptide FK228, natural HDACs (trichostatin (TSA), depudecin, trapoxins, apicidins) as well as sodium butyrate, phenylbutyrate and suberoyl anilide hydroxamic acid (SAHA), while effective in vivo, are inefficient due to instability and low retention. Subsequently, synthetic analogs isolated from screening libraries (oxamflatin, scriptaid) were discovered as havind a common structure with TSA and SAHA: an hydroxamic acid zinc-binding group linked via a spacer (5 or 6 CH2) to a hydrophobic group. Design of a second generation of HDACs was based upon these data affording potent HDACs such as LAQ824 and PDX101 currently under phase I clinical trials. Simultaneously, synthetic benzamide-containing HDACs were reported and two of them, MS-275 and CI-994, have reached phase II and I clinical trials, respectively.
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              Neurological implications of urea cycle disorders.

              The urea cycle disorders constitute a group of rare congenital disorders caused by a deficiency of the enzymes or transport proteins required to remove ammonia from the body. Via a series of biochemical steps, nitrogen, the waste product of protein metabolism, is removed from the blood and converted into urea. A consequence of these disorders is hyperammonaemia, resulting in central nervous system dysfunction with mental status changes, brain oedema, seizures, coma, and potentially death. Both acute and chronic hyperammonaemia result in alterations of neurotransmitter systems. In acute hyperammonaemia, activation of the NMDA receptor leads to excitotoxic cell death, changes in energy metabolism and alterations in protein expression of the astrocyte that affect volume regulation and contribute to oedema. Neuropathological evaluation demonstrates alterations in the astrocyte morphology. Imaging studies, in particular (1)H MRS, can reveal markers of impaired metabolism such as elevations of glutamine and reduction of myoinositol. In contrast, chronic hyperammonaemia leads to adaptive responses in the NMDA receptor and impairments in the glutamate-nitric oxide-cGMP pathway, leading to alterations in cognition and learning. Therapy of acute hyperammonaemia has relied on ammonia-lowering agents but in recent years there has been considerable interest in neuroprotective strategies. Recent studies have suggested restoration of learning abilities by pharmacological manipulation of brain cGMP with phosphodiesterase inhibitors. Thus, both strategies are intriguing areas for potential investigation in human urea cycle disorders.
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                Author and article information

                Journal
                Orphanet J Rare Dis
                Orphanet J Rare Dis
                Orphanet Journal of Rare Diseases
                BioMed Central
                1750-1172
                2012
                29 May 2012
                : 7
                : 32
                Affiliations
                [1 ]University Children’s Hospital Zurich and Children’s Research Centre, Zurich, 8032, Switzerland
                [2 ]Radiologie Hopital Necker, Service Radiologie Pediatrique, 149 Rue De Sevres, Paris 15, 75015, France
                [3 ]Department of Pediatrics, Division of Inborn Metabolic Disease, University Hospital Padua, Via Giustiniani 3, Padova, 35128, Italy
                [4 ]Birmingham Children’s Hospital NHS Foundation Trust, Steelhouse Lane, Birmingham, B4 6NH, United Kingdom
                [5 ]Dietetic Department, Great Ormond Street Hospital for Children, NHS Foundation Trust, London, WC1N 3JH, United Kingdom
                [6 ]Kinderabteilung, LKH Bregenz, Carl-Pedenz-Strasse 2, Bregenz, A-6900, Austria
                [7 ]University Children’s Hospital, Medical University Innsbruck, Anichstrasse 35, Innsbruck, 6020, Austria
                [8 ]Division of Metabolism, Bambino Gesù Children’s Hospital, IRCCS, Piazza S. Onofrio 4, Rome, I-00165, Italy
                [9 ]Division of Pediatric Metabolism, Cruces Children Hospital, Baracaldo, 48903, Spain
                [10 ]Universitätsklinikum Hamburg Eppendorf, Klinik für Kinder- und Jugendmedizin, Martinistr. 52, Hamburg, 20246, Germany
                [11 ]Service de Néphrologie et maladies métaboliques adulte Hôpital Necker 149, rue de Sèvres, Paris, 75015, France
                [12 ]Reference Center for Inherited Metabolic Disorders (MaMEA), Hopital Necker-Enfants Malades, 149 Rue de Sevres, Paris, 75015, France
                [13 ]University Children’s Hospital, Im Neuenheimer Feld 430, Heidelberg, 69120, Germany
                [14 ]Instituto de Biomedicina de Valencia del Consejo Superior de Investigaciones Científicas (IBV-CSIC) and Centro de Investigación Biomédica en Red para Enfermedades Raras (CIBERER), C/ Jaume Roig 11, Valencia, 46010, Spain
                Article
                1750-1172-7-32
                10.1186/1750-1172-7-32
                3488504
                22642880
                ba7b95ce-81a6-4243-9c35-fcc1f233257b
                Copyright ©2012 Häberle et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 November 2011
                : 6 April 2012
                Categories
                Review

                Infectious disease & Microbiology
                n-acetylglutamate synthase,argininosuccinate lyase,arginase 1,ornithine transcarbamylase,ornithine carbamoyl transferase,carbamoylphosphate synthetase 1,hyperammonemia,argininosuccinate synthetase,hyperornithinemia-hyperammonemia-homocitrullinuria syndrome,ucd,urea cycle disorders

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