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Systemic primary carnitine deficiency
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Systemic primary carnitine deficiency
Carnitine
Specialty
Endocrinology
Systemic primary carnitine deficiency (SPCD), also known as carnitine uptake defect, carnitine transporter deficiency (CTD) or systemic carnitine deficiency is an inborn error of fatty acid transport caused by a defect in the transporter responsible for moving carnitine across the plasma membrane. Carnitine is an important amino acid for fatty acid metabolism.[1] When carnitine cannot be transported into tissues, fatty acid oxidation is impaired, leading to a variety of symptoms such as chronic muscle weakness, cardiomyopathy, hypoglycemia and liver dysfunction. The specific transporter involved with SPCD is OCTN2, coded for by the SLC22A5 gene located on chromosome 5. SPCD is inherited in an autosomal recessive manner, with mutated alleles coming from both parents.
Acute episodes due to SPCD are often preceded by metabolic stress such as extended fasting, infections or vomiting. Cardiomyopathy can develop in the absence of an acute episode, and can result in death. SPCD leads to increased carnitine excretion in the urine and low levels in plasma. In most locations with expanded newborn screening, SPCD can be identified and treated shortly after birth. Treatment with high doses of carnitine supplementation is effective, but needs to be rigorously maintained for life.
SPCD is more common in the Faroe Islands than in other countries, at least one out of every 1000 inhabitants of the Faroes has the illness,[2] while the numbers for other countries are one in every 100,000. Around 100 persons in the islands have been diagnosed, around one third of the whole population of 48,000 people have been screened for SPCD. Several young Faroese people and children have died a sudden death with cardiac arrest because of SPCD. Scientists believe that around 10% of the Faroese population are carriers of the gene for SPCD.[3] These people are not ill, but may have a lower amount of carnitine in their blood than non-carriers.
Contents
1 Signs and symptoms
2 Genetics
3 Diagnosis and treatment
4 Incidence
5 History
6 References
7 External links
Signs and symptoms[edit]
The presentation of patient with SPCD can be incredibly varied, from asymptomatic to lethal cardiac manifestations.[4] Early cases were reported with liver dysfunction, muscular findings (weakness and underdevelopment), hypoketotic hypoglycemia, cardiomegaly, cardiomyopathy and marked carnitine deficiency in plasma and tissues, combined with increased excretion in urine.[4] Patients who present clinically with SPCD fall into two categories, a metabolic presentation with hypoglycemia and a cardiac presentation characterized by cardiomyopathy. Muscle weakness can be found with either presentation.[5]
In countries with expanded newborn screening, SPCD can be identified shortly after birth. Affected infants show low levels of free carnitine and all other acylcarnitine species by tandem mass spectrometry.[5] Not all infants with low free carnitine are affected with SPCD. Some may have carnitine deficiency secondary to another metabolic condition or due to maternal carnitine deficiency. Proper follow-up of newborn screening results for low free carnitine includes studies of the mother to determine whether her carnitine deficiency is due to SPCD or secondary to a metabolic disease or diet.[6] Maternal cases of SPCD have been identified at a higher than expected rate, often in women who are asymptomatic.[5][7] Some mothers have also been identified through newborn screening with cardiomyopathy that had not been previously diagnosed.[8] The identification and treatment of these asymptomatic individuals is still developing, as it is not clear whether they require the same levels of intervention as patients identified with SPCD early in life based on clinical presentation.[5]
Genetics[edit]
SPCD is an autosomal recessive condition, meaning a mutated allele must be inherited from each parent for an individual to be affected.[4] The gene responsible for the OCTN2 carnitine transporter is SLC22A5, located at 5q31.1-32. SLC22A5 is regulated by peroxisome proliferator-activated receptor alpha. The transporter, OCTN2, is located in the apical membrane of the renal tubular cells, where it plays a role in tubular reabsorption.[5]
The defective OCTN2 is unable to recapture carnitine prior to its excretion in urine, leading to the characteristic biochemical findings of massively increased urine carnitine levels and significantly decreased plasma carnitine levels.[4] Decreased levels of plasma carnitine inhibit fatty acid oxidation during times of excessive energy demand. Carnitine is needed to transport long chain fatty acids into the mitochondria, where they can be broken down to produce acetyl-CoA. Individuals with SPCD cannot produce ketone bodies as energy due to the interruption of fatty acid oxidation.[5] Although SPCD is an autosomal recessive condition, heterozygotes have been shown to be at an increased risk for developing benign cardiomyopathy compared to wild type individuals.[4]
Diagnosis and treatment[edit]
The first suspicion of SPCD in a patient with a non-specific presentation is an extremely low plasma carnitine level. When combined with an increased concentration of carnitine in urine, the suspicion of SPCD can often be confirmed by either molecular testing or functional studies assessing the uptake of carnitine in cultured fibroblasts.[5]
Identification of patients presymptomatically via newborn screening has allowed early intervention and treatment. Treatment for SPCD involves high dose carnitine supplementation, which must be continued for life.[5] Individuals who are identified and treated at birth have very good outcomes, including the prevention of cardiomyopathy.[4] Mothers who are identified after a positive newborn screen but are otherwise asymptomatic are typically offered carnitine supplementation as well. The long-term outcomes for asymptomatic adults with SPCD is not known, but the discovery of mothers with undiagnosed cardiomyopathy and SPCD has raised the possibility that identification and treatment may prevent adult onset manifestations.[5][8]
Incidence[edit]
The addition of SPCD to newborn screening panels has offered insight into the incidence of the disorder around the world. In Taiwan, the incidence of SPCD in newborns was estimated to be approximately 1:67,000, while maternal cases were identified at a higher frequency of approximately 1:33,000.[8] The increased incidence of SPCD in mothers compared to newborns is not completely understood.[5] Estimates of SPCD in Japan have shown a similar incidence of 1:40,000.[4] Worldwide, SPCD has the highest incidence in the relatively genetically isolated Faroe Islands, where an extensive screening program was instituted after the sudden death of two teenagers. The incidence in the Faroe Islands is approximately 1:200.[9][10]
History[edit]
Carnitine deficiency has been extensively studied, although most commonly as a secondary finding to other metabolic conditions.[4] The first case of SPCD was reported in the 1980s, in a child with fasting hypoketotic hypoglycemia that resolved after treatment with carnitine supplementation. Later cases were reported with cardiomyopathy and muscle weakness. Newborn screening expanded the potential phenotypes associated with SPCD, to include otherwise asymptomatic adults.[5]
References[edit]
Jump up ^ Activation and Transportation of Fatty Acids for Metabolism via Carnitine Shuttle
Jump up ^ Hmr.fo - Faroe Islands Ministry of Health - Information om CTD (Carnitin Transporter Defekt) Archived 2014-02-22 at the Wayback Machine.
Jump up ^ Dr.dk - Livsfarlig sygdom angriber færinge - By Tine Maria Borresø, 17 May 2010
^ Jump up to: a b c d e f g h "#212140; Carnitine Deficiency, Systemic Primary; SPCD". Johns Hopkins University. Retrieved 2012-06-03.
^ Jump up to: a b c d e f g h i j k Stanley, Charles A.; Bennett, Michael J.; Longo, Nicolo (2004). "Plasma Membrane Carnitine Transport Defect". In Scriver, C.W.; Beaudet, A.L.; Sly, W.S.; et al. Metabolic and Molecular Bases of Inherited Disease (8th ed.). New York: McGraw Hill.
Jump up ^ "C0 Free Carnitine Low" (PDF). American College of Medical Genetics. Retrieved 2012-06-03.
Jump up ^ Morris, Andrew A.M.; Spiekerkoetter, Ute (2012). "Disorders of Mitochondrial Fatty Acid Oxidation and Related Metabolic Pathways". In Saudubray, Jean-Marie; van den Berghe, Georges; Walter, John H. Inborn Metabolic Diseases: Diagnosis and Treatment (5th ed.). New York: Springer. pp. 201–216. ISBN 978-3-642-15719-6.
^ Jump up to: a b c Lee, N. C.; Tang, N. L. S.; Chien, Y. H.; Chen, C. A.; Lin, S. J.; Chiu, P. C.; Huang, A. C.; Hwu, W. L. (2010). "Diagnoses of newborns and mothers with carnitine uptake defects through newborn screening". Molecular Genetics and Metabolism. 100 (1): 46–50. doi:10.1016/j.ymgme.2009.12.015. PMID 20074989.
Jump up ^ "Rare genetic disease common in Faroe Islands: expert". Yahoo!. 2010-05-27. Retrieved 2012-06-03.
Jump up ^ Lund, A. M.; Joensen, F.; Hougaard, D. M.; Jensen, L. K.; Christensen, E.; Christensen, M.; Nørgaard-Petersen, B.; Schwartz, M.; Skovby, F. (2007). "Carnitine transporter and holocarboxylase synthetase deficiencies in the Faroe Islands". Journal of Inherited Metabolic Disease. 30 (3): 341–349. doi:10.1007/s10545-007-0527-9. PMID 17417720.
External links[edit]
Classification
D
ICD-10: E71.3
ICD-9-CM: 277.81
OMIM: 212140
DiseasesDB: 31103
External resources
eMedicine: ped/321
GeneReviews/NCBI/NIH/UW entry on Systemic Primary Carnitine Deficiency

hide
v
t
e
Inborn error of lipid metabolism: fatty-acid metabolism disorders (E71.3, 277.81–277.85)
Synthesis
Biotinidase deficiency
Degradation
Acyl transport
Carnitine
Primary
I
II
-acylcarnitine
Adrenoleukodystrophy
Beta oxidation
General
Acyl CoA dehydrogenase
Short-chain
Medium-chain
Long-chain 3-hydroxy
Very long-chain
Mitochondrial trifunctional protein deficiency: Acute fatty liver of pregnancy
Unsaturated
2,4 Dienoyl-CoA reductase deficiency
Odd chain
Propionic acidemia
Other
3-hydroxyacyl-coenzyme A dehydrogenase deficiency
To acetyl-CoA
Malonic aciduria
Aldehyde
Sjögren–Larsson syndrome
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Chain of responsibility
From Wikipedia, the free encyclopedia
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For the Chain of Responsibility Design Pattern, see Chain-of-responsibility pattern.
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The chain of responsibility is a policy concept used in Australian transport legislation to place legal obligations on parties in the transport supply chain or across transport industries generally. The concept was initially developed to apply in the heavy vehicle industry in regulated areas such as speeding, fatigue and mass, loading and dimension. It has since spread to other transport sectors, particularly in Victoria where it has been applied in laws which apply to the rail, bus, marine and taxi industries.
Contents
1 Background
2 Victorian reforms
2.1 Transport Legislation Review
2.2 Rail Safety Act
2.3 National impact
3 See also
4 References
5 External links
Background[edit]
The chain of responsibility concept initially developed out of a recognition that unlawful behaviour by truck drivers is influenced and often controlled by the actions of other parties. Concerns arose that transport laws had often focussed on the actions of drivers while failing to sufficiently recognise and regulate the actions of other key parties. Chain of responsibility laws therefore seek to provide that these other parties cannot encourage, create incentives for, demand or allow drivers to undertake unlawful actions.
Victorian reforms[edit]
Transport Legislation Review[edit]
In recent years, the chain of responsibility concept has been widely used as a basis for the reform of transport laws in the State of Victoria. A major review of policy and legislation in that State, the Transport Legislation Review, has led to the concept being adapted for use in a number of new statutes including the Rail Safety Act 2006, the Bus Safety Act 2009 and the Marine Safety Act 2010.
Rail Safety Act[edit]
Victoria faced the problem of ageing and inadequate transport legislation which failed to reflect modern policy. During his second reading speech for a new rail safety statute in Victoria, the then Minister for Transport explained that -
"It is now recognised that this legislative framework has not kept pace with contemporary developments in safety regulation ... (T) the legislation does not establish a coherent chain of responsibility for the effective management of rail safety risks. For example, unlike other modern safety legislation, the (current) Act does not identify the key parties or individuals who can control risks and does not impose performance-based safety responsibilities."[1]
As a result, the Minister explained that -
"... the Bill now before the House and include the establishment of performance-based rail safety duties for rail operators, managers of rail infrastructure, contractors working on rolling stock or rail infrastructure, and rail safety workers including drivers and maintainers of rolling stock and infrastructure to ensure safety so far as reasonably practicable. This effectively imposes rail safety duties and obligations on each person in the rail industry who is in a position to affect safety and clearly identifies the roles and the safety chain of responsibility between them. The duties emphasise the responsibility of each participant to take steps as far as reasonably practicable to identify hazards and manage risks to safety that are within their control. This includes persons whose influence on safety exists 'upstream', such as persons involved in design, manufacture, maintenance, repair and modification of rail infrastructure and rolling stock."[2]
The Rail Safety Act which emerged from that process therefore imposes a chain of responsibility across all key parties in the rail industry in Victoria who can influence safety outcomes. Accountability at law and sanctions and penalties are allocated according to the level of responsibility each party has for creating and managing safety risks. Similar approaches were taken by the Transport Legislation Review in its work which led to new statutes in Victoria in the bus, marine and taxi industries.
National impact[edit]
The Victorian work has had influence beyond that State. Following the enactment of the Victorian Rail Safety Act in early 2006, Australian Transport Ministers[3] approved a national Model Rail Safety Bill in June 2006 which drew heavily on the Victorian work including its adaption of the chain of responsibility concept. The national Bill proposal has since been adopted by all other States and Territories which have passed Rail Safety Acts reflecting the framework.[4]
See also[edit]
Quintinshill rail crash
Vicarious liability
Department of Transport, Victoria
Transport Legislation Review
Rail Safety Act
Bus Safety Act
Transport Integration Act
References[edit]
Jump up ^ Hon Peter Batchelor MP, Second Reading Speech, Hansard, Legislative Assembly, Parliament of Victoria, 6 October 2005.
Jump up ^ Hon Peter Batchelor MP, Second Reading Speech, Hansard, Legislative Assembly, Parliament of Victoria, 6 October 2005.
Jump up ^ Through their participation on the Australian Transport Council.
Jump up ^ See the article on the Rail Safety Act.
External links[edit]
Essay from the Republic of Letters in re McDonald's case
The Winograd Commission
National Transport Commission
Department of Transport, Victoria
DOT, Transport Legislation Review
Chain of Responsibility
Retrieved from "https://en.wikipedia.org/w/index.php?title=Chain_of_responsibility&oldid=833493086"
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