Biotinidase deficiency is a rare, inherited metabolic disorder characterized by the body’s inability to recycle the vitamin biotin. Biotin is essential for various biochemical processes in the body, particularly in the metabolism of fats, carbohydrates, and certain amino acids.
In individuals with Biotinidase deficiency, the enzyme Biotinidase is either absent or not functioning correctly. This enzyme is crucial for releasing biotin from proteins in the diet and allowing the body to use it.
Biotinidase deficiency is an autosomal recessive genetic disorder, meaning that an affected individual inherits two mutated copies of the gene responsible for producing biotinidase one from each parent.
Epidemiology
Biotinidase deficiency is a relatively rare disorder globally. The prevalence rates is generally estimated to occur in approximately 1 in 60,000 to 1 in 100,000 live births.
The prevalence of Biotinidase deficiency can vary among different ethnic groups and geographic regions.
Biotinidase deficiency follows an autosomal recessive inheritance pattern, meaning that affected individuals inherit two mutated copies of the gene one from each parent. The carrier frequency individuals with one mutated copy may be higher in certain populations.
Biotinidase deficiency does not show a significant gender predilection, affecting males and females equally. The severity of symptoms can vary widely among individuals with biotinidase deficiency.
Anatomy
Pathophysiology
Biotin is obtained from diet or synthesized by gut bacteria. In the body, biotin is often bound to proteins, forming biotinylated proteins.
Biotinidase is the enzyme responsible for cleaving biotin from these biotinylated proteins, making it available for cellular use.
In individuals with biotinidase deficiency, there is a genetic mutation in the BTD gene, which codes for the biotinidase enzyme. Without functional biotinidase, the body is unable to efficiently recycle biotin from biotinylated proteins.
Biotin is a coenzyme for carboxylase enzymes involved in various metabolic pathways. The deficiency of biotin impairs the function of these biotin-dependent carboxylases, affecting critical metabolic processes.
Carboxylases are involved in gluconeogenesis, fatty acid synthesis, and amino acid metabolism. The dysfunction of biotin-dependent enzymes leads to the accumulation of metabolic byproducts that are normally processed in these pathways.
Etiology
Biotinidase deficiency is an autosomal recessive genetic disorder. The specific gene associated with biotinidase deficiency is the BTD gene, which is located on chromosome 3.
Both parents of an affected individual are carriers of a single mutated copy of the BTD gene. Carriers typically do not exhibit symptoms because they have one functional copy of the gene.
Missense mutations result in an altered amino acid sequence of the biotinidase enzyme, affecting its function. Nonsense mutations can lead to the premature termination of protein synthesis.
Genetics
Prognostic Factors
Adherence to lifelong biotin supplementation is critical for maintaining adequate biotin levels and preventing the recurrence of symptoms. Regular monitoring and adjustment of biotin dosage may be necessary to ensure optimal outcomes.
The severity of symptoms at the time of diagnosis can influence the prognosis. Individuals with milder symptoms may respond more quickly to treatment and may have fewer long-term complications.
The presence and severity of neurological symptoms, such as seizures and developmental delays, can impact the long-term prognosis. Early intervention and treatment are essential to prevent or minimize neurological damage.
There can be variability in the clinical presentation and severity of Biotinidase deficiency based on the specific genetic mutations involved.
Access to regular healthcare and monitoring is crucial for individuals with Biotinidase deficiency.
Clinical History
Biotinidase deficiency may be identified through newborn screening, which is routinely conducted in many countries.
Early detection allows for prompt intervention and treatment before symptoms develop.
In some cases, individuals with Biotinidase deficiency may not exhibit symptoms until adolescence or adulthood.
Late-onset cases are generally milder, and symptoms may include neurological problems, such as vision or hearing loss.
Physical Examination
Skin Examination: A characteristic rash, often around the eyes, nose, and mouth, may be present. The rash can be erythematous and scaly.
Ocular Abnormalities: Ophthalmologic examination may reveal abnormalities such as optic atrophy.
Respiratory Examination: Respiratory symptoms, including hyperventilation, may be observed in severe cases.
General Appearance: Evaluation of growth parameters, considering the potential impact of metabolic disturbances.
Age group
Associated comorbidity
Biotin is essential for normal brain function, and Biotinidase deficiency can lead to seizures. Low muscle tone is a common symptom and can affect motor development.
Delayed acquisition of developmental milestones may occur, affecting motor skills, language, and cognitive development.
A characteristic rash, often around the eyes, nose, and mouth, may be present. Individuals with severe Biotinidase deficiency may experience respiratory problems, including hyperventilation.
Biotin is involved in immune system function, and deficiency could potentially compromise immune responses.
Associated activity
Acuity of presentation
Neonatal-onset cases may present with symptoms shortly after birth, leading to rapid recognition of the disorder.
Symptoms such as developmental delays, hypotonia (low muscle tone), and skin rash may become noticeable over the first few months of life.
Late-onset cases tend to be milder, with symptoms such as neurological problems, vision or hearing loss, and skin issues.
Newborn screening programs have been instrumental in identifying affected individuals before the onset of symptoms, allowing for early intervention.
Differential Diagnoses
Glutaric Aciduria Type 1: This disorder affects the metabolism of lysine, hydroxylysine, and tryptophan and can lead to neurological symptoms.
Zellweger Spectrum Disorders: A group of disorders affecting peroxisome function and causing neurological and developmental abnormalities.
Vitamin B12 Deficiency: It can lead to neurological symptoms and developmental delays.
Mitochondrial Disorders: Various mitochondrial disorders can present neurological symptoms, developmental delays, and metabolic disturbances.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Biotin Supplementation: The cornerstone of treatment for biotinidase deficiency is the administration of exogenous biotin.
Biotin is typically given orally in the form of biotin supplements. The dosage varies depending on the severity of the deficiency and individual needs.
Monitoring Phase: Regular monitoring of clinical symptoms, metabolic markers, and biotin levels is essential.
Multidisciplinary Care: Regular follow-up visits are important for ongoing assessment, monitoring, and adjustments to the treatment plan.
Nutritional Support: A balanced and nutritious diet is important for overall health. Ensure that individuals with Biotinidase Deficiency receive a diet that supports their nutritional needs.
Sufficient Hydration: Maintaining proper hydration is important, especially during illness or situations that may lead to increased fluid loss.
Adequate hydration supports general health and helps prevent complications that may arise during illness.
Physical Activity and Therapy: Encourage appropriate physical activity based on an individual’s abilities and preferences.
Neurological Monitoring: Regular neurological monitoring is essential to assess developmental milestones, motor skills, and any potential neurological symptoms.
Skin Care: Individuals with Biotinidase Deficiency may experience skin issues, including rashes. Use gentle and moisturizing skin care products to support skin health.
Use of vitamins and cofactors
The body needs small amounts of organic substances for a variety of metabolic functions. Specific deficiency states are treated and prevented clinically with their use. In cases of Biotinidase deficiency, biotin is the preferred medication.
Biotin: A coenzyme that is vital for the metabolism of fat and other carboxylation processes. The urinary excretion of organic acids and alterations in the skin and hair can be caused by a deficiency in biotin.
Serves as a prosthetic group or coenzyme in all four of the body’s carboxylases. These carboxylases all continue to play vital roles in intermediate metabolism.
Biotinidase deficiency is managed through the administration of biotin supplementation. Biotin is a water-soluble B-vitamin that serves as a cofactor for various enzymes involved in essential metabolic pathways.
Biotin Supplementation: Biotin supplementation aims to provide exogenous biotin, compensating for the deficient biotinidase activity and ensuring that the body has an adequate supply of biotin for various metabolic processes.
use-of-phases-in-managing-biotinidase-deficiency
Newborn Screening Phase: Newborn screening is a critical initial phase for the early detection of Biotinidase Deficiency.
Early Diagnosis Phase: Early diagnosis is essential for initiating treatment before the onset of symptoms, preventing complications, and optimizing long-term outcomes.
Initiation of Biotin Supplementation: Prompt initiation of treatment with biotin supplementation is the cornerstone of management.
Lifelong Treatment: Biotin supplementation is typically a lifelong treatment to maintain optimal biotin levels and prevent the recurrence of symptoms.
Genetic Counselling: Genetic counselling is recommended for affected individuals and their families to discuss the inheritance pattern of Biotinidase Deficiency.
Biotinidase deficiency is a rare, inherited metabolic disorder characterized by the body’s inability to recycle the vitamin biotin. Biotin is essential for various biochemical processes in the body, particularly in the metabolism of fats, carbohydrates, and certain amino acids.
In individuals with Biotinidase deficiency, the enzyme Biotinidase is either absent or not functioning correctly. This enzyme is crucial for releasing biotin from proteins in the diet and allowing the body to use it.
Biotinidase deficiency is an autosomal recessive genetic disorder, meaning that an affected individual inherits two mutated copies of the gene responsible for producing biotinidase one from each parent.
Biotinidase deficiency is a relatively rare disorder globally. The prevalence rates is generally estimated to occur in approximately 1 in 60,000 to 1 in 100,000 live births.
The prevalence of Biotinidase deficiency can vary among different ethnic groups and geographic regions.
Biotinidase deficiency follows an autosomal recessive inheritance pattern, meaning that affected individuals inherit two mutated copies of the gene one from each parent. The carrier frequency individuals with one mutated copy may be higher in certain populations.
Biotinidase deficiency does not show a significant gender predilection, affecting males and females equally. The severity of symptoms can vary widely among individuals with biotinidase deficiency.
Biotin is obtained from diet or synthesized by gut bacteria. In the body, biotin is often bound to proteins, forming biotinylated proteins.
Biotinidase is the enzyme responsible for cleaving biotin from these biotinylated proteins, making it available for cellular use.
In individuals with biotinidase deficiency, there is a genetic mutation in the BTD gene, which codes for the biotinidase enzyme. Without functional biotinidase, the body is unable to efficiently recycle biotin from biotinylated proteins.
Biotin is a coenzyme for carboxylase enzymes involved in various metabolic pathways. The deficiency of biotin impairs the function of these biotin-dependent carboxylases, affecting critical metabolic processes.
Carboxylases are involved in gluconeogenesis, fatty acid synthesis, and amino acid metabolism. The dysfunction of biotin-dependent enzymes leads to the accumulation of metabolic byproducts that are normally processed in these pathways.
Biotinidase deficiency is an autosomal recessive genetic disorder. The specific gene associated with biotinidase deficiency is the BTD gene, which is located on chromosome 3.
Both parents of an affected individual are carriers of a single mutated copy of the BTD gene. Carriers typically do not exhibit symptoms because they have one functional copy of the gene.
Missense mutations result in an altered amino acid sequence of the biotinidase enzyme, affecting its function. Nonsense mutations can lead to the premature termination of protein synthesis.
Adherence to lifelong biotin supplementation is critical for maintaining adequate biotin levels and preventing the recurrence of symptoms. Regular monitoring and adjustment of biotin dosage may be necessary to ensure optimal outcomes.
The severity of symptoms at the time of diagnosis can influence the prognosis. Individuals with milder symptoms may respond more quickly to treatment and may have fewer long-term complications.
The presence and severity of neurological symptoms, such as seizures and developmental delays, can impact the long-term prognosis. Early intervention and treatment are essential to prevent or minimize neurological damage.
There can be variability in the clinical presentation and severity of Biotinidase deficiency based on the specific genetic mutations involved.
Access to regular healthcare and monitoring is crucial for individuals with Biotinidase deficiency.
Biotinidase deficiency may be identified through newborn screening, which is routinely conducted in many countries.
Early detection allows for prompt intervention and treatment before symptoms develop.
In some cases, individuals with Biotinidase deficiency may not exhibit symptoms until adolescence or adulthood.
Late-onset cases are generally milder, and symptoms may include neurological problems, such as vision or hearing loss.
Skin Examination: A characteristic rash, often around the eyes, nose, and mouth, may be present. The rash can be erythematous and scaly.
Ocular Abnormalities: Ophthalmologic examination may reveal abnormalities such as optic atrophy.
Respiratory Examination: Respiratory symptoms, including hyperventilation, may be observed in severe cases.
General Appearance: Evaluation of growth parameters, considering the potential impact of metabolic disturbances.
Biotin is essential for normal brain function, and Biotinidase deficiency can lead to seizures. Low muscle tone is a common symptom and can affect motor development.
Delayed acquisition of developmental milestones may occur, affecting motor skills, language, and cognitive development.
A characteristic rash, often around the eyes, nose, and mouth, may be present. Individuals with severe Biotinidase deficiency may experience respiratory problems, including hyperventilation.
Biotin is involved in immune system function, and deficiency could potentially compromise immune responses.
Neonatal-onset cases may present with symptoms shortly after birth, leading to rapid recognition of the disorder.
Symptoms such as developmental delays, hypotonia (low muscle tone), and skin rash may become noticeable over the first few months of life.
Late-onset cases tend to be milder, with symptoms such as neurological problems, vision or hearing loss, and skin issues.
Newborn screening programs have been instrumental in identifying affected individuals before the onset of symptoms, allowing for early intervention.
Glutaric Aciduria Type 1: This disorder affects the metabolism of lysine, hydroxylysine, and tryptophan and can lead to neurological symptoms.
Zellweger Spectrum Disorders: A group of disorders affecting peroxisome function and causing neurological and developmental abnormalities.
Vitamin B12 Deficiency: It can lead to neurological symptoms and developmental delays.
Mitochondrial Disorders: Various mitochondrial disorders can present neurological symptoms, developmental delays, and metabolic disturbances.
Biotin Supplementation: The cornerstone of treatment for biotinidase deficiency is the administration of exogenous biotin.
Biotin is typically given orally in the form of biotin supplements. The dosage varies depending on the severity of the deficiency and individual needs.
Monitoring Phase: Regular monitoring of clinical symptoms, metabolic markers, and biotin levels is essential.
Multidisciplinary Care: Regular follow-up visits are important for ongoing assessment, monitoring, and adjustments to the treatment plan.
Nutrition
Nutritional Support: A balanced and nutritious diet is important for overall health. Ensure that individuals with Biotinidase Deficiency receive a diet that supports their nutritional needs.
Sufficient Hydration: Maintaining proper hydration is important, especially during illness or situations that may lead to increased fluid loss.
Adequate hydration supports general health and helps prevent complications that may arise during illness.
Physical Activity and Therapy: Encourage appropriate physical activity based on an individual’s abilities and preferences.
Neurological Monitoring: Regular neurological monitoring is essential to assess developmental milestones, motor skills, and any potential neurological symptoms.
Skin Care: Individuals with Biotinidase Deficiency may experience skin issues, including rashes. Use gentle and moisturizing skin care products to support skin health.
Nutrition
The body needs small amounts of organic substances for a variety of metabolic functions. Specific deficiency states are treated and prevented clinically with their use. In cases of Biotinidase deficiency, biotin is the preferred medication.
Biotin: A coenzyme that is vital for the metabolism of fat and other carboxylation processes. The urinary excretion of organic acids and alterations in the skin and hair can be caused by a deficiency in biotin.
Serves as a prosthetic group or coenzyme in all four of the body’s carboxylases. These carboxylases all continue to play vital roles in intermediate metabolism.
Nutrition
Biotinidase deficiency is managed through the administration of biotin supplementation. Biotin is a water-soluble B-vitamin that serves as a cofactor for various enzymes involved in essential metabolic pathways.
Biotin Supplementation: Biotin supplementation aims to provide exogenous biotin, compensating for the deficient biotinidase activity and ensuring that the body has an adequate supply of biotin for various metabolic processes.
Nutrition
Newborn Screening Phase: Newborn screening is a critical initial phase for the early detection of Biotinidase Deficiency.
Early Diagnosis Phase: Early diagnosis is essential for initiating treatment before the onset of symptoms, preventing complications, and optimizing long-term outcomes.
Initiation of Biotin Supplementation: Prompt initiation of treatment with biotin supplementation is the cornerstone of management.
Lifelong Treatment: Biotin supplementation is typically a lifelong treatment to maintain optimal biotin levels and prevent the recurrence of symptoms.
Genetic Counselling: Genetic counselling is recommended for affected individuals and their families to discuss the inheritance pattern of Biotinidase Deficiency.
Biotinidase Deficiency | Baby’s First Test | Newborn Screening | Baby Health (babysfirsttest.org)
medtigo
Biotinidase Deficiency
Updated :
June 26, 2024
Biotinidase deficiency is a rare, inherited metabolic disorder characterized by the body’s inability to recycle the vitamin biotin. Biotin is essential for various biochemical processes in the body, particularly in the metabolism of fats, carbohydrates, and certain amino acids.
In individuals with Biotinidase deficiency, the enzyme Biotinidase is either absent or not functioning correctly. This enzyme is crucial for releasing biotin from proteins in the diet and allowing the body to use it.
Biotinidase deficiency is an autosomal recessive genetic disorder, meaning that an affected individual inherits two mutated copies of the gene responsible for producing biotinidase one from each parent.
Biotinidase deficiency is a relatively rare disorder globally. The prevalence rates is generally estimated to occur in approximately 1 in 60,000 to 1 in 100,000 live births.
The prevalence of Biotinidase deficiency can vary among different ethnic groups and geographic regions.
Biotinidase deficiency follows an autosomal recessive inheritance pattern, meaning that affected individuals inherit two mutated copies of the gene one from each parent. The carrier frequency individuals with one mutated copy may be higher in certain populations.
Biotinidase deficiency does not show a significant gender predilection, affecting males and females equally. The severity of symptoms can vary widely among individuals with biotinidase deficiency.
Biotin is obtained from diet or synthesized by gut bacteria. In the body, biotin is often bound to proteins, forming biotinylated proteins.
Biotinidase is the enzyme responsible for cleaving biotin from these biotinylated proteins, making it available for cellular use.
In individuals with biotinidase deficiency, there is a genetic mutation in the BTD gene, which codes for the biotinidase enzyme. Without functional biotinidase, the body is unable to efficiently recycle biotin from biotinylated proteins.
Biotin is a coenzyme for carboxylase enzymes involved in various metabolic pathways. The deficiency of biotin impairs the function of these biotin-dependent carboxylases, affecting critical metabolic processes.
Carboxylases are involved in gluconeogenesis, fatty acid synthesis, and amino acid metabolism. The dysfunction of biotin-dependent enzymes leads to the accumulation of metabolic byproducts that are normally processed in these pathways.
Biotinidase deficiency is an autosomal recessive genetic disorder. The specific gene associated with biotinidase deficiency is the BTD gene, which is located on chromosome 3.
Both parents of an affected individual are carriers of a single mutated copy of the BTD gene. Carriers typically do not exhibit symptoms because they have one functional copy of the gene.
Missense mutations result in an altered amino acid sequence of the biotinidase enzyme, affecting its function. Nonsense mutations can lead to the premature termination of protein synthesis.
Adherence to lifelong biotin supplementation is critical for maintaining adequate biotin levels and preventing the recurrence of symptoms. Regular monitoring and adjustment of biotin dosage may be necessary to ensure optimal outcomes.
The severity of symptoms at the time of diagnosis can influence the prognosis. Individuals with milder symptoms may respond more quickly to treatment and may have fewer long-term complications.
The presence and severity of neurological symptoms, such as seizures and developmental delays, can impact the long-term prognosis. Early intervention and treatment are essential to prevent or minimize neurological damage.
There can be variability in the clinical presentation and severity of Biotinidase deficiency based on the specific genetic mutations involved.
Access to regular healthcare and monitoring is crucial for individuals with Biotinidase deficiency.
Biotinidase deficiency may be identified through newborn screening, which is routinely conducted in many countries.
Early detection allows for prompt intervention and treatment before symptoms develop.
In some cases, individuals with Biotinidase deficiency may not exhibit symptoms until adolescence or adulthood.
Late-onset cases are generally milder, and symptoms may include neurological problems, such as vision or hearing loss.
Skin Examination: A characteristic rash, often around the eyes, nose, and mouth, may be present. The rash can be erythematous and scaly.
Ocular Abnormalities: Ophthalmologic examination may reveal abnormalities such as optic atrophy.
Respiratory Examination: Respiratory symptoms, including hyperventilation, may be observed in severe cases.
General Appearance: Evaluation of growth parameters, considering the potential impact of metabolic disturbances.
Biotin is essential for normal brain function, and Biotinidase deficiency can lead to seizures. Low muscle tone is a common symptom and can affect motor development.
Delayed acquisition of developmental milestones may occur, affecting motor skills, language, and cognitive development.
A characteristic rash, often around the eyes, nose, and mouth, may be present. Individuals with severe Biotinidase deficiency may experience respiratory problems, including hyperventilation.
Biotin is involved in immune system function, and deficiency could potentially compromise immune responses.
Neonatal-onset cases may present with symptoms shortly after birth, leading to rapid recognition of the disorder.
Symptoms such as developmental delays, hypotonia (low muscle tone), and skin rash may become noticeable over the first few months of life.
Late-onset cases tend to be milder, with symptoms such as neurological problems, vision or hearing loss, and skin issues.
Newborn screening programs have been instrumental in identifying affected individuals before the onset of symptoms, allowing for early intervention.
Glutaric Aciduria Type 1: This disorder affects the metabolism of lysine, hydroxylysine, and tryptophan and can lead to neurological symptoms.
Zellweger Spectrum Disorders: A group of disorders affecting peroxisome function and causing neurological and developmental abnormalities.
Vitamin B12 Deficiency: It can lead to neurological symptoms and developmental delays.
Mitochondrial Disorders: Various mitochondrial disorders can present neurological symptoms, developmental delays, and metabolic disturbances.
Biotin Supplementation: The cornerstone of treatment for biotinidase deficiency is the administration of exogenous biotin.
Biotin is typically given orally in the form of biotin supplements. The dosage varies depending on the severity of the deficiency and individual needs.
Monitoring Phase: Regular monitoring of clinical symptoms, metabolic markers, and biotin levels is essential.
Multidisciplinary Care: Regular follow-up visits are important for ongoing assessment, monitoring, and adjustments to the treatment plan.
Nutrition
Nutritional Support: A balanced and nutritious diet is important for overall health. Ensure that individuals with Biotinidase Deficiency receive a diet that supports their nutritional needs.
Sufficient Hydration: Maintaining proper hydration is important, especially during illness or situations that may lead to increased fluid loss.
Adequate hydration supports general health and helps prevent complications that may arise during illness.
Physical Activity and Therapy: Encourage appropriate physical activity based on an individual’s abilities and preferences.
Neurological Monitoring: Regular neurological monitoring is essential to assess developmental milestones, motor skills, and any potential neurological symptoms.
Skin Care: Individuals with Biotinidase Deficiency may experience skin issues, including rashes. Use gentle and moisturizing skin care products to support skin health.
Nutrition
The body needs small amounts of organic substances for a variety of metabolic functions. Specific deficiency states are treated and prevented clinically with their use. In cases of Biotinidase deficiency, biotin is the preferred medication.
Biotin: A coenzyme that is vital for the metabolism of fat and other carboxylation processes. The urinary excretion of organic acids and alterations in the skin and hair can be caused by a deficiency in biotin.
Serves as a prosthetic group or coenzyme in all four of the body’s carboxylases. These carboxylases all continue to play vital roles in intermediate metabolism.
Nutrition
Biotinidase deficiency is managed through the administration of biotin supplementation. Biotin is a water-soluble B-vitamin that serves as a cofactor for various enzymes involved in essential metabolic pathways.
Biotin Supplementation: Biotin supplementation aims to provide exogenous biotin, compensating for the deficient biotinidase activity and ensuring that the body has an adequate supply of biotin for various metabolic processes.
Nutrition
Newborn Screening Phase: Newborn screening is a critical initial phase for the early detection of Biotinidase Deficiency.
Early Diagnosis Phase: Early diagnosis is essential for initiating treatment before the onset of symptoms, preventing complications, and optimizing long-term outcomes.
Initiation of Biotin Supplementation: Prompt initiation of treatment with biotin supplementation is the cornerstone of management.
Lifelong Treatment: Biotin supplementation is typically a lifelong treatment to maintain optimal biotin levels and prevent the recurrence of symptoms.
Genetic Counselling: Genetic counselling is recommended for affected individuals and their families to discuss the inheritance pattern of Biotinidase Deficiency.
Biotinidase Deficiency | Baby’s First Test | Newborn Screening | Baby Health (babysfirsttest.org)
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