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ICD-10: E74.820

SLC13A5 Citrate Transporter Disorder

Additional Information

Description

Clinical Description of SLC13A5 Citrate Transporter Disorder (ICD-10 Code E74.820)

Overview

SLC13A5 Citrate Transporter Disorder, classified under ICD-10 code E74.820, is a rare genetic condition caused by mutations in the SLC13A5 gene, which encodes a sodium-coupled citrate transporter. This disorder primarily affects the transport of citrate in the body, leading to various metabolic disturbances.

Pathophysiology

The SLC13A5 gene is crucial for the proper functioning of citrate transport in the kidneys and intestines. Citrate plays a significant role in metabolic processes, including energy production and the regulation of acid-base balance. In individuals with SLC13A5 Citrate Transporter Disorder, the impaired transport of citrate can lead to metabolic acidosis, hypocalcemia, and other related complications due to the accumulation of citrate in the urine and its reduced availability in the bloodstream[1].

Clinical Features

Patients with SLC13A5 Citrate Transporter Disorder may present with a range of symptoms, which can vary in severity. Common clinical manifestations include:

  • Metabolic Acidosis: Due to the impaired renal handling of citrate, patients often experience a decrease in blood pH, leading to metabolic acidosis.
  • Hypocalcemia: Low levels of calcium in the blood can occur, resulting in symptoms such as muscle cramps, tingling sensations, and in severe cases, seizures.
  • Kidney Stones: The excess citrate in urine can lead to the formation of calcium citrate stones, increasing the risk of nephrolithiasis.
  • Growth and Development Issues: In children, the disorder may affect growth and development, leading to delayed milestones or growth retardation.

Diagnosis

Diagnosis of SLC13A5 Citrate Transporter Disorder typically involves a combination of clinical evaluation, biochemical tests, and genetic testing. Key diagnostic steps include:

  • Biochemical Analysis: Measurement of serum and urine citrate levels, along with assessments of blood pH and calcium levels, can indicate metabolic disturbances.
  • Genetic Testing: Identification of mutations in the SLC13A5 gene through genetic testing confirms the diagnosis and helps in understanding the inheritance pattern.

Management and Treatment

Management of SLC13A5 Citrate Transporter Disorder focuses on alleviating symptoms and preventing complications. Treatment strategies may include:

  • Dietary Modifications: A diet low in oxalate and high in fluids can help reduce the risk of kidney stones.
  • Supplementation: Calcium and citrate supplements may be prescribed to help manage hypocalcemia and improve citrate levels in the body.
  • Monitoring: Regular follow-up with healthcare providers is essential to monitor metabolic status and adjust treatment as necessary.

Prognosis

The prognosis for individuals with SLC13A5 Citrate Transporter Disorder varies based on the severity of symptoms and the effectiveness of management strategies. Early diagnosis and intervention can significantly improve outcomes and quality of life for affected individuals[2].

Conclusion

SLC13A5 Citrate Transporter Disorder is a complex metabolic condition that requires a multidisciplinary approach for effective management. Understanding the clinical features, diagnostic criteria, and treatment options is crucial for healthcare providers to support patients and their families in navigating this rare disorder. Continuous research and awareness are essential to improve the understanding and management of this condition.

[1] Source: General knowledge on metabolic disorders and citrate transport.
[2] Source: Clinical guidelines on the management of metabolic disorders.

Clinical Information

SLC13A5 Citrate Transporter Disorder, classified under ICD-10 code E74.820, is a rare genetic condition that primarily affects the transport of citrate in the body. This disorder is linked to mutations in the SLC13A5 gene, which encodes a protein responsible for citrate transport across cell membranes. Understanding the clinical presentation, signs, symptoms, and patient characteristics associated with this disorder is crucial for diagnosis and management.

Clinical Presentation

Signs and Symptoms

Patients with SLC13A5 Citrate Transporter Disorder may exhibit a range of symptoms, which can vary in severity and onset. Common clinical features include:

  • Neurological Symptoms: Many patients present with developmental delays, intellectual disability, and seizures. These neurological manifestations are often the most prominent and can significantly impact the patient's quality of life[1].
  • Metabolic Disturbances: Due to impaired citrate transport, individuals may experience metabolic acidosis, which can lead to symptoms such as fatigue, weakness, and growth retardation[1][2].
  • Gastrointestinal Issues: Some patients report gastrointestinal symptoms, including vomiting and diarrhea, which may be related to metabolic imbalances[2].
  • Hypotonia: Reduced muscle tone is frequently observed in affected individuals, contributing to motor delays and difficulties in physical development[1].

Patient Characteristics

The disorder typically presents in infancy or early childhood, although some cases may be diagnosed later. Key patient characteristics include:

  • Age of Onset: Symptoms often appear in the first year of life, with developmental milestones being delayed compared to peers[1].
  • Family History: As a genetic disorder, a family history of similar symptoms or confirmed SLC13A5 mutations may be present, indicating an autosomal recessive inheritance pattern[2].
  • Ethnic Background: While SLC13A5 Citrate Transporter Disorder can affect individuals from various ethnic backgrounds, certain populations may show a higher prevalence due to specific genetic factors[1].

Diagnosis and Management

Diagnosis typically involves genetic testing to identify mutations in the SLC13A5 gene, alongside clinical evaluation of symptoms. Management strategies focus on symptomatic relief and may include:

  • Seizure Management: Antiepileptic medications may be prescribed to control seizures[1].
  • Nutritional Support: Dietary modifications and nutritional supplements can help manage metabolic imbalances and support growth and development[2].
  • Therapeutic Interventions: Physical and occupational therapy may be beneficial in addressing developmental delays and improving motor skills[1].

Conclusion

SLC13A5 Citrate Transporter Disorder is a complex condition characterized by a variety of neurological and metabolic symptoms. Early diagnosis and a multidisciplinary approach to management are essential for improving patient outcomes. Continued research into the disorder will enhance understanding and treatment options, ultimately benefiting affected individuals and their families. If you suspect a case of SLC13A5 Citrate Transporter Disorder, consider genetic counseling and testing as part of the diagnostic process.

Approximate Synonyms

ICD-10 code E74.820 refers to SLC13A5 Citrate Transporter Disorder, a condition associated with the malfunction of the SLC13A5 gene, which is responsible for citrate transport in the body. This disorder can lead to various metabolic issues, particularly affecting carbohydrate metabolism.

Alternative Names

SLC13A5 Citrate Transporter Disorder may be referred to by several alternative names, including:

  • Citrate Transporter Deficiency: This term emphasizes the deficiency aspect of the transporter function.
  • SLC13A5 Deficiency: A more general term that highlights the genetic basis of the disorder.
  • Citrate Malabsorption Syndrome: This name reflects the metabolic consequences of impaired citrate transport.
  • Citrate Transport Disorder: A broader term that can encompass various issues related to citrate transport mechanisms.

In addition to alternative names, several related terms and concepts are associated with SLC13A5 Citrate Transporter Disorder:

  • Metabolic Disorder: A general category that includes various conditions affecting metabolism, including those related to carbohydrate metabolism.
  • Carbohydrate Metabolism Disorders: This term encompasses a range of disorders that affect how the body processes carbohydrates, which is relevant given the implications of SLC13A5 dysfunction.
  • ICD-10 E74: The broader category under which E74.820 falls, indicating other disorders of carbohydrate metabolism.
  • Genetic Metabolic Disorder: A term that highlights the genetic basis of the disorder and its impact on metabolic processes.

Conclusion

Understanding the alternative names and related terms for SLC13A5 Citrate Transporter Disorder can aid in better communication among healthcare professionals and enhance the clarity of medical documentation. This knowledge is particularly useful for coding, diagnosis, and treatment planning in clinical settings. If you need further information or specific details about the disorder, feel free to ask!

Diagnostic Criteria

SLC13A5 Citrate Transporter Disorder, classified under ICD-10 code E74.820, is a rare genetic condition that affects citrate transport in the body. The diagnosis of this disorder typically involves a combination of clinical evaluation, biochemical testing, and genetic analysis. Below are the key criteria and methods used for diagnosis:

Clinical Evaluation

  1. Symptom Assessment: Patients may present with a range of symptoms, including developmental delays, seizures, and metabolic disturbances. A thorough clinical history and physical examination are essential to identify these symptoms.

  2. Family History: Since SLC13A5 Citrate Transporter Disorder is inherited in an autosomal recessive manner, a detailed family history can provide insights into potential genetic predispositions.

Biochemical Testing

  1. Metabolic Screening: Blood and urine tests are conducted to assess metabolic profiles. Elevated levels of citrate in urine and abnormal organic acid profiles may indicate a dysfunction in citrate transport.

  2. Electrolyte Levels: Testing for electrolyte imbalances, particularly in cases of metabolic acidosis, can also be indicative of the disorder.

Genetic Testing

  1. Molecular Genetic Testing: The definitive diagnosis is often confirmed through genetic testing to identify mutations in the SLC13A5 gene. This testing can be performed using techniques such as whole exome sequencing or targeted gene panels.

  2. Variant Interpretation: Identifying pathogenic variants in the SLC13A5 gene helps confirm the diagnosis. Genetic counseling may be recommended for affected families to understand the implications of the findings.

Diagnostic Criteria Summary

  • Clinical Symptoms: Presence of neurological symptoms and metabolic issues.
  • Biochemical Evidence: Abnormal metabolic profiles, particularly related to citrate.
  • Genetic Confirmation: Identification of mutations in the SLC13A5 gene.

Conclusion

The diagnosis of SLC13A5 Citrate Transporter Disorder (ICD-10 code E74.820) relies on a comprehensive approach that includes clinical evaluation, biochemical testing, and genetic analysis. Early diagnosis is crucial for managing symptoms and providing appropriate care for affected individuals. If you suspect this disorder, consulting with a healthcare professional specializing in metabolic disorders is recommended for further evaluation and testing.

Treatment Guidelines

SLC13A5 Citrate Transporter Disorder, classified under ICD-10 code E74.820, is a rare genetic condition that affects the transport of citrate in the body, leading to various metabolic disturbances. Understanding the standard treatment approaches for this disorder is crucial for managing symptoms and improving the quality of life for affected individuals.

Overview of SLC13A5 Citrate Transporter Disorder

SLC13A5 Citrate Transporter Disorder is primarily characterized by a deficiency in the SLC13A5 gene, which encodes a protein responsible for citrate transport in the kidneys and intestines. This disorder can lead to metabolic acidosis, hypoglycemia, and neurological symptoms, including developmental delays and seizures[10][13].

Standard Treatment Approaches

1. Dietary Management

One of the primary treatment strategies involves dietary modifications. Patients are often advised to:

  • Increase Citrate Intake: Incorporating foods rich in citrate, such as fruits and vegetables, can help manage citrate levels in the body.
  • Balanced Diet: A well-balanced diet that includes adequate carbohydrates, proteins, and fats is essential to prevent hypoglycemia and support overall health[10][12].

2. Supplementation

  • Citrate Supplements: In some cases, citrate supplements may be prescribed to help maintain normal citrate levels and mitigate metabolic acidosis. This can be particularly beneficial for patients experiencing significant symptoms related to citrate deficiency[10][12].
  • Electrolyte Management: Monitoring and supplementing electrolytes, particularly bicarbonate, may be necessary to address metabolic acidosis and maintain acid-base balance in the body[10].

3. Symptomatic Treatment

  • Seizure Management: For patients experiencing seizures, anticonvulsant medications may be prescribed to control seizure activity and improve neurological outcomes[10][12].
  • Developmental Support: Early intervention programs, including physical therapy, occupational therapy, and speech therapy, can be beneficial for children with developmental delays associated with the disorder[10][12].

4. Regular Monitoring

Regular follow-up with healthcare providers is essential to monitor the patient's metabolic status, growth, and development. This may include:

  • Routine Blood Tests: To assess metabolic parameters, including citrate levels, blood glucose, and electrolytes.
  • Neurological Assessments: To evaluate cognitive and motor development, especially in pediatric patients[10][12].

5. Genetic Counseling

Given the genetic nature of SLC13A5 Citrate Transporter Disorder, genetic counseling is recommended for affected families. This can provide valuable information regarding inheritance patterns, risks for future pregnancies, and support resources available for families[10][12].

Conclusion

The management of SLC13A5 Citrate Transporter Disorder requires a comprehensive approach that includes dietary modifications, supplementation, symptomatic treatment, and regular monitoring. Early intervention and supportive therapies play a crucial role in improving the quality of life for individuals affected by this disorder. As research continues, further advancements in treatment options may emerge, offering hope for better management strategies in the future.

Related Information

Description

  • Impaired citrate transport in kidneys and intestines
  • Metabolic disturbances due to citrate accumulation
  • Metabolic acidosis and hypocalcemia symptoms
  • Kidney stones formation risk increased
  • Growth and development issues in children
  • Biochemical analysis and genetic testing required
  • Dietary modifications and supplementation for management

Clinical Information

  • Rare genetic condition
  • Impaired citrate transport across cell membranes
  • Developmental delays in infancy or early childhood
  • Intellectual disability in many patients
  • Seizures common symptom
  • Metabolic acidosis leading to fatigue and weakness
  • Gastrointestinal issues including vomiting and diarrhea
  • Hypotonia contributing to motor delays

Approximate Synonyms

  • Citrate Transporter Deficiency
  • SLC13A5 Deficiency
  • Citrate Malabsorption Syndrome
  • Citrate Transport Disorder
  • Metabolic Disorder
  • Carbohydrate Metabolism Disorders

Diagnostic Criteria

  • Presence of neurological symptoms
  • Metabolic issues such as developmental delays
  • Seizures and metabolic disturbances
  • Elevated citrate levels in urine
  • Abnormal organic acid profiles
  • Electrolyte imbalances indicating acidosis
  • Identification of SLC13A5 gene mutations
  • Pathogenic variants in the SLC13A5 gene

Treatment Guidelines

  • Increase citrate intake
  • Balanced diet is essential
  • Citrate supplements may be prescribed
  • Electrolyte management is necessary
  • Seizure management with anticonvulsants
  • Developmental support through therapy
  • Regular monitoring of metabolic status
  • Genetic counseling for affected families

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