Test Directory
| Test Code | ||||||||||||||||||||||||||||||
| 1658 | ||||||||||||||||||||||||||||||
| Test Name | ||||||||||||||||||||||||||||||
| Spondyloepiphyseal Dysplasia With Congenital Joint Dislocations | ||||||||||||||||||||||||||||||
| CPT Codes | ||||||||||||||||||||||||||||||
| 81479 | ||||||||||||||||||||||||||||||
| Expected Turnaround Time | ||||||||||||||||||||||||||||||
| Typically 2 to 4 weeks from receipt of a sample in the laboratory. All cases involving ongoing pregnancies will be expedited. | ||||||||||||||||||||||||||||||
| Clinical Utility | ||||||||||||||||||||||||||||||
| Genetic analysis to provide a molecular diagnosis of this disorder. Recommended for individuals with a personal and/or family history of this disorder to ensure appropriate treatment and establish recurrence risk for family members. | ||||||||||||||||||||||||||||||
| Specimen and Container Info | ||||||||||||||||||||||||||||||
|
Non-Prenatal Specimens
Prenatal Specimens Either specimen type below is acceptable.
NOTE: For specimens from outside of North America, the preferred specimen type is Genomic DNA. HNL Genomics does not recommend shipping whole blood or cultured cells from any location other than the United States, Canada, or Mexico. |
||||||||||||||||||||||||||||||
| Transport Instructions | ||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||
| Stability Requirements | ||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||
| Causes for Rejection | ||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||
| Methodology | ||||||||||||||||||||||||||||||
| Next Generation Sequencing and Copy Number Variation Analysis | ||||||||||||||||||||||||||||||
| Performing Location | ||||||||||||||||||||||||||||||
| Genomics - Snowdrift | ||||||||||||||||||||||||||||||
| Description | ||||||||||||||||||||||||||||||
|
Larsen syndrome, autosomal recessive and spondyloepiphyseal dysplasia with congenital joint dislocations (includes humerospinal dysostosis, spondyloepiphyseal dysplasia, Omani type and chondrodysplasia with multiple dislocations). Larsen syndrome, autosomal recessive (MIM 245600) and spondyloepiphyseal dysplasia with congenital joint dislocations (MIM 143095) which includes humerospinal dysostosis (HSD), spondyloepiphyseal dysplasia, Omani type and chondrodysplasia with multiple joint dislocations are allelic disorders with similar clinical findings. All are caused by mutations in the carbohydrate sulfotransferase 3 gene (CHST3). It has been suggested that they may represent a single disorder with various age dependent manifestations. Alternatively, different loss of function mutations with various severities may cause a clinical spectrum. When patients are evaluated in the neonatal period or as young children, they are often diagnosed with Larsen syndrome, humerospinal dysostosis or chondrodysplasia with multiple dislocations. Patients with Larsen syndrome or humerospinal dysostosis typically have a birth length below the 3rd percentile. Growth often remains below the 3rd percentile throughout childhood and adults typically have short stature. The characteristic feature of patients with CHST3 mutations are congenital dislocations. Almost all patients have congenital knee dislocations and clubfoot. Dislocations or contractures of the elbows and hips are also common. Patients evaluated during childhood typically have features of spondyloepiphyseal dysplasia, Omani type. Older patients have severe degeneration of the intervertebral discs with thoracic kyphoscoliosis. Posterior and inferior scalloping or coronal clefting of lumbar vertebrae and widening of the interpedicular distance from T12 to L1 or L2 are evident on X-ray. Fusion of vertebral bodies eventually occurs. Several patients with CHST3 mutations have also been described with abnormalities of the heart valves. Older patients may present with dislocations that have improved either spontaneously or following surgical intervention. Arthritis of the hips and spine, intervertebral disc degeneration with trunk shortening and rigid kyphoscoliosis also dominates the clinical picture. Patients with CHST3 mutations must be differentiated from patients with classic autosomal dominant Larsen syndrome and Desbuquois dysplasia. Autosomal dominant Larsen syndrome is caused by mutations in the FLNB gene. Those with CHST3 mutations can be differentiated by the lack of facial flattening and the lack of advanced carpal age. In addition, patients with classic Larsen syndrome do not have the vertebral changes seen in patients with CHST3 mutations. Desbuquois dysplasia is an autosomal recessive chondrodysplasia caused by mutations in the CANT1 gene. Individuals with Desbuquois dysplasia have vertebral clefting, facial flattening and advanced carpal age which differentiates these patients from individuals with CHST3 mutations. |
||||||||||||||||||||||||||||||
| Testing Schedule | ||||||||||||||||||||||||||||||
| Monday-Friday | ||||||||||||||||||||||||||||||
| Genes | ||||||||||||||||||||||||||||||
| CHST3 | ||||||||||||||||||||||||||||||
| MIM | ||||||||||||||||||||||||||||||
| 143095 | ||||||||||||||||||||||||||||||
| Disease Group | ||||||||||||||||||||||||||||||
| Skeletal Disorders | ||||||||||||||||||||||||||||||
The American Medical Association (AMA) Current Procedural Terminology (CPT) codes published by HNL Lab Medicine are guidelines and are intended for informational purposes only. CPT coding is the exclusive responsibility of the billing entity. View the Terms.
© 2026 HNL Lab Medicine. All rights reserved.