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Research

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Disease Achondroplasia is the most frequent form of short-limb dwarfism (Nahar R et al 2009). As well as short stature due to shortening of limbs, affected individuals have characteristic facies with frontal bossing and mid-face hypoplasia, exaggerated lumbar lordosis, limitation of elbow extension, genu varum and trident-like hands. Incidence increases with paternal age.
Achondroplasia is caused, in virtually all of the cases, by a G380R mutation in fibroblast growth factor receptor 3 (FGFR3) (Di Rocco F et al 2014). FGFR3 is also important in craniofacial, vertebral and neurological development such that this mutation has multiple effects in an affected individual (Horton WA et al 2007).
Clinical Presentation Gross motor development frequently is delayed. Motor milestones such as head control and independent sitting, standing, and ambulation may lag by 3-6 months. Speech and language problems may be caused by tongue thrust (due to abnormal maxillomandibular relationship) but often resolve spontaneously. Twenty percent of patients experience delayed speech acquisition. Cognitive skills are preserved, and the intelligence level is within normal limits. Cranial enlargement and poor head control place the infant at risk for extension injuries. An Australian study assessed the functional milestones of achondroplasia children aged 3-7 years. The data noted that while milestones were delayed across all ages studied, functioning improved between age 3 and 5 years, although not subsequently. Access to clinicians skilled in achondroplasia management may assist these children to become more independent (Ireland PJ et al 2011).
Standing height is below the third percentile for both sexes. The mean adult standing height for men is 132 cm (52 in), and that for women is 125 cm (49 in). Sitting height, a reflection of trunk length, is within normal limits.
Seventy-five percent of patients have otitis media when younger than 5 years. Recurrent otitis media is common due to poor drainage of the eustachian tubesfrom underdevelopment of the midface, relative hypertrophy of tonsils and adenoids, and temporal bone abnormalities. Conductive hearing loss is present due to ossicular chain stiffness, and may be either congenital or acquired due to recurrent otitis media. Sensorineural hearing loss may be present in a few patients. Maxillary hypoplasia may lead to dental crowding and malocclusion.
Upper airway obstruction, small chest wall, pectus excavatum, and neurogenic effects from brain stem compression reduce the vital capacity. Incidence of pneumonia, cyanotic spells, apnea, and other respiratory complications is increased. Symptoms of airway obstruction include snoring and sleeping with the neck in a hyperextended position.
Abnormal development of the base of the skull results in a foramen magnum that is smaller than in average individuals. Narrowing of the foramen magnum compresses the cervicomedullary region, causing symptoms of respiratory insufficiency, apnea, cyanotic episodes, feeding problems, quadriparesis, and sudden death. These symptoms are common in the first several years of life because of the failure of the anticipated enlargement of foramen magnum during infancy and childhood. Chronic brain stem compression also may be a cause of hypotonia observed in the first 2 years of life.
Stenosis of the spinal canal and intervertebral foramen leads to symptoms such as low back pain, leg pain, dysesthesia, paresthesia, paraparesis, incontinence, and neurogenic claudication. Claudication may present as vague symptoms of aching or tiredness of the lower extremities induced by walking or standing. Symptoms may progress with a sensation of tingling and numbness and, eventually, weakness. Often, the pain is alleviated if the patient assumes a squatting position or bends forward.
More than 50% of patients experience symptoms of lower extremity radiculopathy from nerve root compression or cauda equina syndrome. The mean age of onset of back or lower extremity symptoms is 26 years; one third of patients are younger than 15 years at onset.
Symptoms due to abnormal curvature of the spine (eg, kyphosis, lordosis, scoliosis) may be present, such as deformity, back pain, respiratory dysfunction, neurologic involvement, or symptoms of spinal stenosis. The incidence of kyphoscoliosis may be as high as 33-50% in adults. However, the curve magnitude is generally less than 30° and generally does not require treatment.
Joint laxity may be present in children. Genu recurvatum is common. As the child grows, genu varum (tibial bowing) and lateral tibial torsion become apparent.
Macrocephaly represents ventriculomegaly or arrested hydrocephalus.
Mild but annoying neurologic disturbances can be attributed to local anatomic abnormalities and abnormal stretching of nerves. Examples include hip and knee pain from meralgia paresthetica, ankle pain from irritation of the peroneal nerve, or facial pain due to trigeminal neuralgia.
Fibromyalgia (trigger points located in the lower part of the back) and trochantericbursitis can be seen in some patients (http://emedicine.medscape.com/article/1258401-clinical)
Pathology
A. Normal B. Defect
Achondroplasia is caused by mutations in the fibroblast growth factor receptor-3 (FGFR3) gene (Ezquieta Zubicaray B et al 1999). Mutations within FGFR3 are the only genetic changes known to cause achondroplasia (Schlüter B et al 2011). FGFR3 has been mapped to the short arm of chromosome 4, p16.3 (4p16.3) (Le Merrer M et al 1994). All causal mutations occur at the exact same location within the gene; hence, molecular testing by targeted mutational analysis is easily done and interpreted. The two mutations, G1138A and G1138C, cause increased function of the FGFR3 gene. These mutations cause decreased endochondral ossification, decreased cellular hypertrophy, decreased cartilage matrix production, and inhibited proliferation of chondrocytes in growth plate cartilage.
G1138A and G1138C mutations of FGFR3 account for 99% of the mutational changes in patients with achondroplasia. A specific point mutation results; hence, an amino acid substitution occurs (He X, Xie F, Ren ZR 2012). About 98% of diagnosed patients have the G1138 Amutation, resulting in a G-to-A point change. One percent of cases have a G-to-C point change at nucleotide 1138, causing the G1138 Cmutation. A rare missense mutation (Lys650Met) in the tyrosine kinase region of FGFR3 causes a disorder termed severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) (Bellus GA et al 1999).

Treatment Available The availability of somatotropin (recombinant human growth hormone) has revolutionized the treatment of short stature (Mehta A 2002). Growth hormone is currently being used to augment the height of patients with achondroplasia. The greatest acceleration in growth velocity is seen during the first year of treatment and in those with the lowest growth velocities before treatment. However, no long-term studies exist to determine final height, nor do any randomized controlled studies exist to justify prolonged treatment with growth hormone in patients with short stature. A young age at initiation of therapy (1-6 y) is recommended for maximum benefits (http://emedicine.medscape.com/article/1258401-treatment)

References (1) Nahar R, Saxena R, Kohli S, et al; Molecular studies of achondroplasia. Indian J Orthop. 2009 Apr;43(2):194-6. Retrieved on September 13, 2015. (2) Di Rocco F, Biosse Duplan M, Heuze Y, et al; FGFR3 mutation causes abnormal membranous ossification in achondroplasia. Hum Mol Genet. 2014 Jan 20. Retrieved on September 13, 2015. (3) Horton WA, Hall JG, Hecht JT; Achondroplasia. Lancet. 2007 Jul 14;370(9582):162-72. Retrieved on September 13, 2015. (4) Ireland PJ, McGill J, Zankl A, et al. Functional performance in young Australian children with achondroplasia. Dev Med Child Neurol. 2011 Oct. 53(10):944-50. Retrieved on September 13, 2015. (5) Medscape: Achondroplasia Clinical Presentation http://emedicine.medscape.com/article/1258401-clinical Retrieved on September 13, 2015 (6) Mehta A, Hindmarsh PC. The use of somatropin (recombinant growth hormone) in children of short stature.Paediatr Drugs. 2002. 4(1):37-47. Retrieved on September 13, 2015. (7) Medscape: Achondroplasia Treatment and Management http://emedicine.medscape.com/article/1258401-treatment. Retrieved on September 13, 2015. (8) Ezquieta Zubicaray B, Iguacel AO, Varela Junquera JM, et al. Gly380Arg and Asn540Lys mutations of fibroblast growth factor receptor 3 in achondroplasia and hypochondroplasia in the Spanish population. Med Clin (Barc). 1999 Mar 6. 112(8):290-3. Retrieved on September 13, 2015. (9) Schlüter B, De Sousa G, Trowitzsch E, Andler W. Diagnostics and management of sleep-related respiratory disturbances in children with skeletal dysplasia caused by FGFR3 mutations (achondroplasia and hypochondroplasia). Georgian Med News. 2011 Jul-Aug. 63-72. Retrieved on September 13, 2015. (10) Le Merrer M, Rousseau F, Legeai-Mallet L, et al. A gene for achondroplasia-hypochondroplasia maps to chromosome 4p. Nat Genet. 1994 Mar. 6(3):318-21. Retrieved on September 13, 2015. (11) He X, Xie F, Ren ZR. Rapid Detection of G1138A and G1138C Mutations of FGFR3 Gene in Patients with Achondroplasia Using High-Resolution Melting Analysis. Genet Test Mol Biomarkers. 2012 Feb 17. Retrieved on September 13, 2015. (12) Bellus GA, Bamshad MJ, Przylepa KA, et al. Severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN): phenotypic analysis of a new skeletal dysplasia caused by a Lys650Met mutation in fibroblast growth factor receptor 3. Am J Med Genet. 1999 Jul 2. 85(1):53-65. Retrieved on September 13, 2015. (13) Medscape: Genetics of Achondroplasia; Pathophysiology http://emedicine.medscape.com/article/941280-overview#a5. Retrieved on September 13, 2015.…...

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