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Fulvio Franceschi - One of the best experts on this subject based on the ideXlab platform.
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Towards effective Ponseti Clubfoot care: the Uganda Sustainable Clubfoot Care Project.
Clinical orthopaedics and related research, 2009Co-Authors: Shafique Pirani, Edward Naddumba, Joseph Konde-lule, Titus Beyeza, Richard Mathias, J. Norgrove Penny, Ben Mbonye, Jackson Amone, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations’ healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system’s capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006–2007, 872 children with clubfeet were seen. USCCP-designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the incidence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment protocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.
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The Uganda Sustainable Clubfoot Care Project
2009Co-Authors: Shafique Pirani Frcsc, Edward Naddumba, Richard Mathias Frcpc, Joseph Konde-lule, J. Norgrove Penny Frcsc, Titus Beyeza, Ben Mbonye Frcs, Jackson Amone Mph, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations' healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system's capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006-2007, 872 children with clubfeet were seen. USCCP- designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the inci- dence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment pro- tocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.
Matthew B. Dobbs - One of the best experts on this subject based on the ideXlab platform.
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The 2017 ABJS Nicolas Andry Award: Advancing Personalized Medicine for Clubfoot Through Translational Research
Clinical Orthopaedics and Related Research®, 2017Co-Authors: Matthew B. Dobbs, Christina A. GurnettAbstract:Background Clubfoot is one of the most common pediatric orthopaedic disorders. While the Ponseti method has revolutionized Clubfoot treatment, it is not effective for all patients. When the Ponseti method does not correct the foot, patients are at risk for lifelong disability and may require more-extensive surgery. Questions/Purposes (1) What genetic and morphologic abnormalities contribute to the development of Clubfoot? (2) How can this information be used to devise personalized treatment paradigms for patients with Clubfoot? Methods Human gene sequencing, molecular genetic engineering of mouse models of Clubfoot, MRI of Clubfoot, and development of new treatment methods all have been used by our group to understand the biological basis and improve therapy for this group of disorders. Results We gained new insight into Clubfoot pathogenesis from our discovery that mutations in the PITX1-TBX4-HOXC transcriptional pathway cause familial Clubfoot and vertical talus in a small number of families, with the unique lower limb expression of these genes providing an explanation for the lack of upper extremity involvement in these disorders. MRI studies revealed corresponding morphologic abnormalities, including hypomorphic muscle, bone, and vasculature, that are not only associated with these gene mutations, but also are biomarkers for treatment-resistant Clubfoot. Conclusions Based on an understanding of the underlying biology, we improved treatment methods for neglected and syndromic Clubfoot, developed new treatment for congenital vertical talus based on the principles of the Ponseti method, and designed a new dynamic Clubfoot brace to improve strength and compliance.
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Genetics of Clubfoot.
Journal of pediatric orthopedics. Part B, 2012Co-Authors: Matthew B. Dobbs, Christina A. GurnettAbstract:Clubfoot is one of the most common congenital birth defects, with an estimated birth prevalence of 1 per 1000 live births [1]. In 20% of cases, Clubfoot is associated with distal arthrogryposis, congenital myotonic dystrophy, myelomeningocele, amniotic band sequence, or other genetic syndromes such as trisomy 18 or chromosome 22q11 deletion syndrome [2,3], while in the remaining cases the deformity is isolated and the exact etiology is unknown [4]. Recent studies, however, are beginning to shed light on the importance of early limb developmental pathways in Clubfoot etiology. Many theories of Clubfoot pathogenesis, including intrauterine immobility, neurological, vascular, and connective tissue fibrosis, have been proposed based on specific anatomic abnormalities [5]. Vascular anomalies, consisting most commonly of anterior tibial artery hypoplasia, are present in >80% of Clubfoot patients though the genetic basis of this abnormality is unknown [6,7]. It has also been observed that unilateral Clubfoot is associated with a smaller calf circumference compared to the unaffected limb, resulting in quantitative muscle differences in two series of patients with unilateral Clubfoot [8,9]. Despite quantitative muscle differences, electrophysiological studies of muscle and nerve are most often normal in Clubfoot, and histological evaluations of muscle biopsies from Clubfoot lower extremities typically show nonspecific abnormalities [10–12]. A mild leg length discrepancy can be seen in Clubfoot patients indicating effects on skeletal growth as well [13]. These widespread anatomic abnormalities suggest that Clubfoot is either etiologically heterogeneous or that a single primary cause may be responsible for all of the effects seen on bone and soft tissue. Important insight into the pathogenesis of Clubfoot is being revealed through genetic studies. A genetic basis for isolated Clubfoot is supported by the fact approximately 25% of all patients with isolated Clubfoot report a positive family history for Clubfoot [14]. The role for genetic factors in Clubfoot is also supported by a twin study that demonstrates a higher concordance rate for identical twins compared to fraternal twins (33% versus 3%) [4]. Further evidence for a genetic basis for Clubfoot is the differences in Clubfoot prevalence across ethnic populations, with the lowest prevalence in Chinese (0.39 cases per 1000 live births) and highest in the Hawaiians and Maoris (7 per 1000)[15,16]. The ratio of isolated Clubfoot among males to females is 2:1 and is consistent across ethnic groups [15]. Based on complex inheritance patterns, isolated Clubfoot is unlikely to be due to mutations within a single gene but instead is multifactorial and/or polygenic in nature [1,14]. An argument against a single gene cause of isolated Clubfoot is the fact that there is a sex discrepancy, males more commonly affected than females, in the absence of sex-linked inheritance. A polygenic inheritance model with a dimorphic sex threshold for the affected phenotype would explain this discrepancy. Support for this polygenic threshold model for Clubfoot inheritance has been shown by demonstration of the Carter effect: individuals of the less commonly affected sex carry a higher genetic load and are therefore more likely to transmit the disease to their offspring [17]. The physiological cause of this sex dimorphism, in which males are twice as likely to be affected as females, is currently unknown. There is some evidence to suggest that the common disease-common variant hypothesis applies to Clubfoot [18], in which inheritance of common genetic variants (i.e. single nucleotide polymorphisms present at an allele frequency of > 5%), each conferring a small increase in risk, contributes to Clubfoot susceptibility. Common genetic variants (polymorphisms) near HOX homeobox genes [19], insulin-like growth factor binding protein 3 (IGFBP3) (MIM 146732) [20], and caspase genes [21] have all been reported to be associated with isolated Clubfoot. However, these genetic variants are all of relatively small effect and need to be replicated in larger cohorts to confirm their importance in Clubfoot susceptibility. An alternative to the common disease-common variant hypothesis is that Clubfoot may be explained better by the common disease-rare hypothesis in which rare genetic variants (with allele frequencies of
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genetics of Clubfoot
Journal of Pediatric Orthopaedics B, 2012Co-Authors: Matthew B. Dobbs, Christina A. GurnettAbstract:Clubfoot is one of the most common congenital birth defects, with an estimated birth prevalence of 1 per 1000 live births [1]. In 20% of cases, Clubfoot is associated with distal arthrogryposis, congenital myotonic dystrophy, myelomeningocele, amniotic band sequence, or other genetic syndromes such as trisomy 18 or chromosome 22q11 deletion syndrome [2,3], while in the remaining cases the deformity is isolated and the exact etiology is unknown [4]. Recent studies, however, are beginning to shed light on the importance of early limb developmental pathways in Clubfoot etiology. Many theories of Clubfoot pathogenesis, including intrauterine immobility, neurological, vascular, and connective tissue fibrosis, have been proposed based on specific anatomic abnormalities [5]. Vascular anomalies, consisting most commonly of anterior tibial artery hypoplasia, are present in >80% of Clubfoot patients though the genetic basis of this abnormality is unknown [6,7]. It has also been observed that unilateral Clubfoot is associated with a smaller calf circumference compared to the unaffected limb, resulting in quantitative muscle differences in two series of patients with unilateral Clubfoot [8,9]. Despite quantitative muscle differences, electrophysiological studies of muscle and nerve are most often normal in Clubfoot, and histological evaluations of muscle biopsies from Clubfoot lower extremities typically show nonspecific abnormalities [10–12]. A mild leg length discrepancy can be seen in Clubfoot patients indicating effects on skeletal growth as well [13]. These widespread anatomic abnormalities suggest that Clubfoot is either etiologically heterogeneous or that a single primary cause may be responsible for all of the effects seen on bone and soft tissue. Important insight into the pathogenesis of Clubfoot is being revealed through genetic studies. A genetic basis for isolated Clubfoot is supported by the fact approximately 25% of all patients with isolated Clubfoot report a positive family history for Clubfoot [14]. The role for genetic factors in Clubfoot is also supported by a twin study that demonstrates a higher concordance rate for identical twins compared to fraternal twins (33% versus 3%) [4]. Further evidence for a genetic basis for Clubfoot is the differences in Clubfoot prevalence across ethnic populations, with the lowest prevalence in Chinese (0.39 cases per 1000 live births) and highest in the Hawaiians and Maoris (7 per 1000)[15,16]. The ratio of isolated Clubfoot among males to females is 2:1 and is consistent across ethnic groups [15]. Based on complex inheritance patterns, isolated Clubfoot is unlikely to be due to mutations within a single gene but instead is multifactorial and/or polygenic in nature [1,14]. An argument against a single gene cause of isolated Clubfoot is the fact that there is a sex discrepancy, males more commonly affected than females, in the absence of sex-linked inheritance. A polygenic inheritance model with a dimorphic sex threshold for the affected phenotype would explain this discrepancy. Support for this polygenic threshold model for Clubfoot inheritance has been shown by demonstration of the Carter effect: individuals of the less commonly affected sex carry a higher genetic load and are therefore more likely to transmit the disease to their offspring [17]. The physiological cause of this sex dimorphism, in which males are twice as likely to be affected as females, is currently unknown. There is some evidence to suggest that the common disease-common variant hypothesis applies to Clubfoot [18], in which inheritance of common genetic variants (i.e. single nucleotide polymorphisms present at an allele frequency of > 5%), each conferring a small increase in risk, contributes to Clubfoot susceptibility. Common genetic variants (polymorphisms) near HOX homeobox genes [19], insulin-like growth factor binding protein 3 (IGFBP3) (MIM 146732) [20], and caspase genes [21] have all been reported to be associated with isolated Clubfoot. However, these genetic variants are all of relatively small effect and need to be replicated in larger cohorts to confirm their importance in Clubfoot susceptibility. An alternative to the common disease-common variant hypothesis is that Clubfoot may be explained better by the common disease-rare hypothesis in which rare genetic variants (with allele frequencies of <5%) each confer a moderate risk with higher penetrance [22]. Recent studies supporting this hypothesis have identified a key developmental pathway important in Clubfoot etiology, the PITX1-TBX4 transcriptional pathway responsible for early limb development [23,24]. A missense mutation in PITX1 (MIM 602149), a bicoid-related homeodomain transcription factor, was identified in a large multi-generational family with predominantly isolated Clubfoot segregating with reduced penetrance [23]. Since the PITX1 gene is expressed predominantly in the hindlimb and not the forelimb, this is the first gene implicated in Clubfoot to explain the specific involvement of the foot. Though mutations in PITX1 are not a common cause of isolated Clubfoot, recurrent chromosome 17q23 copy number variants involving the T-box transcription factor TBX4, a transcriptional target of PITX1 [24–26], are responsible for ~5% of all patients with familial isolated Clubfoot[24]. Both duplications and deletions of the chromosome 17q23 region result in Clubfoot, highlighting the critical importance of TBX4 gene dosage. Similar to PITX1, TBX4 is uniquely expressed in the hindlimb, explaining the foot phenotype. The chromosomal microarray (CMA) genetic study can detect the chromosome 17q23 copy number variants, which are clinically significant for their possible association with both severe, treatment-refractory Clubfoot and hip dysplasia [24]. The implication of genes specifically involved in hindlimb development in Clubfoot etiology makes other commonly hypothesized genes for Clubfoot, such as the muscle contractile genes implicated in distal arthrogryposis less likely, as mutations in these genes cause both upper and lower extremity involvement and have not been identified in isolated Clubfoot patients [27,28]. Future studies are needed to develop animal models to determine the exact mechanisms by which these genetic abnormalities cause Clubfoot and to test other hypotheses of Clubfoot pathogenesis.
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Pitx1 haploinsufficiency causes Clubfoot in humans and a Clubfoot-like phenotype in mice
Human molecular genetics, 2011Co-Authors: David M. Alvarado, Matthew B. Dobbs, Kevin Mccall, Hyuliya Aferol, Matthew J. Silva, Joel R. Garbow, William M. Spees, Tarpit K. Patel, Marilyn J. Siegel, Christina A. GurnettAbstract:Clubfoot affects 1 in 1000 live births, although little is known about its genetic or developmental basis. We recently identified a missense mutation in the PITX1 bicoid homeodomain transcription factor in a family with a spectrum of lower extremity abnormalities, including Clubfoot. Because the E130K mutation reduced PITX1 activity, we hypothesized that PITX1 haploinsufficiency could also cause Clubfoot. Using copy number analysis, we identified a 241 kb chromosome 5q31 microdeletion involving PITX1 in a patient with isolated familial Clubfoot. The PITX1 deletion segregated with autosomal dominant Clubfoot over three generations. To study the role of PITX1 haploinsufficiency in Clubfoot pathogenesis, we began to breed Pitx1 knockout mice. Although Pitx1+/− mice were previously reported to be normal, Clubfoot was observed in 20 of 225 Pitx1+/− mice, resulting in an 8.9% penetrance. Clubfoot was unilateral in 16 of the 20 affected Pitx1+/− mice, with the right and left limbs equally affected, in contrast to right-sided predominant hindlimb abnormalities previously noted with complete loss of Pitx1. Peroneal artery hypoplasia occurred in the Clubfoot limb and corresponded spatially with small lateral muscle compartments. Tibial and fibular bone volumes were also reduced. Skeletal muscle gene expression was significantly reduced in Pitx1−/− E12.5 hindlimb buds compared with the wild-type, suggesting that muscle hypoplasia was due to abnormal early muscle development and not disuse atrophy. Our morphological data suggest that PITX1 haploinsufficiency may cause a developmental field defect preferentially affecting the lateral lower leg, a theory that accounts for similar findings in human Clubfoot.
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familial isolated Clubfoot is associated with recurrent chromosome 17q23 1q23 2 microduplications containing tbx4
American Journal of Human Genetics, 2010Co-Authors: David M. Alvarado, Matthew B. Dobbs, Kevin Mccall, Hyuliya Aferol, Jason B Huang, Matthew Techy, Jillian G Buchan, Janet Cady, Patrick R GonzalesAbstract:Clubfoot is a common musculoskeletal birth defect for which few causative genes have been identified. To identify the genes responsible for isolated Clubfoot, we screened for genomic copy-number variants with the Affymetrix Genome-wide Human SNP Array 6.0. A recurrent chromosome 17q23.1q23.2 microduplication was identified in 3 of 66 probands with familial isolated Clubfoot. The chromosome 17q23.1q23.2 microduplication segregated with autosomal-dominant Clubfoot in all three families but with reduced penetrance. Mild short stature was common and one female had developmental hip dysplasia. Subtle skeletal abnormalities consisted of broad and shortened metatarsals and calcanei, small distal tibial epiphyses, and thickened ischia. Several skeletal features were opposite to those described in the reciprocal chromosome 17q23.1q23.2 microdeletion syndrome associated with developmental delay and cardiac and limb abnormalities. Of note, during our study, we also identified a microdeletion at the locus in a sibling pair with isolated Clubfoot. The chromosome 17q23.1q23.2 region contains the T-box transcription factor TBX4, a likely target of the bicoid-related transcription factor PITX1 previously implicated in Clubfoot etiology. Our result suggests that this chromosome 17q23.1q23.2 microduplication is a relatively common cause of familial isolated Clubfoot and provides strong evidence linking Clubfoot etiology to abnormal early limb development.
Jose A. Morcuende - One of the best experts on this subject based on the ideXlab platform.
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Descriptive epidemiology of Clubfoot in Romania: a clinic-based study.
European review for medical and pharmacological sciences, 2016Co-Authors: L Mcconnell, Dan Cosma, Dana Vasilescu, Jose A. MorcuendeAbstract:OBJECTIVE Congenital Clubfoot affects 1 per 1000 live births per year in Romania. To date, no epidemiological studies have been conducted in this country to assess risk factors associated with the deformity. The aim of this study was to evaluate specific environmental and socio-demographic factors that may increase the risk of an infant to be born with Clubfoot. PATIENTS AND METHODS A descriptive clinic-based study over a twelve-week period was conducted using structured questionnaires given to biological parents of clinically confirmed Clubfoot and control subjects. 62 parents of probands and 66 parents of control patients were enrolled for risk factor questionnaires. Phenotypic data from Clubfoot children was also collected. RESULTS We found that males were twice as likely to have Clubfoot and half of Clubfoot subjects were affected bilaterally. There was no significant difference in the rate of left versus right Clubfoot. Infant and maternal characteristics showing a strong association with Clubfoot included breech presentation and old maternal age at conception. CONCLUSIONS Our results support reported literature data that males are two times as likely to have Clubfoot which indicates a genetic influence. Previous reports suggest Clubfoot babies are born to young mothers but in Romania advanced maternal age (≥ 35 years) was an indicator which may suggest genetic influence. This clinic-based study does not support previously recorded data of a positive association for maternal or household smoking. Data from this Romanian population also does not support previous data suggesting strong associations with maternal diabetes.
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long term results of comprehensive Clubfoot release versus the ponseti method which is better
Clinical Orthopaedics and Related Research, 2014Co-Authors: Peter A Smith, Jose A. Morcuende, Ken N Kuo, Adam Graf, Joseph Krzak, Ann Flanagan, Sahar Hassani, Angela Caudill, Fredrick R Dietz, Gerald F HarrisAbstract:Background Clubfoot can be treated nonoperatively, most commonly using a Ponseti approach, or surgically, most often with a comprehensive Clubfoot release. Little is known about how these approaches compare with one another at longer term, or how patients treated with these approaches differ in terms of foot function, foot biomechanics, or quality-of-life from individuals who did not have Clubfoot as a child.
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Descriptive epidemiology of Clubfoot in Peru: a clinic-based study.
The Iowa orthopaedic journal, 2013Co-Authors: Melissa Palma, Thomas Cook, Julio Segura, Augustin Pecho, Jose A. MorcuendeAbstract:congenital Clubfoot is the most common birth defect of the musculoskeletal system and affects 1 in every 1000 live births each year.(1) Although there have been numerous studies of investigation, the etiology and pathogenesis of Clubfoot remains unknown. To date, no epidemiological studies have been conducted in Peru to assess possible genetic and environmental risk factors associated with this deformity. The purpose of this study was to evaluate specific environmental and socioeconomic factors that may increase the risk of Clubfoot. A descriptive clinic-based study was conducted using structured questionnaires given to biological mothers of clinically confirmed Clubfoot patients (n=72) and biological mothers of children between ages 0-18 with no first or second degree family history of Clubfoot as controls (n=103). Phenotypic data from Clubfoot subjects were also collected. We found that males were twice as likely to have Clubfoot as females, and half of all Clubfoot patients had bilateral Clubfoot. There was no significant difference in the rate of left vs. right Clubfoot. Infant birth in the winter months correlated with an increased risk of Clubfoot (p=0.01476). Maternal characteristics found to be significantly associated with increased risk of Clubfoot were young maternal age at conception (p=0.04369) and low maternal education (p=0.003245). Young paternal age also had a correlation with increased risk of Clubfoot in the child (p=0.0371). Both paternal smoking (p=0.00001) and the presence of any household smoking (p=0.00003) were strongly associated with an increased risk of Clubfoot.
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Mutation screening of muscle development genes in patients with idiopathic Clubfoot
Open Journal of Genetics, 2012Co-Authors: Christopher L. Groth, Valerie Buffard, Jose A. Morcuende, Val C. SheffieldAbstract:Background: Congenital idiopathic Clubfoot is a very common musculoskeletal birth defect, but with no known etiology. Dietz et al. have shown possible linkage in chromosome 3 and 13 in a large, multigenerational family with congenital idiopathic Clubfoot. Current evidence suggests that muscle development is impaired in patients with congenital idiopathic Clubfoot, therefore we hypothesized that mutations in genes related to muscle development could be associated with this deformity. From the areas identified in the linkage study, candidate genes SPRY2, RAF1, IQSEC1, LMO7, and UCHL3 were selected based upon their presence in skeletal muscle as well as their involvement in muscle development. Methods: The exons and splice sites of the five genes were screened via sequence-based analysis in a group of 24 patients with congenital idiopathic Clubfoot. All single nucleotide polymorphisms (SNPs) found were compared to public databases to determine allelic frequency and amino acid modification. Results: While many SNPs were found, none proved to be significantly associated with the phenotype of congenital idiopathic Clubfoot. The SNPs found were shown to be common amongst a non-Clubfoot population and to follow the allelic frequency of the general population. Conclusions: Based upon these results, SPRY2, RAF1, IQSEC1, LMO7, and UCHL3 are not likely to be the major causes of congenital idiopathic Clubfoot. Given the complexity of myogenesis, many other candidate genes remain that could cause defects in the hypaxial musculature that is invariably observed in congenital idiopathic Clubfoot. Clinical Relevance: This study further identifies genes which are unlikely to be the direct cause of congenital idiopathic Clubfoot. It also helps to eliminate suspected genes found within the given bounds of chromosome 3 and 13.
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Descriptive Epidemiology of Clubfoot in Vietnam: A Clinic-Based Study
The Iowa orthopaedic journal, 2012Co-Authors: Michelle C. Nguyen, Huynh Manh Nhi, Vo Quang Dinh Nam, Van Thanh, Paul A. Romitti, Jose A. MorcuendeAbstract:congenital Clubfoot is the most common birth defect of the musculoskeletal system and affects 1 in every 1000 live births each year.1 Although there have been numerous studies of investigation, the etiology and pathogenesis of Clubfoot remains unknown. To date, no epidemiological studies have been conducted in Peru to assess possible genetic and environmental risk factors associated with this deformity. The purpose of this study was to evaluate specific environmental and socioeconomic factors that may increase the risk of Clubfoot. A descriptive clinic-based study was conducted using structured questionnaires given to biological mothers of clinically confirmed Clubfoot patients (n=72) and biological mothers of children between ages 0-18 with no first or second degree family history of Clubfoot as controls (n=103). Phenotypic data from Clubfoot subjects were also collected. We found that males were twice as likely to have Clubfoot as females, and half of all Clubfoot patients had bilateral Clubfoot. There was no significant difference in the rate of left vs. right Clubfoot. Infant birth in the winter months correlated with an increased risk of Clubfoot (p=0.01476). Maternal characteristics found to be significantly associated with increased risk of Clubfoot were young maternal age at conception (p=0.04369) and low maternal education (p=0.003245). Young paternal age also had a correlation with increased risk of Clubfoot in the child (p=0.0371). Both paternal smoking (p=0.00001) and the presence of any household smoking (p=0.00003) were strongly associated with an increased risk of Clubfoot.
Edward Naddumba - One of the best experts on this subject based on the ideXlab platform.
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Towards effective Ponseti Clubfoot care: the Uganda Sustainable Clubfoot Care Project.
Clinical orthopaedics and related research, 2009Co-Authors: Shafique Pirani, Edward Naddumba, Joseph Konde-lule, Titus Beyeza, Richard Mathias, J. Norgrove Penny, Ben Mbonye, Jackson Amone, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations’ healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system’s capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006–2007, 872 children with clubfeet were seen. USCCP-designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the incidence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment protocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.
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The Uganda Sustainable Clubfoot Care Project
2009Co-Authors: Shafique Pirani Frcsc, Edward Naddumba, Richard Mathias Frcpc, Joseph Konde-lule, J. Norgrove Penny Frcsc, Titus Beyeza, Ben Mbonye Frcs, Jackson Amone Mph, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations' healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system's capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006-2007, 872 children with clubfeet were seen. USCCP- designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the inci- dence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment pro- tocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.
Titus Beyeza - One of the best experts on this subject based on the ideXlab platform.
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Towards effective Ponseti Clubfoot care: the Uganda Sustainable Clubfoot Care Project.
Clinical orthopaedics and related research, 2009Co-Authors: Shafique Pirani, Edward Naddumba, Joseph Konde-lule, Titus Beyeza, Richard Mathias, J. Norgrove Penny, Ben Mbonye, Jackson Amone, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations’ healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system’s capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006–2007, 872 children with clubfeet were seen. USCCP-designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the incidence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment protocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.
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The Uganda Sustainable Clubfoot Care Project
2009Co-Authors: Shafique Pirani Frcsc, Edward Naddumba, Richard Mathias Frcpc, Joseph Konde-lule, J. Norgrove Penny Frcsc, Titus Beyeza, Ben Mbonye Frcs, Jackson Amone Mph, Fulvio FranceschiAbstract:Neglected Clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti Clubfoot treatment has high efficacy in correcting the Clubfoot deformity in ideal conditions but is demanding on parents and on developing nations' healthcare systems. Its effectiveness and the best method of care delivery remain unknown in this context. The 6-year Uganda Sustainable Clubfoot Care Project (USCCP) aims to build the Ugandan healthcare system's capacity to treat children with the Ponseti method and assess its effectiveness. We describe the Project and its achievements to date (March 2008). The Ugandan Ministry of Health has approved the Ponseti method as the preferred treatment for congenital Clubfoot in all its hospitals. USCCP has trained 798 healthcare professionals to identify and treat foot deformities at birth. Ponseti Clubfoot care is now available in 21 hospitals; in 2006-2007, 872 children with clubfeet were seen. USCCP- designed teaching modules on Clubfoot and the Ponseti method are in use at two medical and three paramedical schools. 1152 students in various health disciplines have benefited. USCCP surveys have (1) determined the inci- dence of Clubfoot in Uganda as 1.2 per 1000 live births, (2) gained knowledge surrounding attitudes, beliefs, and practices about Clubfoot across different regions, and (3) identified barriers to adherence to Ponseti treatment pro- tocols. USCCP is now following a cohort of treated children to evaluate its effectiveness in the Ugandan context.