Congenital Dislocation of the Hip in the American Black

Burke, Stephen W.; Macey, Theodore I.; Roberts, John M.; Johnston, Charles E.

doi:10.1097/00003086-198501000-00015

Cited by 14 publications

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“…Genetic mixing between Africans and other races with a higher incidence of DDH (e.g., Caucasians in the United States) [ 48 , 159 ] results in a higher but still comparatively low incidence of DDH. Quoted incidences in African Americans are 0.21 [ 51 ] and 0.46 [ 50 ] compared to 1.5 in American Caucasian infants [ 50 ]. Using weighted averages, the incidence of DDH is 0.06 in Africans in Africa and 0.40 in the United States.…”

Section: Resultsmentioning

confidence: 99%

The Epidemiology and Demographics of Hip Dysplasia

2011

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The etiology of developmental dysplasia of the hip (DDH) is unknown. There are many insights, however, from epidemiologic/demographic information. A systematic medical literature review regarding DDH was performed. There is a predominance of left-sided (64.0%) and unilateral disease (63.4%). The incidence per 1000 live births ranges from 0.06 in Africans in Africa to 76.1 in Native Americans. There is significant variability in incidence within each racial group by geographic location. The incidence of clinical neonatal hip instability at birth ranges from 0.4 in Africans to 61.7 in Polish Caucasians. Predictors of DDH are breech presentation, positive family history, and gender (female). Children born premature, with low birth weights, or to multifetal pregnancies are somewhat protected from DDH. Certain HLA A, B, and D types demonstrate an increase in DDH. Chromosome 17q21 is strongly associated with DDH. Ligamentous laxity and abnormalities in collagen metabolism, estrogen metabolism, and pregnancy-associated pelvic instability are well-described associations with DDH. Many studies demonstrate an increase of DDH in the winter, both in the northern and southern hemispheres. Swaddling is strongly associated with DDH. Amniocentesis, premature labor, and massive radiation exposure may increase the risk of DDH. Associated conditions are congenital muscular torticollis and congenital foot deformities. The opposite hip is frequently abnormal when using rigorous radiographic assessments. The role of acetabular dysplasia and adult hip osteoarthritis is complex. Archeological studies demonstrate that the epidemiology of DDH may be changing.

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Section: Resultsmentioning

confidence: 99%

The Epidemiology and Demographics of Hip Dysplasia

2011

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“…The proportion of DDH in Blacks being ~1/3 of that expected in Indiana is similar to that in New York state [~1/2 of that expected (2.4 vs. 5.1 %)] [ 7 ]. DDH was previously considered to be extremely rare in those of African descent [ 58 – 66 ]. Our study suggests that this is no longer true.…”

Section: Discussionmentioning

confidence: 99%

The demographics of developmental hip dysplasia in the Midwestern United States (Indiana)

Loder

Shafer

2015

Journal of Children's Orthopaedics

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BackgroundToday’s society is much more mobile than in the past. This increased mobility has resulted in different marriage/parenting groups. We wished to study the demographics of developmental dysplasia of the hip (DDH) in our area and compare/contrast our findings with those in the literature and specifically look for new findings compared to previous studies.MethodsA retrospective review of all children with DDH from 2003 through 2012 was performed. The age at first visit, gestational age, pregnancy number, gender, race, and family history of DDH was collected. Statistical significance was a p-value < 0.05.ResultsThere were 424 children (363 girls, 61 boys). Ethnicity was White in 80.8 %, Hispanic in 13.8 %, Black in 4.0 %, and Indo-Malay and Indo-Mediterranean in 0.7 % each; 66.8 % were unilateral; 14.2 % had a positive family history. The average gestational age was 38.1 weeks; 94.4 % were full term. The child was vertex presentation in 67.6 % and breech in 32.4 %; 52.8 % were delivered vaginally and 47.2 % by Cesarean section. The child was the first-born in 48.3 %. When compared to the birth statistics of our state, there was a higher proportion of Whites and Hispanics with DDH, and a lower, but not inconsequential, proportion of Blacks (p = 0.0018).ConclusionMixing of gene pools and infant carrying methods (lack of swaddling or marked abduction) occurring with societal change likely explains the higher than expected proportion of DDH amongst those of Hispanic ethnicity and a lower than expected, but not rare, proportion in those of African ancestry.Level of evidenceLevel IV—retrospective case series.

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“…16 The prevalence of hip dysplasia in our series of patients is therefore 7 per 1000, which is higher than the prevalence in the general population (0.7 to 1.2 per 1000 live births). 9 , 18 , 19 Sponseller et al 13 reported an incidence of hip dysplasia of 2% in association with Marfan syndrome. Our case series included 4 boys (80%) and only 1 girl (20%), which is in contrast with the female predominance for hip dysplasia (81% female predominance) in the general population.…”

Section: Discussionmentioning

confidence: 99%

Hip Dysplasia in Children With Osteogenesis Imperfecta: Association With Collagen Type I C-Propeptide Mutations

Kishta

Abduljabbar

Gdalevitch

et al. 2017

Journal of Pediatric Orthopaedics

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Background:Osteogenesis imperfecta (OI) is a heritable skeletal disorder characterized by bone fragility and short stature that is usually due to mutations in 1 of the 2 genes that code for collagen type I α-chains. The association between hip dysplasia and OI has not been systematically investigated. In this single-center study, we retrospectively reviewed all cases of OI associated with hip dysplasia to describe clinical characteristics and the effect of therapy.Methods:We reviewed the charts of 687 patients with OI who were seen at the Shriners Hospital for Children in Montreal between 1999 and 2013 to identify patients with a diagnosis of hip dysplasia. Clinical characteristics and the course after therapeutic interventions were extracted from the charts.Results:Hip dysplasia was diagnosed in 8 hips of 5 patients (4 boys, 1 girl; age at diagnosis ranged between 3 wk and 27 mo old). The prevalence of hip dysplasia and OI was therefore 0.87% (per patient). In 4 of the 5 patients (80%), OI was caused by mutations affecting the C-propeptide of collagen type I, which is otherwise rare in OI. Among the 26 patients with C-propeptide mutations followed at our institution, 4 (15%) had hip dysplasia. Pavlik harness treatment was attempted in 2 patients (3 hips) but was not effective in either case and resulted in avascular necrosis of 1 hip. Femoral varus derotational shortening osteotomies using a telescopic rod were performed in all 8 hips along with a closed reduction in 4 hips and an open reduction in 4 hips. Concomitant pelvic osteotomies were performed in 2 hips (1 patient). Surgery resulted in redislocation of 1 hip; all other surgically treated hips remained reduced.Conclusions:Clinical screening for hip dysplasia is difficult in OI owing to the bowing of the proximal femur and the risk of causing fractures. OI patients with positive C-propeptide mutation should therefore be screened for hip dysplasia by use of ultrasound. Presence of a C-propeptide mutation appears to be a risk factor for hip dysplasia (80%). It appears that Pavlik harness treatment is not useful in children with OI. The usual treatment of children with OI who pull to stand or started walking with femoral deformity is femoral osteotomy and rodding. In case of associated hip dysplasia with a dislocation, open reduction of the hip and a possible concomitant pelvic osteotomy appears to be a valid management option.Level of Evidence:Level IV.

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Congenital Dislocation of the Hip in the American Black

Cited by 14 publications

References 0 publications

The Epidemiology and Demographics of Hip Dysplasia

The Epidemiology and Demographics of Hip Dysplasia

The demographics of developmental hip dysplasia in the Midwestern United States (Indiana)

Hip Dysplasia in Children With Osteogenesis Imperfecta: Association With Collagen Type I C-Propeptide Mutations

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