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Analysis of human genetic linkage

Chronic Cough Due to Gastroesophageal Reflux Disease: ACCP Evidence-Based Clinical Practice Guidelines

https://www.gastrojournal.org/article/S0016-5085(02)56599-9/pdf

Gastroesophageal reflux disease in monozygotic and dizygotic twins

Background: Although familial clusters of Barrett’s oesophagus and oesophageal adenocarcinoma have been reported, a familial predisposition to these diseases has not been systematically investigated. Aims: To determine whether Barrett’s oesophagus and oesophageal (or oesophagogastric junctional) adenocarcinoma aggregate in families. Patients and methods: A structured questionnaire eliciting details on reflux symptoms, exposure history, and family history was given to Caucasian case (n=58) subjects with Barrett’s oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma, and to Caucasian control (n=106) subjects with symptomatic gastro-oesophageal reflux disease without Barrett’s oesophagus. Reported diagnoses of family members were confirmed by review of medical records. Results: The presence of a positive family history (that is, first or second degree relative with Barrett’s oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma) was significantly higher among case subjects compared with controls (24% v 5%; p v 43% male; p Conclusions: Individuals with Barrett’s oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma are more likely to have a positive family history of Barrett’s oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma than individuals without Barrett’s oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma. A positive family history should be considered when making decisions about screening endoscopy in patients with symptoms of gastro-oesophageal reflux.

https://gut.bmj.com/content/gutjnl/51/3/323.full.pdf

Familial aggregation of Barrett's oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults.

Gastroesophageal reflux is a physiological phenomenon, occurring with different severity and duration in different individuals. Reflux occurs when this normal event results in the occurrence of symptoms/signs or complications. The pathophysiology of gastroesophageal reflux is complex and diverse, since it is influenced by factors that are genetic, environmental (e.g., diet smoking), anatomic, hormonal, and neurogenic. However, many mechanisms remain incompletely understood. Future research should focus on a better understanding of the physiology of the upper and lower esophageal sphincters, and of gastric motility. The afferent and efferent neural pathways and neuropharmacologic mediators of transient lower esophageal sphincter relaxations and gastric dysmotility require further study. The role of anatomic malformations such as hiatal hernia in children has been underestimated. While therapeutic possibilities are greater in number and largely improved, the outcomes of some treatments are far from satisfactory in many cases. In addition to development of new forms of treatment, research should address better use of currently available medical and surgical treatments.

Mechanisms of gastroesophageal reflux and gastroesophageal reflux disease.

ContextGastroesophageal reflux (GER) has not previously been widely regarded
as a hereditary disease. A few reports have suggested, however, that a genetic
component may contribute to the incidence of GER, especially in its severe
or chronic forms.ObjectiveTo identify a genetic locus that cosegregates with a severe pediatric
GER phenotype in families with multiple affected members.DesignA genome-wide scan of families affected by severe pediatric GER using
polymorphic microsatellite markers spaced at an average of 8 centimorgans
(cM), followed by haplotyping and by pairwise and multipoint linkage analyses.SettingGeneral US community, with research performed in a university tertiary
care hospital.SubjectsAffected and unaffected family members from 5 families having multiple
individuals affected by severe pediatric GER, identified through a patient
support group.Main Outcome MeasuresDetermination of inheritance patterns and linkage of a genetic locus
with the severe pediatric GER phenotype by logarithm-of-odds (lod) score analysis,
considering a lod score of 3 or greater as evidence of linkage.ResultsIn these families, severe pediatric GER followed an autosomal dominant
hereditary pattern with high penetrance. A gene for severe pediatric GER was
mapped to a 13-cM region on chromosome 13q between microsatellite markers
D13S171 and D13S263. A maximum multifamily 2-point lod score of 5.58 and a
maximum multifamily multipoint lod score of 7.15 were obtained for marker
D13S1253 at map position 35 cM when presumptively affected persons were modeled
as unknown (a maximum multipoint score of 4.88 was obtained when presumptively
affected persons were modeled as unaffected).ConclusionThese data suggest that a gene for severe pediatric GER maps to chromosome
13q14.

https://jamanetwork.com/journals/jama/articlepdf/192899/joc91307.pdf

Mapping of a gene for severe pediatric gastroesophageal reflux to chromosome 13q14.

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Mapping of a gene for severe pediatric gastroesophageal reflux to chromosome 13q14.