Gallstone formation is the result of a complex interaction between genetic and nongenetic factors. We searched and reviewed the available literature to define how the primary prevention of gallstones (cholesterol gallstones in particular) could be applied in general practice. Electronic bibliographical databases were searched. Prospective and retrospective cohort studies and case-controlled studies were analyzed and graded for evidence quality. The epidemiological data confirmed that genetic factors are estimated to account for only approximately 25% of the overall risk of gallstones, while metabolic/environmental factors are at least partially modifiable in stone-free risk groups, and are thus modifiable by primary prevention measures related to diet, lifestyle, and environmental factors (i.e., rapid weight loss, bariatric surgery, somatostatin or analogues therapy, transient gallbladder stasis, and hormone therapy). There is no specific recommendation for the secondary prevention of recurrent gallstones. Family physicians can contribute to preventing gallstones due to their capability to identify and effectively manage several risk factors discussed in this study. Although further studies are needed to better elucidate the involvement of epigenetic factors that may regulate the effect of environment and lifestyle on gene expression in the primary prevention of gallstone formation, preventive interventions are feasible and advisable in the general practice setting.
Bariatric Surgery ; Bile Acids and Salts ; Case-Control Studies ; Cohort Studies ; Diet ; Epigenomics ; Gallbladder ; Gallstones* ; Gene Expression ; General Practice ; Humans ; Life Style ; Mental Competency* ; Obesity ; Physicians, Family* ; Primary Prevention ; Prospective Studies ; Retrospective Studies ; Risk Factors ; Secondary Prevention ; Somatostatin ; Weight Loss

Background: Gastroesophageal reflux disease is a digestive disorder characterized by nausea, regurgitation, and heartburn. Gastroesophageal reflux is the primary cause of laryngeal symptoms, especially chronic posterior laryngitis. The best diagnostic test for this disease is esophageal impedance-pH monitoring; however, it is poorly employed owing to its high cost and invasiveness. Salivary pepsin measured using a lateral flow device (Pep-test) has been suggested as an indirect marker of laryngopharyngeal reflux (LPR). The present study tested the reliability of Pep-test in diagnosing LPR in uninvestigated primary care attenders presenting with chronic laryngeal symptoms, and evaluated the raw pepsin concentration in patients with LPR. Methods: A multicenter, non-interventional pilot study was conducted on 86 suspected patients with LPR and 59 asymptomatic subjects as controls in three Italian primary care settings. A reflux symptom index questionnaire was used to differentiate patients with LPR (score >13) from controls (score <5). Two saliva samples were collected, and comparisons between the groups were performed using two-sided statistical tests, according to variable distributions. Results: There was no statistical difference in the salivary pepsin positivity between LPR patients and controls, whereas the pepsin intensity value was higher in controls than in LPR patients. Conclusion A high prevalence of pepsin positivity was observed in asymptomatic controls. Pepsin measurement should not be considered as a diagnostic test for LPR in primary care patients.