Epidemiology and genetics of peptic ulcer

At the turn of the century, duodenal ulcer rose from rarity to affect 10% of males in their life time, subsequently declining in some countries such as UK, levelling off in others such as Germany, and continuing to increase in still others such as Hong Kong. The annual incidence per 1000 population varies from about 1 in Japan to 1.5 in Norway, 1.8 in USA and 2.7 in Scotland, and the frequency also varies within many individual countries, such as Australia, China and India, and among races such as a higher prevalence among whites than blacks in USA and among Chinese than Javanese in Indonesia. Ulcer frequency is higher in winter months, and this appears universal, being true in cold as well as in warm countries. Most places report a rise of ulcer rates among the elderly in recent decades. The male to female ratio also varies geographically, for example from 1:1 in USA to 18:1 in India, and with time such as moving from 2:1 to 1:1 in the last two decades in USA, and the duodenal ulcer to gastric ulcer ratio varies widely from place to place, for example from 0.8 in Japan to 19:1 in Africa and 32:1 in India. Placebo healing rates also differ geographically, ranging from 5% in Philippines to 78% in Mexico. These epidemiological data can only be explained by the presence of multiple aetiological factors, including analgesics, society stress, cigarette smoking, Helicobacter pylori, dietary factors, and genetic factors. Three lines of evidence support a genetic role: family studies, twin studies and blood group studies. Family aggregation occurs more commonly in patients with early-onset (< 30 yr) of symptoms. Blood group O prevalence is more associated with late-onset of symptoms. Other genetic markers include nonsecretor status, HLA antigens, phenylthiocarbamide taste sensitivity, and alpha-1-antitrypsin. Genetic syndromes such as MEN I also support a genetic role and give insight into pathogenetic mechanisms. The best physiological marker is still hyperpepsinogenemia I, which is transmitted by autosomal dominance, despite recent report of lower serum pepsinogen 1 after healing of Helicobacter pylori associated gastritis.