[Naming and classification of steroids and human stress ulcers. Articles of historic significance published by Hans Selye 70 years ago]. / A szteroidok elnevezése, felosztása és az emberi stresszfekélyek. Selye János 70 éve megjelent történelmi jelentoségu cikkei.

The name of Hans Selye is mostly known worldwide as the discoverer of stress reaction. Yet, he made numerous other seminal and clinically relevant discoveries. Namely, since he had a focused research on steroid hormones originating from the adrenal cortex that play a crucial role in stress response, he was the first who introduced about 70 years ago the first classification of steroids that is still valid nowadays. This is based on three objective facts: (a) the names of steroid groups are identical with their organ of origin (e.g., corticoids from the adrenal cortex, testoids/androgens from the testis); (b) chemical structures of the steroids are identical within a group (e.g., all corticoids have pregnane nucleus with 21 carbon atoms); and (c) the biological effects are homogenous within a group (e.g., all glucocorticoids exert catabolic effect, while androgens are anabolic). It should be emphasized that Selye also discovered in animal models the pro-inflammmatory effect of mineralocorticoids and the anti-inflammatory properties of glucocorticoids, about 8-10 years before Nobel Prize was awarded to a physician for the first clinical use of adrenocorticotrop hormone and cortisone. Last, but not least, Selye was the first who recognized about 70 years ago the occurence of stress ulcers in humans, based on clinical reports on the huge increase in the number of perforated gastric anti-duodenal ulcers during bombings of London in World War II. The subsequent ulcer research by Selye`s former students and their contemporaries resulted in the recognition of anti-duodenal ulcer effect of dopamine, and the central gastroprotective actions of thyreotrop releasing hormone and endogenous opioids. Thus, Hans Selye made much more contributions to medical science and clinical practice than 'just' the discoverer of biologic stress response.

History of Helicobacter pylori, duodenal ulcer, gastric ulcer and gastric cancer.

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician's believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for "surgical disease" or for "Sippy" diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

[The problems of etiology and pathogenesis of ulcer disease: rereading V. Kh. Vasilenko].

The author discusses the views of V. Kh. Vasilenko on etiology and pathogenesis of ulcer disease expounded in his last publications and compares them with modern concepts of the origin of this condition. The nature of ulcer disease as a systemic gastrointestinal pathology is considered with special emphasis on its difference from secondary (symptomatic) ulceration, pathogenetic significance of H. pylori infection, hereditary and environmental (non-infectious) factors. Much attention is given to the conditions facilitating the development of ulcer diseases at different combinations of internal and environmental factors including such poorly known ones as immune and sanogenetic mechanisms.

Time trends of mortality from gastric cancer in Europe.

BACKGROUND: The time trends of gastric and duodenal ulcer disease are shaped by a birth-cohort phenomenon. AIMS: The aim of this study was to assess the extent by which a birth-cohort phenomenon also affected the long-term time trends of gastric cancer among different European countries. METHODS: Mortality data from France, Germany, Netherlands, Scotland, Spain, and Sweden of the past 56-85 years were analyzed. The age-specific death rates were plotted against the period of death as period-age contours and against the period of birth as cohort-age contours. RESULTS: The long-term time trends of gastric cancer mortality were found to have risen among generations born during the 18th century until the mid-19th century and then to have declined in all subsequent generations. The rise and fall of gastric cancer preceded similar birth-cohort patterns of gastric and duodenal ulcer by about 10-30 years. With the exception of gastric cancer in Germany, similar birth-cohort phenomena were found in all countries, as well as in men and women. CONCLUSIONS: The time trends of mortality from gastric cancer and peptic are shaped by birth-cohort patterns that have affected all countries of Europe. It remains an enigma why mortality associated with gastric cancer and peptic ulcer suddenly started to rise within a short time period during the 19th century.

The possible causes of the pandemic of peptic ulcer in the late 19th and early 20th century.

Helicobacter pylori is established as a cause of peptic ulcer (PU). Less well recognised is that an epidemic of PU began around the middle of the 19th century, reached a peak at the turn of the century, and is now on the wane. As the epidemic developed, the risk of PU increased in successive generations throughout life. Then the epidemic diminished in successive generations. The risk of gastric ulcer (GU) was highest in people born around 1885, while the risk of duodenal ulcer (DU) was highest in those born about 10-30 years later. H. pylori infection offers an inadequate explanation of the PU epidemic. Although the epidemic coincided with a major rise in cigarette smoking, PU then declined in spite of an increased incidence of smoking. None of the other possible causes of ulcer (non-steroidal anti-inflammatory drugs, stress or diet) satisfactorily explains the epidemics of GU and DU and their asynchronicity. The best, but inadequate, explanation for the epidemic is the coincidence of the acquisition of a new potent strain of H. pylori in childhood and the uptake of smoking in adult life.

Three centuries of stomach symptoms in Scotland.

BACKGROUND: Stomach pain and discomfort have been reported since antiquity. AIM: To follow the time trends since the 18th century of dyspepsia, gastric ulcer, duodenal ulcer, and benign oesophageal disease to test when dyspepsia started to become a major clinical problem. METHODS: The annual in- and out-patient records of the last three centuries from the Scottish Royal Infirmaries of Edinburgh, Aberdeen, Glasgow and Dundee were analysed. In addition, dispensary attendances, clinicians' casebooks, students' notebooks and medical texts have been scrutinized for historic statistics of upper gastrointestinal disease. RESULTS: Dyspepsia was first recorded in the 1750s and increased markedly subsequently. Such dyspepsia persisted after gastric and duodenal ulcers appeared in the late 19th century and then declined again in the late 20th century. Non-ulcer dyspepsia has remained the commonest diagnosis made after endoscopy for stomach pain in the beginning of the 21st century. CONCLUSION: The current commonest diagnosis of stomach pain, dyspepsia dates from the mid-18th century. Any explanations of its causation need to consider this timing.

[Perforated stomach and duodenal ulcers at St Jósef's Hospital in Reykjavík up to 1948. 1950]. / Sprungin maga- og skeifugarnarsár. I St. Jósefsspítala í Reykjavík til ársloka 1948.

The St. Josephs Hospital in Reykjavík opened on the 1st of Sept. 1902. Until 1930 it was the main hospital of South Iceland. During the first 21 year period or until October 22nd 1923, not a single case of perforated peptic uncer seems to have been diagnosed nor treated in this hospital nor in any other hospital in the country. Neither is there any death from perforated pept. ulcer reported in the public health register of this period with only one exception in the year 1912. During the following 25 year period (1923-1948) 27 cases of an acute perforation and 8 cases of a subacute perforations (perf. larvata) of peptic ulcerations were admitted to and operated on in the St. Josephs Hospital and further 8 cases were given surgical treatment (reoperation) for the sequelae of an acute perforations that primarily had been operated on in other hospitals. There is thus a total of 42 cases as one of them is counted twice (in group 1 and 3).--In the first group there were two women, in the second group one woman and in the third group none.--The relation between the sexes thus being 39:3 for all three groups. Ulcers of the duodenum and pylorus were prevalent in all 3 groups (being 35 cases against 7 gastric ulcers). Two cases had perforated twice and 3 had perforated in the hospital. The treatment was surgical in all cases.--A simple closure of the ulcerperforation was made in 26 cases of the first group, but in one case a costal resection was done and no laparotomy. The immediate operative fatalities amongst those who underwent a laparotomy were 2 i. e. 7, 8 percent (or 7, 4 percent amongst all 27 cases). Eleven of the remaining 25 cases had to be reoperated on later because of the same disease or its complications (with one immediate fatality). Two more of them are dead, one from cancer of the stomach 5 years later (39 years old) and the other from a recurrent intestinal obstruction, the others (9) are still alive (1949) and are enjoying good health. Of the 14 not operated, 9 had a good or a fairly good result from the primary operation, 2 had a bad result and 2 have succumbed late on, one fram apoplexia, the other from an accident.--On couldn't be traced (foreigner). In the 2nd and 3rd group a G. E. anast. was done en 12 cases, an excision of the ulcer and G. E. anast., a gastrectomy and an exploratory laparatomy in one case each. In 14 cases the result has been good, bad in one case, they are all alive, with one exception, who died from cancer of the stomach five years later, at the age of 28. Approximately some 100 cases of an acute perforation of peptic ulceration are known to have had surgical treatment in all the hospitals of Iceland during this 25 year period (1923-1948). The immediate operative mortality as far as the author could trace amongst 87 of the cases does not seem to exceed 13 percent.

[Development of diagnostic methods in upper gastrointestinal tract bleeding]. / Rozwój diagnostyki krwawien z górnego odcinka przewodu pokarmowego.

Since the first description of upper gastrointestinal bleeding, presented as ground coffee vomiting and melena by Galen Claudius in 200 A.D., we have been observing dynamic progress in the diagnostics of this disease. This article presents modern methods and diagnostic examinations used to detect and localise the bleeding source.

Hospital admissions for peptic ulcer and indigestion in London and New York in the 19th and early 20th centuries.

The occurrence of peptic ulcer increased rapidly in all Western countries from the 19th to the 20th century, attributed to a possible epidemic of Helicobacter pylori, a new pathogenic strain, or a change in host susceptibility. The early trends in hospital admissions for peptic ulcer and dyspepsia in London and New York during the 19th century are reviewed to test these hypotheses.

Period- and cohort-age contours of deaths from gastric and duodenal ulcer in New York 1804-1998.

OBJECTIVES: Mortality data of peptic ulcer are mostly national and limited to the 20th century. The New York City data from 1804 have therefore been examined by both year of death and year of birth (cohort analysis), to consider whether the increases and subsequent decreases in deaths from gastric, followed by duodenal ulcer, can be attributed to Helicobacter pylori. METHODS: The annual mortality reports of New York City described gastric ulcer from 1838 and duodenal ulcer from 1931. The age-specific death rates per 100,000 population were calculated in 10-yr periods both by year of death and by year of birth for each disease according to age and sex. RESULTS: For gastric ulcer the period-of-death-age contours from the 1850s to the 1990s showed an increase to a mid-19th century plateau, but the cohort-age contours revealed a peak mortality for those born in the 1870s. Women born between about 1770 and 1880 showed a faster increase in mortality. For duodenal ulcer the period of birth contours showed a decline from a peak for those born in the 1880s and 1890s, with no sex difference. CONCLUSIONS: This urban study with data regarding deaths from gastric ulcer registered from 1838 and in those born from the 1770s, revealed by cohort analysis a peak in the 1870s, and for duodenal ulcer in the 1880s, comparable to national data worldwide. These time changes in fatalities are compatible with a change in the environment of children born in these decades, as, for example infection by a pathogenic strain of H. pylori.