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Enf. Asocioadas con úlcera: Epoc, corrosis, insuficiencia renal crónica, todas =hipergastrinemia. Síndrome Zollinger Ellison: hipergastrinemia x tumor en páncreas o duodeno, producción incontrolada de gastrina produce hipersecreción de ac. y pepsina y produce 1) úlcera duodenal severa, 2) indigestión, esofagtis, duodenoyeynitis y diarrea.
Ulceras: lesión que sobrepasa la muscular de la mucosa
The discovery by Marshall and Warren of a ‘spiral bacterium’ on the gastric mucosa of patients with gastritis1, 2 has radically changed our understanding and clinical management of peptic ulcer disease. H. pylori is now known to be closely involved in the pathogenesis of gastroduodenal disease. Most patients with peptic ulcer disease are infected with H. pylori, and eradication of the bacterium is essential to obtain long-term remission of the disease.
1 Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983;1:1273–5.
2 Marshall B, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984;1:1311–14.
The prevalence of H. pylori infection differs between developed and developing countries
H. pylori infection is one of the most common chronic infections in the normal population, with 7 out of 10 people infected globally.3,4 Low socioeconomic status predicts infection and the prevalence of infection is much greater in developing than in developed countries.5 Older generations tend to carry long-standing infections acquired early in life, and even in developed countries the prevalence of infection generally increases with age, such that about 50% of adults over 60 years of age may be infected. As living standards and hygiene improve, rates of infection fall, and the infection rate in adults today is probably only 1–2% in developed countries.6 However, infection is usually acquired in childhood, and indeed, most children in a southern USA study were shown to be infected by 7 years of age, with infection being more persistent in blacks than whites.7 In Ireland, H. pylori-positive children under 5 years of age, from whom the bacterium had been successfully eradicated, commonly became reinfected.8 Furthermore, in Japan, it has been shown that an increasing number of siblings is a risk factor for H. pylori infection.9 Person-to-person spread of the bacterium is poorly understood, but both faecal–oral and oral–oral routes may be involved.10
3 Mégraud F, Brassens-Rabble MP, Denis F et al. Seroepidemiology of Campylobacter pylori infections in various populations. J Clin Microbiol 1989;27:1870–3.
4 Dixon MF. Moderator's introduction II – pathological consequences of Helicobacter pylori infection. Scan J Gastroenterol 1996;31 Suppl:21.
5 Marshall BJ. Helicobacter pylori. Am J Gastroenterol 1994;89:S116–28.
6 Meihlke S, Bayerdörffer E, Lehn N et al. Helicobacter pylori reinfection in duodenal and gastric ulcer patients after antibacterial treatment. Gut 1995;37:A54.
7 Malaty HM, Berenson GS, Wattington WA et al. Helicobacter pylori acquisition in childhood: a 12-year follow-up cohort study in a bi-racial community. Gut 1997;41 Suppl:A33.
8 Rowland M, Kumar D, O'Connor P et al. Reinfection with Helicobacter pylori in children. Gut 1997;41 Suppl:A33.
9 Kikuchi S, Sakiyam T, Kurosawa M. Risk factors for H. pylori infection in Japan. Gut 1997;41 Suppl:A36.
10 Mendall MA, Pajares-Garcia J. Epidemiology and transmission of Helicobacter pylori. Current Opinions in Gastroenterology 1995;11 Suppl:1–4.
A range of disease-inducing factors contribute to epithelial damage
Several disease-inducing factors may contribute to epithelial damage as H. pylori infection of the gastroduodenal mucosa persists, though our understanding of the damage process is incomplete.12 H. pylori can reduce gastric mucus secretion, making the mucosa more susceptible to gastric acid, while stimulating pepsinogen – and hence pepsin – production. Bacterial phospholipases may make the mucus less hydrophobic, and urease-induced ammonia may also damage the tissues. Damaging vacuolation of epithelial cells may be caused by the ammonia, and may also occur independently through the activity of vacuolating cytotoxin (VacA), which is expressed in 50–60% of H. pylori strains.12 Production of the toxin is associated with the presence of an antigenic protein encoded by the cytotoxin-associated gene A (CagA).
12 Moran AP. Pathological properties of H. pylori. Scand J Gastroenterol 1996;3 Suppl:22–31.
Diagnosis of H. pylori
Techniques for the diagnosis of H. pylori infection can be broadly divided into invasive and non-invasive types. Invasive tests usually involve multiple biopsies from the antrum and corpus, so as to maximise the chances of finding an infected area of mucosa.
In the rapid or biopsy urease test, any ammonia produced by urease in the sample is detected by a pH indicator. Dark-field microscopy can detect the bacterium in smears, and histology can be highly accurate but is dependent on the skill of the operator. Culturing also requires specialist expertise, but can be highly sensitive and allows strains to be typed and antibiotic resistance determined. H. pylori DNA can also be detected in biopsy specimens by the highly sensitive polymerase chain reaction (PCR) technique.
Non-invasive tests for the diagnosis of H. pylori
The two principal non-invasive tests for diagnosing H. pylori infection are the urea breath test (UBT) and serology. The UBT is based on the measurement of 13CO2 or 14CO2 in the patient’s breath, due to the activity of bacterial urease in the stomach after ingestion of a radiolabelled urea test meal. The UBT is highly accurate and, unlike serological tests, can be used to either confirm presence or eradication of H. pylori. The test can predict not only intragastric bacterial load and severity of inflammation,37 but is also widely used to assess the effectiveness of different eradication regimens.38, 39
Serological tests on blood samples can rapidly detect anti-H. pylori antibodies in a primary-care setting, but need careful interpretation when assessing the success of eradication therapies because circulating antibodies persist for months after bacterial elimination.
Furthermore, as well as being an invasive test, PCR can also be used non-invasively, on faeces or saliva, for example.
37 Perri F, Clemente R, Bisceglia M et al. The 13C-urea breath test (UBT) correlates with the bacterial load and the severity of inflammation in H. pylori (HP) gastritis. Gut 1997;41 Suppl:A81.
38 Perri F, Clemente R, Ghoos Y et al. The relationship between results of pre-treatment urea breath test (UBT) and the efficacy of eradication of H. pylori infection. Gut 1997;41 Suppl:A73.
39 Lind T, Bardhan KD, Bayerdörffer E et al. The MACH 2 study: optimal Helicobacter pylori therapy needs omeprazole and can be reliably assessed by UBT. Gastroenterology 1997;112:A200.