The South African national drug policy (NDP) was implemented in 1994 to ensure the availability and accessibility of essential drugs to all citizens. The NDP also hoped to ensure the safety, efficacy and quality of drugs as well as to promote the concepts of individual responsibility for health, preventative care and informed decision making. However, drug utilisation studies performed after the implementation of the national drug policy showed that South Africa's pharmaceutical sector was characterised by indiscriminate and irrational drug use, high drug prices and polypharmacy. A retrospective study that was done in 2001 in the clinics supplied by Evander Hospital showed that only 11.9% of prescriptions for acid-related disorders complied with the standard treatment guidelines (STG). It became evident that there was need for an intervention. The general objective of this study was to determine the effect of an education intervention, implemented in 2003, on the prescribing patterns of drugs for acid-related disorders in the Govan Mbeki municipal clinics serviced by Evander Hospital. An empirical pre-intervention and post-intervention study using primary data obtained from patient files at the clinics was done. A quantitative survey of the use of the drugs included in the study (magnesium trisilicate, aluminium hydroxide/magnesium trisilicate combination tablets, cimetidine or omeprazole) was conducted. To determine a baseline, all prescriptions where the drugs selected for this study were prescribed from 1 July 2001 to 31 December 2001 were collected. For the period I January 2002 to 31 December 2002 retrospective data was collected in the form of all prescriptions where the relevant drugs were prescribed. Additional retrospective data was collected for the period January 2002 to 30 June 2003 to determine the outcome of treatment given. The phi coefficient was calculated, and although statistical correlation could not be proven, important tendencies could be detected in the data. Only 8% of the prescriptions adhered to the STG before the presentation of the face to face education intervention. In the first six months following the intervention, STG compliance increased to 15.2%. In the following six-month period, the STG compliance decreased to 14.1 %. The assumption was made that patients were cured if they did not return with the same complaint. Based on this assumption the conclusion was drawn that, before the intervention, 50.2% of the patients were cured. In the first six months after the intervention had taken place the percentage patients who did not return increased from 50.2% to 60.6%. In the second six months after the intervention the percentage of patients who did not return increased to 70.7%. It may be concluded that compliance with the STG improved as a result of the face to face education intervention. Moreover, it was found that cost efficiency improved in parallel and the cure rate seemed to be positively affected by the intervention. / Thesis (M.Pharm. (Pharmacy Practice))--North-West University, Potchefstroom Campus, 2007.

INTRODUÇÃO: A prevalência da úlcera péptica e outras afecções esofagogastroduodenais associadas à infecção pelo H. pylori foram alteradas em decorrência da erradicação desta infecção e uso de inibidores de secreção gástrica ácida. OBJETIVO: Determinar a prevalência da infecção pelo Helicobacter pylori associada às afecções diagnosticadas pela endoscopia digestiva alta e analisar fatores de risco. MÉTODOS: Foram analisados dados de 1478 pacientes, e as informações dos achados endoscópicos foram correlacionadas com resultado de teste de urease, faixa etária e gênero. Os pacientes com exame endoscópico normal foram considerados como grupo controle para análise estatística dos fatores de risco, perfazendo um total de 272 indivíduos. RESULTADOS: A prevalência da infecção por H. pylori foi de 53% (n=786), e maior na faixa etária entre 31 e 40 anos. Os achados endoscópicos mais frequentes foram gastrites (n=810; 54,8%), úlceras pépticas duodenais e gástricas (n=494; 33,4%), duodenites (n=287; 19,4%) e esofagites (n=217; 14,7%). Apenas a gastrite nodular e úlcera péptica foram associadas com infecção por H. pylori (p<0,05). Gastrite erosiva no antro (n=644, 78,5%) predominou em relação à pangastrite (n=166; 20,2%) e aquelas no corpo (n=19; 2,3%). Entre os casos de úlcera péptica, 103 (7%) foram gástricas, 343 (23,2%) foram duodenais e 48 (3,2%) foram gástrica e duodenal. A esofagite geralmente foi leve (grau A; 63,1%), 23,5% foram moderada (grau B) e 13,3% foram intensa (graus C e D). Infecção por H. pylori aumentou o risco de úlceras gástrica e duodenal em 1,9 e 1,6 vezes, respectivamente. Gênero masculino e maior idade foram riscos de todas as outras afecções. CONCLUSÃO: Infecção pelo H. pylori associada com maior idade e gênero masculino foram determinantes importantes para evolução de afecções gastrintestinais / Introduction: Peptic ulcer prevalence and other esophageal and gastroduodenal disorders associated with H. pylori infection changed as a consequence of its eradication and the use of gastric acid secretor inhibitors. Purpose: To establish H. pylori infection prevalence associated with clinical disorders diagnosed by upper gastrointestinal endoscopy, and determine the risk factors. Methods: Data from 1478 patients were analyzed, and the endoscopic findings were correlated with the urease test results, age and gender. Patients with normal endoscopy were considered control group for statistical analysis of the risk factors, comprising a total of 272 individuals. Results: The overall prevalence of H. pylori infection was 53% (n=786), being higher between 31 and 40 years old. The most frequent endoscopic findings were gastritis (n=810, 54.8%), peptic ulcer (n=494, 33.4%), duodenitis (n=287, 19.4%) and esophagitis (n=217, 14.7%). Only nodular gastritis and peptic ulcer were associated with H. pylori infection (p<0.05). Erosive gastritis (70%) in the antrum (n=644; 78.5%) predominated in relation to pangastritis (n=166, 20.2%) and the ones in the corpus (n=19, 2.3%). Among peptic ulcer cases, 103 (7%) were gastric, 343 (23.2%) were duodenal and 48 (3.2%) were gastric and duodenal. Esophagitis usually was mild (grade A in 63.1%), 23.5% were moderate (grade B) and 13.3% were intense (grades C and D). H. pylori infection increased the risk of gastric and duodenal ulcers by 1.9 and 1.6-fold, respectively. Male gender and being older were risks of all the other conditions. Conclusion: H. pylori infection associated with older age and male gender were important determinants to gastrointestinal diseases outcome

Bakgrund: Infektion med Helicobacter pylori är vanligt förekommande världen över. Forskning pekar på att låg socioekonomisk status, trångboddhet och dålig hygien tycks gynna smitta med Helicobacter pylori. Helicobacter pylori infekterar magsäckens och/eller tolvfingertarmens slemhinna, vilket kan resultera i magsår och gastrit. Därmed bör behandling sättas in efter påvisad infektion med Helicobacter pylori, för att förebygga risken att magsäckscancer utvecklas. Behandling vid infektion orsakad av Helicobacter pylori innefattar oftast trippelterapibehandling bestående av protonpumpshämmare samt två olika antibiotikum. Forskning pekar på att probiotika har positiva effekter i behandling mot Helicobacter pylori. Syfte: Uppsatsen syftar till att undersöka och redogöra för om trippelterapibehandling i kombination med probiotika är en effektivare behandling hos patienter infekterade med Helicobacter pylori, än enbart trippelterapibehandling. Metod: Studien är designad som en litteraturstudie. I studien granskades sex stycken vetenskapliga, randomiserade, kliniskt prövade originalartiklar. Litteratursökningen genomfördes i databasen PubMed. Resultat: Fyra av studierna visade en signifikant skillnad mellan interventionsgruppen som tilldelats probiotika + trippelterapibehandling, och kontrollgruppen som enbart tilldelats trippelterapibehandling. Slutsats: Slutsatsen är att probiotika kombinerat med trippelterapibehandling är något effektivare än enbart trippelterapibehandling. För- och efterbehandling med probiotika i samband med en trippelterapibehandling gav störst effekt. Ytterligare studier krävs för att säkerställa effekten av probiotika vid en trippelterapibehandling. / Background: Being infected by Helicobacter pylori is very common all around the world. Research indicates that low socioeconomic status, overcrowding and bad hygiene most likely increases the risk of being infected by Helicobacter pylori. Helicobacter pylori infects the stomach and/or duodenal mucosa, which can result in a gastric ulcer and gastritis. Therefore, treatment should be instituted directly after Helicobacter pylori has been detected, to reduce the risk of developing gastric cancer. Treatment for a infection caused by Helicobacter pylori often involves a triple therapy treatment consisting of a proton-pump inhibitor and two different types of antibiotics. Research indicates that probiotics could have positive effects regarding treatment against Helicobacter pylori. Aim: The aim of this study is to examine if triple therapy treatment in combination with probiotics is a more effective treatment for patients infected by Helicobacter pylori, than with triple therapy treatment alone. Method: This study is designed as a literature study. Six different scientific, randomized, clinically tested original articles were examined. The literature search was conducted in the database PubMed. Result: There was a significant difference in four studies between the intervention group, which was assigned probiotics + triple therapy, and the control group, which was assigned only triple therapy treatment. Conclusion: The conclusion is that probiotics combined with triple therapy treatment is somewhat more effective than triple therapy treatment alone. A treatment with probiotics before and after a treatment with triple therapy treatment gave the largest effect. Further studies are needed to ensure the effect of probiotics with a triple therapy treatment.

Introdução: A reinfecção pelo Helicobacter pylori em países em desenvolvimento parece ser maior do que nos países desenvolvidos. O retratamento da bactéria e o controle periódico de cura são necessários, quando elevadas taxas de reinfecção são verificadas. O objetivo do trabalho foi determinar a taxa anual de reinfecção, em pacientes brasileiros com úlcera péptica, num seguimento de cinco anos. Métodos: Pacientes com úlcera péptica, diagnosticada por endoscopia digestiva alta e infecção pelo Helicobacter pylori documentada por histologia, teste da urease, reação em cadeia da polimerase e teste respiratório, foram tratados para erradicação da bactéria. A cura da infecção foi verificada com os mesmos exames, três meses após o término do tratamento. Avaliação clínica e teste respiratório foram realizados aos seis e nove meses. Com um ano de seguimento, endoscopia, exame histológico, teste da urease, reação em cadeia da polimerase e teste respiratório foram novamente realizados. Até o quinto ano de seguimento, foram feitas consultas semestrais e testes respiratórios anuais. Na inclusão dos pacientes e nos reinfectados foram estudados 15 diferentes genes da bactéria. Resultados; Cento e quarenta e sete pacientes foram seguidos: 19 por um ano, oito por dois anos, quatro por três anos, cinco por quatro anos e 98 por cinco anos, num total de 557 pacientes/ano. Não ocorreu reinfecção no primeiro ano. No segundo ano, dois pacientes se reinfectaram, no terceiro quatro pacientes, no quarto três pacientes e no quinto um paciente, num total de 10 reinfecções. A taxa anual de reinfecção por pacientes/ano foi de 1,8%. Conclusão: O Brasil, um país em desenvolvimento com alta prevalência da infecção pelo Helicobacter pylori, apresenta uma taxa de reinfecção semelhante à dos países desenvolvidos / Introduction: The Helicobacter pylori reinfection rate seems to be higher in developing countries, than in developed ones. If a high reinfection rate is verified, periodical exams and bacterial retreatment would be necessary. The objective of this study was to determine the annual reinfection rate of Helicobacter pylori, in Brazilian patients with peptic ulcer disease, in a five year follow-up. Methods: Patients, with peptic ulcer disease diagnosed by upper digestive endoscopy and Helicobacter pylori infection verified by histological examination, rapid urease test, polymerase chain reaction and urea breath test, were treated for bacterial eradication. The infection cure was determined by the same proceedings, three months after the treatments end. Clinical evaluation and urea breath test were performed at sixth and ninth months of the follow-up. At one year of the follow-up, upper digestive endoscopy, histological examination, rapid urea test, polymerase chain reaction and urea breath test were repeated. Up to the fifth year of follow-up semester clinical evaluation and annual urea breath test were performed. All the patients included in the study and all the reinfected patients were tested for fifteen different genes of the Helicobacter pylori. Results: One hundred and forty-seven patients were followed: nineteen patients for one year, eight patients for two years, four patients for three years, five patients for four years and ninety-eight patients for five years. The total of patients/years follow-up was 557. Reinfection did not occur in the first year of the follow-up. In the second year, two patients became reinfected; in the third year, four patients; in the fourth, three and in the fifth, one patient. The total of reinfected patients was 10. The annual reinfection rate was 1,8%. Conclusion: Brazil, a developing country, presents a high prevalence of Helicobacter pylori infection. Nonetheless, the reinfection rate is similar to the developed countries.

Introdução: A reinfecção pelo Helicobacter pylori em países em desenvolvimento parece ser maior do que nos países desenvolvidos. O retratamento da bactéria e o controle periódico de cura são necessários, quando elevadas taxas de reinfecção são verificadas. O objetivo do trabalho foi determinar a taxa anual de reinfecção, em pacientes brasileiros com úlcera péptica, num seguimento de cinco anos. Métodos: Pacientes com úlcera péptica, diagnosticada por endoscopia digestiva alta e infecção pelo Helicobacter pylori documentada por histologia, teste da urease, reação em cadeia da polimerase e teste respiratório, foram tratados para erradicação da bactéria. A cura da infecção foi verificada com os mesmos exames, três meses após o término do tratamento. Avaliação clínica e teste respiratório foram realizados aos seis e nove meses. Com um ano de seguimento, endoscopia, exame histológico, teste da urease, reação em cadeia da polimerase e teste respiratório foram novamente realizados. Até o quinto ano de seguimento, foram feitas consultas semestrais e testes respiratórios anuais. Na inclusão dos pacientes e nos reinfectados foram estudados 15 diferentes genes da bactéria. Resultados; Cento e quarenta e sete pacientes foram seguidos: 19 por um ano, oito por dois anos, quatro por três anos, cinco por quatro anos e 98 por cinco anos, num total de 557 pacientes/ano. Não ocorreu reinfecção no primeiro ano. No segundo ano, dois pacientes se reinfectaram, no terceiro quatro pacientes, no quarto três pacientes e no quinto um paciente, num total de 10 reinfecções. A taxa anual de reinfecção por pacientes/ano foi de 1,8%. Conclusão: O Brasil, um país em desenvolvimento com alta prevalência da infecção pelo Helicobacter pylori, apresenta uma taxa de reinfecção semelhante à dos países desenvolvidos / Introduction: The Helicobacter pylori reinfection rate seems to be higher in developing countries, than in developed ones. If a high reinfection rate is verified, periodical exams and bacterial retreatment would be necessary. The objective of this study was to determine the annual reinfection rate of Helicobacter pylori, in Brazilian patients with peptic ulcer disease, in a five year follow-up. Methods: Patients, with peptic ulcer disease diagnosed by upper digestive endoscopy and Helicobacter pylori infection verified by histological examination, rapid urease test, polymerase chain reaction and urea breath test, were treated for bacterial eradication. The infection cure was determined by the same proceedings, three months after the treatments end. Clinical evaluation and urea breath test were performed at sixth and ninth months of the follow-up. At one year of the follow-up, upper digestive endoscopy, histological examination, rapid urea test, polymerase chain reaction and urea breath test were repeated. Up to the fifth year of follow-up semester clinical evaluation and annual urea breath test were performed. All the patients included in the study and all the reinfected patients were tested for fifteen different genes of the Helicobacter pylori. Results: One hundred and forty-seven patients were followed: nineteen patients for one year, eight patients for two years, four patients for three years, five patients for four years and ninety-eight patients for five years. The total of patients/years follow-up was 557. Reinfection did not occur in the first year of the follow-up. In the second year, two patients became reinfected; in the third year, four patients; in the fourth, three and in the fifth, one patient. The total of reinfected patients was 10. The annual reinfection rate was 1,8%. Conclusion: Brazil, a developing country, presents a high prevalence of Helicobacter pylori infection. Nonetheless, the reinfection rate is similar to the developed countries.

Abstract Gastric erosions are superficial mucosal breaks. With the exception of bleeding, they are considered harmless, but their aetiology, histopathology and long-term course have remained unknown and even the evolution of gastritis in patients with gastric erosions is unclear. The present study aimed to solve clinical significance and pathology of gastric erosions in a long-term follow-up study. Initially, 117 patients and 117 controls were studied in 1974–1981, and a follow-up study was performed in 1996. We evaluated the presence of Helicobacter pylori and Herpes simplex virus (HSV) infections, use of NSAIDs and alcohol, smoking, and assessed features of gastric histopathology. For follow-up, 52 patients and 66 controls were available. In the follow-up visit, 39% patients still had gastric erosions while 11% of the controls had developed erosions (p&#160;=&#160;0.001). In H. pylori-positive subjects, peptic ulcer or a scar was more common in patients (17%) than in controls (4%, p&#160;=&#160;0.006), but otherwise no increased morbidity or mortality was seen. High antibody titres against HSV predicted the persistence of erosions (p&#160;=&#160;0.000), but H. pylori infection, use of NSAIDs, alcohol or smoking were not associated. Initially, inflammation was more active in the region of erosions than elsewhere in the antral mucosa, and more active inflammation in the erosion was associated with HSV seropositivity, H. pylori infection and the recent use of NSAIDs. Initially, H. pylori-positive subjects with chronic or recurrent erosions had higher scores of neutrophils compared to those with non-chronic/non-recurrent erosions. In H. pylori-positive subjects, body gastritis was initially less active in the patient group. With time, antral gastritis worsened only in the patient group. In H. pylori-negative subjects, there was no evolution of gastritis. These results show that a significant proportion of gastric erosions are chronic/recurrent but mostly without serious complications. However, H. pylori-positive patients have a significant risk to develop a peptic ulcer. A significant proportion of chronic gastric erosions is related to HSV infection. Focally enhanced inflammation modified by HSV or NSAID may be important in the pathogenesis of gastric antral erosions. Active inflammation in the erosions seems to predict their chronicity/recurrency. Patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype. / Tiivistelmä Eroosiot ovat mahalaukun pinnallisia limakalvovaurioita. Niitä pidetään vaarattomina lukuun ottamatta niihin liittyvää verenvuototaipumusta. Niiden etiologiaa, histopatologiaa ja taudinkulkua ei tunneta. Ei myöskään tiedetä eroosiopotilaiden mahan limakalvon tulehduksen kulkua. Tämän tutkimuksen tavoitteena oli selvittää mahalaukun eroosioiden kliininen merkitys ja patologia pitkäkestoisena seurantatutkimuksena. Alkujaan 117 potilasta ja 117 kontrollihenkilöä tutkittiin vuosina 1974–1981, ja seurantatutkimus tehtiin vuonna 1996. Selvitimme helikobakteerin ja Herpes simplex -viruksen (HSV) aiheuttamien infektioiden, tulehduskipulääkkeiden (NSAID) ja alkoholin käytön, sekä tupakoinnin esiintymistä. Lisäksi tutkimme histopatologisesti mahalaukun limakalvoa. Lopulta oli 52 potilaan ja 66 kontrollihenkilön aineisto käytettävissä. Seurantakäynnillä 39 prosentilla potilaista oli yhä mahalaukun eroosioita, kun taas kontrolliryhmästä vain 11 prosentilla oli kehittynyt eroosioita. Helikobakteeri -infektoituneilla maha- tai pohjukaissuolen haava/arpi oli yleisempää eroosioryhmässä (17&#160;%) kuin kontrolleilla (4&#160;%), mutta muuten ei esiintynyt lisääntynyttä sairastuvuutta tai kuolleisuutta. Tulehdus oli aktiivisempaa eroosioissa kuin viereisellä limakalvolla, ja tämä tulehdus liittyi korkeisiin HSV-vasta-ainetasoihin, helikobakteeri-infektioon ja NSAID:n käyttöön. Korkeat HSV-vasta-ainetasot ennustivat eroosioiden pysyvyyttä. Ensimmäisellä käynnillä aktiivinen tulehdus eroosioissa oli voimakkaampaa niillä helikobakteeri-infektoituneilla, joilla eroosiot olivat pysyviä kuin niillä, joilla eroosiot eivät uusineet. Helikobakteeri-infektoituneilla eroosiopotilailla mahalaukun runko-osan limakalvon tulehdus oli aluksi vähemmän aktiivista kuin vastaavilla kontrolliryhmän henkilöillä, mutta ajan myötä mahalaukun corpusosan limakalvon tulehdus voimistui vain eroosioryhmällä. Limakalvotulehdus ei edennyt helikobakteeri-infektoitumattomilla henkilöillä. Tulokset osoittavat, että merkittävä osa mahalaukun eroosioista on kroonisia/toistuvia, mutta enimmäkseen ilman vakavia komplikaatioita. Kuitenkin helikobakteeri-infektoituneilla eroosiopotilailla on merkittävä riski saada maha- tai pohjakaissuolen haava. HSV- infektio liittyy merkittävään osaan kroonisia mahalaukun eroosioita. Paikallisella tulehdusaktiivisuudella, jota HSV ja NSAID:n käyttö muokkaavat, saattaa olla tärkeä rooli eroosioiden synnyssä ja niiden kroonistumisessa. Eroosiopotilailla on samanlainen mahalaukun limakalvon tulehduksen jakauma kuin pohjakaissuolihaavaa sairastavilla.

Abstract Helicobacter pylori is a Gram-negative bacterium, which infects the stomach of more than 50% of the population worldwide. In addition to being the most important risk factor for gastric cancer and peptic ulcers, H. pylori infection is a risk factor for several extra-digestive diseases including dyslipidemia. The consequences of having an H. pylori infection are significantly influenced by the inflammatory response of the host. The pattern recognition receptor Toll-like receptor 4 (TLR4) and the cytokine interleukin 6 (IL6) are important mediators of inflammation in H. pylori related diseases. We have analyzed a series of control subjects and patients with dyspepsia, peptic ulcers or gastric cancer for frequent genetic polymorphisms of the TLR4 and IL6 genes. The prevalence of H. pylori infection, the histologic features of gastritis and cancer and serum endocrine markers and lipid concentrations were also analyzed. Furthermore, the expression of TLR4 was analyzed in specific cell types of gastric mucosa by immunohistochemistry. The TLR4 wild type genotypes of polymorphisms +896 and +1196 were associated with an increased risk of peptic ulcers. The same genotypes also associated with higher serum gastrin levels, but not with atrophy or other features of gastritis. The TLR4 expression was seen in the gastrin and somatostatin secreting cells of gastric mucosa. These results suggest a regulatory link between TLR4 and gastrin secretion. Such a link indicates the presence of a novel effector mechanism for innate immunity in modifying the host endocrine function. The IL6 -174 polymorphism associated significantly with a risk of the diffuse type of gastric carcinoma but not with the intestinal type or its precursor conditions. Finally, we demonstrated that H. pylori infections modify HDL serum levels significantly only in IL6 -174 CC genotype patients, which suggests that the detrimental effects of H. pylori infections on HDL levels are transmitted through IL6. These results clarify the mechanisms of H. pylori related diseases and open new possibilities for research on peptic ulcer disease, gastric cancer and dyslipidemia. / Tiivistelmä Helicobacter pylori on yleinen ihmisen mahalaukussa esiintyvä Gram-negatiivinen bakteeri. Helikobakteeri on tärkein mahasyövän ja maha- ja pohjukaissuolihaavan riskitekijä ja se on myös muun muassa rasva-aineenvaihdunnan häiriöiden riskitekijä. Ihmisen tulehdusvaste vaikuttaa merkittävästi helikobakteeri-infektion seurauksiin. Tollin kaltainen reseptori 4 (TLR4), joka on hahmontunnistusreseptori ja tulehduksenvälittäjäaine interleukiini 6 (IL6) ovat tärkeitä ihmisen tulehdusvasteeseen osallistuvia proteiineja. Olemme tutkineet dyspepsiaa, maha- ja pohjukaissuolihaavaa ja mahasyöpää sairastavilta potilailta sekä kontrollihenkilöiltä TLR4:n ja IL6:n geenien yleisiä emäsjärjestyksen polymorfioita. Tutkimme myös helikobakteeri-infektion yleisyyttä ja histologisia piirteitä, mahasyövän histologisia piirteitä ja seerumin merkkiaineita ja lipidipitoisuuksia. Lisäksi tutkimme TLR4:n ilmenemistä mahan limakalvolla immunohistokemiallisesti. TLR4:n polymorfismien +896 ja +1196 villin tyypin genotyypit liittyivät kohonneeseen maha- ja pohjukaissuolihaavan riskiin. Samat genotyypit liittyivät myös korkeampiin gastriinitasoihin. TLR4:ä esiintyi mahalaukun limakalvolla gastriinia tai somatostatiinia ilmentävissä soluissa. Täten TLR4:n ja maha- pohjukaissuolihaavariskin yhteys näyttää välittyvän gastriinin erityksen kautta, mikä viittaa uuteen säätely-yhteyteen luontaisen immuniteetin ja mahalaukun umpieritysjärjestelmän välillä. IL6 -174 -polymorfismi yhdistyi diffuusin tyypin mahakarsinooman riskiin mutta ei intestinaalisen tyypin karsinooman riskiin. Helikobakteeri-infektio yhdistyi pienentyneisiin HDL-kolesterolipitoisuuksiin vain potilailla, joilla oli IL6 -174 CC genotyyppi, mikä viittaa helikobakteerin kolesterolitasoille haitallisen vaikutuksen välittyvän IL6:n kautta. Nämä tulokset antavat lisätietoa helikobakteerin aiheuttamien sairauksien mekanismeista ja avaavat uusia tutkimuspolkuja myös mahahaavan, mahasyövän ja rasva-aineenvaihdunnan häiriöiden kliiniseen tutkimukseen.

Atualmente, muitas são as diretrizes na literatura quanto à influência do Helicobacter pylori na Doença do Refluxo Gastroesofágico. Alguns autores acreditam que o H. pylori poderia ter um efeito protetor para o desenvolvimento na DRGE e outros até mesmo concluem que o agente possa ser um fator agravante na doença. Muitas publicações nos alertam para o desenvolvimento de sintomas da DRGE, ou mesmo da esofagite, em uma porcentagem razoável de pacientes erradicados pelo esquema tríplice para tratar o H. pylori, sendo que aproximadamente 10% teriam DRGE. Na verdade, por essas dúvidas, ainda não foi estabelecido um consenso quanto à importância do H. pylori na etiopatogenia da DRGE e suas complicações. Fato também discutido, seria a importância das cepas para a formação da esofagite em pacientes submetidos à erradicação. Talvez as mais virulentas, assim como a presença da “ilha de patogenicidade"(cagA) ou algumas cepas vacuolizantes (vacA), teriam uma maior relação com a prevenção da esofagite. Outro mecanismo importante, apontado por muitos, para a formação da esofagite em pacientes erradicados seria a elevação do índice de Massa Corpórea nesse grupo de pacientes erradicados associados ou não à presença da hérnia hiatal e justificados pela melhor qualidade de vida após melhora dos sintomas depois da erradicação. Em nosso estudo, 148 pacientes com úlcera péptica ativa ou cicatrizada receberam esquema tríplice de erradicação para o Helicobacter pylori e foram submetidos a exame endoscópico e ao teste histopatológico das amostras colhidas por biópsias de corpo e antro, teste respiratório com Carbono 14 e urease, antes e após o tratamento. Realizamos a genotipagem do agente, através do PCR, separando amostras de corpo e de antro, para determinar as cepas do agente. Os pacientes foram seguidos ambulatorialmente por um ano e avaliados quanto à melhora ou piora dos sintomas relacionados a DRGE (pirose) e sintomas considerados inespecíficos como a dor epigástrica; também procuramos quantificar o ganho ou perda do IMC. Encontramos 28 pacientes (18,9%) com esofagite erosiva (24 grau A e 4 grau B de Los Angeles) endoscópica após o tratamento do agente. Deste grupo, somente 3 pacientes que não tinham sintomas desenvolveram pirose (2%). A grande maioria dos pacientes se beneficiou com o tratamento, mostrando que 69 46,6%) melhoraram da pirose e outra grande maioria melhorou dos sintomas inespecíficos. Em 18 pacientes ulcerosos com esofagite, a análise de fragmentos de corpo foi cagA positiva (64,3%) e em amostras de antro 21 eram cagA positivos (75%). Assim como no grupo geral, as cepas vacuolizantes s1b/m1 e s1b foram, respectivamente, as mais encontradas no grupo da esofagite endoscópica. Houve ligeiro aumento nos Índices de Massa Corpórea em pacientes com e sem esofagite, sendo estatisticamente mais significativo nos 120 pacientes sem esofagite. Apesar do aparecimento da esofagite erosiva endoscópica em número razoável de pacientes, a sintomatologia não foi fator determinante, pois muitos melhoraram dos sintomas após o tratamento, e a erradicação não foi importante para determinar o grau de esofagite erosiva. Não foi encontrada nenhuma relação entre a genotipagem do agente e o desenvolvimento de esofagite endoscópica. O aumento de IMC, também não justifica, em nosso estudo a esofagite em pacientes ulcerosos tratados contra o H. pylori. / Nowadays, there are many directrixes in literature as to the influence of Helicobacter pylori, in the Disease of Gastroesophagic reflux. Some authors believe that H. pylori could have a protective effect to the development of GERD, and others even conclude that the agent may be an aggravating factor in the disease. Many publications allert us to the development of symptoms of GERD, or even the esophagitis,in a reasonable percentage of erradicated patients by the triplicit scheme to treat H. pylori, and 10%, approximately, would have GERD. In fact, due to these doubts, a consensus has not been established yet to the importance of H. pylori in the GERD’s etiopathogenic and its complications. The strains importance to the formation of esophagitis in patients submitted to erradication is another fact that has also been discussed. Maybe the most virulent ones, as the presence of “pathogenical island"(cagA) or some other vacuolating cytotoxin (vacA), would have a larger relation in the esophagitis prevention. Another important mechanism, pointed by many, to the formation of esophagitis in erradicated patients would be the elevation of Body Mass Index in this group of eradicated patients associated or not to the presence of hiatal hernia and justified by a better quality of life due to symptoms’ improvement after erradication. In our studies, 148 patients with active or healed peptic ulcer received triplicit scheme of erradication to the Helicobacter pylori and were submitted to endoscopic exams and histopathologic test of gathered samples by body and antro biopsies, respiratory test with carbon 14 and ureasis, before and after treatment. We have done the agent genotyping, through the PCR, separating samples of body and antro, to determine the agent Cepas. The patients have been followed ambulatorially for a year and evaluated as to the improvement or worsening of the symptoms related to GERD (pyrosis) and symptoms considered non-specific as epigastric pain; we have also tried to quantify the gain or loss of Body Mass Index. We found 28 patients(18.9%) with endoscopic erosive esophagitis (24 degree A and 4 degree B of Los Angeles) after agent’s treatment. In this group, only three patients who had no symptoms developed pyrosis (2%). Most of the patients benefitted from treatment showing that 69 (46.6%) presented improvement in pyrosis and another great majority improved non-specific symptoms. In 18 ulcered patients with esophagitis, the body analysis fragments was positive cagA (64.3%)and in antro samples of 21 were positive cagA (75%). As in the general group, the vacuolizing cepas slb/ml and slb were, respectivelly, the most found in the endoscopic esophagitis group. There was a slight raise in the BMI in patients with and without esophagitis, and it is, statistically more meaningful in the 120 patients without esophagitis. Even though there was the appearance of endoscopic erosive esophagitis in a reasonable number of patients, the symptmology was not a determining factor, because many have got better after the treatment, and erradication was not important to determine the erosive esophagitis. It was not found any relation between the agent genotyping and the development of endoscopic esophagitis. The raise of BMI does not justify in our study the esophagitis in ulcered patients treated against H. pylori.

Atualmente, muitas são as diretrizes na literatura quanto à influência do Helicobacter pylori na Doença do Refluxo Gastroesofágico. Alguns autores acreditam que o H. pylori poderia ter um efeito protetor para o desenvolvimento na DRGE e outros até mesmo concluem que o agente possa ser um fator agravante na doença. Muitas publicações nos alertam para o desenvolvimento de sintomas da DRGE, ou mesmo da esofagite, em uma porcentagem razoável de pacientes erradicados pelo esquema tríplice para tratar o H. pylori, sendo que aproximadamente 10% teriam DRGE. Na verdade, por essas dúvidas, ainda não foi estabelecido um consenso quanto à importância do H. pylori na etiopatogenia da DRGE e suas complicações. Fato também discutido, seria a importância das cepas para a formação da esofagite em pacientes submetidos à erradicação. Talvez as mais virulentas, assim como a presença da “ilha de patogenicidade”(cagA) ou algumas cepas vacuolizantes (vacA), teriam uma maior relação com a prevenção da esofagite. Outro mecanismo importante, apontado por muitos, para a formação da esofagite em pacientes erradicados seria a elevação do índice de Massa Corpórea nesse grupo de pacientes erradicados associados ou não à presença da hérnia hiatal e justificados pela melhor qualidade de vida após melhora dos sintomas depois da erradicação. Em nosso estudo, 148 pacientes com úlcera péptica ativa ou cicatrizada receberam esquema tríplice de erradicação para o Helicobacter pylori e foram submetidos a exame endoscópico e ao teste histopatológico das amostras colhidas por biópsias de corpo e antro, teste respiratório com Carbono 14 e urease, antes e após o tratamento. Realizamos a genotipagem do agente, através do PCR, separando amostras de corpo e de antro, para determinar as cepas do agente. Os pacientes foram seguidos ambulatorialmente por um ano e avaliados quanto à melhora ou piora dos sintomas relacionados a DRGE (pirose) e sintomas considerados inespecíficos como a dor epigástrica; também procuramos quantificar o ganho ou perda do IMC. Encontramos 28 pacientes (18,9%) com esofagite erosiva (24 grau A e 4 grau B de Los Angeles) endoscópica após o tratamento do agente. Deste grupo, somente 3 pacientes que não tinham sintomas desenvolveram pirose (2%). A grande maioria dos pacientes se beneficiou com o tratamento, mostrando que 69 46,6%) melhoraram da pirose e outra grande maioria melhorou dos sintomas inespecíficos. Em 18 pacientes ulcerosos com esofagite, a análise de fragmentos de corpo foi cagA positiva (64,3%) e em amostras de antro 21 eram cagA positivos (75%). Assim como no grupo geral, as cepas vacuolizantes s1b/m1 e s1b foram, respectivamente, as mais encontradas no grupo da esofagite endoscópica. Houve ligeiro aumento nos Índices de Massa Corpórea em pacientes com e sem esofagite, sendo estatisticamente mais significativo nos 120 pacientes sem esofagite. Apesar do aparecimento da esofagite erosiva endoscópica em número razoável de pacientes, a sintomatologia não foi fator determinante, pois muitos melhoraram dos sintomas após o tratamento, e a erradicação não foi importante para determinar o grau de esofagite erosiva. Não foi encontrada nenhuma relação entre a genotipagem do agente e o desenvolvimento de esofagite endoscópica. O aumento de IMC, também não justifica, em nosso estudo a esofagite em pacientes ulcerosos tratados contra o H. pylori. / Nowadays, there are many directrixes in literature as to the influence of Helicobacter pylori, in the Disease of Gastroesophagic reflux. Some authors believe that H. pylori could have a protective effect to the development of GERD, and others even conclude that the agent may be an aggravating factor in the disease. Many publications allert us to the development of symptoms of GERD, or even the esophagitis,in a reasonable percentage of erradicated patients by the triplicit scheme to treat H. pylori, and 10%, approximately, would have GERD. In fact, due to these doubts, a consensus has not been established yet to the importance of H. pylori in the GERD’s etiopathogenic and its complications. The strains importance to the formation of esophagitis in patients submitted to erradication is another fact that has also been discussed. Maybe the most virulent ones, as the presence of “pathogenical island”(cagA) or some other vacuolating cytotoxin (vacA), would have a larger relation in the esophagitis prevention. Another important mechanism, pointed by many, to the formation of esophagitis in erradicated patients would be the elevation of Body Mass Index in this group of eradicated patients associated or not to the presence of hiatal hernia and justified by a better quality of life due to symptoms’ improvement after erradication. In our studies, 148 patients with active or healed peptic ulcer received triplicit scheme of erradication to the Helicobacter pylori and were submitted to endoscopic exams and histopathologic test of gathered samples by body and antro biopsies, respiratory test with carbon 14 and ureasis, before and after treatment. We have done the agent genotyping, through the PCR, separating samples of body and antro, to determine the agent Cepas. The patients have been followed ambulatorially for a year and evaluated as to the improvement or worsening of the symptoms related to GERD (pyrosis) and symptoms considered non-specific as epigastric pain; we have also tried to quantify the gain or loss of Body Mass Index. We found 28 patients(18.9%) with endoscopic erosive esophagitis (24 degree A and 4 degree B of Los Angeles) after agent’s treatment. In this group, only three patients who had no symptoms developed pyrosis (2%). Most of the patients benefitted from treatment showing that 69 (46.6%) presented improvement in pyrosis and another great majority improved non-specific symptoms. In 18 ulcered patients with esophagitis, the body analysis fragments was positive cagA (64.3%)and in antro samples of 21 were positive cagA (75%). As in the general group, the vacuolizing cepas slb/ml and slb were, respectivelly, the most found in the endoscopic esophagitis group. There was a slight raise in the BMI in patients with and without esophagitis, and it is, statistically more meaningful in the 120 patients without esophagitis. Even though there was the appearance of endoscopic erosive esophagitis in a reasonable number of patients, the symptmology was not a determining factor, because many have got better after the treatment, and erradication was not important to determine the erosive esophagitis. It was not found any relation between the agent genotyping and the development of endoscopic esophagitis. The raise of BMI does not justify in our study the esophagitis in ulcered patients treated against H. pylori.

Thesis (M.Pharm. (Pharmacy Practice))--North-West University, Potchefstroom Campus, 2008.