Influência do óxido nítrico na cicatrização da esofagite erosiva em fumantes / Influence of nitric oxide in healing of erosive oesophagitis in smokers

INTRODUÇÃO: O cigarro é citado como um possível fator externo que influencia sobre a fisiopatologia e a evolução da doença do refluxo gastroesofágico (DRGE). O cigarro contém uma quantidade significativa de óxido nítrico (NO). Os objetivos deste trabalho foram avaliar, em pacientes fumantes com DRGE erosiva, o papel do NO, pela análise de seus precursores: nitratos salivar (SNO3) e gástrico (GNO3) e nitrito salivar (SNO2), nos resultados de cicatrização após tratamento clínico, bem como comparar esta cicatrização com não-fumantes. MATERIAIS E MÉTODOS: 31 pacientes (grupo GF) adultos fumantes, com sintomas típicos de DRGE e endoscopia digestiva alta (EDA) mostrando esofagite A ou B de Los Angeles e 10 adultos não-fumantes, com mesmas características de DRGE em sintomas e EDA (grupo GNF) realizaram manometria esofágica, pHmetria de 24 horas, dosagens de bicarbonato salivar, dosagens de SNO3, GNO3 e SNO2. Foram tratados com pantoprazol 40 mg/dia por oito semanas e repetiram a EDA. Comparou-se os grupos GF e GNF e também os grupos que cicatrizaram (grupo GC=18 pacientes) e não cicatrizaram (grupo GNC=23 pacientes). RESULTADOS E DISCUSSÃO: A cicatrização da esofagite erosiva ocorreu em dez pacientes (32,2%) em GF e oito pacientes (80%) em GNF (p<0,05). A manometria esofágica não mostrou diferenças estatísticas na avaliação do esfíncter inferior do esôfago (EIE) entre GF e GNF (p=0,517). A pHmetria de 24 horas mostrou maior intensidade de refluxo ácido em fumantes, com diferença estatisticamente significativa entre GF e GNF (p<0,05), com médias em GF: escore de DeMeester: 35,26, porcentagem de tempo com pH<4: 8,67 e tempo total com pH <4: 120,42 no GF, e médias no GNF: escore de DeMeester: 12,53, porcentagem de tempo com pH<4: 2,97 e tempo total com pH <4: 2,97. Bicarbonato salivar médio foi 4,54 uM/L em GF e 2,90 uM/L em GNF (p<0,05), portanto fumantes têm maior depuração esofágica. SNO2 média foi...

INTRODUCTION: Cigarettes are one of the possible external factors to influence the physiopathology and the evolution of the gastroesophageal reflux disease (GERD). Cigarettes contain a significant amount of nitric oxide (NO). The objectives of this work were, in smokers with erosive esophagitis, to evaluate the role of the nitric oxide (NO), carrying out an assessment of its precursors: salivary nitate (SNO3), gastric nitrate (GNO3) and salivary nitrite (SNO2), in the healing after clinical treatment, as well as to compare healing between smokers and non-smokers. MATERIALS AND METHODS: 31 adults smokers (group GS), who had typical GERD symptoms and an upper endoscopy which showed Los Angeles grade A or B esophagitis and ten non-smoker adults patients, with the same GERD symptoms and with similar esophagitis (group GNS), were submitted to esophageal manometry, 24-hour pHmetry, salivary bicarbonate count, and counts of SNO3, GNO3 and SNO2. Then they were treated with pantoprazole 40 mg/day for eight weeks and repeated upper endoscopy. We compared the groups GS and GNS, and the group where healing was observed (group GH=18 patients) with the group with no healing (GNH=23 patients). RESULTS/ DISCUSSION: Erosive esophagitis healing occured in ten patients (32.2%) of the GS and eight patients (80%) of the GNS (p <0.05). Esophageal manometry didn't show significantly statistical differences in the evaluation of the lower esophageal sphincter (LES), between GS and GNS (p=0.517). 24-hour pHmetry showed a more intense reflux in smokers, with significantly statistical differences between GS and GNS (p <0.05) in DeMeester score averages of: 35.26, percent of time with pH <4: 8.67 and total time with pH <4: 120.42 in GS, and DeMeester score averages of: 12.53, percent of time with pH <4: 2.97 and total time with pH <4: 2.97 in GNS. Mean salivary bicarbonate was 4.54 uM/L in GS and 2.90 uM/L in GNS (p <0.05), so smokers have more...

Effect of gastric bypass on Barrett's esophagus and intestinal metaplasia of the cardia in patients with morbid obesity.

Gastric bypass in patients with morbid obesity should be an excellent antireflux procedure, because no acid is produced at the small gastric pouch and no duodenal reflux is present, due to the long Roux-en-Y limb. Five hundred fifty-seven patients with morbid obesity submitted to resectional gastric bypass, and routine preoperative upper endoscopy with biopsy samples demonstrated 12 patients with Barrett's esophagus (2.1%) and three patients with intestinal metaplasia of the cardia (CIM). An endoscopic procedure was repeated twice after surgery, producing seven patients with short-segment Barrett's esophagus (BE) and five patients with long-segment BE. Body mass index (BMI) decreased significantly, from 43.2 kg/m(2) to 29.4 kg/m(2) 2 years after surgery. Symptoms of reflux esophagitis, which were present in 14 of the 15 patients, disappeared in all patients 1 year after surgery. Preoperative erosive esophagitis and peptic ulcer of the esophagus healed in all patients. There was regression from intestinal metaplasia to cardiac mucosa in four patients (57%) with short-segment BE, and in one patient (20%) with long-segment BE. Two (67%) of three cases with CIM had regression to cardiac mucosa. There was no progression to low- or high-grade dysplasia. Gastric bypass in patients with Barrett's esophagus and morbid obesity is an excellent antireflux operation, proved by the disappearance of symptoms and the healing of endoscopic esophagitis or peptic ulcer in all patients, which is followed by an important regression to cardiac mucosa that is length-dependent and time-dependent.

Doença do refluxo gastroesofágico: influência da cepa cagA do Helicobacter pylori na resposta terapêutica à inibição da bomba protônica em pacientes com esofagite erosiva leve / Gastroesophageal reflux disease: influence of cagA strains of Helicobacter pylori in the proton pump inhibition therapeutic response in patients with low grade erosive esophagitis

Foram estudados 83 pacientes com esofagite erosiva graus I e II, pela classificação de Savary-Miller modificada, divididos em 3 grupos. Um sem Helicobacter pylori, dois outros com Helicobacter pylori, com e sem o gene cagA. Avaliou-se a participação da bactéria e de seu gene cagA, associados à estudo histopatológico de antro e corpo e à gastrinemia basal, na cicatrização da mucosa do esôfago após tratamento com pantoprazol 40 mg ao dia por 6 semanas. Verificou-se que a presença do Helicobacter pylori, independentemente da presença do gene cagA, facilita a cicatrização esofágica. Indivíduos com gastrinemias maiores também tendem a cicatrizar melhor. Não houve relação do resultado do estudo histopatológico com a resposta terapêutica / Eighty three patients with grade I-II of the modified Savary-Miller classification have been studied. They were divided in three groups. One without Helicobacter pylori infection, two with the bacterium, one with and other without the cagA gene. We verified the influence of cagA status, histopathology of antrum and body of the stomach and gastrinemia in the esophageal healing rates after treatment with pantoprazole 40 mg once a day for six weeks. Helicobacter pylori presence but not cagA status and gastrinemia led to better healing rates. Histopathology of the gastric mucosa did not influence the response...

[Peptic stricture of the esophagus: long term outcome of conservative treatment]. / Estenosis péptica del esófago: resultados alejados del tratamiento conservador.

BACKGROUND: Endoscopic dilatation of esophageal strictures is a simple and safe procedure. AIM: To analyze the long term outcome of conservative treatment for esophageal peptic stricture in patients with high surgical risk. PATIENTS AND METHODS: Twenty consecutive patients, 13 male, whose mean age was 75.2 years, with a peptic stricture of the esophagus and high surgical risk were prospectively studied. All were subjected to endoscopic esophageal dilatation and treated with continuous medical antireflux therapy thereafter. RESULTS: Only five patients complied with antireflux treatment on a regular basis. The remaining 15 were non compliant or abandoned it. A total of 56 dilatations were done (mean 2.8 per patient, range 1-6). No complications were observed after the procedure. With a mean follow up period of 49 months, the outcome of the conservative treatment was classified as excellent or good in all the cases. Eight patients (40%) died of causes unrelated to the treatment. Two patients had an organic foreing body impactation. This situation was solved endoscopically in both. CONCLUSION: In high risk patients, endoscopic dilatation, with or without regular antireflux medical treatment is a simple, safe and effective therapy in the management of peptic oesophagel stenosis.

Estenosis péptica del esófago: resultados alejados del tratamiento conservador / Peptic stricture of the esophagus: long term outcome of conservative treatment

BACKGROUND: Endoscopic dilatation of esophageal strictures is a simple and safe procedure. AIM: To analyze the long term outcome of conservative treatment for esophageal peptic stricture in patients with high surgical risk. PATIENTS AND METHODS: Twenty consecutive patients, 13 male, whose mean age was 75.2 years, with a peptic stricture of the esophagus and high surgical risk were prospectively studied. All were subjected to endoscopic esophageal dilatation and treated with continuous medical antireflux therapy thereafter. RESULTS: Only five patients complied with antireflux treatment on a regular basis. The remaining 15 were non compliant or abandoned it. A total of 56 dilatations were done (mean 2.8 per patient, range 1-6). No complications were observed after the procedure. With a mean follow up period of 49 months, the outcome of the conservative treatment was classified as excellent or good in all the cases. Eight patients (40 per cent) died of causes unrelated to the treatment. Two patients had an organic foreing body impactation. This situation was solved endoscopically in both. CONCLUSION: In high risk patients, endoscopic dilatation, with or without regular antireflux medical treatment is a simple, safe and effective therapy in the management of peptic oesophagel stenosis.

Resultados imediatos da eletrocoagulaçäo com argônio no tratamento do esôfago de Barrett em pacientes com e sem displasia / Endoscopic argon plasma coagulation (Beamer) of Barrett`s esophagus in patients with and without dysplasia

Intoduçäo e objetivo: O esôfago de Barrett (EB) é uma lesäo comprovadamente pré-maligna. As cirurgias anti-refluxo ou o tratamento farmacológico nem o revertem para epitélio escamoso, nem diminuem o risco de câncer associado a esta lesäo metaplásica. Recentemente, alguns estudos têm demonstrado reversäo do EB com diferentes técnicas endoscópicas associadas à inibiçäo ácida. Neste estudo os autores pretendem verificar se a reversäo completa do EB é possível através da APC. Métodos: foram tratados 32 pacientes -20M/12F, média etária =55,2 (21-84)- com EB demonstrado histologicamente com extensäo média de 3,9cm (0,5-6). Quatorze casos apresentavam displasia de baixo grau. Toda a extensäo do EB era cauterizada em cada sessäo usando o APC com uma potencia de 65-70W. Todos os pacientes recebiam 60mg de omeprazol durante o período de tratamento. Resultados: Reversäo completa do EB foi obtida em todos os pacientes após média de 1,9 sessäo (1-3). Esses resultados foram confirmados histologicamente por meio de múltiplas biópsias que evidenciaram epitélio escamoso. Dezessete (53por cento) pacientes sofreram dor retroesternal de forte a moderada intensidade com odinofagia por dois a dez dias após cada sessäo. Febre alta e derrame pleural ocorreram em cinco e estenose de esôfago em três desses 17 casos. Conclusäo: A eletrocoagulaçäo por argônio associada a supressäo ácida com omeprazol é um método efetivo em eliminar o EB, pelo menos, a curto prazo. Apenas estudos com seguimento a longo prazo desses pacientes, juntamente com alívio permanente do refluxo ( por cirurgia ou medicaçäo), poderäo determinar se essa técnica reduz ou elimina o risco de câncer associado ao EB

La funduplastia posterior: valoración a treinta años / Posterior fundoplasty: a thirty year evaluation

La funduplastia posterior constituye una técnica antirreflujo introducida en 1966 por uno de los autores (Guarner), después de un largo estudio experimental. El presente artículo valora un seguimiento de uno a 30 años en un grupo de 1499 pacientes, con una incidencia global de recidivas de 9.6 por ciento y una frecuencia reducida de efectos indeseables. Los autores establecen comparaciones con un grupo de 68 pacientes operados, también por ellos mismos, con la técnica original de Nissen y seguidos por un periodo similar. Comparan la funduplastia posterior con las principales operaciones en uso y ponen de manifiesto la efectividad del procedimiento. Una valoración con una serie tan amplia de casos y a tan largo plazo resulta poco frecuente en la literatura médica.

Revision actualizada del tratamiento de la esofagitis por reflujo y de sus complicaciones / Treatment of reflux esophagitis and its complications

Se presenta la revisión actualizada de la enfermedad por reflujo gastroesofágico, usando la clasificación clásica de la esofagitis por grados y mediante la endoscopia y la biopsiarelacionar los aspectos macroscopicos con los microscopicos. Luego en tratamiento se señala las modificaciones en el estilo de vida y tratamiento farmacológico, segun el grado de esofagitis haciendo especial enfasis en los casos del lactante , la gestante y el anciano. Si el paciente con esofagitis de reflujo evoluciona negativamente a pesar de un buen tratamiento, se indica el tratamiento quirurgico (operación antireflujo) actualmente se usa la via laparoscópica. En cuanto a las complicaciones puede ocurrir que en la esofagitis grado III a ulcera(s) al reepitelizarse lo hagan con epitelio cilindrico-ulcera de Barret. La estenosis (grado IV) previa endoscopia y biopsia si procede la dilatación se hace en forma progresiva (sonda de Savary G.) o el tratamiento quirurgico (reseccion de la zona estenosada). La otra complicación es el esofago de Barrett, en este caso la metaplasia (lesión premaligna) debe ser controlada, con energico tratamiento médico; con rayos laser y/o resección quirurgica. Sabemos que la displasia y cáncer guardan relación, y si la displasia es de alto grado debera indicarse la esofaguectomia y segun estudios mostrados en el ultimo Congreso Mundial de Gastroenterología 1994, la citometria de flujo es un indicador de mucho valor, ya que indica en gran porcentaje cancer intramucoso, cuando la endoscopía, biopsia y citología aun no lo detectan

Gastroesophageal reflux: one reason why baby won't eat.

Gastroesophageal reflux (GER) is the movement of gastric contents retrograde into the esophagus. Sometimes the refluxate is seen as emesis, but often reflux is "silent," meaning that there are no discrete symptoms during an episode. In adults, the most common symptom of GER is heartburn, whereas in infancy excessive crying and malaise are symptoms that prompt investigation for GER, with or without esophagitis. Symptoms of esophagitis in infancy may include arching (hyperextension) of the torso and refusal of feedings. Tube feedings may be required to treat infants with failure to thrive who refuse oral feedings. Paradoxically, tube feedings increase the number of GER episodes. A hypothetical explanation for refusal of food in infancy is that pain with swallowing (odynophagia) or heartburn are consequences of peptic esophagitis. As a result, infants will learn to refuse food if it hurts or if they fear that it will hurt to eat. Another possible mechanism is visceral hyperalgesia, a neuropathic condition in which prior experience changes sensory nerves so that previously innocuous stimuli are perceived as painful. Some infants may have especially sensitive sensory nerves in the upper gastrointestinal tract, which predisposes visceral hyperalgesia to develop. Thus pain occurs from luminal distension or acid reflux in the absence of tissue damage. The evaluation of babies who won't eat includes a careful history and physical examination to exclude the possibility of chronic systemic illness. Refusal to feed is an unusual manifestation of a common condition: GER disease. The initial tests for GER usually include a barium swallow study to assess the upper gastrointestinal anatomy, endoscopy and esophageal biopsy to assess esophagitis, and an intraesophageal pH study, which is useful in "silent" reflux to quantitate the duration of esophageal acid exposure and to correlate discrete symptom episodes with periods of reflux. The treatment of infants and toddlers who refuse to eat because of pain resulting from visceral hyperalgesia or reflux esophagitis involves removing the pain associated with eating and making eating a pleasurable experience. Treatment for esophagitis may include maintaining an upright posture after meals and thickened feeds, medication to improve gastrointestinal motility or to decrease acid secretion, or fundoplication.

[Reflux esophagitis]. / Esofagitis de reflujo.

Chronic Esophageal reflux induces reflux esophagitis, which is a common finding in gastroenterological practice. Reflux esophagitis produce symptoms like pirosis, regurgitation and in some cases respiratory complains resembling asthma or angina-like chest pain. The pathophysiology of this disease is based on a multifactorial origin, which usually results in the chronic evolution of the disease. In recent years, there have appeared new evidences pointing out to alterations in the relaxing mechanisms of the lower esophageal sphincter; however, some patients having reflux esophagitis show normal shincteric pressure. The sweep action of esophageal smooth muscle is a key point for sending back to stomach the eventually refluxed material; it has been demonstrated that this sweeping action is impaired in many patients having reflux esophagitis. Incompetence of lower esophageal sphincter seems to be related a local to neural alteration rather than to smooth muscle functional disturbance. Recent findings stablis a link between local nitric oxide release and relaxation of the lower esophageal sphincter. Esophageal mucosaldisplay an intrinsic resistance to HCL, pepsin, bilis and enzymes deleterious action by a blockade of back-defusion of hydrogen ions contained in the refluxed material. Nevertheless, some other luminal and non-luminal factors are involved in this mucosalprotection. When these intrinsic resistance factors are abated, tisular lesions like ersion, ulcer and Barret's mucosal changes can occur; is of particular interest because its potential malignant evolution. Esophageal reflux usually resolves with medical treatmen, but in some particular cases surgical correction is indicated for improving the antireflux barrier.

[Gastroesophageal reflux in pediatrics]. / Reflujo gastroesofágico en pediatría.

The frequency of gastroesophageal reflux disease in pediatrics has increased. There is not a clear explanation, some believe there is more awareness of the disease, others believe that new formulas, which are richer in nutrients, may irritate the gastrointestinal tract of the infant. Clinically, children present with regurgitation-malnutrition, respiratory disease, and esophagitis. The medical treatment aims to improve the eating techniques, to decrease the gastric acid output, and to improve the motility function of the esophago-gastrointestinal tract. Surgical treatment is rarely needed.