Lymphocytic esophagitis is a rare, poorly understood disease. This case report presents a patient with a history of squamous cell carcinoma of the tongue who presented with dysphagia. He received esophageal dilation that unfortunately resulted in perforation. Biopsies showed lymphocytic esophagitis. There are very few cases in the literature describing perforation in lymphocytic esophagitis. In addition, management and treatment have been challenging for physicians; however, this case represents a complete symptomatic improvement in four to six weeks with a proton pump inhibitor.

Many causes of esophagitis exist in immunocompromised patients. Uncommon pathogens must be considered to facilitate timely and appropriate therapy. A limited number of cases of esophageal actinomycosis have been reported. This report describes an unusual case of esophageal actinomycosis in a patient with persistent dysphagia. The broad differential may have delayed definitive diagnosis in the case study patient. Biopsy and culture are essential for accurate diagnosis. Although actinomycosis is a rare disease, it should be included in the differential diagnosis of patients presenting with oral or esophageal complaints. It may also be considered as an opportunistic infection in immunocompromised patients. The treatment of choice is parenteral penicillin G, 18 to 24 million units for 2 to 6 weeks followed by oral therapy for 6-12 months.

Diss. (sammanfattning)--Göteborg : Göteborgs universitet, 2007. / Härtill 3 uppsatser.

No description available.

This thesis provides a description of reflux disease, especially its nature, diagnosis and treatment, followed by the analysis of the costs of this disease and the procedure for the patient as an example.

Percutaneous endoscopic gastrostomy (PEG) is currently a popular method of administering enteral feeding. Most of these patients are elderly, debilitated, and chronically ill. They are on a number of medications and have multiple diseases. With impaired consciousness and swallowing disability, these patients are prone to develop pneumonia. In order to identify possible risk factors, we followed 24 men who underwent PEG for the occurrence of pneumonia or until they died. We then analyzed the medical records of these patients for potential risk factors for pneumonia. The presence of esophagitis during PEG placement endoscopy and history of pneumonia prior to PEG were significant risk factors. Advanced age and cerebrovascular accident (CVA) tended to indicate a higher risk of pneumonia. Taking these risk factors into consideration may be beneficial in the management of such patients.

No description available.

No description available.

No description available.

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 maior em GF (69,60 uM) que GNF (38,60 uM) (p<0,05), que pode estar relacionada à aquisição de NO diretamente da fumaça do cigarro e sua provável oxidação a SNO2 quando entra em contato com bicarbonato salivar (básico). SNO3 média foi 226,88 ?M em GF e 197,02 uM em GNF (p=0,304). GNO3 média foi 134,56 uM em GF e 125,63 uM em GNF (p=0,699). Comparando-se GC e GNC houve diferença estatística (p<0,05) somente em SNO3 (médias - GC: 172,36 uM e GNC: 256,57 uM). Este se mostrou relacionado à manutenção da erosão na mucosa esofágica, grupo (GNC) com 91,3% dos pacientes sendo fumantes. A manometria e a pHmetria tiverem, respectivamente, p=0,935 na avaliação do EIE e p=0,235 para escore de DeMeester, p=0,194 para porcentagem de tempo total com pH<4 e p=0,214 para tempo total com pH<4. GNO3 teve média em GC de 112,09 uM e em GNC de 148,26 uM (p=0,157). SNO2 foi em média de 62,07 uM em GC e 61,67 uM em GNC (p=0,977). Bicarbonato salivar teve média de 3,88 uM/L em GC e 4,36 uM/L em GNC (p=0,491). CONCLUSÕES: O cigarro pode ser considerado como uma co-morbidade capaz de piorar os resultados do tratamento clínico da esofagite erosiva, e o NO do cigarro está relacionado a esta piora. / 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 esophageal clearance. Mean SNO2 was higher (69.60 uM) in GS than in GNS (38.60 uM) (p <0.05), that can be related to the acquisition of NO directly from the cigarette smoke and its probable oxidation to SNO2 when it gets in touch with bicarbonate in the saliva (basic). Mean SNO3 was 226.88 uM in GS and 197.02 uM in GNS (p=0.304). Mean GNO3 was 134.56 uM in the GS and 125.63 uM in GNS (p=0.699). When comparing GH and GNH significantly statistical differences were found (p <0.05) only in SNO3 (mean - GH: 172.36 uM and GNH: 256.57 uM). Higher doses of SNO3 were related to the maintenance of the erosion in the esophageal mucuosae, group (GNH) with 91.3% of patients being smokers. Manometry and pHmetry were, respectively, p=0.935 in evaluation of the lower esophageal sphincter (LES) and p=0.235 for DeMeester score, p=0.194 for percentage of total time with pH <4 and p=0.214 for total time with pH <4 between GH and GNH. Mean GNO3 in GH was of 112.09 uM and in GNH of 148.26 uM (p=0.157). Mean SNO2 was on average 62.07 uM in the GH and 61.67 uM in the GNH (p=0.977). Mean salivary bicarbonate was 3.88 uM/L in GH and 4.36uM/L in GNH (p=0.491). CONCLUSIONS: Cigarette smoking can be considered as a co-moribidity factor capable of worsening results of erosive esophagitis results, and its NO is related to this worsening.