Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty two patients (mean age 45.6 years) were assessed for oral hygiene and periodontal disease by dental examination before endoscopy. Information about oral care, smoking, and dentures was obtained and samples of dental plaque collected. The presence of Helicobacter pylori in plaque as sought by culture and polymerase chain reaction (PCR), and gastric antral biopsy specimens were taken for histological examination. Although H pylori was detected in the antral specimens of 34 patients (54%) all of the cultures of dental plaque were negative, and PCR was only positive from the dentures of one patient. Smokers had poor oral hygiene, visited their dentist less often, and brushed their teeth less frequently. There was no correlation of H pylori gastritis with either dental hygiene or periodontal disease. These results suggest that dental plaque or dentures are not an important reservoir for H pylori and are probably not a significant factor in transmission of the organism. The conflicting results in published works may be caused by differences in sample collection, culture techniques, or oral contamination from gastric juice as a result of gastro-oesophageal reflux at the time of endoscopy.
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PMID:Helicobacter pylori infection and dental care. 767 79

Helicobacter pylori is a microaerophilic, motile bacterium, especially adapted to life in the human stomach. The presence of H. pylori in the stomach is strongly associated with chronic gastritis and ulcer disease and is a risk factor for gastric cancers. The microorganism may be transmitted orally and has been detected in dental plaque, saliva, and feces, but the hypothesis that oral microflora may be a permanent reservoir of H. pylori is still controversial. A review of the literature suggests that the recovery of H. pylori in the mouth is probably intermittent, associated with gastroesophageal reflux but not with specific oral disease. Nonetheless, the PCR identification of oral H. pylori may become helpful, particularly in cases of gastritis or ulcer relapse after antimicrobial therapy. Eradication of oral H. pylori by local medication or periodontal procedures would rely on the precise identification of its ecological niche. Within family groups, prophylactic methods should be practiced to avoid oral carriage of H. pylori. The risk of iatrogenic transmission during dental care, however, is already circumscribed by standard professional hygiene procedures.
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PMID:Oral carriage of Helicobacter pylori: a review. 902 44

H. pylori is found in the stomach of patients with chronic gastritis. The infection is usually transmitted by the gastro-oral route and bacteria could be identified in saliva and dental plaque. An essential cause of chronic laryngitis is gastroesophageal reflux. The aim of the study was to evaluate if a H.pylori-associated chronic laryngitis exists. 38 patients with chronic laryngitis underwent gastroscopy. Biopsies were taken from the gastric antrum and body, lower, middle and upper esophagus. H. pylori was diagnosed by rapid urease test and histology. 14 of the patients (36.8%) were H.pylori-positive, but the bacteria could not be identified between stomach and larynx. 24 patients were H. pylori-negative. Seven patients (18.4%) suffered from esophagitis, six of these patients were H. pylori-negative. The H. pylori-infected patients received triple therapy for one week, in case of esophogitis Omeprazole 20 mg BID was prescribed. Six weeks later a follow-up endoscopy was performed. The eradication rate was 12/14 (85.7%), in all patients with reflux the esophagitis was cured. The laryngitis was clinically and endoscopically unchanged in ten of the twelve (83.3%) patients after successful treatment for H. pylori; in the remaining two patients as well as in the two H. pylori-positive patients the laryngitis was improved. In six out of the seven patients with esophagitis the laryngitis had healed completely and was improved in the remaining patient. It may be concluded that there is no evidence for the existence of H. pylori-associated laryngitis, suggesting that acid reflux is the underlying etiology.
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PMID:[Is chronic laryngitis associated with Helicobacter pylori? Results of a prospective study]. 965 3

Acute febrile neutrophilic dermatosis or Sweet's syndrome is a well-described acute condition with possible paraneoplastic and inflammatory associations. A case of a 49-year-old man with a prior history of Hodgkin's disease is described, who underwent a laparotomy for operative treatment of a small intestinal stricture and therapy-refractory gastroesophageal reflux. Incidentally, mild mesenteric lymphadenopathy was encountered, and a biopsy confirmed the presence of a new, unrelated low-grade follicular lymphoma. Two weeks postoperatively, the patient developed a tender erythematous plaque at the site of the Bovie electrocautery pad on the proximal thigh. Over the following week, the affected area extended in size, and became markedly edematous and infiltrated, with hemorrhagic surface studding. Multiple small plaques, some with annular arrays of pustules, were found on the opposite lower extremity, the lower back, and the arms. A skin biopsy suggested the presence of Sweet's syndrome, and corticosteroid treatment was initiated. All cutaneous manifestations disappeared within 48 h except for the presence of postinflammatory erythema. Acute neutrophilic dermatoses have not been previously described in this postoperative presentation. The differential diagnostic importance of this emergent entity and the potential for it being caused by surgical trauma are discussed.
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PMID:Acute postoperative dermatosis at the site of the electrocautery pad: sweet diagnosis of a burning issue. 1066 52

Barrett's esophagus is an acquired condition characterized by a progressive columnar metaplasia of the distal esophagus caused by longstanding gastroesophageal reflux and reflux esophagitis. Barrett's esophagus is a premalignant condition associated with a significantly increased risk of developing esophageal adenocarcinoma. The purpose of this article is to provide an overview of the radiologic aspects of Barrett's esophagus and esophageal adenocarcinoma. Review of the literature shows that some findings on esophagography that are relatively specific for Barrett's esophagus are not sensitive, while others that are sensitive have a low specificity. Specific radiologic features allowing a confident diagnosis of Barrett's esophagus are a high esophageal stricture or ulcer associated with a hiatal hernia and/or gastroesophageal reflux. A reticular mucosal pattern is a relatively specific sign particularly if located adjacent to a stricture and is highly suggestive of Barrett's esophagus. Unfortunately, these findings are only present in a minority of cases. More common but nonspecific findings include gastroesophageal reflux, hiatal hernia, reflux esophagitis and/or peptic stricture in distal esophagus. These findings may also be present in patients with uncomplicated reflux disease. Barrett's esophagus carries a risk of malignant change. Early adenocarcinoma may appear as a plaque-like lesion or with focal irregularity, nodularity, and ulceration of the esophageal wall. Invasive adenocarcinoma may be seen as an infiltrating ulcerated mass. The radiologic diagnosis of Barrett's esophagus is limited by lack of criteria that are both sensitive and specific. The major value of double-contrast esophagography is its ability to classify patients into high risk (high stricture, ulcer or reticular pattern), moderate risk (esophagitis and/or distal peptic strictures), and low-risk (absence of esophagitis or stricture) for Barrett's esophagus determining the relative need for endoscopy and biopsy. Endoscopy and biopsy are generally advocated to make a definitive diagnosis. Endoscopic ultrasound plays a role in the early detection of invasive carcinoma and the staging of proven carcinoma but has no role in the surveillance of Barrett's esophagus.
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PMID:The value of medical imaging in uncomplicated and complicated Barrett's esophagus. 1090 15

Children with esophageal burns due to toxic ingestion are medically compromised in many ways. They have problems like strictures in esophagus, dysphagia, gastroesophageal reflux and necessity to be fed with a special soft diet. Taking these distinctive features into consideration, we aimed to study these children with special focus on the dental caries risk. The experimental group consisted of 33 children between 2 and 14 years old (mean age 6.42 +/- 0.56) who had received stricture treatment in the Pediatric Surgery Department of our university. The control group consisted of 20 healthy children aged between 3 and 14 (mean age 7.25 +/- 0.7) who applied to the Pedodontics department for dental treatment. While mean dfs (+/- SE) was 11.13 +/- 2.30 and mean DMFs (+/- SE) was 9.79 +/- 4.76 in the experimental group, mean dfs (+/- SE) was found as 11.53 +/- 2.16 and mean DMFS (+/- SE) was 1.90 +/- 0.56 in control group. For the determination of Streptococcus mutans (SM), Lactobacilli (LB) and Buffer capacity (BC), salivary tests of Dentocult SM (Vivacult SM Vivadent-Liechtenstein), Dentocult LB (Vivacult LB-Vivadent-Liechtenstein) and Dentobuff (Vivacult BC-Vivadent-Liechtenstein) were applied to both groups. Our findings were evaluated statistically and compared by the Mann Whitney Confidence Test. The amount of Streptococcus mutans, Lactobacilli and the level of buffering capacity in the children with esophageal burns showed a high caries risk. Positive correlations were found between SM and LB, SM and dfs, LB and dfs levels and DMFs and duration of stricture treatment (p < 0.05). However, negative correlations were found between BC and DMFs, DMFs and tooth brushing habit, dental visit and DMFs (p < 0.05). The mean DMFs, LB and SM levels were lower and BC levels were higher in the control group. Although a significant difference was found between DMFs scores (p < 0.05), no significant difference was found between LB, BC, SM and dfs levels (p > 0.05). It could be concluded that children with esophageal burns have high dental caries risk and for this reason parental counseling about oral hygiene, diet, dental plaque controlling and preventive dental regimens have an importance in these medically compromised children.
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PMID:Salivary Streptococcus mutans, Lactobacilli levels and buffer capacity in children with esophageal burns. 1131 25

Helicobacter pylori infections of the stomach are common worldwide and may cause serious medical problems, ranging from gastritis and its sequelae to gastric carcinoma or lymphoma. Current studies indicate that H. pylori is present in dental plaque, although the number of organisms in individual samples is very low, and these numbers appear to vary from one site to another within the mouth. The presence of this organism in plaque may be intermittent, perhaps occurring as the result of gastroesophageal reflux. It is still unclear if the low numbers of H. pylori present in the mouths of most patients would be sufficient to serve as a source of infection or reinfection for gastric conditions. Whether dental plaque is a significant source for reinfection of the gastric mucosa among patients with fair to poor oral hygiene remains to be confirmed. It has been suggested that attempting to improve oral hygiene through standard periodontal procedures would be prudent as an ancillary measure to conventional ulcer therapy, especially in patients whose gastric infections have proven recalcitrant. H. pylori may also be a cofactor in the recurrence of aphthous ulceration, especially in patients sensitized through gastric colonization and mucosal attachment.
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PMID:Dental implications of Helicobacter pylori. 1232 5

A 43-year-old white man presented with an 8-month history of redness and swelling on the back of the neck. He also noted a decrease in range of motion of his upper body. There was no improvement with a 4-week course of topical corticosteroids. Review of systems was negative for polydipsia, polyuria, polyphagia, and bone pain. His medical history included depression, gastroesophageal reflux disease, and microdiscectomy. His medications included sertraline and omeprazole. Physical examination revealed a 20-cm erythematous, indurated plaque on the posterior part of the upper back and neck (Figure 1). A lack of skin wrinkling was noted with lateral pressure. Biopsy revealed a periadnexal and mild interface dermatitis with an increase in connective tissue mucin as demonstrated with colloidal iron (Figures 2A and 2B). Serum protein electrophoresis, hemoglobin A1C, and antinuclear antibody titer were within normal limits. A diagnosis of tumid lupus erythematosus mimicking scleredema was made. Hydroxychloroquine therapy was started at a dose of 200 mg and, at 2 months' follow-up, the patient's symptoms and appearance were improved.
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PMID:Tumid lupus erythematosus: an unusual scleredema-like presentation. 1660 43

Helicobacter pylori (H. pylori) is one of the frequently encountered micro-organisms in the aerodigestive tract. Although infections caused by H. pylori are this common, the exact mode of transmission has not been fully understood yet. Oral-oral, fecal-oral and gastrointestinal-oral routes are the possible modes of transmission. This infection is usually acquired in childhood and may persist for the whole life of the patient. However, about 80% of the infected humans are asymptomatic. Human stomach was considered to be the only reservoir of H. pylori until bacteria were discovered in human dental plaque, in oral lesions, in saliva, in tonsil and adenoid tissue. It is suggested that H. pylori enters the nasopharyngeal cavity by gastroesophageal reflux and colonize in the dental plaques, adenoid tissues and tonsils. From these localizations, the bacteria ascend to the middle ear and to the paranasal sinuses directly or by the reflux again and may trigger some diseases, including otitis, sinusitis, phyrangitis, laryngitis and glossitis. But still, the exact mechanism remains unclear.
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PMID:Role of Helicobacter pylori in pathogenesis of upper respiratory system diseases. 1894 85

Two aspiration syndromes have been identified: Aspiration pneumonia is infectious caused by micro-aspiration of oral bacteria secondary to neurogenic dysphagia or sedation. Infectious bacteria may also be aspirated from the stomach. Aspiration pneumonitis classically follows large bolus aspiration of food, acid, or digestive enzymes and is initially noninfectious. Large bolus gastric aspiration events may have an acute/dramatic onset. This article discusses (1) prevention of recurrent aspiration events caused by 2 common motility disorders: neurogenic dysphagia and gastro esophageal reflux; (2) mechanical source control (debridement/drainage) of sites that may harbor large collections of bacteria protected from antibiotics in biofilm including dental plaque, coated tongue, and chronic sinusitis.
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PMID:Preventing aspiration in the nursing home: the role of biofilm and data from the ICU. 2012 17


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