Esophageal white sponge nevus associated with severe dysphagia and odynophagia.
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Biomedical subjects
Publications and source records attributed to R Timmer.
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Barrett's oesophagus is often considered an end stage of gastro-oesophageal reflux disease. In its pathogenesis increased oesophageal acid exposure, disturbed oesophageal motility and decreased oesophageal mucosal sensitivity are thought to be of importance. In this review the role of each of these factors will be discussed and an update of the recent literature will be given.
Hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, is a hereditary disorder leading to easily bleeding telangiectases on skin and mucosal surfaces, and it is associated with the presence of arteriovenous malformations (AVMs) in multiple organ systems. These AVMs may cause serious complications when they are located in the lungs, liver, or brain. The prevalence of AVMs in patients with HHT might be higher than previously estimated. Nowadays, treatment is often possible. In some families, mutations have been shown in the gene encoding for a transforming growth factor receptor, endoglin. Genetic heterogeneity has been demonstrated, suggesting involvement of other transforming growth factor receptors. This might explain the variable clinical expression of the disease. In view of the high prevalence of pulmonary and cerebral AVMs, all patients with HHT should be screened for their presence, and relatives of patients with HHT should be investigated for presence of the disease.
A 49-year-old female with rheumatoid arthritis developed liver cirrhosis after a cumulative dosage of 6 g methotrexate (MTX). There were mild liver enzyme abnormalities, decreased liver synthesis function and possible signs of portal hypertension. After stopping MTX all laboratory abnormalities disappeared except for a mild thrombocytopenia. Risk factors and guidelines for monitoring liver toxicity during MTX treatment in rheumatoid arthritis are discussed.
STUDY OBJECTIVE: The prevalence of esophageal disorders (dysmotility and/or gastroesophageal reflux) in patients with chest pain newly referred to a cardiologic clinic is unknown. The aims of our study were to investigate the prevalence of esophageal abnormalities in these patients and to assess the value of medical history in predicting the origin of the patient's chest pain. DESIGN: We evaluated 28 consecutive patients who were newly referred to the cardiologist because of angina-like chest pain. Patients with evidence of severe myocardial ischemia were excluded. Cardiologic evaluation included medical history, physical examination, ECG, and exercise testing; further cardiologic workup was carried out only when considered necessary. Gastroenterologic evaluation consisted of medical history, esophageal manometry, endoscopy, and 24-h ambulatory monitoring of esophageal pH and pressure. MEASUREMENTS AND RESULTS: In five patients a diagnosis of ischemic coronary artery disease was made. In only two of these five patients, the cardiologic history strongly suggested a cardiac origin of the pain. Twelve patients had a pathologic 24-h pH profile, four of whom also had reflux esophagitis. Ten patients had symptomatic reflux. In only three of these ten patients, the history was judged to be indicative of an esophageal origin of the chest pain. No motility disorders were found. CONCLUSIONS: Thirty-six percent of the patients with chest pain newly referred to a cardiologic out-patient clinic have symptomatic gastroesophageal reflux. Neither cardiologic nor gastroenterologic history data have a high predictive value with respect to the origin of the chest pain.
This case report presents a patient with progressive dysphagia, accompanied by weight loss, in the absence of organic disease. Esophageal motility studies initially failed to reveal a diagnosis. At simultaneous manometry and fluoroscopy, with bread/barium boluses, the diagnosis of esophageal spasm in a relatively weak esophagus was made. All conservative treatment modalities failed. Thoracoscopic myotomy resulted in partial field of symptoms. Finally, an esophagectomy was performed because of sever dysphagia accompanied by persisting weight loss.
BACKGROUND: Nissen fundoplication reduces gastro-oesophageal reflux effectively, but the mechanisms through which this effect is brought about have remained rather obscure. METHODS: In this study the effect of fundoplication on oesophageal acid exposure, oesophageal body motility, and lower oesophageal sphincter pressure (LOSP) was assessed prospectively. Eleven patients were studied before and 3 months after a floppy Nissen fundoplication. A Dent sleeve was used to measure LOSP, and ambulatory pH and pressure monitoring were used to evaluate oesophageal motor function. RESULTS: Gastro-oesophageal reflux was significantly decreased after fundoplication without an increase in LOSP. The motor function of the oesophageal body was not affected by the antireflux procedure. CONCLUSIONS: Nissen fundoplication is an effective antireflux operation, even though the procedure does not increase LOSP, and the motility pattern of the oesophageal body is not affected by the construction of a floppy fundic wrap.
Using conventional manometry and 24-hr ambulatory pressure and pH monitoring, we investigated esophageal motility and the esophageal motor response to reflux in 11 patients with reflux esophagitis Savary-Miller grade III and IV, and an age- and sex-matched group of 11 healthy controls. The patients had a significantly increased esophageal acid exposure. Conventional manometry showed a significantly decreased LES pressure and distal peristaltic amplitude in patients. The 24-hr monitoring yielded a significant decrease in peristaltic contraction duration and peristaltic propagation velocity in the patient group. Distal peristaltic amplitude was not decreased. Analysis of the contractions occurring in the 2-min period after each reflux episode showed a reduced number of contractions during the upright period, caused by a significantly decreased number of peristaltic contractions. During the supine period, there was a trend towards an increased number of contractions. It is concluded that esophageal motor activity and the response to reflux are impaired in patients with high-grade reflux esophagitis. However, the abnormalities found are only minor and are unlikely to play an important role in the pathogenesis of reflux esophagitis.
In this study 24 hour oesophageal pH and pressure monitoring was used to assess oesophageal motility and acid clearance in 27 patients with reflux oesophagitis (Savary-Miller grades I-IV), before and after healing of oesophagitis. After the first 24 hour study patients were treated with omeprazole 40 mg for 8-24 weeks. After endoscopically verified healing and withdrawing omeprazole for four days 24 hour monitoring was repeated. A total of 106,630 pressure events was analysed. No significant differences were found for any of the motility variables, especially the number and the type of contractions, the peristaltic amplitude, duration, and propagation velocity did not show any changes. Separate analysis of motility variables before and after healing in the low and high grade oesophagitis groups yielded similar results. Oesophageal motor response to reflux was investigated by analysis of all contractions occurring in the two minute period after the onset of each reflux episode. Both motor response and oesophageal acid exposure (% time pH < 4, number of reflux episodes) did not change after healing of oesophagitis, thus implying that acid clearance remained unchanged. These results indicate that impaired motility in reflux oesophagitis is either an irreversible consequence of oesophageal inflammation, or a (pre-existent) factor in its pathogenesis.
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Whether the oesophageal motor response to reflux, as recorded over 24 hours, is impaired in patients with reflux oesophagitis was investigated. Twenty three patients with oesophagitis (Savary-Miller grades I-IV) and 23 control subjects matched for age and sex underwent 24 hour ambulatory pH and pressure monitoring. All contractions occurring in the 2 minute period after the onset of each reflux episode were analysed automatically using dedicated computer algorithms. A total of 2085 reflux episodes occurred--1513 in patients and 572 in controls. Oesophageal acid exposure was greater (p < 0.01) in patients than in controls (mean (SEM) % time pH < 4 13.3 (1.7) and 5.3 (0.9)%, respectively). The mean duration of the supine reflux episodes was longer (p < 0.01) in patients (11.2 (2.8) minutes) than in controls (5.1 (1.8) minutes). In the upright period, no significant differences in the motor response to reflux were found. In the supine period, the patients showed a higher number of reflux induced contractions (4.40 (0.61) v 1.62 (0.31), p < 0.01), a higher contraction amplitude (4.55 (0.42) v 2.99 (0.71) kPa, p < 0.02) and longer contractions (1.86 (0.19) v 1.32 (0.29) seconds, p < 0.05). The percentages of peristaltic and simultaneous contractions that occurred in response to supine reflux did not differ between the two groups. In patients with reflux oesophagitis the motor response of the oesophagus to reflux is not impaired. During the supine period the response is even stronger than in healthy controls.
Whereas previous studies have unequivocally shown that esophageal motility is abnormal in patients with severe reflux esophagitis, the results of motility testing in patients with low-grade esophagitis are inconsistent. We studied 27 patients with Savary grade I and II esophagitis and 24 healthy controls matched for age and sex. Both underwent conventional manometry and 24-h ambulatory pH and pressure monitoring. Esophageal acid exposure was greater in patients than controls. The mean lower esophageal sphincter pressure was significantly lower in esophagitis patients [1.46 +/- 0.09 vs. 1.79 +/- 0.11 kPa (10.98 +/- 0.68 vs. 13.46 +/- 0.83 mm Hg)]. The total number of contractions recorded in the 24-h period was not different in the patient group (2168 +/- 108.4 vs. 2033 +/- 130.5), but esophagitis patients had an increased number of nontransmitted contractions (968 +/- 39.4 vs. 773 +/- 50.2, p < 0.01). A tendency toward a decreased prevalence of peristaltic contractions just failed to reach statistical significance (p = 0.07). Both conventional manometry and 24-h monitoring showed no significant difference in peristaltic amplitude between the two groups. Differences in contraction duration (2.02 +/- 0.08 vs. 2.39 +/- 0.12 s, p < 0.01) and velocity of the peristaltic wave (3.65 +/- 0.10 vs. 4.63 +/- 0.13 cm/s, p < 0.01) were only detected by 24-h monitoring. The findings made in this study do not support the concept that impaired esophageal peristalsis is a major factor in the pathogenesis of low-grade esophagitis.
Eosinophilic pneumonia and skin rash developed in a 21-yr-old man while taking sulphasalazine. After discontinuation of the drug and treatment with steroids the pulmonary infiltrates and rash resolved completely. A short review of the literature concerning sulphasalazine-induced lung disease is presented.
The efficacy of subchronic (3 weeks) treatment with the long-acting somatostatin analogue octreotide was studied in four patients with symptomatic benign insulinoma. No clinical or biochemical effect on serum glucose, insulin, C-peptide or glucagon was observed in all four patients despite clearly detectable serum levels of octreotide. The resistance to octreotide therapy in these patients might be explained by the absence of somatostatin analogue receptors on their tumours.