Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154059 (Esophagus)
 2,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drinks that contain phosphoric acid have been shown to have erosive effects and cola drinks are strongly acidic (pH 2.5). Gingivitis may be caused by dietary acids. Therefore, this study analyses the interaction of Coca Cola consumption and oral mucosal damage. Thirty rats were divided into three groups of 10. The animals received saline (pH 7.0) or HCl acid buffered to pH 2.6 or Coca Cola (pH 2.6) per os with 24-h free access to these solutions. A biopsy was taken from the front of the gingiva and the tongue. Histopathological analysis showed no specific lesion and there were no differences among saline, Coca Cola and HCl groups. Flow cytometric analysis was used to assess proliferative activity. In the HCl acid and Coca Cola groups, cell cycle analysis showed that the effects of Coca Cola and HCl acid in inducing oral mucosal damage are similar. In both Coca Cola [G0/G1, 70.38+/-7.9; S, 28.06+/-10.13; G2/M, 1.62+/-2.80; proliferative index (PI), 28.68+/-7.981 and HCI (G0/G1, 67.7+/-18.9; S, 27.8+/-17.5; G2/M, 4.4+/-3.8; PI, 30.9+/-20.98), the rat cell population G0/G1 and G2/M phases were found to be low (p < 0.05) and the cell population S and PI phases were found to be significantly elevated compared with the control group (p < 0.05) (G0/G1, 86.92+/-8.69; S, 9.8+/-1.21; G2/M, 3.25+/-2.87; P1, 13.2+/-8.7). This result was reflected in the proliferative index, which is used as a measure of the regeneration index. The data show that Coca Cola and HCl acid have similar proliferative and regenerative effects on oral mucosa, and it is possible that their regenerative effects are caused as a result of an irritant effect.
Dis Esophagus 2000
PMID:The effect of cola consumption on oral mucosa in rats. 1100 35

Dilated intercellular spaces (DIS) within esophageal epithelium (EE) is a histopathologic feature of non-erosive reflux disease and early lesion in acid-damaged rabbit EE associated with increased paracellular permeability. Its cause remains unknown, but the lesion's morphology suggests a significant fluid shift into the intercellular spaces (ICS). Since water follows osmotic forces and consequently ion movements, we explored the role of active (ion) transport and ion gradients in its pathogenesis. This was done by quantifying the effect of inhibited active transport and altered ion gradients on electrical resistance (R(T)) and ICS diameter in acid-exposed Ussing-chambered rabbit EE. Compared with normal Ringer, pH 7.5, 30 minutes of luminal HCl (100 mmol/L), pH 1.1, increased permeability (R(T): +5 +/- 4% vs-52 +/- 4%) and ICS diameter (0.25 +/- 0.01 microm vs 0.42 +/- 0.02 microm), but had no effect on cell morphology or diameter. Ouabain pretreatment significantly reduced active transport but had no effect on the acid-induced changes. However, negating the chloride gradient created by luminal HCl either by adding choline chloride, 100 mmol/L, serosally or by replacing luminal HCl, pH 1.1, with luminal H(2)SO(4), pH 1.1, prevented the development of DIS while maintaining the increase in permeability. DIS was also prevented in the presence of a 100 mmol/L (choline) chloride gradient by luminal exposure at neutral pH. DIS in HCl-damaged EE is caused by an H(+)-induced increase in epithelial permeability; this enables Cl(-) to diffuse along its gradient into the ICS, creating an osmotic force for water movement into and (hydrostatic) dilation of the ICS.
Dis Esophagus 2008
PMID:Physicochemical basis for dilated intercellular spaces in non-erosive acid-damaged rabbit esophageal epithelium. 1852 36

The aim of this study was to determine the necessity of endoscopy in cases in which a corrosive substance was ingested and to find a practical way to avoid unnecessary endoscopies for similar cases in the future. The clinical records of 458 hospitalized cases with clinical histories of corrosive substance ingestion between January 2007 and December 2013 were retrospectively reviewed. The demographics of the cases, the ingested substances, and the rigid endoscopy findings were evaluated. The three most commonly ingested corrosive agents were household bleach (22.9%), household degreaser (15.9%), and drain cleaner (13.1%). Rigid esophagoscopy was performed in 367 of the 458 cases. Corrosive agents were grouped according to their purpose of household use; eight groups were created. The degree of corrosive injury observed in the different groups was compared with the degree of injury caused by household bleach. Among the corrosive agent groups, dishwashing machine products (Gr.1), laundry products (Gr.2), liquid cleaners (Gr.3), and household bleach (Gr.4) did not cause high-grade injuries. The resulting injuries and esophagoscopy results among the above groups, whether symptomatic or not, did not differ from one another. Corrosive agents such as drain cleaner (Gr.6), household degreaser (Gr.7), and several other acidic products (Gr.8) caused high-grade injuries in the esophagus; however, lime remover/HCl (Gr.5) did not. Thus, hospitalization and rigid endoscopy seem unnecessary to assess esophageal injury in most cases, if the ingested corrosive agent fits into group 1, 2, 3, or 4 and if the patient can be easily fed. Esophagoscopy is useful to shorten the hospitalization times in cases where strong corrosive agents were ingested, such as those in groups 5, 6, 7, and 8.
Dis Esophagus 2017 Feb 01
PMID:Is rigid endoscopy necessary with childhood corrosive ingestion? a retrospective comparative analysis of 458 cases. 2682 61