21 January 2021: Articles
A 61-Year-Old Woman with Chronic Iron-Deficiency Anemia Due to a Cameron Lesion and a Response to Oral Application of Combined Poloxamer 407 with Hyaluronic Acid and Chondroitin Sulfate Following Single Treatment with Pantoprazole: A Case Report
Challenging differential diagnosis, Unusual setting of medical care, Rare disease
Iliyan Emilov Iliev D* , Almute Loidl BDOI: 10.12659/AJCR.928021
Am J Case Rep 2021; 22:e928021
Table 2. Pathogeneses of Cameron lesions. Each factor is accompanied by a short explanation of its significance and role in the development of Cameron lesions.
| Commentary | |
|---|---|
| Presence of a diaphragmatic hernia (axial or paraesophageal) | This is the most important factor. There are no Cameron lesions without a hiatal hernia. Larger hiatal hernias are associated with a greater risk of their occurrence (10–20% in axial hiatal hernias ≥5 cm) []4 |
| Extraluminal rubbing of the upper stomach and lower esophagus against the diaphragmatic hiatus | An important role is played by the permanent extraluminal rubbing of the upper stomach and lower esophagus against the diaphragmatic hiatus (the repeated ascending and descending movement associated with breathing and swallowing) and the intraluminal friction of the mucosal folds within the hiatal hernia against each other and at the level of the distal hernial ring. The gradient between the positive intraabdominal and negative intrathoracic pressure probably provokes an additional sliding movement of the gastro-esophageal junction between both cavities, resulting in mucosal distress with edema, petechiae, and ulcers. This effect is stronger in paraesophageal hiatal hernias |
| Ratio between hernial opening and hernial size | From the physical point of view, the ratio between the hernial opening () and the hernial size appears to be most important. A significant trauma should be expected in smaller hiatal hernias and a greater friction in larger hernias []. The configuration of a hiatal hernia may change with time, which is why erosions or ulcers may appear at different locations []5 |
| Dual-hit hypothesis | Multiple studies showed that the mechanical trauma from outside is insufficient to cause mucosal defects. Cameron lesions occur only when the external compression on the gastric wall is combined with an aggressive influence from inside. According to the so-called ‘dual-hit hypothesis’ additional intraluminal and mucosal factors also play a substantial role: gastric acid, gastro-esophageal reflux, and the oral intake of NSAID for 3 days/week within a month. One study demonstrated that in large hiatal hernias, intraluminal lesions occur only when the gastro-esophageal flap valve is intact. This valve counteracts the reflux and affects the role of gastric acid [,]7 |
| Helicobacter pylori | There is no clear correlation between HP and Cameron lesions. Only 1/3 of all patients with Cameron lesions are HP-positive [–]9 |
| Gastric ischemia and stasis | Additional independent factors for the occurrence of Cameron lesions could be the so-called gastric ‘ischemia’ and ‘stasis’. In some patients, the diaphragmatic hiatus could be narrow enough to cause an intermittent venous stasis in the gastric wall when the diaphragm contracts (e.g., sneezing, coughing, choking). The pathogenesis of Cameron lesions is multifactorial and probably comprises patient’s genotype and phenotype, their comorbidities, and the oral intake of drugs. Patients with Cameron lesions often take iron supplements because the gastric stasis tablets and secretions can remain longer in the herniated stomach and cause pressure erosions [,]12 |
| NSAID – Non-steroidal anti-inflammatory drugs; HP – . | |