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Pathophysiology

The initial studies of esophageal acid clearance in patients with reflux esophagitis suggested that acid clearance time was almost invariably longer in the patients than in normal subjects.

Subsequent studies, however, demonstrated that substantial overlap in acid clearance times occurred between patients and controls.
Thus, some patients with reflux symptoms exhibit normal esophageal acid clearance times whereas in other patients acid clearance is abnormally long.
What accounts for delayed acid clearance in some of the patients?
One obvious candidate as a cause for delayed esophageal clearance is an abnormal esophageal motor function.
Abnormal esophageal motility is generally associated with prolonged acid clearance.

Not all individuals with delayed acid clearance, however, have overt peristaltic dysfunction.
Regrettably, the subject of esophageal-body motor function in patients with reflux esophagitis has received negligible attention.
Earlier reports based on manometry with non-infused catheters suggested that the majority of patients manifest disordered esophageal motor activity after deglutition.
The predominant motor abnormality appeared to be an increased incidence of nonperistaltic contractions, often repetitive, in the distal esophagus.
These contractions were believed to cause ineffective esophageal emptying in recumbent subjects.
Subsequent studies using infused-catheter manometry suggest that many, if not the majority, of patients with reflux esophagitis, have overtly normal primary peristalsis.
A recent study suggests that that patients with reflux esophagitis and controls have a similar high frequency of swallowing in the awake state and low frequency while asleep .

Additional data are needed, however, about swallowing frequency and incidence of intact primary peristaltic sequences in the esophagitis patients.
Even less is known about secondary peristalsis in patients with reflux esophagitis.
In patients with reflux esophagitis accompanied by esophageal-body motor dysfunction, the motor abnormality may either antedate the reflux esophagitis or be caused by the esophagitis.
Again, the choice need not be "either-or." We have observed both types of circumstances.
In some patients, esophageal motor abnormalities improve or disappear after healing of reflux esophagitis.

This sequence argues that the motor abnormality was secondary.
In other patients, esophageal motor dysfunction persists after complete resolution of reflux esophagitis.
This finding suggests that the motor dysfunction either preceded reflux esophagitis or the esophagitis was sufficiently severe to cause permanent damage to esophageal muscle or nerves.
Regardless of whether esophageal motor dysfunction is primary or secondary, this feature, once present, may create a vicious cycle whereby esophageal motor dysfunction leads to increasingly severe reflux esophagitis that in turn further impairs esophageal motor function.

A second factor that could cause delayed acid clearance is abnormal salivation.
Diminished salivation would decrease: (a) swallowing frequency and (b) the volume of saliva available to dilute, neutralize, and washout esophageal acid.
Another possible abnormality of saliva is a decreased capacity for acid neutralization.
Although salivation is known to be defective in certain disease entities such as Sjogren's syndrome, salivary flow and content remain to be comprehensively analyzed in patients with reflux esophagitis.
Regardless of the underlying cause, delayed esophageal clearance promotes esophageal exposure to the refluxed material. Some patients with reflux esophagitis may have the same frequency of GE reflux as healthy subjects, but sustain an excessive esophageal exposure to acid because of an abnormality in esophageal acid clearance.