Impaired Accommodation a Target for Functional Dyspepsia Therapy
Impaired Accommodation a Target for Functional Dyspepsia Therapy
Several important pathophysiological mechanisms have been identified in functional dyspepsia, however a complete understanding of these mechanisms and beneficial therapeutic strategies are still lacking. Based on the currently available literature we aimed at providing a critical view on one of these pathophysiological mechanisms, impaired accommodation.
Although impaired gastric accommodation is identified as a major pathophysiological mechanism, the clinical evidence supporting its role as an important therapeutic target is currently still lacking. Treatment with fundic relaxant drugs has shown conflicting results and has been rather disappointing in general.
These negative findings could be explained by the fact that impaired fundic accommodation is part of a more complex disorder involving other regions of the proximal gut or by the increasing insight that central mechanisms may play an important role. Future studies of impaired accommodation should take these considerations into account.
Functional dyspepsia (FD) is a common disorder characterized by persistent or recurrent pain or discomfort centered in the upper abdomen without evidence of organic disease likely to explain the symptoms. A broad variety of symptoms such as fullness, bloating, early satiety, epigastric pain, nausea, weight loss, belching and vomiting have been reported by patients with FD. Although symptoms can occur at any time, patients often relate the onset or aggravation of their symptoms to meal intake.
Several pathophysiological mechanisms underlying FD such as delayed gastric emptying, abnormal antroduodenal motility, altered sensitivity to duodenal lipid or acid exposure, visceral hypersensitivity and impaired fundic accommodation have been identified. However, the current knowledge of these pathophysiological mechanisms has not led to a complete understanding of FD. Furthermore, attempts to develop therapeutic strategies based on this knowledge have thus far not banned dyspepsia from our midst.
Together with visceral hypersensitivity and delayed gastric emptying, impaired accommodation is the most frequently observed pathophysiological mechanism in patients with FD. All three mechanisms have independently been reported in approximately 40% of the functional dyspeptic patients. In this paper we aim at providing a critical view of the current knowledge regarding one of these pathophysiological mechanisms involved in FD, namely impaired fundic accommodation and its potential as a therapeutic target in the treatment of FD.
Several important pathophysiological mechanisms have been identified in functional dyspepsia, however a complete understanding of these mechanisms and beneficial therapeutic strategies are still lacking. Based on the currently available literature we aimed at providing a critical view on one of these pathophysiological mechanisms, impaired accommodation.
Although impaired gastric accommodation is identified as a major pathophysiological mechanism, the clinical evidence supporting its role as an important therapeutic target is currently still lacking. Treatment with fundic relaxant drugs has shown conflicting results and has been rather disappointing in general.
These negative findings could be explained by the fact that impaired fundic accommodation is part of a more complex disorder involving other regions of the proximal gut or by the increasing insight that central mechanisms may play an important role. Future studies of impaired accommodation should take these considerations into account.
Functional dyspepsia (FD) is a common disorder characterized by persistent or recurrent pain or discomfort centered in the upper abdomen without evidence of organic disease likely to explain the symptoms. A broad variety of symptoms such as fullness, bloating, early satiety, epigastric pain, nausea, weight loss, belching and vomiting have been reported by patients with FD. Although symptoms can occur at any time, patients often relate the onset or aggravation of their symptoms to meal intake.
Several pathophysiological mechanisms underlying FD such as delayed gastric emptying, abnormal antroduodenal motility, altered sensitivity to duodenal lipid or acid exposure, visceral hypersensitivity and impaired fundic accommodation have been identified. However, the current knowledge of these pathophysiological mechanisms has not led to a complete understanding of FD. Furthermore, attempts to develop therapeutic strategies based on this knowledge have thus far not banned dyspepsia from our midst.
Together with visceral hypersensitivity and delayed gastric emptying, impaired accommodation is the most frequently observed pathophysiological mechanism in patients with FD. All three mechanisms have independently been reported in approximately 40% of the functional dyspeptic patients. In this paper we aim at providing a critical view of the current knowledge regarding one of these pathophysiological mechanisms involved in FD, namely impaired fundic accommodation and its potential as a therapeutic target in the treatment of FD.
