Viral gastroparesis: a subgroup of idiopathic gastroparesis--clinical characteristics and long-term outcomes.

OBJECTIVES: Viral gastroparesis has been regarded as a subgroup of idiopathic gastroparesis. METHODS: We have reviewed the medical records of 143 patients diagnosed as having gastroparesis. Fifty-two patients were regarded as idiopathic in origin, of which 12 were identified as consistent with a postviral etiology. Their follow-up and current status were assessed by interview. Available for interview were 32 patients: 11 from the viral group and 21 from idiopathic group. RESULTS: All "viral gastroparesis" patients reported gradual improvement of their symptoms, no hospitalizations during the previous 6 months, stable weight, were not disabled, and remained professionally active. In comparison, 21 "idiopathic" patients had an indolent, slowly progressive clinical presentation. The idiopathic group had a significantly longer duration of illness (p < 0.05) with greater symptom score of abdominal pain, early satiety, and anorexia, and overall worse quality of life (p < 0.05). CONCLUSIONS: A viral etiology should be considered in gastroparesis patients when their illness is characterized by an acute onset, initial severe illness and slow resolution toward a satisfactory quality of life. Idiopathic gastroparesis is a more slowly progressive illness, and patients remain significantly more symptomatic for a longer period of time.

Esophagoprotective potential of cisapride. An additional benefit for gastroesophageal reflux disease.

Cisapride is a novel prokinetic agent that releases acetylcholine at the level of the myenteric plexus. Acetylcholine also plays a role in the secretory function of salivary glands evoked by intraesophagal mechanical and chemical stimulation, mediated through the esophagosalivary reflex. The impact, however, of cisapride on salivary protective components mediated by esophagosalivary reflex remains unknown. Therefore, we have studied salivary pH, bicarbonate, nonbicarbonate, glycoconjugate, protein, EGF, TGF-alpha, and PGE2 before and after the administration of cisapride. The study was conducted in 20 asymptomatic volunteers (9 women and 11 men, mean age 36, range 26-52). Salivary secretions were collected under basal conditions and during masticatory, mechanical, and chemical stimulation before and after four days of cisapride administration (10 or 20 mg four times a day). Cisapride administration resulted in a 45% increase in salivary volume during the basal condition (P < 0.01), a 32% increase during mastication (P < 0.05), a 53% increase during mechanical (P < 0.05), and a 51% increase during chemical (P < 0.01) stimulation. Cisapride administration resulted also in a significant increase in salivary protein output (P < 0.05), salivary bicarbonate (P < 0.05), and nonbicarbonate buffers (P < 0.05), and salivary EGF (P < 0.05). Salivary glycoconjugate significantly increased only during mechanical stimulation with the catheter and at the end of the esophageal perfusion procedure (P < 0.05). Although a similar trend was also recorded during the analysis of salivary PGE2, this difference did not reach statistical significance. Salivary pH and TGF-alpha before and after cisapride administration remained unchanged. The stimulatory impact of cisapride on salivary volume and inorganic (bicarbonate and nonbicarbonate buffers) and organic (protein, glycoconjugate, and EGF) protective components would benefit patients with GERD and would also be potential therapy for xerostomia.