Reductions in symptom distress reported by patients with moderately severe, nonerosive gastroesophageal reflux disease treated with rabeprazole.

Gastroesophageal reflux disease (GERD) is characterized by heartburn and related symptoms that are distressing to patients and interfere with everyday functioning and well-being. A measure of symptom distress, the GERD Symptom Assessment Scale (GSAS), was included in two randomized, placebo-controlled trials of rabeprazole among patients with nonerosive GERD. The age (mean +/- SD) of the 223 patients was 43.5 +/- 11.9 years, and most were female (67%) and Caucasian (78%). Significantly greater reductions in symptom distress were observed among patients receiving rabeprazole 20 mg daily for 4 weeks relative to those receiving placebo (-0.62 vs -0.36, P < 0.0001). The magnitude of this treatment difference was comparable to the differences observed between levels of overall symptom improvement on the patient global rating (0.2 and 0.3 points; P < 0.0001). In conclusion, reducing symptom distress is an important goal of therapeutic interventions for GERD. Rabeprazole significantly reduced the distress associated with a broad range of GERD symptoms, and the magnitude of this effect was meaningful to patients.

Not a usual suspect; rabeprazole therapy presenting as a severe neuropsychiatric illness: case report.

We report the case of a patient who, as a result of exposure to the proton pump inhibitor rabeprazole, developed a severe and disabling admixture of neuropsychiatric symptoms. Because of its widely appreciated placebo-like side effect profile, rabeprazole was never suspected as being the cause of his symptoms. Instead, a somatoform spectrum disorder was assigned based on the patient's atypical symptom presentation, progressive course, subjective psychological distress, intemperate consumption of healthcare resources over a relatively brief period of time and lack of any medical explanation for his symptoms at that time, despite exhaustive laboratory and radiologic work-ups. This case report reinforces the notion that even a medication such as rabeprazole, with an established safety and tolerability profile, may be associated with side effects severe enough to mimic disabling neuropsychiatric illness.

H(+)-dependent ATPase and K+ channel activities in the rat thyroid cell strain FRTL-5.

Using the fluorescent indicators 2',7'-bis(2-carboxyethyl)-5'-(6')-carboxyfluorescein and Oxonol V to monitor intracellular pH (pHi) and cell membrane potential respectively, we have investigated the involvement of H(+)-dependent ATPase and H(+)-dependent K+ channels in the recovery of the rat thyroid cell strain FRTL-5 from experimentally induced cytosolic acidification and membrane hyperpolarization events. Following exposure of cells to the weak acid sodium butyrate (24 mmol/l) under bicarbonate-free incubation conditions, cytoplasmic acidification was maximal after 3 min, attaining a pHi of 6.42. The subsequent recovery of pHi was unimpaired by the absence of extracellular K+, but was reduced in the presence of the Na+ antagonist amiloride (1 mmol/l), recovering by 0.11 +/- 0.003 units, compared with 0.27 +/- 0.02 units under amiloride-free conditions. In the presence of the H(+)-dependent ATPase antagonist N,N'-dicyclohexylcarbodiimide (DCC), the pHi recovery observed in amiloride-containing, K(+)-free buffer was abolished. The recovery of pHi in Na(+)- and K(+)-containing buffer was accompanied by hyperpolarization of the cell membrane, the later stage of which was reduced after blockade of K+ channels with BaCl2, implying a major contribution of transmembrane K+ movement to such events. In contrast to its attenuating effect on pHi recovery, DCC was ineffective in reducing butyrate-dependent membrane hyperpolarization, suggesting that H(+)-dependent ATPase may not be a major contributory factor to this event. However, when K+ channels were blocked by addition of BaCl2, addition of DCC abolished the butyrate-induced membrane depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)