The Tohoku journal of experimental medicine
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Tohoku J. Exp. Med. · Mar 2015
Late-onset glucocorticoid-responsive circulatory collapse in preterm infants: clinical characteristics of 14 patients.
Preterm infants may develop acute systemic hypotension that responds to glucocorticoid therapy, but not to volume loading or vasopressors, during the postnatal period. This condition is termed late-onset circulatory collapse (LCC) that develops a few weeks after birth in relatively stable infants. LCC may cause periventricular leukomalacia, periventricular necrosis in the white matter. ⋯ There was no evidence of periventricular leukomalacia in any of the infants. None of the infants developed adrenal insufficiency during the follow-up period. During the acute stage of LCC, the main priority is the early initiation of glucocorticoid therapy.
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Tohoku J. Exp. Med. · Mar 2015
Randomized Controlled TrialEsomeprazole inhibits the pentagastrin-stimulated secretion of gastric acid in healthy Japanese volunteers.
Gastroesophageal reflux disease (GERD) is a common disease, in which the reflux of gastric acid causes mucosal damage of the esophagus and/or troublesome symptoms. Esomeprazole, a proton pump inhibitor, has been used for treatment of GERD in Japan since 2011; namely, only little is known about its effect on gastric acid secretion in Japanese. We, therefore, assessed the relationship between dose and timing of esomeprazole administration and gastric acid inhibition in 11 healthy male Japanese volunteers by directly examining gastric acid secretion capacity. ⋯ At trough states, esomeprazole 20 mg b.i.d. showed significantly higher gastric acid inhibition (99.6%, IQR 99.0-100%) than did 20 mg q.d. (84.2%, IQR 76.4-88.8%, P = 0.002) or 10 mg q.d. (64.9%, IQR 59.1-76.7%, P = 0.001). Thus, esomeprazole 20 mg b.i.d. was sufficient to inhibit > 99% gastric acid secretion in healthy subjects. We propose that esomeprazole 20 mg b.i.d. is effective for treating Japanese patients with refractory GERD who require long-lasting gastric acid inhibition.