Extraordinary cause of acute gastric dilatation and hepatic portal venous gas: Chronic use of synthetic cannabinoid.

Addiction to synthetic cannabinoids (SCs) is a growing social and health problem worldwide. Chronic use of SCs may cause adverse effects in the gastrointestinal system. We describe a very rare case of acute gastric dilatation (AGD) and hepatic portal venous gas (HPVG), with findings of acute abdomen resulting from chronic use of a SC, Bonzai. AGD and HPVG were detected by computerized tomography examination. Patchy mucosal ischemia was seen in endoscopic examination. Despite the findings of an acute abdomen, a non-surgical approach with nasogastric decompression, antibiotic therapy, and close radiologic and endoscopic follow-up was preferred in the presented case. Clinical and radiologic findings decreased dramatically on the first day, and endoscopic findings gradually disappeared over 7 d. In conclusion, this case shows that chronic use of a SC may cause AGD and accompanying HPVG, which can be managed non-surgically despite the findings of acute abdomen.

Ecabet sodium induces neuronal nitric oxide synthase-derived nitric oxide synthesis and gastric adaptive relaxation in the human stomach.

BACKGROUND: Gastric adaptive relaxation (GAR) is a major factor of functional dyspepsia (FD). Nitric oxide (NO) could be the key molecule responsible for GAR. We previously reported that the physiological gastric reservoir ability can be evaluated by measuring the cross-sectional area of the proximal stomach by abdominal ultrasonography (US). Ecabet sodium (ES), a gastro-protective antiulcer agent, has been shown to improve symptoms in FD patients. We examined the effects of ES on GAR in humans and on NO synthesis in vitro. METHODS: GAR was measured by US in 14 subjects, 8 of whom had a pressure sensor inserted into their stomach, after treatment with ES, placebo, or no drugs. NO was measured in SH-SY 5Y cells using a fluorescent indicator. Neuronal, endothelial and inducible NO synthase (nNOS, eNOS and iNOS, respectively) expressions were examined in SH-SY 5Y cells by Western blotting. RESULTS: Compared to placebo, ES induced significantly greater dilatation of the proximal stomach after the subjects drank 300-400 ml water (P < 0.05). After ES intake, the intragastric pressure did not change significantly, but it tended to be lower (n = 8; P = 0.15). ES increased NO production and nNOS expression, but not iNOS or eNOS expression, in SH-SY 5Y cells in vitro. Pretreatment with non-selective NO synthase (NOS) inhibitor, but not with iNOS-selective inhibitor, reduced NO production by ES. CONCLUSION: ES may promote GAR in humans through nNOS-related NO; therefore, it may be useful for patients with FD.

Poor tolerability of high dose ascorbic acid in a population of genetically confirmed adult Charcot-Marie-Tooth 1A patients.

BACKGROUND: Preclinical studies have suggested that ascorbic acid (AA) treatment in a mouse model of Charcot-Marie-Tooth type 1A (CMT1A) improves motor function and prolongs lifespan. AIMS: I sought to determine the safety and tolerability of AA in adult patients with CMT1A. METHODS: An open-label cohort-controlled 2-year pilot study was used to evaluate the tolerability of 5 g of AA daily. Secondary measurements consisted of clinical and electrophysiological measurements at 0, 12, and 24 months in CMT1A patients. RESULTS: Twelve CMT1A patients received AA and 10 CMT1A patients formed a cohort group followed in identical manner. Five (42%) patients tolerated this dose of AA for the entire 2-year span, with six patients (50%) developing intolerable gastrointestinal side effects. No significant differences in clinical, disability, or electrophysiological measurements occurred between baseline and final follow-up in patients receiving AA when compared with cohorts. CONCLUSIONS: High dose AA was not well tolerated in all adult CMT1A patients who may be susceptible to gastrointestinal adverse effects of AA. Studies with greater powers to detect efficacy will be required to test the validity of AA as a therapy in CMT1A patients. Doses lower than 5 g of AA daily may be required for maintenance of tolerability in the CMT1A population.

Acute gastric dilatation complicating the use of mydriatics in a preterm newborn.

A 2-month-old girl who had been born at 27-weeks' gestation was admitted for her screening examination for retinopathy of prematurity and given two drops each of cyclopentolate 0.5% and phenylephrine 2.5%. Approximately 2 h after completion of the examination, the infant had episodes of apnoea and vomiting. She was noted to be distended, and an abdominal radiograph demonstrated acute gastric dilatation. Apnoea, vomiting and distension resolved after 18 h and a repeat abdominal radiograph demonstrated resolution of the gastric dilatation.

Role of central oxytocin in the inhibition by endotoxin of distension-stimulated gastric acid secretion.

The gastric acid hyposecretory state associated with endotoxemia is mediated by a nervous reflex involving the central nervous system. The aim of the present study was to analyse the central effects of different peptides on distension-stimulated gastric acid secretion and the endogenous role of such peptides on the hyposecretory effects of endotoxin. The effect of an intracisternal (i.c.) administration of oxytocin, vasopressin, corticotropin releasing factor (CRF), bombesin, somatostatin and the opioid receptor agonist BW443C or an intravenous (i.v.) injection of a small dose of endotoxin on distension-stimulated gastric acid secretion was studied in the continuously perfused stomach of anaesthetised rats. In some animals, specific receptor antagonists for oxytocin (Compound VI [d(CH2)5, Tyr(Me)2, Thr4, Tyr-NH2(9)]-OVT, 0.01-1 microg/rat), vasopressin (des-Gly9-[beta-Mercapto-beta,beta-cyclopentamethylene-propiony l1, O-Et-Tyr2, Val4, Arg8]-VP, 20 microg/rat), CRF (alpha-helical CRF [9-41], 50 microg/rat) or bombesin (D-Phe12-Bombesin, 20 microg/rat) were administered i.c. before endotoxin. Distension-stimulated acid secretion was significantly inhibited by central oxytocin (0.2, 2 or 4 nmol/rat, 45+/-16%, 69+/-10% and 79+/-5% reduction, respectively), CRF (0.5, 1 or 2 nmol/rat, 52.2+/-15.6%, 74.3+/-9.1% and 93.2+/-1.6% reduction, respectively) and bombesin (2 nmol/rat, 79.1+/-5.8% reduction). The hyposecretory effect induced by endotoxin (5 microg/kg, 60.2+/-2.3% reduction) was reversed in a dose-dependent manner by pretreatment with the oxytocin receptor antagonist (0.01, 0.1 and 1 microg/rat, 65.2+/-14.4%, 88.0+/-22.5% and 112.4+/-25.2% of control response, respectively) while the vasopressin (20 microg/rat), CRF (50 microg/rat) or bombesin (20 microg/rat) receptor antagonists had no effect. The present results support a role for the endogenous release and action in the central nervous system of oxytocin in the inhibitory effect of endotoxin on gastric acid secretion.

Role of delayed gastric emptying in the pathogenesis of cysteamine-induced duodenal ulcer in the rat.

Cysteamine is a potent duodenal ulcerogen in rats. It has been demonstrated to inhibit gastric empyting, whose role in ulcer formation is unknown. In the present study the effect of cysteamine on gastric motility and emptying rate in rats was studied by direct fluoroscopic observation. The delayed gastric empyting was due to a pronounced relaxation of the stomach and a complete blocking of gastric peristalsis. These effects have their maximum within the first 4 h after administration of cysteamine. Thereafter peristalsis and gastric empyting slowly return. In controls contrast medium administered intragastrically was completely discharged from the stomach within 30 min. After cysteamine the first small amounts of contrast medium were discharged into the duodenum after 4 h, and contrast medium remained in the stomach for at least 12 h after administration. The size of the stomach reached a maximum after 3 h and approached normal values again after 12 h. Because of complete gastric retention the acid gastric secretions provoked by cysteamine probably accumulate in the stomach during the first 4 h after cysteamine administration, and because of the absence of peristalsis they are not mixed with gastric contents. After 4 h this pool of undiluted gastric secretions gradually is emptied into the duodenum, where the mucosal resistance is reduced by inhibition of the secretory activity of Brunner's glands, and ulceration rapidly develops. The time relationship is supported by histopathologic findings and measurements of gastric acid secretions after cysteamine. Vagotomy augmented the inhibitory effect of cysteamine on gastric motility. The relaxation was even more pronounced, and contrast medium was not discharged from the stomach within 24 h. In these rats cysteamine induced ulcerations in the stomach.

A peculiar toxicity manifested by platinum(II)amines in rats: gastric distension after intraperitoneal administration.

Metoclopramide i.p. reduces the gastric distension consistently seen in rats given cisplatin i.p. at effective immunosuppressant doses (6 mg/kg). Many other immunosuppressant/oncolytic platinum amines also engendered gastric distension but certain dimers and 1,2-cyclohexanediaminoplatinum (II) compounds did not. This phenomenon appears to be due to paralysis of gastric emptying (without appetite suppression).

cis-Platinum(II) amine complexes: some structure-activity relationships for immunosuppressive, nephrotoxic and gastrointestinal (side) effects in rats.

A local graft-versus-host reaction was established to elicit lymphoid hypertrophy in F1 hybrid PVG X Lew rats. cis-Di(amine)platinum(II) complexes were given i.p. on days 1--4 in divided doses. Overnight proteinuria and measurements of renal hypertrophy on day 5 reflected the nephrotoxicity of the test compound. Stomach weights indicated the peculiar effect on pyloric stasis causing gastric distension. Weights of thymus' and spleens together with lymph-nodes showed the lymphodepressant/immunosuppressive properties of platinum compounds. Structure activity relationships for immunosuppressant, nephrotoxic and gastric-distending activities were investigated with: (a) cis-diaquo, cis-hydroxyaquo- and cis-dichlorodi(amine)platinum(II) complexes; (b) dinuclear mu-dihydroxo-bridged di(amine)platinum(II) complexes; (c) carboxylatodi(amine)platinum(II) complexes. Nephrotoxicity was minimised (with retention of immunosuppressant activity) by (a) the use of certain N-substituted amines e.g. Dach, Me4en; (b) co-administration of selected adjuncts e.g. citrate, salicylate; (c) auxiliary treatment with a penicillin mixture (Triplopen). In vitro effects of some platinum(II) compounds on isolated rat kidney tubules were also investigated.