methimazole and Stomach-Ulcer

Topics: Abdominal Pain; Adult; Anti-Inflammatory Agents, Non-Steroidal; Depressive Disorder; Desvenlafaxine Succinate; Drug Synergism; Duloxetine Hydrochloride; Duodenal Ulcer; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Male; Melena; Methimazole; Naproxen; Selective Serotonin Reuptake Inhibitors; Stomach Ulcer

We report successful anesthetic management of a 38-year-old man with thyroid storm using an ultra-short acting beta blocker, landiolol. The patient was admitted to the hospital for severe abdominal pain. An emergency laparotomy was scheduled for perforated gastric ulcer under a condition of uncontrolled thyrotoxicosis. On arriving the operating room, he showed tachycardia of 140 beats x min(-1) and blood pressure of 140/75 mmHg and high fever of 39 degrees C with tremor, sweating and diarrhea. He was anesthetized with oxygen, nitrous oxide, sevoflurane and fentanyl. Heart rate was around 130 beats x min(-1), and the landiolol was given continuously at a rate of 0.02-0.04 microg x kg(-1) x min(-1). Heart rate was controlled bellow 120 beats x min(-1) without hypotension during anesthesia. Thiamazole and inorganic iodine were given through an enterostomy tube postoperatively, and heart rate decreased gradually. He was extubated on the third postoperative day without any sequelae.

Topics: Adrenergic beta-Antagonists; Adult; Anesthesia, Inhalation; Humans; Infusions, Intravenous; Male; Methimazole; Morpholines; Peptic Ulcer Perforation; Perioperative Care; Stomach Ulcer; Thyroid Crisis; Treatment Outcome; Urea

This investigation was undertaken to study the effect of methimazole (MMI) on gastric acid secretion and stress and chemically induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with MMI (10-100 mg/kg, i.p.). The effect of orally administered MMI on water-immersion restraint (WIR) stress, indomethacin and ethanol-induced gastric ulcers was also tested. The level of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a dose-dependent inhibition of gastric acid secretion and ulcerogen induced gastric lesion formation in the MMI treated rats. Our morphological and histological studies showed a complete prevention of ethanol-induced lesions in the rats treated with high dose (100 mg/kg) of MMI. A significant attenuation of ethanol-induced increase in gastric MPO activity, depletion of NP-SH and reduction of gastric wall mucus was also observed in MMI treated rats. These findings clearly suggest the involvement of endogenous pro-inflammatory agents and oxidative stress in mediating the gastroprotective effect of MMI.

Topics: Animals; Antithyroid Agents; Disease Models, Animal; Dose-Response Relationship, Drug; Ethanol; Female; Gastric Acid; Gastric Mucosa; Indomethacin; Injections, Intraperitoneal; Ligation; Male; Methimazole; Pylorus; Rats; Rats, Wistar; Stomach; Stomach Ulcer; Stress, Physiological; Sulfhydryl Compounds

The plausible mechanism by which dexamethasone makes the gastric mucosa susceptible to ulceration has been studied. As acid aggravates ulcer, the role of dexamethasone on acid secretion was first investigated. Dexamethasone stimulates both basal and drug (mercaptomethylimidazole)-induced gastric acid secretion by 100 and 50% respectively in male Wister rats 24 h after intramuscular administration at the dose of 1 mg/kg body wt. This stimulated acid secretion is 93% blocked by cimetidine indicating increased liberation of histamine in the process. Pretreatment of dexamethasone before 24 h produces ulcer in 30% of the pylorus- ligated rats and aggravates the ulcer index by 82% in both pylorus and esophagus ligated rats. The incidence of ulceration in the latter cases is also increased by 25%. As mucosal prostaglandin synthetase and peroxidase play an important role in gastroprotection through biosynthesis of prostaglandin and by scavenging endogenous H2O2 respectively, the effect of dexamethasone on the activities of these gastroprotective enzymes were studied. Prostaglandin synthetase and peroxidase activities of the mucosa are significantly inhibited by 87 and 83% respectively by 24-h pretreatment with dexamethasone. The results indicate that dexamethasone makes the mucosa prone to ulceration by inhibiting the activity of prostaglandin synthetase to block the gastroprotective action of prostaglandin and also by inhibiting the peroxidase, thereby elevating the endogenous H2O2 level to generate more reactive hydroxyl radical responsible for the mucosal damage.

Topics: Animals; Cimetidine; Cyclooxygenase Inhibitors; Dexamethasone; Gastric Acid; Gastric Mucosa; Histamine Release; Imidazoles; Male; Pepsin A; Peroxidases; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Wistar; Stomach Ulcer