Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 32 years old female was admitted to hospital due to acute abdominal pain, nausea, vomiting and liquid stools. Physical examination was normal except for pain on her left inferior abdominal quadrant without peritoneal irritation signs. An abdominal CAT-scan suggested thrombosis at celiac trunk, although the echo Doppler showed no alterations except for signs of ischemia in the distal branch of the superior mesenteric artery. An exploratory laparotomy was performed disclosing a necrosis of the distal ileum and cecum, diffuse peritonitis and thrombosis of the ileocecoapendiculocolic artery. No vasculitis lesions were found in the arteries of medium size examined. A history of intermittent claudication for the past 3 years as well as acrocyanosis, asymmetry of pulses and blood pressure in the superior extremities was ascertained after the surgery. A MRI angiogram showed multiple stenoses and irregularities at the celiac trunk, hepatic, superior mesenteric and fibular arteries. No abnormalities at the aortic arch and its main branches were documented. A sepsis due to Candida sp complicated her postoperative period. After recovery, prednisone 1 mg/kg/day was started and the anticoagulation continued. The abdominal pain, intermittent claudication and superior limb acrocyanosis disappeared. This is an unusual case of type IV Takayasu's arteritis with acute abdominal signs as the first manifestation.
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PMID:[Intestinal necrosis as clinical presentation of Takayasu arteritis]. 1249 34

This study compares remifentanil/propofol (remi/prop) with isoflurane/fentanyl (iso/fen) anesthesia to determine which provides the greater hemodynamic stability, lesser myocardial ischemia, and morbidity with better postoperative outcomes after carotid endarterectomy. Sixty patients undergoing unilateral carotid endarterectomy were randomized to receive either a remi/prop or iso/fen anesthetic. Hemodynamic variables were recorded during the surgical procedure. In addition, transesophageal echocardiography was used to assess evidence of intraoperative regional wall motion abnormalities suggestive of cardiac ischemia. Emergence and extubation times, recovery from anesthesia, hemodynamic instability, nausea, vomiting, and pain in post anesthesia recovery, discharge delays, ICU admittance, hospital discharge, and preoperative and postoperative troponin levels were compared using appropriate statistical methods with P < 0.05 considered significant. The groups were demographically alike. Hemodynamic variables were similar during intubation and throughout surgery. Twenty-two percent of patients receiving iso/fen developed intraoperative regional wall motion abnormalities suggestive of ischemia, whereas no remi/prop patients had changes (P < 0.05). There was no difference in ST-T wave changes after surgery, and no patient had an elevation in troponin I levels. Postoperative variables were similar except that patients who received iso/fen had lower Stewart recovery scores during the first 15 minutes after post anesthesia care unit admission and a higher incidence of nausea and vomiting the day after surgery, whereas patients receiving remi/prop had discharge delays secondary to hypertension. ICU admittance, time to first void, oral intake, and time to hospital discharge were similar between the groups. At 9 times the cost of an iso/fen anesthesia technique, remi/prop offers little advantage over inhalational anesthesia for carotid endarterectomy.
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PMID:Hemodynamic stability, myocardial ischemia, and perioperative outcome after carotid surgery with remifentanil/propofol or isoflurane/fentanyl anesthesia. 1282 64

Gastric neuromuscular disorders encompass a spectrum of dysfunction in nerve and smooth muscle that includes gastric visceral hypersensitivity, gastric dysrhythmias, fundic dysfunction, antral hypomotility, and gastroparesis. Patients with each disorder may present with such vague dyspepsia symptoms as early satiety, upper abdominal discomfort, bloating, or nausea with or without vomiting. A careful history and physical examination may suggest a gastric neuromuscular disorder, but symptoms are nonspecific. Gastroparesis is the most severe form of neuromuscular dysfunction. Such reversible causes of gastroparesis as mechanical obstruction of the stomach and chronic mesenteric ischemia must be excluded. Gastroparesis, gastric dysrhythmias, and hypersensitivity may follow viral infection or be due to degenerative processes that affect the gastric enteric neurons, smooth muscle, or interstitial cells of Cajal. Commonly, the cause of these gastric neuromuscular disorders is unknown. An approach to the diagnosis and treatment of gastric neuromuscular disorders is reviewed, including dietary counseling, drugs, and medical devices.
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PMID:Diagnosis and treatment of neuromuscular disorders of the stomach. 1286 63

The temporal association of symptoms consistent with ephedrine toxicity after ingestion of ephedrine-containing dietary supplements is heavily relied upon to confirm exposure. Few reports in the literature attempt to associate toxicity with serum levels of these drugs. We report a case of ephedrine-induced cardiac ischemia confirmed by a plasma level. A 22-year-old woman ingesting an ephedrine- and caffeine-containing product for 2 days presented with multiple symptoms, including palpitations, nausea, tremulousness, abdominal pain, and vomiting. The initial electrocardiogram (ECG) revealed a normal sinus rhythm with 1 mm of ST segment depression in leads V3 and V4, along with inverted T waves in leads V1-V4. Her symptoms and ST segment depression resolved over several hours with medical management. The amplitude of her T wave inversions notably diminished with therapy; however, they did not completely resolve. Troponins at presentation and the following morning were negative, and an echocardiogram showed only trace tricuspid regurgitation. A serum ephedrine level, drawn approximately 6 to 7 hr after ingestion, was 150 ng/mL. She was discharged from the hospital after being instructed to avoid ephedrine-containing products.
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PMID:Ephedrine-induced cardiac ischemia: exposure confirmed with a serum level. 1467 95

Severe ethylene glycol toxicity can cause profound morbidity and is almost universally fatal if untreated. Central nervous system depression with intoxication, pulmonary edema, and acute oliguric renal failure with crystalluria are among the most commonly encountered complications of ingestion. The previously reported gastrointestinal side effects of ethylene glycol toxicity are mostly nonspecific, including nausea, abdominal pain, and cramping. In addition, hepatic damage due to calcium oxalate deposition has been reported. We describe a patient who developed acute colonic ischemia following ethylene glycol intoxication. Three months after the ingestion, the patient presented with severe abdominal pain secondary to a colonic stricture and perforation, necessitating emergent colectomy. Histology of the resected colon revealed polarizable polyhedral crystals suggestive of oxalate deposition. The pathophysiology underlying ethylene glycol intoxication, treatment strategies, and gastrointestinal toxicity are discussed.
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PMID:Ethylene glycol toxicity associated with ischemia, perforation, and colonic oxalate crystal deposition. 1510 May 24

We report a case of a dissecting vertebral aneurysm with subarachnoid hemorrhage (SAH) after ischemic onset on the same day. A 48-year-old man had abrupt vertigo and nausea. CT & MRI on admission showed no abnormality, but he complained of left hemiparesis after admission. Twelve hours after the ischemic onset he suddenly complained of severe headache and his consciousness deteriorated. The follow-up CT showed diffuse SAH. Cerebral angiography showed occlusion of the right vertebral artery at the origin of the posterior inferior cerebellar artery (PICA) and segmental stenosis of the left vertebral artery at the portion distal to the vertebral PICA junction. We treated the patient conservatively. Four days later, he suddenly fell into a coma, but CT showed no bleeding. Because of this we suspected brain stem ischemia due to deterioration of vertebral dissection. The patient died 8 hours after the ischemic reattack. We report difficulty of treatment of a dissecting vertebral aneurysm with simultaneous ischemia and subarachnoid hemorrhage.
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PMID:[Dissecting vertebral aneurysm with subarachnoid hemorrhage after ischemic onset on the same day: a case report]. 1546 62

The sudden onset of hearing impairment or hearing loss can be a characteristic sign of a vertebrobasilar circulatory disturbance. We report on a 65 year old male patient with an acute left-sided tinnitus followed by hearing loss as an initial symptom of an infarction of the left anterior inferior cerebellar artery (AICA). Successively, additional symptoms with vertigo, nausea, vomiting and a transient dysarthria and ataxia of the left upper extremity occurred. In the course of the illness, the hearing loss, ataxia and dysarthria completely recovered. MRI of the brain showed an infarction in the area of the anterior inferior cerebellar artery; neurosonographic examination of the basilar and vertebral arteries was normal. Therefore, in patients with acute hearing impairment or hearing loss, an AICA-ischemia should be considered and the patient carefully examined for additional brainstem symptoms, since this can be the first sign of an life-threatening basilar artery thrombosis.
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PMID:[Sudden hearing loss as the leading symptom of an infarction of the left anterior inferior cerebellar artery]. 1565 56

We reviewed the medical records of 62 patients with systemic small and medium-sized vessel vasculitides and gastrointestinal tract involvement followed at our institution between 1981 and 2002. This group included 46 men and 16 women (male:female ratio, 2.9), with a mean age of 48 +/- 18 years. Vasculitides were distributed as follows: 38 polyarteritis nodosa (21 related to hepatitis B virus), 11 Churg-Strauss syndrome, 6 Wegener granulomatosis, 4 microscopic polyangiitis, and 3 rheumatoid arthritis-associated vasculitis. Gastrointestinal manifestations were present at or occurred within 3 months of diagnosis in 50 (81%) patients and were mainly abdominal pain in 61 (97%), nausea or vomiting in 21 (34%), diarrhea in 17 (27%), hematochezia or melena in 10 (16%), and hematemesis in 4 (6%). Gastroduodenal ulcerations were detected endoscopically in 17 (27 %) patients, esophageal in 7 (11%), and colorectal in 6 (10%), but histologic signs of vasculitis were found in only 3 colon biopsies. Twenty-one (34%) patients had a surgical abdomen; 11 (18%) developed peritonitis, 9 (15%) had bowel perforations, 10 (16%) bowel ischemia/infarction, 4 (6%) intestinal occlusion, 6 (10%) acute appendicitis, 5 (8%) cholecystitis, and 3 (5%) acute pancreatitis. (Some patients had more than 1 condition.) Sixteen (26%) patients died.The respective 10-month and 5-year survival rates were 71% (95% confidence interval [CI], 52-90) and 56% (95% CI, 35-77) for the 21 surgical patients; and 94% (95% CI, 87-101) and 82% (95% CI, 70-94) for the 41 patients without surgical abdomen (p = 0.08). Peritonitis (hazard ratio [HR] = 4.3, p < 0.01), bowel perforations (HR = 5.7, p < 0.01), gastrointestinal ischemia or infarctions (HR = 4.1, p < 0.01), and intestinal occlusion (HR = 5.5, p < 0.01) were the only gastrointestinal manifestations significantly associated with increased mortality in multivariate analysis. For this subgroup of 15 patients, 6-month and 5-year survival rates were 60% (95% CI, 35-85) and 46% (95% CI, 19-73), respectively (p = 0.003). None of the other gastrointestinal or extraintestinal vasculitis-related symptoms, or angiographic abnormalities (seen in 67% of the 39 patients who underwent angiography), was predictive of surgical complications or poor outcome. However, prognosis has dramatically improved during the past 30 years, probably owing to better management of these more severely ill patients, with prompt surgical intervention when indicated, and the combined use of steroids and immunosuppressants.
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PMID:Presentation and outcome of gastrointestinal involvement in systemic necrotizing vasculitides: analysis of 62 patients with polyarteritis nodosa, microscopic polyangiitis, Wegener granulomatosis, Churg-Strauss syndrome, or rheumatoid arthritis-associated vasculitis. 1575 41

Gastrointestinal complications are frequent in renal transplant recipients and can include oral lesions, esophagitis, peptic ulcer, diarrhea, colon disorders and malignancy. Oral lesions may be caused by drugs such as cyclosporine and sirolimus, by virus or fungal infections. Leukoplakia may develop in patients with Epstein-Barr virus (EBV) infection. The commonest esophageal disorder is represented by fungal esophagitis usually caused by candida. A number of patients may suffer from nausea, vomiting and gastric discomfort. These disorders are more frequent in patients treated with mycophenolate mofetil (MMF). Peptic ulcer is more rare than in the past. Patients with a history of peptic ulcer are particularly prone to this complication. Other gastroduodenal disorders are caused by cytomegalovirus (CMV) and herpes simplex infection. Diarrhea is a frequent disorder which may be caused by pathogen microorganisms or by immunosuppressive agents. The differential diagnosis may be difficult. Colon disorders mainly consist of hemorrhage, usually sustained by CMV infection, or perforation which may be caused by diverticulitis or intestinal ischemia. Colon cancer, anal carcinoma, and EBV-associated lymphoproliferative disorders are particularly frequent in transplant recipients. A particular gastric lymphoma called mucosa-associated lymphoid tissue (MALT) lymphoma may develop in renal transplant patients. It usually responds to the eradication of Helicobacter pylori.
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PMID:Gastrointestinal complications in renal transplant recipients. 1591 Feb 87

Mildronate (3-(2,2,2-trimethylhydrazinium)propionate; MET-88; meldonium, quaterine) is an antiischemic drug developed at the Latvian Institute of Organic Synthesis. Mildronate was designed to inhibit carnitine biosynthesis in order to prevent accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues and to block this highly oxygen-consuming process. Mildronate is efficient in the treatment of heart ischemia and its consequences. Extensive evaluation of pharmacological activities of mildronate revealed its beneficial effect on cerebral circulation disorders and central nervous system (CNS) functions. The drug is used in neurological clinics for the treatment of brain circulation disorders. It appears to improve patients' mood; they become more active, their motor dysfunction decreases, and asthenia, dizziness and nausea become less pronounced. Since the brain does not utilize fatty acids as fuel other mechanisms of action of mildronate in CNS should be considered. Several reports indicate the possible existence of an alternative, non-carnitine dependent mechanism of action of mildronate. Our recent findings suggest that CNS effects of mildronate could be mediated by stimulation of the nitric oxide production in the vascular endothelium by modification of the gamma-butyrobetaine and its esters pools. It is hypothesized that mildronate may increase the formation of the gamma-butyrobetaine esters. The latter are potent cholinomimetics and may activate eNOS via acetylcholine receptors or specific gamma-butyrobetaine ester receptors. This article summarizes known pharmacological effects of mildronate, its pharmacokinetics, toxicology, as well as the proposed mechanisms of action.
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PMID:Mildronate: an antiischemic drug for neurological indications. 1600 37


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