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)

This article presents an analysis of acute gastroduodenal mucosal lesions (AGML) based on a review of current literature and the personal experience of the authors. The pathology of AGML involes two distinct types of lesions, namely, superficial erosions confined to the acid-secreting gastric mucosa and presenting as erosive hemorrhagic gastritis, and acute ulcers that occur in the alkaline gastric mucosa and duodenum. The etiology of these two lesions is very likely different. Acut gastroduodenal ulcers, best known as stress ulcers, are probably "peptic" lesions, whereas erosive hemorrhagic gastritis appears to be due to pathologic back diffusion of hydrogen ions caused by a breakdown of the gastric mucosal barrier as a result of endogenous factors, such as gastric mucosal ischemia, and sometimes exogenous factors, such as alcohol, urea, and acetylsalicylic acid. Catecholamine hypersecretion resulting from severe stress, such as occurs in hypovolemia, sepsis, and hypercapnea, contributes to ischemia of the gastric mucosa by producing splanchnic vasoconstriction. The key to the diagnosis of AGML is early endoscopy in all cases of upper gastrointestinal bleeding. Therapy for AGML should begin with a trial of medical measures directed at restoring effective perfusion of tissues and removing hydrogen ions from the stomach by gastric washing. Medical therapy is effective in 80% of patients with erosive hemorrhagic gastritis, but surgical treatment is usually required in acute gastroduodenal ulcer. When surgery is necessary for either type of lesion, vagotomy with hemigastrectomy appears to be the most effective operation. The personal experience of the authors has involved 36 patients with AGML who were treated in three periods between 1968 and 1976. The mortality rate of patients with AGML has been reduced from 50% in the first 2 years to zero in the last 2 years by the use of emergency endoscopy for diagnosis, appropriate medical therapy, properly timed and executed surgery, and, most recently, selective angiography.
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PMID:Progress in the treatment of acute gastroduodenal mucosal lesions (AGML). 1 30

A zinc-carnosine chelate compound, Z-103, attenuates gastric mucosal injuries and inhibits the increase of lipid peroxide in the gastric mucosa induced by burn shock or ischemia-reperfusion. However, the exact mechanism of the antioxidative effect of Z-103 is not clear. The antioxidant properties of a novel anti-peptic ulcer agent Z-103 in vitro were compared with those of zinc ion and L-carnosine. Z-103 scavenged superoxide anion radicals. Z-103 and ZnSO4, but not L-carnosine, inhibited the superoxide generation from polymorphonuclear leukocytes stimulated by opsonized zymosan, and also inhibited the generation of hydroxyl radicals by the Fenton reaction. The increase of lipid peroxides produced by rat brain homogenates and liver microsomes was also inhibited by Z-103 and ZnSO4. These findings indicate that the strong anti-ulcer and antioxidative actions of Z-103 in vivo are due to a combination of these antioxidant actions in vitro.
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PMID:The antioxidant properties of a novel zinc-carnosine chelate compound, N-(3-aminopropionyl)-L-histidinato zinc. 165 10

Rare instances of intestinal ischemia subsequent to cocaine use have been reported. Crack abuse, linked to gastroduodenal ulcer perforation, has not been associated with mesenteric infarction until this case report.
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PMID:Crack-induced enteric ischemia. 227 Jan 46

The authors report the surgical management of 19 patients with chronic intestinal ischemia over the last ten years. There were 11 women and 8 men (mean age 59 years). Most patients (13/19) suffered from widespread generalized atheromatosis. Fifteen patients had symptoms which were mostly aspecific and insidious in onset. In 8 cases, there was previous misdiagnosis when pain was considered as peptic ulcer or cholecystitis, which explains a mean delay of 18 months between the onset of symptoms and angiographic evidence of coeliomesenteric stenosis. Four patients were asymptomatic and underwent a prophylactic splanchnic revascularization during aorto-iliac or aorto-renal surgery. Obstructive lesions were limited to one single digestive artery in 9 patients, 2 arteries in 7 patients and all 3 arteries in 3 patients. Twenty-two operations for coeliomesenteric revascularization were performed: 16 venous bypasses, 1 prosthetic bypass, 6 thrombendarterectomies, and 5 arterial reimplantations. Nine bypasses were retrograde versus 8 anterograde. A mean of 1.5 visceral arteries was revascularized per patient. Complete revascularization of all 3 splanchnic vessels was obtained in 73% of the cases. Operative mortality (30 days) was 16% (3 cases). Mean follow-up is 3 years. There was no single late mesenteric infarction. Four patients died of non-related causes (3 cardiac, 1 cerebrovascular), and 84% of the survivors are completely symptom free since the operation.
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PMID:[Surgical treatment of chronic mesenteric ischemia]. 248 11

Nineteen patients with a prosthetic infrarenal aortic graft and gastrointestinal bleeding were managed over a 7 year period. Graft-to-enteric fistula, identified in five patients, was the most common cause of bleeding. Other causes included bowel ischemia (four patients) and peptic ulcer disease (three patients). Clinical signs of infection, such as fever and leukocytosis, were common in patients with graft-to-enteric fistula and bowel ischemia. Most of these patients will benefit from a prompt evaluation and expedient operation.
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PMID:Clinical spectrum of patients with infrarenal aortic grafts and gastrointestinal bleeding. 349 91

Bowel ischemia and infarction are diseases primarily of, but not confined to, the elderly. Insidiously developing bowel ischemia may mimic more common gastrointestinal disturbances, such as peptic ulcer disease or malignancy, and go undiagnosed for long periods. Bowel infarction is a catastrophic event: Mortality rates approach 90%. Chronic intestinal ischemia may precede infarction, or infarction may occur with no warning. Laboratory and radiologic studies have minimal value in diagnosis of these disorders. A high index of suspicion must be maintained in patients complaining of abdominal pain if these diagnoses are to be made promptly.
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PMID:Bowel ischemia and infarction. Chronic and acute causes of abdominal pain. 368 21

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.
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PMID:The pathophysiology of peptic ulcer disease. 405 22

The basic mechanisms underlying cytoprotection of gastrointestinal mucosae against damage are not understood. One hypothesis is that the initial and primary system affected by a cytoprotective agent is the local circulation of the tissue that is being protected. According to this circulatory hypothesis, a cytoprotective prostaglandin would increase gastric mucosal blood flow, thereby ameliorating the effect of topical damaging agents, such as ethanol, aspirin or bile salts. Four questions need to be considered in order to evaluate the circulatory hypothesis: (i) What degree of ischemia is necessary to break the gastric mucosal barrier? (ii) Is peptic ulcer disease due to local ischemia of the mucosa? (iii) Do mucosal damaging agents invariably reduce gastric blood flow? (iv) Do cytoprotective agents invariably increase gastric blood flow? A survey of available literature concerning blood flow and damage to the gastric mucosa suggests that: (i) severe degrees of gastric ischemia are necessary to impair vital functions of the epithelial cells of the stomach; (ii) peptic ulcer disease is not a manifestation of isolated gastric ischemia; (iii) mucosal damaging agents do not invariably reduce gastric blood flow; and (iv) cytoprotective drugs do not invariably increase gastric mucosal blood flow. The weight of available evidence does not support the circulatory hypothesis about the mechanism of cytoprotection.
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PMID:Gastric blood flow and the gastric mucosal barrier. 405 27

Peptic ulceration is a known complication of hepatic arterial chemotherapy for metastatic disease. We report a case of peptic ulceration associated with marked epithelial atypia initially interpreted as carcinoma, probably metastatic in nature. Subsequent partial gastric resection proved the lesion benign. Examination of other gastric biopsies from ulcerated and nonulcerated mucosa from similarly treated patients has revealed similar marked atypical changes. The etiology of the epithelial atypia and ulceration remains unanswered, but is probably related to locally enhanced chemotherapeutic cytotoxicity or ischemia. Care should be taken not to interpret the marked epithelial atypia as carcinoma in this clinical setting.
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PMID:Peptic ulceration with marked epithelial atypia following hepatic arterial infusion chemotherapy. A lesion initially misinterpreted as carcinoma. 622 Jun 16

Acute primary ulcer of the small intestine is an exceptional occurrence. Diagnosis is established only after a complication occurs. In most instances, this complication is perforation of the gut. Acute primary ulcer of the small intestine is accurately defined by specific histologic criteria. It can be unequivocally distinguished from the many other causes of spontaneous perforation of the small intestine. Experimental studies, although numerous, have not improved understanding of pathophysiology. Nosologic classification remains unclear. Many features are similar to those encountered in acute peptic ulcer but stress is usually absent. Other features resemble those of transient necrotizing enterocolitis ; acute primary ulcer of the small intestine may be a very localized form of this latter condition. Ischemia seems to be the most significant factor. However, for an ulcer and finally perforation to occur, ischemia must probably be associated with a number of other factors.
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PMID:[Acute primary ulcer of the small intestine. Present concepts (author's transl)]. 628 93


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