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 elderly male with a long history of alcohol abuse presented with an acute pleural trauma and hemopneumothorax, which may have served as the precipitating medical illness for cecal volvulus. He subsequently developed bacterial peritonitis as a complication of his bowel obstruction. It is probable that his pleural cavity was seeded hematogenously via a bacteremia from his peritonitis, thus accounting for the empyema with species typical of bowel flora. Cecal bascule is a type of cecal volvulus that causes intestinal obstruction. Diagnosis is difficult, but a delay in recognition may result in intestinal ischemia, perforation, sepsis, and even death. Cecal ischemia or gangrene cannot always be determined based on physical examination or laboratory findings. Plain films of the abdomen may be helpful, and barium enema has been advocated by some authors. However, laparotomy is often necessary for definitive diagnosis and therapy. While cecal volvulus has not been reported to occur frequently in the elderly, the relatively common occurrence of anatomic predisposition in addition to the widespread use of respirators and the increasing age and number of medical illnesses of our population make it possible that cecal volvulus will be seen with increasing frequency in the future.
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PMID:Cecal bascule: an overlooked diagnosis in the elderly. 172 51

A pilot case-control quantitative study of the hippocampus in patients with severe status epilepticus was performed to identify specific patterns of pyramidal cell loss. Pyramidal cell densities from five patients who died following status epilepticus were compared with five normal controls and five controls matched for age, hypoxia/ischemia, previous epilepsy, and alcohol abuse. Neuronal densities were greatest in the normal control group and least in patients with status epilepticus. Significant reductions were identified in Sommer's sector (prosubiculum and CA1) as well as in CA3 when compared to normal controls.
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PMID:Hippocampal pyramidal cell loss in human status epilepticus. 173 57

Rhabdomyolysis leading to acute renal failure necessitating hemodialysis is described in three chronic alcoholics. In each case an acute medical or surgical event, but not alcoholic intoxication, was implicated. Renal biopsies demonstrated acute tubular necrosis with intraluminal deposits consisting of Tamm-Horsfall protein and myoglobin. After recovery all three patients were demonstrated to have proximal muscle weakness with similar electromyographic abnormalities but nerve-conduction was impaired in only two. Muscle biopsies showed mixed, but predominantly type II fiber atrophy and reduced muscle phosphorylase levels. In the one patient tested the lactate response to forearm muscle ischemia was abnormal. It is postulated that chronic alcoholics may be predisposed to rhabdomyolysis and acute renal failure following acute medical and surgical stress as well as acute alcohol abuse. The muscle damage in these patients may be due to impaired intra cellular glycogen metabolism.
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PMID:Rhabdomyolysis and acute renal failure in chronic alcoholics with myopathy, unrelated to acute alcohol ingestion. 673 97

The classic features of idiopathic femoral head necrosis - increased roentgenologic density, the subchondral crescent-fracture and distortion of the femoral head - are now known to be late manifestations of the disease. The early changes have been studied prospectively in 34 patients receiving corticosteroids in high dosage and 11 patients with femoral head necrosis attributed to alcohol abuse. In five patients with unilateral femoral head necrosis, intraosseous pressure studies and core biopsy were carried out on the apparently unaffected side. The earliest pathologic changes were a relative increase in cancellous bone fat at the expense of myeloid tissue, swelling and necrosis of the fat cells, and variable areas of cell death in the trabeculae. All of these were fairly widespread throughout the proximal femur. Intraosseous pressures were raised, suggesting the presence of venous stasis. Fat cell size was measured in undistorted femoral heads with osteonecrosis and in a comparable series with osteoarthritis. There was a significant (P less than 0.001) increase in fat cell size and a virtual absence of sinusoids in histologic sections from those with osteonecrosis. It is posited that idiopathic osteonecrosis results from the following sequence: fatty accumulation and replacement of myeloid tissue, followed by compression of vascular sinusoids, venous stasis, ischemia, fat necrosis and then bone necrosis. The earliest stages in this chain of events are clinically asymptomatic and produce no radiologic abnormality. The results of treatment by core decompression in 22 hips are discussed. This is an effective prophylactic measure in all early cases and it has a place even in the management of more advanced cases, especially if the patient is considered too young for hip arthroplasty.
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PMID:Idiopathic necrosis of the femoral head: pathogenesis and treatment. 732 18

Between 1978 and 1991, 116 of 19,246 patients (0.6%) undergoing cardiac surgery developed abdominal complications (renal/hepatic failure excluded) within 30 days of their cardiac operation. Comparison with a randomly selected control group of 217 patients operated upon over the same period of time was also undertaken. Compared to the control group, the study patients were older (mean age, 63.3 +/- 12.5 years vs 57.5 +/- 21.5 years; P = 0.03), more likely to have a history of alcohol abuse (10% vs 4%; P = 0.03), and more likely to have a previous history of gastrointestinal problems (43% vs 17%; P = 0.0001). There was also a trend towards a greater number of patients having valvular surgery, particularly reoperative surgery, in the study group. Postoperatively, patients with marked low cardiac output, requiring the intra-aortic balloon pump, were more likely to develop abdominal complications. These complications included complicated peptic ulcer disease in 54 (47%), intestinal obstruction and/or perforation in 19 (16%), biliary tract disease in 13 (11%), mesenteric ischemia in 13 (11%), acute pancreatitis in 3 (3%), and miscellaneous complications in the remaining 14 (12%). Forty-three patients were treated medically and 73 patients required operative intervention. The surgical procedures performed were truncal vagotomy and drainage (12), oversewing of a perforation or a bleeding vessel (6), gastrectomy (2), intestinal resection (14), laparotomy only (14), cholecystectomy (14), and other (11). Mortality was 26% (30/116) with the mortality for medical and surgical treatment being 16% vs 32%, respectively (P = 0.112). Intestinal ischemia had the highest mortality, with a rate of 85% (11/13). Despite intensive monitoring and care of cardiac surgical patients, abdominal complications do occur, although rarely. Risk factors include older age, a positive history of gastrointestinal disease, reoperative valve surgery, and severe postoperative low cardiac output.
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PMID:Abdominal complications following cardiac surgery. 820 26

Central pontine myelinolysis (CPM) is a rare syndrome generally linked to hyponatremia. Autopsy and imaging studies described demyelination in the central pons, in some cases combined with thalamic, internal capsular, hemispheric and cerebellar white matter lesions. The clinical syndrome and prognosis spans from asymptomatic patients displaying only imaging lesions to coma and death. Frequent findings are pyramidal tract and pseudobulbar signs. No effective treatment is known. Alcohol abuse is often associated. The imaging pattern of CPM is unique and generally accepted as diagnostic when other causes such as ischemia, multiple sclerosis, tumors, radiation, or pharmacological effects are ruled out. However, the exact mechanism of this selective process of demyelination remains obscure. The current major controversy concerns the role of therapeutic efforts of sodium level restoration in the etiology of CPM. We present a case of CPM where no hyponatremia was found. We hypothesize that (1) iatrogenic sodium restoration may not in all cases of CPM be the putative mechanism, (2) the clinical onset of CPM may in some patients represent a delayed response to an initially asymptomatic demyelination, and (3) normal admission sodium levels do not exclude the diagnosis of CPM.
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PMID:Central pontine myelinolysis: clinical syndrome with normal serum sodium. 938 79

Because of the unique demographics of our patient population, we have had the opportunity to dedicate further studies of the management of hepatitis B and hepatitis C. We have experienced a very low HBV recurrence rate with the use of HBIG in patients transplanted for hepatitis B. Investigations, including the use of new antiviral agents, and the development of approaches to minimize or abrogate disease recurrence such as lower levels of immunosuppression are ongoing. Using a standardized approach to the proper evaluation and selection of patients for liver transplantation with alcoholic liver disease or other liver diseases with coexistent alcohol abuse, we report favorable long-term results in these patients. We have reviewed our results and our approach to the management of EBV and posttransplant lymphoproliferative disorder. There is a firm commitment in our laboratories and outpatient clinics to the investigation of disease prevention, reliable detection and screening methods, and treatment modalities for EBV-related disease. We have addressed specific technical considerations to pediatric liver transplant and have discussed unique aspects of postoperative management in these patients. One-third of the transplants performed at Stanford are in children, 42% of whom are less than one year old. Results with our pediatric transplant recipients compare favorably with those of our adult recipients with patient and graft survival rates approaching 90% at one year and exceeding 80% at 46 months for both groups. As a response to the limited organ supply, we have extended our criteria for suitable donors. Most notably, we have utilized older donors and grafts with significant microsteatosis and have observed good results with these grafts as long as ischemia time is minimized. We have also successfully used reduced size grafts for our pediatric patients with good results and are continuing to expand the use of living-related partial grafts and split allografts.
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PMID:Liver transplantation at Stanford University Medical Center. 1050 6

Acute pancreatitis is a disorder that has numerous causes and an obscure pathogenesis. Bile duct stones and alcohol abuse together account for about 80% of acute pancreatitis. Most episodes of biliary pancreatitis are associated with transient impaction of the stone in the ampulla (that causes obstruction of the pancreatic duct, with ductal hypertension) or passage of the stone though and into the duodenum. Other causes of acute pancreatitis are various toxins, drugs, other obstructive causes (such as malignancy or fibrotic sphincter of Oddi), metabolic abnormalities, trauma, ischemia, infection, autoimmune diseases, etc. In 10% of cases of acute pancreatitis, no underlying cause can be identified; this is idiopathic pancreatitis. Occult biliary microlithiasis may be the cause of two thirds of the cases of "idiopathic" acute pancreatitis. Intra-acinar activation of trypsinogen plays a central role in the pathogenesis of acute pancreatitis, resulting in subsequent activation of other proteases causing the subsequent cell damage. Ischemia/reperfusion injury is increasingly recognized as a common and important mechanism in the pathogenesis of acute pancreatitis and especially in the progression from mild edematous to severe necrotizing form. Increased intracellular calcium concentration also mediates acinar cell damage. Oxygen-derived free radicals and many cytokines (e.g., interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor-alpha, platelet activating factor) are considered to be principal mediators in the transformation of acute pancreatitis from a local inflammatory process into a multiorgan illness.
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PMID:Etiology and pathogenesis of acute pancreatitis: current concepts. 1087 61

The etiology of acute pancreatitis, apart from alcohol abuse and cholelithiasis may also include a vascular component responsible for pancreatic ischemia. It is now acknowledged that chronic pancreatitis may be a consequence of the acute variant, but it remains unclear what factors influence this sequence of morphological changes. In order to clarify this issue we proposed a model of experimental acute pancreatitis in rats induced by a 30 min reduction of blood flow in inferior splenic artery followed by reperfusion. Rats were sacrificed at 1 h, 12 h, 24 h, and 2, 3, 5, 7, 14, 21, 28 days after cessation of ischemia. We performed histopathological examination of pancreatic tissue and measured pancreatic blood flow, plasma amylase activity and interleukin-1 beta concentration. The present findings indicate that transient pancreatic ischemia leads to the development of acute necro-haemorrhagic pancreatitis. The morphological features of acute inflammation are correlated positively with functional disorders. In some cases the features of chronic pancreatitis may appear transiently after the acute phase, whereas the repair of postinflammatory injury involves the regeneration of acinar cells.
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PMID:Morphological changes and morphological-functional correlations in acute experimental ischemia/reperfusion pancreatitis in rats. 1124 88

Different tissues display distinct sensitivities to defective mitochondrial oxidative phosphorylation (OXPHOS). Tissues highly dependent on oxygen such as the cardiac muscle, skeletal and smooth muscle, the central and peripheral nervous system, the kidney, and the insulin-producing pancreatic beta-cell are especially susceptible to defective OXPHOS. There is evidence that defective OXPHOS plays an important role in atherogenesis, in the pathogenesis of Alzheimer's disease, Parkinson's disease, diabetes, and aging. Defective OXPHOS may be caused by abnormal mitochondrial biosynthesis due to inherited or acquired mutations in the nuclear (n) or mitochondrial (mt) deoxyribonucleic acid (DNA). For instance, the presence of a mutation of the mtDNA in the pancreatic beta-cell impairs adenosine triphosphate (ATP) generation and insulin synthesis. The nuclear genome controls mitochondrial biosynthesis, but mtDNA has a much higher mutation rate than nDNA because it lacks histones and is exposed to the radical oxygen species (ROS) generated by the electron transport chain, and the mtDNA repair system is limited. Defective OXPHOS may be caused by insufficient fuel supply, by defective electron transport chain enzymes (Complexes I - IV), lack of the electron carrier coenzyme Q10, lack of oxygen due to ischemia or anemia, or excessive membrane leakage, resulting in insufficient mitochondrial inner membrane potential for ATP synthesis by the F0F1-ATPase. Human tissues can counteract OXPHOS defects by stimulating mitochondrial biosynthesis; however, above a certain threshold the lack of ATP causes cell death. Many agents affect OXPHOS. Several nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit or uncouple OXPHOS and induce the 'topical' phase of gastrointestinal ulcer formation. Uncoupled mitochondria reduce cell viability. The Helicobacter pylori induces uncoupling. The uncoupling that opens the membrane pores can activate apoptosis. Cholic acid in experimental atherogenic diets inhibits Complex IV, cocaine inhibits Complex I, the poliovirus inhibits Complex II, ceramide inhibits Complex III, azide, cyanide, chloroform, and methamphetamine inhibit Complex IV. Ethanol abuse and antiviral nucleoside analogue therapy inhibit mtDNA replication. By contrast, melatonin stimulates Complexes I and IV and Gingko biloba stimulates Complexes I and III. Oral Q10 supplementation is effective in treating cardiomyopathies and in restoring plasma levels reduced by the statin type of cholesterol-lowering drugs.
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PMID:Mitochondrial medicine--molecular pathology of defective oxidative phosphorylation. 1131 62


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