Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disodium edetate (ethylenediaminetetraacetic acid, disodium salt; disodic EDTA), 3 g, was given, via an intravenous normal saline drip of 30 min, to 25 patients in order to assess a benefit for anaesthesia practice. A significant reduction of both volume and acidity of the gastric secretion was found in all the 10 patients with peptic ulcer having received the drug. The peak of the change was 1 h after administration. In other 10 non-ulcer patients undergoing orthopaedic surgeries under epidural anaesthesia with lidocaine 2%, 5 mg kg-1, pH of the gastric juice unanimously rose, from 2.24 +/- 0.28 to 4.10 +/- 0.21 1 h after EDTA with a P derived from paired difference analysis of less than 0.001. A similar group of patients receiving only normal saline showed no important changes in pH (from 2.37 +/- 0.24 to 2.34 +/- 0.19). The pH of the fundic surface, measured directly under fiberscopic control in further 5 patients suffering from peptic ulcer, was found also to rise from 1.84 +/- 0.21 to 4.62 +/- 0.34 1 h after EDTA, P less than 0.001. Total and ionized calcium changed unsignificantly. Disodic EDTA in the dose and manner used in this study showed no clinical side-effects. The constant and obvious effect of inhibition of the gastric secretion as well as the dynamics of such an action recommend disodic EDTA to be tried in reducing the aspiration pneumonia morbidity.
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PMID:Inhibitory effect of disodium edetate on gastric secretion. 308 72

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

Factors that predispose to infection in general, of course, may predispose to infection with anaerobes. Included in this category are diabetes mellitus, neutropenia, hypogammaglobulinaemia, malignancy, splenectomy, collagen vascular disease, cytotoxic drug therapy, corticosteroid therapy and other immunosuppression. However, even with these situations there may be certain, more specific, associations: anaerobic cholecystitis and anaerobic osteomyelitis in diabetics, neutropenic colitis, and the increased incidence of local anaerobic infections associated with carcinoma of the lung, colon and uterus. Conditions that lead to decreased redox potential more specifically predispose to infection with anaerobes. Included in this category are obstruction and stasis, tissue anoxia, tissue destruction, vascular insufficiency, prior aerobic infection, burns, foreign body implantation, and calcium salts in a wound (in association with fractures). Other specific clinical situations that predispose to anaerobic infections include leukaemia; oral, gastrointestinal, and female pelvic surgery; trauma at other sites; childbirth; aspiration pneumonia; human and animal bites; and therapy with agents with poor activity against anaerobes (e.g. aminoglycosides, quinolones). AIDS patients appear to be predisposed to severe periodontal disease and its complications.
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PMID:Host factors predisposing to anaerobic infections. 851 53

Esophageal reflux is a common condition that affects children and 1 in 10 adults, and if untreated may result in chronic esophagitis, aspiration pneumonia, esophageal strictures, and Barrett's esophagus, a premalignant condition. Although esophagitis is a multifactorial disease that may depend on transient lower esophageal sphincter (LES) relaxation, speed of esophageal clearance, mucosal resistance, and other factors, impairment of LES pressure is a common finding in patients complaining of chronic heartburn. Our data suggest that esophageal and LES circular muscle utilize distinct Ca2+ sources, phospholipid pools, and signal transduction pathways to contract in response to acetylcholine (ACh): (1) In esophageal muscle ACh-induced contraction requires influx of extracellular Ca2+ and may be linked to phosphatidylcholine metabolism, production of diacylglycerol (DAG) and arachidonic acid, and activation of a protein kinase C (PKC)-dependent pathway. (2) In LES muscle ACh-induced contraction utilizes intracellular Ca2+ release arising from metabolism of phosphatidylinositol (PI), and a calmodulin-myosin light chain kinase-dependent pathway. Resting LES tone, on the other hand, may be due to relatively low basal PI hydrolysis resulting in submaximal levels of inositol triphosphate (IP3)-induced calcium release and interaction with DAG to activate PKC. (3) After induction of experimental esophagitis, basal levels of PI hydrolysis and intracellular calcium stores are substantially reduced, resulting in a reduction of resting tone. In addition the signal transduction pathway responsible for LES contraction in response to ACh changes from one that depends on IP3 production, calcium release, and calmodulin activation to one that relies on influx of extracellular calcium and activation of PKC.
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PMID:Signal transduction pathways in esophageal and lower esophageal sphincter circular muscle. 942 18

We report here three patients with intractable epilepsy who developed urinary lithiasis during zonisamide (ZNS) treatment. Abdominal pain due to left-sided hydronephrosis was the initial symptom in the first patient, and it was resolved after the excretion of a stone. The second patient, who had no specific symptoms, was found to have a thick sludge of calcium phosphate in the bladder when he suffered from aspiration pneumonia and dehydration. The third patient, who had a history of recurrent urinary obstruction, was also found to have a thick sludge of calcium oxalate in the bladder. The urinalysis of the three patients revealed alkaline urine and hypercalciuria. Although their urinary lithiasis was resolved by discontinuation of ZNS and supportive therapy, routine examination of urine parameters such as pH and sediments, and daily urine-output checks are thought to be necessary during treatment with ZNS, especially for patients who are bedridden for a long time and receive multiple antiepileptic drugs.
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PMID:Zonisamide - induced urinary lithiasis in patients with intractable epilepsy. 1122 4

Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110-120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed.
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PMID:Ultrafiltration and dry weight-what are the cardiovascular effects? 1266 7

A 99-year-old woman was admitted to Shizuoka Shimizu Municipal Hospital because of fever and anasarca. Imaging and laboratory tests showed pneumonia, urinary tract infection, and cardiac failure. The patient died 20 days after admission. An autopsy revealed marked diffuse dilations of the biliary tree ranging from the lower common bile duct to intrahepatic bile ducts. Intrahepatic calcium bilirubinate stones and biliary sludges were recognized within the dilated bile ducts. A unilocular cyst (2 cm in diameter) was present in the pancreatic head adjacent to the lower common bile duct, and it appeared to compress the common bile duct. Histologically, the walls of the dilated biliary tree showed proliferation of peribiliary glands, fibrosis, and infiltration of lymphocytes and neutrophils (cholangitis). The lumens of the dilated biliary ducts contained neutral and acidic mucins, fibrinous materials, bacteria, neutrophils, and Aspergillus fungi, in addition to the calculi and sludges. The background liver showed atrophy (400 g). The pancreatic unilocular cyst was composed of mucous columnar cells with a few infoldings, and the pancreas also showed foci of mucinous duct hyperplasia and ectasia; the pathological diagnosis of the cyst was cystic dilations of a pancreatic duct branch (mucinous ductal ectasia or mucinous cyst). Other lesions included aspiration pneumonia, emaciation, atrophy of systemic organs, gastric leiomyoma, serous cystadenoma of the right ovary, and arteriosclerotic nephrosclerosis. The present case suggests that a mucinous cyst of the pancreas may compress the biliary tree and lead to marked diffuse dilations of the biliary tree. Alternatively, the dilations of the bile ducts may be associated with aging or may be of congenital origin. The dilated bile ducts may, in turn, give rise to bacterial and fungal cholangitis and formation of biliary sludges and intrahepatic calcium bilirubinate stones.
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PMID:Marked diffuse dilations of the biliary tree associated with intrahepatic calculi, biliary sludges and a mucinous cyst of the pancreatic head in a 99-year-old woman. 1289 37

A lot of oral diseases, including marginal periodontitis, are infectious diseases that caused by the oral biofilm-forming bacteria for example dental biofilm (dental plaque). The oral biofilm is paid to attention as a risk factor of the systemic disease such as metabolic syndrome, osteoporosis, aspiration pneumonia, diabetics, and the infective endocarditises. It had been shown that 500 bacterial species inhabited with symbiosis and antagonization within the oral biofilm and communication among bacteria is essential for initial colonization and subsequent biofilm formation on human teeth and oral mucosa. The feature and the realities of the biofilm to cause the bone absorption were outlined in this manuscript and speculated how the biofilm-forming bacteria approach to the alveolar bone, although it was difficult to clarify the whole contents of human oral biofilm that presented a various aspect.
Clin Calcium 2007 Feb
PMID:[Oral Biofilms and bone resorption]. 1727 74

Idiopathic basal ganglia calcification (IBGC) is a syndrome in which bilateral cerebral calcification occurs despite the absence of abnormal calcium metabolism. A 17-year-old Japanese female was admitted for investigation of intermittent proteinuria from the age of 12 years. On admission, her blood pressure was 126/60 mmHg and her serum creatinine was 0.8 mg/dL. Although computed tomography revealed bilateral striopallidodentate calcinosis, her level of intelligence and neurological findings were normal, as were the results of endocrine tests including parathyroid hormone. Asymptomatic IBGC was diagnosed. Renal biopsy showed membranoproliferative glomerulonephritis. Peritoneal dialysis was started for end-stage renal failure when she was 24 years old. Pyramidal and extrapyramidal signs started to develop at the age of 27 years and progressed, resulting in death from aspiration pneumonia at the age of 32 years. Post-mortem revealed bilateral calcification of the basal ganglia, dentate nucleus, thalamus, and centrum semiovale. On light microscopy, there was circumferential calcification of the media and intima of affected vessels in the brain, including small arteries, small veins, and capillaries, and luminal narrowing was seen. On electron microscopy, layers of differing electron density were arranged in concentric laminae. This is the first report of IBGC with bilateral and symmetrical cerebral calcification accompanied by membranoproliferative glomerulonephritis resulting in end-stage renal failure.
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PMID:A case of idiopathic basal ganglia calcification associated with membranoproliferative glomerulonephritis. 2200 64

Seven goats and one ram presented with clinical signs including regurgitation, obtundation, anorexia, apparent pain, and bloat. The animals had escaped from their barn, and it was discovered that they had ingested leaves of Pieris japonica, Japanese pieris, a grayanotoxin-containing plant. Animals were treated with antibiotics, calcium borogluconate, B vitamins, and activated charcoal within the first 24-h postexposure, which was followed by the recovery of the ram and two goats and the death of two goats. Approximately 36 h after Japanese pieris ingestion, one of the three remaining anorectic goats was dosed with intravenous lipid emulsion (ILE). This goat recovered within a few hours. The remaining two goats were given ILE the next day and appeared to recover, but one died a week later of aspiration pneumonia.
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PMID:Treatment of pieris ingestion in goats with intravenous lipid emulsion. 2519 85


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