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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

This paper calls attention to the methodologies designed to investigate the higher cortical functions in order to elicit signis of encephalopathy in apparently normal conditions. This can be done by testing the blobal hemispheric funcionts or the interhemispheric functional balance. This shows up the clinical sequels that may precede or be the outcome both of transient pathological disorders, such as transient global anemia, migraine, TIAs and subarachnoid hemorrhage without apparent clinical consequences and of nontransient pathological conditions, such as epilepsy, occupational diseases, arterial hypertension and cerebral revascularization.
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PMID:Neurobehavioral investigation as a tool for revealing preclinical disorders. 332 25

Accumulation of aluminum occurs in children with renal failure and can cause anemia, disabling osteodystrophy, and encephalopathy. Effects on bone mineralization are of particular concern in pediatric patients with growth potential. We measured plasma aluminum levels in 36 patients on continuous ambulatory peritoneal dialysis (CAPD) and 22 on hemodialysis under surveillance at a single pediatric center. The levels were above normal in 35 and 21 patients, respectively, and the values correlated with the oral dose of aluminum-containing phosphate-binding medications (r = 0.57; P less than 0.001). Younger and smaller children had higher plasma aluminum levels and also received larger doses of oral aluminum-containing compounds. Mean plasma aluminum levels (57.2 +/- 52.8 and 48.7 +/- 32.1 micrograms/liter, respectively) and the daily oral doses of elemental aluminum (47.3 +/- 37.6 and 39.2 +/- 26.7 mg/kg, respectively) were not statistically different in patients on CAPD and those on hemodialysis. Plasma aluminum levels did not correlate with estimated cumulative oral intake of aluminum, total duration of dialysis, serum calcium and phosphorus concentrations, N-terminal parathyroid hormone levels, or transfusion requirements. Retention of aluminum is common in children undergoing dialysis, correlates with the amount of aluminum administered orally, and results in similar elevations of plasma aluminum with CAPD and hemodialysis. Younger and smaller children are at increased risk for accumulation of aluminum. Alternative methods for control of serum phosphorus are needed in children with end-stage renal disease.
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PMID:Plasma aluminum levels in pediatric dialysis patients: comparison of hemodialysis and continuous ambulatory peritoneal dialysis. 356 Oct 41

The records of 54 patients with documented cirrhosis who underwent colectomy between January 1970 and January 1984 were studied to assess the operative risk and to determine the preoperative predictive risk factors. In-hospital mortality was 24 percent (13 patients), and postoperative complications occurred in 48 percent (26 patients). The risk of surgical intervention was significantly increased if encephalopathy, ascites, anemia, or hypoalbuminemia was present before operation. A simple operative risk index involving the presence of encephalopathy and ascites and the levels of hemoglobin and albumin is proposed to help distinguish a low-risk subgroup in whom postoperative mortality was 12.8 percent from a high-risk subgroup in whom postoperative mortality was 53.3 percent.
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PMID:The surgical risk of colectomy in patients with cirrhosis. 359 74

Kidneys of patients on hemodialysis therapy often undergo structural changes leading to acquired cystic disease. A wide variety of chemical compounds are known to induce experimental renal cystic disease. Since aluminum intoxication has been implicated in the development of encephalopathy, osteomalacia and anemia in uremic patients, this study was designed to investigate whether aluminum administration to normal rats could induce renal morphological changes. Male Wistar rats were divided into three groups; Animals of the Low-dose aluminum (LDA) group received 0.2 mg/day of aluminum, animals of the high-dose aluminum (HDA) group received 2 mg/day of aluminum; the third group consisted of controls (C). Aluminum was injected intraperitoneally as aluminum chloride (6 days a week). 13 weeks later, the kidneys were removed and examined by light and electron microscopy. The findings on eight-microscopic examination were normal in all groups. Electron-microscopic examination was unremarkable in the C and LDA group. In HDA rats, ultrasections of the cortex and outer medulla showed changes in the proximal tubules with increased size and number of lysosomes, osmiophilic granular material inside the lysosomes, vacuolisation of organelles and mitochondrial damage of varying degree. No cystic changes were found.
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PMID:Effect of long-term aluminum administration on the renal structure of the rat. 362 36

In a cohort analysis of Silastic vacuum extractor deliveries, 65% were completed with the vacuum extractor alone, 24% with outlet forceps, 3% with midforceps, and 7% with cesarean section (vacuum extractor-cesarean). Control groups were formed by using the next sequential forceps delivery, spontaneous vaginal delivery, and every second cesarean section after a trial of labor. The infants were examined using a neurobehavioral scale, an encephalopathy assessment, cranial ultrasound, and indirect ophthalmoscopy. In the combined vacuum extractor and forceps delivery subgroup (vacuum extractor-forceps), all but 3% were converted from a high mid-forceps delivery to outlet forceps by the initial vacuum extractor procedure, thus eliminating many difficult midforceps deliveries. The study yielded no significant difference in maternal morbidity between vacuum extractor-forceps and forceps delivery, no difference in vaginal trauma for vacuum extractor-cesarean versus vacuum extractor delivery, and no greater hospital stay, infection rate, or need for transfusion for either vacuum extractor-forceps versus forceps delivery or vacuum extractor-cesarean versus cesarean delivery. Neonatal morbidity did not differ between successful and unsuccessful trial of vacuum extractor, except for an increased frequency of retinal hemorrhage. The frequency of scalp trauma, including cephalohematoma, did not differ between vacuum extractor-forceps and forceps delivery, or between vacuum extractor-cesarean and vacuum extractor delivery. For vacuum extractor-forceps versus forceps delivery and vacuum extractor-cesarean versus cesarean section, there were no significant differences in neurobehavioral or encephalopathy scores, or in the frequency of neonatal jaundice, facial palsy, anemia, fractures, or mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cohort study of Silastic obstetric vacuum cup deliveries: II. Unsuccessful vacuum extraction. 376 80

In the presence of normal renal function, a high concentration of aluminum in drinking water has been implicated as a factor in the etiology of a neurological syndrome in one specific geographical area. The role of aluminum as a toxic agent in other neurological disorders, where renal function is normal, is controversial. Aluminum is absorbed from the gastrointestinal tract and is normally excreted by the kidneys in the urine. In patients with chronic renal failure, aluminum appears to be of proven toxicological importance. In these patients the accumulation of aluminum in tissues causes an encephalopathy (dialysis encephalopathy or dialysis dementia), a specific form of metabolic bone disease (osteomalacic dialysis osteodystrophy), and an anemia and also plays an etiological role in some of the other complications associated with end-stage chronic renal disease. A failure in the normal renal excretory mechanism accounts for the tissue accumulation in chronic renal failure. The majority of chronic renal failure patients who develop aluminum toxicity are on long-term treatment with either hemo- or peritoneal dialysis; some patients develop toxicity who are only on treatment with aluminum-containing phosphate-binding agents. Aluminum in the dialysate appears to be the major source of the metal in chronic renal failure patients who develop aluminum toxicity. The aluminum content of the dialysate depends primarily on the content of the water with which it is prepared; there may be some contribution from the chemicals used in the concentrate which is added to the water. Some domestic tap-water supplies contain aluminum in high concentration, either naturally or because aluminum has been added as a flocculant in the purification process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Water content of aluminum, dialysis dementia, and osteomalacia. 390 86

A survey of 67 pregnancies in 51 professional women (physicians, psychologists, nurses, administrators, etc.) revealed the occurrence of symptoms of cognitive dysfunction such as forgetfulness, disorientation, confusion and reading difficulties in 28 pregnancies occurring in 21 women. These were unrelated to such factors as age of delivery, percentage weight gain, the baby's sex or birth weight, alcohol consumption, smoking, a history of migraine or allergy or other symptoms occurring during pregnancy such as sleepiness and lack of concentration, irritability, loss of interest in job or nightmares. Nor was there any correlation with hypertension, proteinuria, glycosuria, ketonuria, anemia, or morning sickness. Furthermore, these cognitive disturbances were not related to depression or sleep deprivation. Despite these symptoms, none of the women suffering from them were forced to interrupt their professional activities during pregnancy. The syndrome of benign encephalopathy of pregnancy should be recognized so that simple precautions can be taken to prevent any interference with professional or other activities. The etiology of the syndrome is unknown.
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PMID:Benign encephalopathy of pregnancy. Preliminary clinical observations. 395 58

Of 38 children investigated between 1966 and 1971 who had a blood lead concentration greater than 37 mug/100 ml eight had encephalopathy and one died; all these eight had a blood lead concentration of 99 mug/100 ml or above. Blood lead levels are related to haemoglobin concentrations and anaemia is common in children with blood lead concentrations of 37-60 mug/100 ml, levels previously accepted as harmless.Children with blood lead concentrations greater than 60 mug/100 ml show radiological evidence of lead intoxication, and treatment for this should be considered when blood lead concentration exceeds 37 mug/100 ml. Children presenting with unexplained encephalopathy should be radiographed for evidence of lead intoxication.
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PMID:Lead intoxication in children in Birmingham. 469 Oct 65

Bleeding from esophageal varices may be a serious or lethal complication of portal hypertension in children. The standard therapy over the past 30 years has been to create a portosystemic shunt. In children physiologic complications leading to high rates of perioperative morbidity and early and late thrombosis with recurrence and encephalopathy have been common. Over a 42 month period, we treated six patients aged 5 to 18 years, with endoscopic injection of 3 percent sodium tetradecyl sulfate into the varix. Five patients required only injection, whereas one underwent direct oversewing of gastric varices followed by endoscopic sclerosis of the esophageal varices which remained. A total of 38 endoscopic procedures were performed. There has been complete cessation of bleeding in two patients, minimal subsequent bleeding in two others, and anemia requiring transfusion in the last two treated. These last two patients, although still requiring occasional transfusions, have been free from hypotensive or exsanguinating hemorrhage since beginning sclerotherapy. No deaths or serious complications were encountered in this series. Follow-up has ranged from 18 to 42 months (mean 26 months). The results of this trial suggest that repeated endoscopic sclerotherapy of varices, combined with operative oversewing of gastric varices when necessary, offered a viable alternative therapy for patients with esophageal varices.
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PMID:Treatment of esophageal varices by sclerotherapy in children. 660 73


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