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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).
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PMID:Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. 50 43

Occupational lead poisoning and environmental contamination were evaluated at a lead scrap smelter. Thirty of 37 employees (81 per cent) has blood lead levels of greater than or equal to 80 mug/100 ml, indicating unacceptable absorption, and 35 had free erythrocyte protoporphyrin (FEP) levels greater than 60mug/100ml rbc, indicating toxicity of lead on heme metabolism in red blood cells; eight current and previous employees had been hospitalized with lead colic, and another with encephalopathy. Levels of lead in surface soil (1,800 ppm) and vegetation (20,000 ppm) at the smelter were high and decreased with distance. Animals on nearby pasture had died, and lead levels in the blood, milk, and hair of large and small animals were elevated. Adults living within 100 meters of the smelter had higher blood and hair lead levels than controls, who lived at greater distances, but there was no evidence in them of lead toxicity.
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PMID:Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter. 93

Although the toxicity of lead was recognized centuries ago, concern was restricted to overt symptoms: colic, encephalopathy, anemia, or renal disease. Two major reasons for lack of progress in restricting toxicity were that interest was limited to occupational exposures and there was lack of awareness of specific biochemical or metabolic effects. Identification of subclinical effects has been possible the last 15 or 20 years because of the development of sensitive measures to detect cognitive and behavioral changes that are not apparent clinically and because of methods to measure the reduced activity of heme enzymes. This progress was driven by basic and clinical research that resulted in a better understanding of cellular toxicology. The new awareness prompted the lowering of acceptable occupational exposures, as measured by blood lead from 80 to 40 to 60 micrograms/dL range, and the establishment of maximum recommended exposures in children to a blood lead level of 25 micrograms/dL. Lowering the lead content in gasoline has been accomplished by a nearly 50% decrease in average blood levels of persons in the United States (NHANES II data). Current research implicates lead as a contributing etiologic factor in a number of common diseases affecting large portions of the population such as subtle cognitive and neurological deficits, hypertension, congenital malformations, immunotoxicity, and deficits in growth and development. For each of these disorders there may be multiple etiologic factors; the scientific challenge is to develop sensitive methodology to detect the specific role of lead. Other potential subtle health effects include the influence of small amounts of lead on cell proliferation and lead as a cofactor in carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lead toxicity: from overt to subclinical to subtle health effects. 220 87

Six infants, three of them neonates, were diagnosed as having acute lead poisoning; four of them had acute encephalopathy. All had been given an indigenous preparation, 'Bint Al Zahab' (Daughter of Gold), for abdominal colic and early passage of meconium after birth. Chemical analysis of this powder revealed a lead content of 82.5%. The index case had anaemia with punctate basophilia, dense metaphysial lines on X-ray and markedly raised blood lead levels, arousing a strong index of suspicion for the early diagnosis of subsequent cases. Computerized axial tomography (CAT) scan in three cases showed signs of early cerebral cortical atrophy. The picture of cerebral oedema was absent in the four cases of acute lead encephalopathy. The importance of prevention and the ideal management is discussed.
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PMID:Lead poisoning in infancy--unusual causes in the U.A.E. 243 May 14

Encephalopathy is an unusual manifestation of lead poisoning in an adult, the more common presentation being abdominal colic, anaemia and limb palsy. We report a case of adult lead encephalopathy and describe the use of a simple screening test for lead poisoning together with the increasing number of cases associated with imported ceramics.
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PMID:Lead encephalopathy from an imported Toby mug. 260 65

Essential mesocaval shunt is very rare entity. A case of chronic cholecystitis with mesocaval shunt from the branch of superior mesenteric vein was reported. This rare hepatofugal pathway was clearly demonstrated by percutaneous transhepatic portography. Selective middle colic venography showed that the branch of this vein was directly connected to the inferior vena cava. After ligation and resection of the shunt, the level of patient's blood ammonia was decreased and the pressure of portal vein was increased. This rare case indicate that the possibility of early diagnosis and interventional radiology for +hepatic encephalopathy.
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PMID:[A case of essential mesocaval shunt]. 274 59

The authors present a case of tyrosinemia type 1, 3 years old girl at the time of diagnosis. The presenting symptoms were 3 times colic, obstipation, acute encephalopathy, hypertension, hyponatremia, according to the porphyric crisis. Her kidney function tests gave normal results during illness, only once an increased calcium turnover was observed. She has no singe of rachitis. Cirrhosis of the liver was proved by biopsy because of progressively rising gammaGT and alfa-fetoprotein levels. A new ensime-blocker (NTBC) treatment was started in an international collaboration. The authors compare the history of this case to that of others published in the literature. They summarize the pathomechanism of the disease.
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PMID:[Late onset type I tyrosinemia]. 928 Aug 76

The authors, on performing a critical analysis of reported data on clinical manifestations of lead intoxication, suggest that the initial manifestations thereof presenting as changes in no other indices but laboratory ones, be regarded as a preclinical stage. Aside from generally recognized concepts of "mild" and "prominent" stages in lead intoxication the authors consider it logical and expediant to introduce a moderately severe stage manifested by vegetosensory polyneuropathy, astheno-vegetative syndrome, dyskinesia of the biliary and intestinal tracts, spastic colitis. It is in this very stage of lead intoxication that the patient, to the author's thinking, is to be assigned to some other job where he/she will not be exposed to lead or other adverse occupational factors. This will, we believe, permit preventing development of a clinically significant stage of lead intoxication manifested by encephalopathy, motor form of polyneuropathy, lead colic, anemia and hepatitis.
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PMID:[Clinical stages of lead intoxication]. 1258 28

This report describes 4 fatal cases of serum hepatitis associated with the administration of commercial plasma in the horse. Serum hepatitis in the horse is characterized by acute hepatic central lobular necrosis, and it has been associated with the administration of biological products of equine origin. None of these horses had a recent history of equine biologic-origin vaccination; however, they had received 1.5-5 L of commercial plasma, and in I horse, an additional 8 L of fresh blood. Acute, severe colic unresponsive to medical therapy, lethargy, or sudden death developed in these 4 horses 41 to 60 days later. Two of the horses developed encephalopathy, confirmed in 1 horse by the presence of severe diffuse Alzheimer type II astrocytes in the brain. Although the prevalence of serum hepatitis associated with the administration of commercial plasma appears to be low in the horse, it should be considered an uncommon but potentially fatal risk factor.
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PMID:Serum hepatitis associated with commercial plasma transfusion in horses. 1571 60

A 13-year-old Standardbred gelding was referred for evaluation of continuous abdominal pain. Rectal examination revealed a dislocated large colon (Dislocatio coli ad dextram). The horse showed muscle fasciculations and appeared lethargic. It was sent to surgery because of persistent colic. In transit the gelding showed an unstable walk and immediately prior to surgery a wide-based stance in the hindlimbs. Laparotomy revealed a retroflexion of the large colon and a secundary mesenterial volvulus. After surgery the horse remained recumbent. Due to the comatose state and poor prognosis the gelding was euthanized after 15 hours of recumbency. Necropsy indicated hyperaemic meninges, edema of gliacells and submeningeal tissue with vacuolization and loss of several cerebellar Purkinjecells as well as multiple conglomerates of Alzheimer type II astrocyte groups within the grey matter. Further findings included marked hepatolipidosis, multiple gastric ulcers, small intestinal hyperaemia with mild mononuclear inflammation, tapeworm-infestation of the caecum and moderate chronic enteritis with eosinophilic component in the large intestine. To the best of our knowledge, this was the first case of a horse with colic and concurrent encephalopathy without primary liver disease described in a German-speaking country.
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PMID:[Encephalopathy and Alzheimer type II astrocytes in a post laparotomy recumbent horse]. 1953 45


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